Full Name:  Rhianon Price
Username:  rprice@brynmawr.edu
Title:  Human Mother-Infant Bonds
Date:  2005-04-05 15:06:45
Message Id:  14327
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip



It is probably common knowledge to many people that mother-infant bonding occurs in nonhuman animals. Ducklings and many other types of birds imprint on the first moving thing they see, which is usually their mother, following her or it wherever it may go (1); baby monkeys express much anxiety and display social inadequacies when separated from their mothers (2). In most nonhuman species, it is critical for this bonding to occur if the baby is to survive; the mother is the baby's caretaker and protects it from dangers in the surrounding environment, so both the infant's desire to maintain physical proximity to her and the mother's desire to have her baby with her act in the infant's overall best interest. It is perhaps not a surprising concept to mention, then, that human animals, too, develop mother-infant bonds.


Peripartum is the most important time for the human mother-infant bond to develop. During the time immediately post-delivery, when in a natural childbirth setting the mother is holding her baby for the first time without it having been taken away from her, endorphins, oxytocin and endogenous opiates are released in the mother's brain. This produces an intense pleasure or gratification, which is then associated with the nurturing process, helping mothers want to be with their infants (bond with them) (3); this is ultimately beneficial for the newborn, which requires its mother's protection and care in order to survive. Furthermore, mothers who have been separated from their infants immediately postpartum often express feelings of lack of affection for, alienation from, and disinterest in the baby, as well as the accompanying infamous postpartum depression. In fact, some studies suggest that lack of uninterrupted postpartum mother-infant bonding can be linked to incidences of maternal child abuse (5).


Physical proximity of infant to mother immediately postpartum is also very important for not only bonding to occur, but also for the development of the infant's senses. The infant's senses are stimulated by the sounds, scents, and feel of the mother's body. Physical contact not only allows the baby to eventually identify the caress of its mother (and its father, too, eventually), it also stimulates the baby's nervous system (7). Encouraged by the ability to physically touch its mother's skin, the infant soon begins to nurse (5). Babies learn their mother's scent by during nursing; at first, the infant is attracted to the breast because the breast produces a scent very similar to the infant's own, so it is familiar, but then during active nursing, the infant learns the scent that is specifically its mother's (6). Also during nursing, the mother and baby often gaze into each other's eyes, stimulating the infant's developing sense of sight and familiarizing the baby with the mother's facial features and human expressions (key for later development in the ability to mimic these expressions [7]), and the mother will talk softly to her new baby, identifying the mother auditorially to the infant and stimulating its developing sense of hearing, as well (5). Mothers learn their baby's scent and sounds during this interval, too (4).


Bonding does not always occur peripartum. In many hospitals, it is still routine practice for the baby to be taken away for testing and cleaning immediately after delivery, or perhaps the baby actually does have an emergency medical condition and requires time in the Intensive Care Unit (7). It is not impossible for mother-infant bonds to develop after this key interval. However, bonding is most easily established during this time, and many mothers describe bonding as far more difficult to achieve after initial senses of disconnectedness from, disinterest in, and alienation from the baby have occurred. It can take weeks in these cases for attunement and bonding to occur (5).


Many studies still dispute the importance and relevance of peri- and postpartum mother-infant bonding. Despite evidence that infants not allowed peripartum bonding time with their mothers smile less frequently, respond more slowly and with less seeming-comprehension to sensory data, are more prone to developing colic, and cry more frequently, research scientists, very often male, discount this critical bonding window as far less important than weighing, measuring, and administering tests to the baby (8). Infants develop attachments to inanimate objects (security blanket, anyone?) and this goes unremarked upon – what would that infant have been clinging to one or two hundred years ago? Its mother?


It seems very clear that, like so many animals in the world, human infants and mothers are wired for bonding to occur; yet medical technology and scientific studies seem more geared to disprove than to see any validity in the assertion of this. Chemicals released in our brains promoting joy and contentment, sensory and neurological responses to identifying aspects of mother and baby, and the sad imprinting of babies to teddy bears and security blankets all support the fact that human mothers and babies are both designed to and need the opportunity to bond peri- and postpartum; why does our society choose to ignore this fact?

References


(1)Wild Ducks of North America, from The Humane Society of the United States..

(2)Forcibly Breaking the Maternal Bond, from the Animal Welfare Institute Quarterly.

(3)Lecture 8 Notes, from the University of Newcastle Upon Tyne.

(4)Professor finds that nonhuman primates have evolutionary reason to bond with their offspring, from The University of Chicago Chronicle.

(5)Bonding Period, from Birth Messages.

(6)Unique Salience of Maternal Breast Odors for Newborn Infants, from Science Direct.

(7)Bonding With Your Baby, from Kids Health.

(8)Breaking the Bond, from Gentlebirth.org.



Full Name:  Xuan-Shi, Lim
Username:  xlim@brynmawr.edu
Title:  Television: A Weapon of Mind Destruction?
Date:  2005-04-05 16:19:14
Message Id:  14329
Paper Text:
<mytitle> Biology 202, Spring 2005 Second Web Papers On Serendip

Although little is known about changes that occur in the brain when children watch TV, much has been written in print and on the web about the negative cognitive and behavioral outcomes associated with TV viewing. The claim that watching TV adversely impacts children's imagination is of special interest in this paper. In his poem "Charlie and the Chocolate Factory," written in the early 1960s, Roald Dahl warned about the destructive effects of TV viewing: "It kills the imagination dead!" and children's "powers of thinking rust and freeze! (1)" How may TV viewing affect children's imagination? Are children who watch more TV less imaginative than those who watch little or no TV? How has imagination been defined and studied? This paper examines the relationship between TV viewing and children's imagination to evaluate whether watching TV undermines children's capacity to think imaginatively and creatively.

Johnson observed that watching TV does not require the use of imaginative thinking because the viewer passively takes in pictures on the screen (2). When children read, however, they generate their own mental images (2). Here, imaginative thinking refers to the spontaneous generation of mental images in response to incoming visual and/or auditory information. Johnson's claim merely states that watching TV does not promote imaginative thinking during the act of TV viewing itself, when compared to reading. Thus, regardless of their supposed educational value, TV programs generally leave no room for imagination because they supply abundant images to direct or dominate children's thinking. Johnson's claim seems reasonable but could TV viewing also have some benefits for children's imagination? It is not uncommon for children to "imagine" themselves as the cartoon superheroes they adore and create hypothetical scenarios related to the characters' powers during play. Therefore, the content of TV shows could stimulate a child's imagination after viewing.

While Johnson stated that the neocortex is inactive when children watch TV, she did not cite data from scientific studies (2). Interestingly, her observation that TV viewing does not promote imaginative thinking appears to be supported by a biological phenomenon that occurs when people watch TV. Researchers found that TV viewing triggers the activation of the orienting response in humans, which functions to increase the sensitivity of one's visual and auditory senses to any novel or sudden stimuli in the environment (3). When the TV is turned on, people's attention naturally diverts to the screen because it sends out a changing sequence of images often accompanied by sudden noises (3). Both adults and children would "sit and stare, and stare and sit" in front of the television as if they were hypnotized (1) because the orienting response is continually activated during TV viewing (3). Upon activation, alpha waves in the brain are blocked for a few seconds as the body rests and the alert brain becomes preoccupied with gathering more information about the source of disturbance (3); alpha waves would be recorded in the brain of an awake and relaxed person.

With their orienting response active most of the time, it is no wonder that children do not engage in imaginative thinking while they watch TV. Excessive TV viewing would also prolong the activation of a child's orienting response, thereby causing the child to experience headaches, dizziness, and tiredness (3). Consequently, children may be less likely to engage in activities that require cognitive or mental effort after watching TV. Clearly, excessive TV viewing per se does not seem to impair children's capacity for imaginative thinking by causing certain areas of the brain to atrophy from the lack of use; it simply tires the mind. Logically, TV viewing may adversely impact imaginative thinking by taking up time that could be better spent in other activities, such as reading and play, which stimulate thought processes.

Valkenburg & van der Voort (1994) concluded in their review of 17 studies that watching TV reduces creative imagination among children of a wide range of ages, most of whom were older than age 6 (4). Creative imagination is narrowly defined as "the capacity to generate many different novel or unusual ideas" (4). Experimental studies typically present a story to the children in video, print, or audio; after the presentation, children are asked several questions about the story (4). In most studies, children in the video condition gave responses that contained more elements derived from the story, and/or fewer novel or original elements, when compared to children in other conditions (4). Assuming that information shown on video was as well remembered as that presented in audio or print, there is reason to believe that children who watched the video displayed less creative imagination on this task.

Could one then extrapolate from these findings that TV images dominate children's mind, making it difficult for them to mentally put these images away while engaging in a thought process (4)? Given that it is unclear whether children's creative imagination shows a reduction on other unrelated tasks, such as story writing and divergent thinking tests, there is little reason to believe that TV viewing would lead to a decline in children's creative imagination. Also, although creativity is often associated with originality and novelty, individuals may also display creativity by drawing on elements from different sources of information to create something new. Therefore, it may not be sufficient to measure creative imagination only by comparing the number of borrowed and/or novel elements in children's responses. In reality, children probably watch TV programs that interest them in the first place. Consequently, their talk and drawings may exhibit a preoccupation with a program's plot and scenes. Should this preoccupation be construed as a child's fad or a reduction in creative imagination?

Correlational studies included in the 1994 review usually use divergent thinking tests, teacher ratings, and/or inkblot tests to measure creative imagination (4). Verbal divergent thinking tests consist of open-ended problems for which children have to generate as many solutions as possible (4). For instance, they may be asked to provide alternative uses for a common object such as rubber-band. Generally, responses are scored for the number of ideas, conceptual categories, and original ideas generated. Of 7 correlational studies, 5 studies found that children who watched more TV had lower scores on the creative imagination measure/s that were used (4). Does this suggest that TV viewing decreases children's creative imagination? As Valkenburg & van der Voort (1994) pointed out, correlational studies assumed that TV viewing and creative imagination are related in a linear fashion (4). It is probable that TV viewing diminishes creative imagination only beyond a certain threshold of viewing hours.

Taken together, these findings suggest that children's creative imagination is affected by exposure to any type of material shown on TV. Although the content of TV shows may affect whether TV viewing would positively or negatively impact creative imagination, this factor was not examined by studies included in the 1994 review. In terms of neurobiology, what does it mean to have a reduced capacity for creative imagination? Given a task such as the divergent thinking test, would children who watch little or no TV show greater overall brain activation compared with children who watch more TV or excessive TV? Would there also be significant differences in brain activity at the neocortex, as well as brain areas related to memory? Unless there is evidence to suggest that young viewers show a specific pattern of brain activity indicative of decreased creative imagination, when compared to non-viewers, there should be little cause for concern over whether TV viewing reduces creative imagination.

Clearly, TV viewing has become an integral part of modern life and almost every child grows up watching some TV. Generally, information presented on TV seems to leave a deeper impression on children's mind, which explains why they may readily draw from elements in TV presentations. However, there appears to be no conclusive evidence suggesting that TV viewing per se adversely impacts a child's ability to think imaginatively and creatively. Having said so, there is some support for the claim that TV viewing does not promote imaginative thinking. Spending many hours in front of the TV would tire the mind and displace other intellectual or social activities which would promote imaginative thinking. Therefore, children who watch excessive TV may possibly be less imaginative and creative than children whose TV viewing hours are carefully regulated by adults.

References

1)Michael's Most Excellent Home Page, "Charlie and the Chocolate Factory" by Roald Dahl

2)TV Allowance, "Strangers in Our homes: TV and Our Children's Minds" by Susan R. Johnson

3)Total Obscurity, "Television Addiction is No Mere Metaphor" by Robert Kubey and Mihaly Csikszentmihalyi (2002), in Scientific American.

4) Valkenburg, P. M., & van der Voort, T. H. A. (1994). Influence of TV on Daydreaming and Creative Imagination: A Review of Research. Psychological Bulletin, 116, 316-339.

5)Parenting Information, "The Parent's Guide: Use TV to Your Child's Advantage" by Dorothy G. Singer, Jerome L. Singer, and Diana M. Zuckerman



Full Name:  Jenna Rosania
Username:  jrosania@brynmawr.edu
Title:  Lead Poisoning, Delinquency, and Mitigation of Criminal Culpability
Date:  2005-04-06 16:36:40
Message Id:  14356
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Jenna Rosania
4/7/05
Neurobiology and Behavior
Prof. Grobstein

Lead Poisoning, Delinquency, and Mitigation of Criminal Culpability

For decades, lead, chemically referred to as pb24, has been known to be a hazardous toxicant particularly detrimental for children (1). It is estimated that 2.2 percent of all preschoolers in the US, totaling approximately 434,000 children, have elevated lead levels sufficient to interfere with their neurological development (2). The children who are usually exposed to lead tend to live in older homes and come from poorer families who cannot afford to replace the two most common sources of lead to children in their homes, lead paint and lead plumbing (3). Although lead can affect several areas of the body, the neurological damage is often quite severe for individuals exposed to even slight amounts of lead during brain development. This damage often results in behavioral problems, reasoning and attention deficits, and low IQ and mental retardation; conditions that occasionally lead to deviant behavior. In neighborhoods where lead exposure is so common and unavoidable due to the impoverished state of the inhabitants, the lead exposure of the children that develop neurological deficits and subsequently exhibit deviant behavior must be considered when determining their degree of culpability for a crime. If the physical state and composition of the brain determine the behavior of an individual, a brain damaged by lead poisoning can be the source of socially abnormal behavior.

The most common sources of exposure to lead in the household are chips or dust from lead paint, commonly used between the years1900 and 1977 until the federal government banned lead as an additive to paint used for housing in 1978 (3). It has been estimated that 38 million homes in which children are raised have deteriorating lead surfaces, and in about 24 million homes, or 25% of the nation's housing, the lead paint is extremely hazardous (4). This state of the nation's housing stock underscores that although lead paint has been banned from use since 1978, the problem still exists for occupants of homes built before then, particularly urban, low-income occupants.

Lead is referred to as xenobiotic, meaning it is a foreign substance with no useful role in human physiology, toxic even in minute quantities. Rather than breaking down to be eliminated as a waste product, lead accumulates in the body's bones and tissues because the body recognizes it as if it were calcium. It may be absorbed from the gastrointestinal tract or through the respiratory system. Lead exposure can result in low sperm counts in men and can increase the risk of miscarriage or stillbirth among women. It damages the kidneys and gastrointestinal tract, and can lead to a host of neurological problems including decreased cognitive abilities (5). and increased behavior problems in children (6). The current trigger level for lead, decreased over the years as scientific understanding about lead's effects increased, is 10µg/dL (7).

Although lead can cause harm to children and adults alike, children still developing mentally and physically experience the most seriously deleterious effects of lead poisoning. Children are more likely to be exposed to lead because their exposure to certain toxins increases as they play outdoors. They are shorter than adults, which means they can breathe dust, soil, and vapors close to the ground. Children are smaller than adults, therefore childhood exposure results in higher doses of chemicals per body weight (8). They are more likely to be irrevocably damaged by lead poisoning because lead causes damage to the nerve cells of the brain while the brain is still developing. Once ingested, lead inhibits a child's ability to absorb iron, necessary for brain, nerve and bone development (3). The dendrites of nerve cells in developing brains are cut short by lead, thereby reducing the connections between axons among adjacent neurons. Dendrites are most plentiful during the early years of childhood, especially between the ages of 1 and 5, and thin naturally with age. Thus it is crucial for healthy development to establish as many connections between neurons in the brain as possible through education and stimulation between the ages of 1 and 5. When children are exposed to lead which limits the connections being made during this important developmental period, the brain is irrevocably disadvantaged, resulting in decreased amounts of gray matter (9).(10). Chelation therapy, which involves reducing the lead concentrations in the bloodstream by orally administering succimer, or injecting ethylenediaminetetraacetic acid (EDTA), a ligand that binds metals, has been shown to be ineffective at increasing already damaged neurons and increasing diminished IQ (11). Therefore, even when individuals undergo treatment during childhood, the damaged areas cannot be recovered.

The neurological damage resulting from exposure to lead can result in abnormal behavior, exhibited through increased irritability and violence, learning disabilities, mental retardation, and other functional difficulties. The social effects of these abnormal behaviors through disciplinary actions, peer isolation, falling behind in school, drug abuse, domestic abuse, and a lack of understanding about the basis of an individual's impairments may also compound the neurological damage, resulting in psychological trauma, which studies show can cause other types of brain damage (12). Additionally, lead exposure is known to cause attention problems for children (13). making academic success and effectively adapting to society difficult. All these conditions have been known to result in an individual's inability to function in society or possess adaptive skills. Inability to function in society often results in deviancy of various kinds, and at times the deviancy that is a symptom of an individual's neurological damage is so seriously a breach of the mores of social structure that it is viewed by our legal system as criminal.

Dr. Herbert Needleman of the Psychiatry Department at University of Pittsburgh has conducted several studies in the past decades dealing with children's exposure to lead, sources of lead exposure, and social, behavioral, and neurological consequences of lead exposure. In 2002 he examined 194 youths convicted in the Juvenile Court of Allegheny County, PA, and 146 non-delinquent controls from high schools in Pittsburgh, PA. Lead levels measured from the tibias of the subjects using K X-ray fluorescence spectroscopy revealed substantially higher lead levels in the bones of the delinquent youths at an average of 11 parts per million (ppm) compared to 1.5 ppm in the non-delinquent group (14). Dr. Needleman described this study, which was the first to show lead exposure is higher in convicted delinquents than in non-delinquents, as a positive step towards connecting lead poisoning with delinquency. (15).

Dr. Needleman's groundbreaking work in the area of lead exposure and behavior warrants further investigation into the area of responsibility for behavior when an affected individual commits crime. According to all the studies, lead poisoning is a disease of poverty and is in no way the fault of the person afflicted. Therefore, the effects of lead poisoning, increased aggressive behavior, low intelligence, learning disabilities, and anti-social behavior, all of which are known predictors of crime, should be mitigation of the culpability of offenders afflicted with lead poisoning.

Lead poisoning has been epidemic in the city of Philadelphia for decades. Although it would seem the problem of lead in the US as well as in Philadelphia is being ameliorated and that the numbers of children being exposed is decreasing, the children who were affected by the high doses of lead far more common and rampant in the last century are now adults, trying to function in society with the effects of their exposure. In addition, those children who are currently being exposed to lead need a society that will be able to better understand the implications of this environmental toxin for delinquency and execute justice more effectively when they become adults. Human exposure to lead continues to be a crisis of public health, criminal justice, and environmental racism, and what is necessary for its complete elimination in schools and housing is a change in people's attitudes about the extent of lead poisoning in order to gain more public and federal support and make this problem of poor minorities in the inner-city everyone's problem.


References


1) US Department of Health and Human Services, The Nature and Extent of Lead Poisoning in Children in the United States: A Report to Congress 1 (July 1988). 2) Centers for Disease Control and Prevention. 2003. Second National Report on Human Exposure to Environmental Chemicals. NCEH Pub. No. 02-0716.
3) Center for Disease Control and Prevention. 1991. Preventing Lead Poisoning in Young Children: A Statement by the Centers for Disease Control. Atlanta, GA.
4)US Department of Housing and Urban Development (HUD), accessed: 4/4/05
5) Thacker, S.B. et al.. 1992. Effects of Low-Level Body Burdens of Lead on the Mental Development of Children. Archives of Environmental Health, Vol. 47.
6) Konopka, Allan. 2003. The Secret Life of Lead, Living on Earth and World Media Foundation.
7) Needleman, Herbert L.. The Poisoning of America's Children: Lead Exposure, Children's Brains, and the Ability to Learn. National Health/ Educational Consortium, Occasional Paper #6. November 1992
8) Rodier, Patricia M.. 1994. Developing Brain as a Target of Toxicity, in symposium: "Preventing Child Exposures to Environmental Hazards: Research and Policy Issues." University of Rochester, New York.
9) Hrdina, P.D., et al..1980. Neurochemical Correlates of Lead Toxicity. In eds. Singhal, R.L.; Thomas, J.A.; Lead Toxicity. Baltimore, MD, Urban and Schwarzenberg.
10) Nathanson, J.A. 1977. Lead-inhibited Adenylate Eyclase, a Model for the Evaluation of Chelating Agents in the Treatment of Lead Toxicity. Journal of Pharmacy and Pharmacology, Vol. 29.
11) Rogan W. J., Dietrich K. N., et al.. 2001. The Effect of Chelation Therapy with Succimer on Neuropsychological Development in Children Exposed to Lead, New England Journal of Medicine, 344.
12) Rosen J. F., Mushak P.. 2001. Primary Prevention of Childhood Lead Poisoning — The Only Solution, New England Journal of Medicine, 344.
13) Minder, Barbara, et al.. 1994. Exposure to Lead and Specific Attentional Problems in Schoolchildren. Journal of Learning Disabilities, Vol. 27.
14) Needleman, Herbert L., et al.. 2002. Bone Lead Levels in Adjudicated Delinquents: A Case Control Study. Neurotoxicology and Teratology, Vol. 24.
15)Lead link to youth crime," BBC News Online, 7 January, 2003



Full Name:  Camilla Culler
Username:  cculler@brynmawr.edu
Title:  Functional Magnetic Resonance Imaging (fMRI): Much Ado About What?
Date:  2005-04-11 00:14:48
Message Id:  14441
Paper Text:
<mytitle> Biology 202, Spring 2005 Second Web Papers On Serendip

A cursory review of research in cognitive neuroscience reveals how widespread the use of neuroimaging technologies has become during the last ten years. Of these relatively new neuroimaging methods, functional magnetic resonance imaging (fMRI) has occupied the dominant role (1). As opposed to PET, which requires the use of radioactive markers that limit the frequency of exposures for a single participant, fMRI is a non-invasive method that purports to measure neural activity while a person engages in cognitive tasks (2). Unlike MRI which provides a static picture of the structure of the brain, fMRI provides both structural and functional images of the brain (3). The fMRI technique that has been used most frequently in cognitive neuroscience research is the BOLD (Blood Oxygen Level Dependent) method. The assumption that underlies BOLD is that neural activation is correlated with changes in blood flow and blood oxygenation and that the magnetic properties of oxygenated and deoxygenated blood are not the same (4). Banich (4) has referred to a "veritable explosion of research" that has appeared using the BOLD method of fMRI.

It would be hard to overstate the enthusiasm with which the neuroscientific community has embraced the use of fMRI methods. Gazzaniga and Heatherton (5) believe that fMRI has contributed to a "biological revolution" in psychology permitting scientists to begin to answer "some of the most central questions of human experience." Gazzaniga, Ivry, and Mangun (1) report that between 1998, when the first edition of their text appeared, and 2002, when the second edition was published, there have been an "explosion" of brain imaging studies with "dozens of dozens" of academic and clinical centers doing research with MRI scanners and close to 1500 brain imaging studies published for each of the four years. Posner and Raichle (3) refer to fMRI as the "most promising" of the new brain imaging technologies and Bear, Connors, and Paradiso (6) report that the advent of fMRI techniques has provided an "extraordinary opportunity" for scientists to witness the inner workings of the thinking, feeling, and responding brain.

But all is apparently not rosy in the neuroimaging world. There have been a growing number of cautionary voices that are beginning to appear in print that address the limitations of fMRI. Specific, technical concerns are about what conclusions can be made about the relation between fMRI and neuronal activity, and how neuronal activity, blood flow in the brain, and fMRI signals are connected (7). For example Heeger and Ress (7) point out the fMRI is an indirect measure of brain activation (brain cells firing) and address some of the weaknesses of the "linear transformation model". This model uses a mathematical formula to interpret fMRI results, and states that the strength of the fMRI signal is proportional to local neuronal activity that has been averaged over a space of several millimeters and over a time period of several seconds. Although Heeger and Ress conclude that the linear transformation model is a "reasonable and useful approximation" for what is actually taking place in the brain, they qualify this conclusion by stating that it applies to only some recording sites, in only some brain areas, and only when using select experimental protocols.

Heeger and Ress also cite several factors that may influence the relationship between the variables of the neural activity, the fMRI signal and the blood flow in the brain. These include the fMRI acquisition technique (BOLD results sometimes differ from other non-BOLD methods), the behavioral and stimulus protocols that are used (one working memory task may produce different fMRI results than another working memory task), the data analysis method that is used, and lastly how the neuronal activity itself is quantified and measured.

A recent article (8) refers to the "growing controversy over fMRI scans" and quotes several prominent neuroscientists who cite a range of concerns about the use of fMRI, the limitations of the method, and the reliability and validity of the conclusions that have been made on the basis of fMRI data. The initial excitement over fMRI and the great expectations may have been in part due to the fact that it does provide both spatial and temporal improvements in image resolution when compared with the older and more expensive PET scan (4). More than one researcher has referred to fMRI data as "gross" claiming that the localization of cognitive functioning is not consistent with the notion that brain activity for even simple cognitive activities is distributed in neural networks (8). This search for the localization of function has led some critics of fMRI to dismiss it as a 21st century variety of 19th century phrenology (8). There is also speculation that some of the false confidence in fMRI results may be due to the fact that the vivid, colorful graphics that fMRI produces, suggest a level of precision in measurement that is misleading (8).

Others have voiced concerns over fMRI's imaging power, the ability to make generalizations about individual brains when using fMRI data that are based on group averages, questionable forensic applications (using fMRI results as evidence in a court of law), as well as neuromarketing applications (using fMRI results to tell how consumers respond to certain products) that raise a host of neuroethical concerns (9). For example, in one study where six different people were given the same spatial memory task to perform, the fMRI scans for each of the six yielded extremely varied patterns of activation (8). In another study that looked at the findings of 38 different fMRI studies that purported to locate the region in the brain responsible for "executive functioning" the areas that were identified varied considerably from study to study (8). Therefore fMRI results cannot be generalized to entire populations, as each individual's result is different.

Recent efforts to create new lie detectors based on fMRI technology are being made while at the same time they have been subject to considerable criticism. Preliminary fMRI results show that when subjects lie, their anterior cingulate cortex and superior frontal gyrus are activated. Yet other studies show that activation of the anterior cingulate occurs when people are making decisions about a variety of things, not just whether to tell the truth or not (10). Langleben, who conducted these studies on fMRI and lie detection, concedes that the development of an fMRI lie detector that works effectively outside the controlled laboratory environment will take many years before it is realized (9).

These apparent contradictions mean that the use of fMRI is controversial. On the one hand, fMRI is touted as "revolutionary" and literally thousands of neuroscience studies during the past few years have made use of this method, while on the other hand, considerable criticism of fMRI has begun to appear. These criticisms, at the very least, call into question some of the conclusions that have been reached in studies making use of this technology, and suggest that the future of fMRI research and application is not so certain. What does fMRI reveal about brain-mind relations? What are its limitations? To what extent does the application of fMRI to forensics, the marketplace, etc., raise legitimate bioethical concerns? Although these questions, and related ones have yet to be completely answered, they raise serious concerns and present new challenges to neuroscientists. At least for now, "where fMRI is concerned, 'a penny for your thoughts' is currently more like 'a million pennies for a group-averaged hemodynamic response to highly constrained stimuli under entirely artificial conditions" (9).

References:
1) Gazzaniga, M., Ivry, R. & Mangun, G. Cognitive Neuroscience: The Biology of the Mind. New York: W.W. Norton, 2002.
2) Stirling, J. Cortical Functions. London: Rutledge, 2000.
3) Posner, M. & Raichel, M. Images of Mind. New York: W.H. Freeman, 1997.
4) Banich, M. Cognitive Neuroscience and Neuropsychology. New York: Houghton Mifflin, 2004.
5) Gazzaniga, M., & Heatherton, T. Psychological Science: Mind, Brain, and Behavior. New York: W.W. Norton, 2003.
6) Bear, M., Connors, B., & Paradiso, M. Neuroscience: Exploring The Brain. Baltimore: Lippincott Williams & Wilkins, 2001.
7) What Does fMRI Tell Us About Neuronal Activity?, an article by Heeger, D. & Ress, D. Nature Reviews/Neuroscience 2002, 3:142-151.
8) Fact Or Phrenology?, an article by Dobbs, D. Scientific American Mind, 2005, 16: 24-31
9)fMRI Beyond The Clinic: Will It Ever Be Ready for Prime Time?, an article by Robinson, R. PLOS Biology, 2004.
10) The New Lie Detectors , an article by Tancredi, L. Scientific American Mind, 2005, 16: 46-47e.



Full Name:  Sonnet Loftus
Username:  sloftus@brynmawr.edu
Title:  Can Sex Cure Insomnia???
Date:  2005-04-11 02:02:26
Message Id:  14443
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip



I am constantly reminded that I am no stranger to insomnia. There have been countless nights that I lay in bed staring at the ceiling while my mind is racing. Even if I am unable to hold my head up one more minute to finish reading that last paragraph or to find the answer to that one question I have difficulty with in my problem set, I cannot manage to fall asleep. A number of things run through my head--I think about what I have done earlier in the day, I think about what I am doing the next day, but most importantly, I think about ways to solve my sleeping problem. I have heard all the theories of reducing insomnia from limiting caffeine and food intake prior to the hours of sleep to using the bed only for what is meant to be used for...sleep and sex. This got me to thinking, how are sleep and sex related? Could it be that sex is a cure for insomnia?

Insomnia is quite a problem. Statistics show that 90% of people experience insomnia to some degree during their life, while 30% of the population are plagued with chronic insomnia (1). Many illnesses can potentially lead to insomnia such as; ulcers, diabetes, kidney disease, heart failure, Parkinson's disease, hyperthyroidism, and depression (1).

Depression is one of the main causes of chronic insomnia. This leads me to think more about the relationship between sex and sleep. If an individual is unable to sleep because they are unhappy or stressed, then what exists that can change their mood or feelings? Sex may be the solution as it has many benefits for the mind, body, and soul. I had never thought about it too closely, but the brain is the largest sex organ because of the vital role it plays in sexual arousal (2).

The hypothalamus sends a signal to the brain to release certain sexual hormones such as oxytocin, dopamine, norepinephrine, endorphins, estrogen and testosterone into the blood stream (2). If the transmission of neural signals from neuron to neuron has an effect on how we feel, then it seems increasingly obvious that sex can decrease depression which in turn can decrease problems falling asleep.

Endorphins are natural pain relievers. They make us feel content, relaxed, perhaps in a state of bliss. If a woman is able to orgasm, then she is privileged to experience a release of endorphins which remain active in the body for several hours after climax. In addition, the male sex hormone prostaglandin which is found in sperm serves as a regulator for female hormones by maintaining a balance and decreasing mood swings and depression. The processes therefore involved with sex are healing. If the problem with insomnia is that an individual is unable to relax or stop the thoughts running through their head, then perhaps sex is the needed solution. There is an experience to be had in a woman's orgasm and a man's ejaculation. This is one of the few times that people allow themselves to let go, surrender, and relax (3).

I was therefore intrigued to learn other ways in which to "let go, surrender, and relax." I have been told by my parents since I was a little kid to just clear my head and count sheep until I could not count anymore. This sort of behavioral technique used to improve sleep is often referred to as relaxation therapy. Relaxation therapy is meant to eliminate anxiety and body tension by allowing the muscles to relax, which can be done by a repeating of words, sounds, or muscular activities such as tensing and releasing muscles (4). As I have allowed myself to become more educated on the subject, I can see how 'relaxation therapy' is similarly related to sex. A repeating of breaths, sounds, and muscle contractions all add to the pleasure of sex. The pleasure and emotional passion of sex occurs once a sensorial impulse travels up the spinal cord to the sensory cortex and the limbic system (2).

There is an intimate connection between sexuality and the limbic system (5). Sexual smells are associated with the cooling of the limbic system. If it is therefore the case that when the limbic system cools we are put in the 'mood' for love, whereas when there is limbic over-activity, we are put in a depressed mood (5). It now seems clearer to me that limbic over-activity has a positive relationship with insomnia because of its connection with depression. If the limbic system is receiving sensorial impulses that aid in its cooling, then the body is getting prepared for sex, which essentially prepares the body for sleep by way of making the body relaxed and the mind content.

I am now convinced of the potentiality of sex to cure insomnia, but I worry if this is possible even if an individual has not been able to orgasm. The orgasm greatly adds to the pleasure of sex. Speaking on behalf of a woman, I tend to think that if a woman has been unable to orgasm that she may not be able to fully relax and let go. Is it possible for a woman's limbic system to cool and then warm if she is unable to climax? A female orgasm occurs when all tension is released in the form of involuntary and pleasurable muscular contractions (6).. If this does not occur, I am less convinced of the power of sex to decrease problems with falling asleep. It seems that if a woman is experiencing a mounting of sexual tension that she is unable to release, then her mind will be left in a state of discontent. I do however think that the actual emotions and feelings evoked with a sexual experience are very personal and differ amongst couples, which makes it seemingly possible that even if a woman is unable to orgasm that maybe she has still experienced enough pleasure to compensate for the lack of release.

In conclusion, I think that further research is needed to fully understand what correlation does or does not exist between the orgasm and insomnia. In addition, I think that it would also be interesting to learn what role gender might play. Are males better inclined to deal with tension? Perhaps it is unfair to simply say that 'sex' can cure insomnia, as there are many facets to sex.


References

WWW Sources

1.) http://www.health24.com/medical/Head2Toe/777-778-781,12339.asp; a website devoted to the development of health, diet, fitness and wellness-related content.
2.) http://www.queendom.com/sex-files/orgasm/orgasm-physiology.html; a website devoted to the discussion of issues that matter most, such as health and love,
3.) http://www.tantra-sex.com/ummsummer00.html; a website containing writings about sex, tantra, and relationships.
4.) http://www.sleepnet.com/insomnia.html; a website containing information on sleep disorders.
5.) http://www.brainplace.com/bp/brainsystem/limbic.asp; a website devoted to information and resources on the brain.
6.) http://www.coolnurse.com/orgasm_female.htm; a website created to help today's teens and young adults achieve and maintain a high level of health, fitness and well-being.



Full Name:  Joanna Scott
Username:  jscott@brynmawr.edu
Title:  More Than a Cup of Joe: Clinical Implications for the Neurobiology of Caffeine
Date:  2005-04-11 21:18:36
Message Id:  14475
Paper Text:
<mytitle> Biology 202, Spring 2005 Second Web Papers On Serendip

Caffeine is perhaps best associated with its 'energy-boosting' powers—its effects on alertness and memory. Many avid coffee drinkers swear they cannot function properly without it. Indeed, its benefits have been touted for years and new studies are further expanding the list of its useful properties. Understanding caffeine's mechanism of action in the brain is a helpful start in determining its relationship to different aspects of health and overall functioning. When the majority of coffee drinkers go to the office coffee pot or to line up at Starbucks, however, chances are their motivation is not to reduce their risk of Parkinson's disease. Therefore, understanding the neurobiology behind caffeine and its benefits or risks is only the first step. We must next consider how to use this information in a clinical setting.

Caffeine is a widely used central nervous stimulant found most commonly in coffee, tea, soda, and chocolate, but also in such over-the-counter medications as pain relievers and cold medicines. Current consumption levels average 200 mg/daily for adults (2). Caffeine belongs to the pharmacological class of compounds called methylxanthines. Its primary mechanism is as an adenosine receptor antagonist. Adenosine is involved in important biochemical processes such as energy transfer and signal transduction (12). The inhibitive effects of caffeine on adenosine are fairly specific, occurring mainly in the A2A receptor subtype in dopamine-rich areas of the brain (1). Activation of adenosine receptors, such as A2A, inhibits the neurotransmitter dopamine. Dopamine is involved in carrying out motor movements, and has also been implicated in (4) Caffeine indirectly increases levels of dopamine in such areas as the meso-limbic and nigra-strital pathways through its suppression of adenosine (8). Observational studies have found that caffeine may have a neuroprotective effect against Parkinson's disease (PD). Depleted levels of dopamine in such areas a(10). Ross et. al (2000) noted that nondrinkers of coffee had a risk for developing PD 2-3 times higher than that of coffee-drinkers. Similarly, Gale and Martyn (2003) reported a 30% risk reduction for PD in coffee drinkers compared to non-drinkers. Whether or not increases in dopamine related to caffeine intake will help clinicians to treat Parkinsonian symptoms has yet to be determined; for now, the data is restricted to the observational and correlative.

Regular coffee drinkers have also shown a decreased risk for diabetes, gallstones, and colon cancer, along with improvements in cognitive functioning (6). While the wide held belief that drinking coffee will help treat a hangover appears unfounded, caffeine's effects on general arousal and on more specific perceptual, attentional, and motor processes are not just a myth. This is the 'upper' the general public associates with caffeine and these benefits have been supported by previous research (11). Most of these effects are transient, however, usually lasting only a few hours. Both a stimulant and diuretic, caffeine has a half-life of several hours. That is, half of the amount consumed is leaves the bloodstream in 3-4 hours. Caffeine may have other uses beyond the effects of mere consumption. Sheppard, Grace, Cole, & Klein (2005) gave a group of students a decaffeinated beverage, but told them the study was examining the effects of caffeine on academic performance. In one condition, the students were told, prior to receiving feedback on performance, that the coffee they drank was highly caffeinated and that they may experience some trembling, increased perspiration, and feelings of anxiety. This was part of a misattribution paradigm in which the students were led to attribute any anxiety they felt to the coffee. The researchers found the misattribution paradigm successfully boosted students' optimism and helped them cope with their apprehension (p. 273). When given an external 'cause' for their anxious feelings, participants attributed their sensations to that 'cause'—the caffeine—and not to the anticipation of negative feedback.

The misattribution paradigm might be a useful tack for clinicians to try when working with ruminators or prior to giving patients results of medical exams. The very experience of anxious symptoms can trigger further anxiety about those symptoms (positive feedback loop). For example, patients might feel their heart race or shortness of breath and then worry they are going to die or have a panic attack, and that increases the heart rate and so forth. Perhaps the coffee can be used to interrupt such a cycle; patients can reassure themselves that their feelings have a tangible cause and will pass soon. If a patient is worried about test results, such a paradigm could allow them to attribute their anxiety to the caffeine and feel more optimistic about their tests. One important caveat: caffeine is associated with increases in agitation and anxiety. While this makes it a believable cause for anxious feelings, it might exacerbate some patients' conditions and so clinicians should encourage anxiety sufferers to limit their caffeine intake. Another consideration is that of interactions between caffeine and medications such as SSRIS and MAOIs (antidepressants). As mentioned above, caffeine is linked to increases in dopamine. Monoamine oxidase inhibitors (MAOIs) also increase dopamine levels, by interfering with the enzyme (MAO) which breaks down dopamine at the synapse. Abnormalities in neurotransmitter functioning are believed to be at the root of many mental disorders; long-term use of caffeine may further disrupt this functioning and complicate pharmacological treatments. In summary, the misattribution paradigm may be useful, but better suited to another external cue than caffeine or for patients without chronic anxiety concerns.

Caffeine intake will soon be relevant to clinicians for another reason: addictive potential. There are plans to include caffeine withdrawal in the upcoming DSM-V, expected to be released in 2011 (5). A study by Johns Hopkins University concluded that caffeine withdrawal is "a veritable syndrome"; as many as half of regular consumers of caffeine will experience withdrawal in the absence of their usual dose (6). Headache, fatigue, nausea, irritability, and difficulty concentrating are the common symptoms associated with caffeine withdrawal. These symptoms are the result of adenosine. If we think of the effects of caffeine as the opposite of adenosine, withdrawal can be viewed as the "reversal of those effects with a vengeance" (6). While adenosine dilates the blood vessels, caffeine restricts them. When the caffeine leaves the bloodstream, the blood flow increases again, causing the unpleasant feelings of a headache. In regular consumers, the desire for caffeine may be more of an attempt to reduce the unpleasant side effects of withdrawal than to experience its benefits. Physiological dependence has two components: withdrawal and tolerance. Regular caffeine users do exhibit tolerance. Compared to infrequent users, who get a 'buzz' from one cup of coffee, regular coffee- drinkers will often need two or three cups to produce the same response (2). This is the very definition of tolerance—requiring more of the substance over time to produce the same effect. People show varying levels of sensitivity to caffeine. Interestingly, dependency is not correlated with amounts of caffeine consumed in either adults or adolescents. Some adults showing tolerance and withdrawal actually drink less than the national average (1). Despite these 'addictive' properties, caffeine consumption is socially accepted and, at times, even encouraged. Visiting Starbucks is trendy, and the notion of 'coffee hour' or 'coffee talk' has established a firm relationship between caffeine consumption and social interaction. Potentially reinforcing properties of caffeine include such social interaction, as well as the increases in dopamine, the energy boost (or 'buzz'), and even the pleasant aroma.

At first glance, caffeine withdrawal does not seem overly alarming, just mildly unpleasant. The real concern arises from the studies suggesting that caffeine could be a gateway drug. Animal studies support that caffeine facilitates the effect of self- administration of other drugs, such as nicotine and cocaine (1). There is a potential confound here, however, as nicotine increases the metabolism of caffeine (7). Smokers may therefore have more tolerance to caffeine. The theory of an 'addictive personality' is not a new one. Different addictions do overlap, or co-occur in predictable ways. For example, Christo, et al. (2003) noted that college students' use of alcohol, nicotine, caffeine, chocolate, exercise, and gambling were highly correlated. Individuals showing addiction to one substance or activity seem to have an increased risk for developing further addictive behaviors. A common, underlying pathway—such as dopamine-- might be involved in all such behaviors. Psychoactive substances and behaviors that increase physiological arousal (gambling or exercise) may be linked to increased sensation-seeking or impulsivity in general. Christo, et al. (2003) found that one-third of bulimics indicated "problematic use of caffeine". The same was true for 36.8% of alcohol and drug users (p. 236).

Whether or not caffeine constitutes a gateway drug is still highly debatable. Caffeine is currently the most commonly ingested psychoactive substance (1). This means that by sheer numbers alone, regular caffeine users are well represented in most populations. The actual percentage of such consumers that go on to develop more serious addictions, to the point of hurting loved ones and neglecting their responsibilities, is presumably low. Coffee drinking is not usually associated with guarding of the supply, or stealing in order to attain coffee, and so forth. Problematic psychological caffeine addiction may be qualitatively different from physiological dependence on caffeine and represent a population at risk for other addictive behaviors. Clinicians should be aware of the correlation, and assess their clients' intake of various substances, as well as their motivation for such use. On the positive, the social aspects of caffeine could be used constructively in some clients who would benefit from the basic human interactions that occur in such places as the coffee shop. And if there are concerns about anxiety and insomnia, they can even make it a decaf!

References

1)Bernstein, G. A., Carroll, M. E., Thuras, P. D., Cosgrove, K. P., & Roth, M. E. (2002). Caffeine dependence in teenagers. Drug and Alcohol Dependence, 66, pp. 1-6. Article Online

2)Caffeine and Health: Clarifying the Controversies. 1993.International Food Information Council.

3)Christo, G., Jones, S. L., Haylett, S., Stephenson, G. M., Lefever, R. M. H., & Lefever, R. (2003). The shorter PROMIS Questionnaire: Further validation of a tool for simultaneous assessment of multiple addictive behaviors. Addictive Behaviors, 28, pp. 225-248. Article Online.

4) Dopamine - A Sample Neurotransmitter. , University of Texas at Austin's Review of DA

5)The DSM-V Prelude Project. , The APA's Updates on the DSM-V

6) Crazy for Coffee. , Psychology Today's Overview of Coffee

7)Gale, C. and Martyn, C. (2003). Tobacco, caffeine, and Parkinson's disease. British Medical Journal, 326, 561-562. Article Online.

8)Ross, G. W., Abbott, R. D., Petrovich, H., Morens, D. M., Grandinetti, A., Tung, K., Tanner, C. M., Kamal, H. M., Blanchette, P. L., Curb, J. D., Popper, J. S., & White, L. R. (2000). Association of coffee and caffeine intake with the risk of Parkinson Disease. Journal of the American Medical Association, 283 (20), pp. 2674-2679.

9)Sheppard, J. A., Grace, J., Cole, L. J., & Klein, C. (2005). Anxiety and outcome predictions. Personality and Social Psychology Bulletin, 31(2), pp. 267-274.

10)The Substantia Nigra in PD., from WEMOVE--Worldwide Education and Awareness for Movement Disorders

11)Tieges, Z., Ridderinkhof, K. R., Snel, J., & Kok, A. (2004). Caffeine strengthens action monitoring: Evidence from the error-related negativity. Cognitive Brain Research, 21, pp. 87-93. Article Online

12) Image of the Molecule Adenosine, from Wikipedia Online



Full Name:  Kara Gillich
Username:  Kgillich@brynmawr.edu
Title:  The Limitations of Testing, and the Million Dollar Challenge
Date:  2005-04-11 21:25:23
Message Id:  14476
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


YOUR TEXT. REMEMBER TO SEPARATE PARAGRAPHS WITH A BLANK LINE (OR WITH

, BUT NOT BOTH). REFERENCES (IF ANY) GO IN A NUMBERED LIST AT THE END (SEE BELOW). TO CITE A REFERENCE IN THE TEXT, USE THE FOLLOWING AT EACH NEEDED LOCATION:
(YOUR REFERENCE NUMBER).

References

Want a million dollars? The James Randi Educational Foundation, run out of Florida since 1996, is currently offering any person who can display paranormal activity before a panel of real researchers and scientists, a million dollar reward. Up to this point no one has passed the preliminary testing in order to try for the million dollars, but the search is still eagerly pursued by the foundation ((1)).
There has been a long history equated with the phenomenon of extra sensory perception and other types of paranormal activity. ESP has been defined loosely as the "form of information transfer in which all known sensorial stimuli are absent" ((2)). This definition also assumes that the mechanism by which these interactions are occurring are neither known nor understood. Extra sensory perception has been placed together in the all-encompassing category called phi, which also included telepathy, precognition, psychokinesis, and clairvoyance.
Humans abilities to detect stimuli outside the main five senses have only relatively recently in our history begun to be experimental tested. However testing has been unable to prove that it does exist, because of the nature of what they are studying. One of the first researchers to conduct such experiments was Joseph Rhine in the 1930's. He asked people to try and identify what was on the back of five varying playing cards. He concluded that ESP did indeed exist; however in light of new experimental procedures his research was found to be inconclusive at best because of lack of proper technique.
One current innovation in the search for proof of ESP is the Mind Machine in 2002. This highly sophisticated computer program asks its user to predict the random flip of a coin on the screen and records the user's data for analysis. Designed to gather and process a lot of data within a short amount of time, while eliminating any chance for clues given to the tester, the Mind Machine was tested all over Britain's colleges and malls. However this newest wave of "out of the laboratory testing" still found results that were consist with those of chance guessing ((3)). Can this be proof that even when the human element is removed to avoid miscalculations and the experiment is taken out of the lab, that ESP still can not be proven? Believers still say that there are mistakes in the system, the crowds were too noisy, and there was still not enough of random sampling.
There have been many experiments conducted about ESP with little success or inconclusive data since the Rhine experiments. One limitation that all ESP experimenters face, regardless of technique, is the fact that trying to force ESP to occur under experimental conditions is in and of itself a difficult task. Much in the way that animals are known to do opposite or contradictory things when placed in captivity, as compared to when in their natural habitat, humans could work the same way. One newspaper journalist comments, "it is still controversial as a science because any positive results cannot be replicated in the lab, we can't make people be psychic under observed conditions" ((4)). Again this raises the question that if it is so hard to produce successful results in an experimental setting, this hinders the chance that ESP could ever be proven or further studied.
Another limitation that exists is the danger level at which this testing is being conducted. Most or all of the ESP occurrences that occur outside of laboratory testing happen when a family member or close friend is in trouble. Most people claim to get a "feeling in their gut" that something just is not right. This is evidence that ESP might only be working by a mechanism that allows for easier transmittance of unnerving thoughts/events rather than happy ones. However testing this would be very difficult, because most people are not willing to put family members in danger, for the sake of science. So the idea that ESP might only work in extreme and alarming cases, might again mean that may never be able to be prove in a laboratory that ESP exists.
As seen in nature, animals are capable of sensing when earthquakes or storms are coming, and have ample time to get to safety. Can this be considered a form of ESP or precognition? If animals are capable of this type of transmittance why would humans not be as equally able? Humans may potentially be able to respond to environmental stimuli, but we might be blocking such signals with our I-function, or other parts of the nervous system by closing off receptors to everything but our traditional five senses. In an effort to put a more of a focus on these other senses, scientists have proposed the concept of hypnotism to help fine tune the chance of finding information about ESP in the body.
Many successful experiments have used hypnotism to test for ESP, that way the person is more open to suggestion. Again, these types of experiments are believed to work because the subconscious can be focused on, rather than the conscious. Hypnotism allows the body to let the nervous system enter a more relaxed state, potentially allowing for the detection of stimuli below the normal threshold, which can create an action potential and the body can receive the stimuli. One of the major theories of hypnotism applies here: that during hypnotism the ego is suppressed, so that one is more likely to act on natural instincts rather than the rational side ((5)). This theory links the idea that it might be necessary for people who receive ESP to be in a trance-like state that allows their nervous system to essentially suppress or bypass the I-function and focus more on stimuli they are receiving from the subconscious.
In conclusion, the limitations of ESP testing give rise to many implications for future research. As discussed there exist many factors that have hindered and continue to inhibit experiments that could potentially ever give legitimate proof for the existence of ESP. Whether or not ESP exists in animals or humans is debatable, but the most feasible ways for accurately testing would be the continuation of using hypnotism on people. There seems little or no chance for testing ESP in terms of ability of sensing threatening or dangerous conditions, unless there was a way to fake a dangerous situation. Another serious consideration could be to emphasis why animals can sense things humans can not, and then to try and isolate a certain receptor, gene or area of the nervous system that is involved in accepting these stimuli, and relate it back to humans. Research on this highly controversial topic will continue and its only chances for survival as a field of research require reconsiderations of the testing practices and the limitations ESP presents.


Works cited
1. 1)official foundation website, Site with lots of enthusiasm for research
2. 2)official research foundation website

3. 3) Newpaper article

4. 4)

5. 5), an insightful website on hypnotism

Works consulted
1. http://www.painstudy.com/NonDrugRemedies/Painp14.htm; website about hypnotism



Full Name:  Shu-Zhen Kuang
Username:  skuang@brynmawr.edu
Title:  Hunger and Obesity: Are We Really Hungry?
Date:  2005-04-11 21:37:28
Message Id:  14477
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


My mother always said that being overweight is a blessing because only the rich can afford to be fat. Having lived most of her life in a rural countryside in China, my mother never thought there could be other reasons why people are overweight. America is the richest country in the world, and obesity has become a major health concern. A person is considered obese if their body weight is 20% over the normal weight (1). With obesity on the rise, the health problems that come along with being overweight are major concern in most American households. Being obese carries with it the predisposition to get diabetes, heart disease, and many other serious illnesses (2). Our bodies have biological mechanisms that tell us when we are hungry and when we are full. Do obese people have a defect in their biological mechanisms that control their weight or are other issues, such as lifestyle and psychology, affecting their weight?

From a biological prospective, our body must have a way of telling us when we need to eat to ensure survival. People are usually aware of their hunger when their stomach starts making noises. These noises are stomach contractions, but this sign is not the most important indication of hunger (2). The feeling of hunger comes from the hypothalamus, which is responsible for maintaining our body weight by telling us to consume more or less calories in order to have a properly functioning body (4). The mechanism starts when blood glucose levels are low. Then the liver, which changes food into glucose, sends a signal to the lateral hypothalamus. In order to increase the blood glucose levels, the lateral hypothalamus activates the behavior that each individual has for finding and consuming food (2). Low levels of leptin, a hormone released by fat cells, when detected by the hypothalamus, have also been showed to generate the feeling of hunger (4).

The hypothalamus controls the sensation of hunger, but it also plays a role in the amount of food consumed. Satiety is when we feel full, and as a result, we stop eating. When food begins to move from the stomach to the intestines, certain hormones are released from the stomach that signals the ventromedial hypothalamus to stop consumption (1), (5). Leptin is also released from fat cells in response to increased levels in caloric storage (4).

Each individual has a similar mechanism that controls his or her body weight, but some people are predisposed to be obese. Forty to 70% of body mass can be associated with genetics (2). An example of genetic predisposition is indicated in studies that show adopted children's weight being similar to their biological parents' weight instead of their adoptive parents (5). A case where genetics severely affects hunger is in the rare genetic disorder called Prader-Willi Syndrome. Because the hypothalamus functions abnormally, people with this syndrome are constantly hungry and can never be satisfied no matter how much is consumed. Unless parents set up a controlled diet early on in the child's life, obesity will be one of the results of this syndrome (6).

Another biological aspect that relates to hunger is the set point hypothesis. This is the idea that the weight of every individual is determined and maintained by their hypothalamus. As a result, when a person tries to lose weight, the hypothalamus resists these changes. When people are on a diet, their leptin levels decrease and in turn cause the hypothalamus to trigger the feeling of being hungry. In other words, this continual cycle is the downfall of many people who attempt dieting. In addition, the set point for obese people may be higher than for healthy individuals. Studies have found that satiety point, which is determined by the hypothalamus, is higher in obese individuals compared to average weight individuals (5). Therefore, the biological mechanisms that maintain a certain weight may be different for obese individuals compared to healthy individuals.

Although genetics plays an important role in regulating our weight, a large portion of our body mass is determined by the daily choices we make. The time, amount and type of food we consume are selected by us. For some people, it is the lack of willpower that leads to the path of obesity. Although the extra snack eaten every day may not seem to contribute to the overall weight gain, the extra calories from this snack gets converted to fat and build up overtime (3).

Since most people who tried dieting have failed, many physicians have resorted to treating the side effects of obesity such as diabetes instead of a cause of the diabetes which is obesity (2). Because not enough emphasis has been placed on diet and exercise, there is an increasing trend toward obesity. One national study states that 65% of American adults are overweight compared to 56% in 1994 (3). This study shows that genetics is not to blame for all cases of obesity. Part of the increase can be associated with our inability stay with the regimen of diet and exercise. The way our culture chooses to deal with this problem is not working since the continuation of fad diets still persists along with obesity.

For others, unhealthy eating habits are developed from upbringing and culture. In America, advertisers spend a great deal money promoting unhealthy foods to children and adults. This temptation is hard to resist for many who have grown accustomed to eating these foods. However, other parts of the world are also experiencing the same obesity trend as America (2). Perhaps, the spreading of Western culture is influencing the diets of other cultures as well.

There is more than just the biological explanation of hunger. Physical hunger and psychological hunger are very different things. Some people have developed the habit of eating during a certain time of the day ever since they were children. The time of day can be a component that triggers the feeling of hunger for many people. For others, the smell of certain foods could instantaneously make the person feel hungry even though they may have just consumed a meal not long ago. As most people have experienced, these sudden urges are not satisfied until the certain type of food is consumed. Many people also use food as a way to suppress an emotional problem in order to avoid dealing with the actual problem (5). These people find that by eating food, their emotional problems become temporarily solved. High fat and sweet foods have been found to give off a pleasurable sensation through the brain after consumption (7). These external stimuli provide other ways to signal the hypothalamus to make us feel hungry even though the signals are not physiological.

There has been much debate about whether biology or other aspects play a greater role in obesity. Genetics is only one of the many factors that are involved in determining a person weight. Subconsciously, most people know that living a healthy lifestyle through diet and exercise is the best way to avoid obesity whether you are genetically predisposed or not. However, our culture is providing conflicting messages about weight control. The food and snack industry continually promotes fattening foods while it promotes diet foods at the same time (2). Among scientists, there is still a difference of opinion on whether genetics or self-control affects a person's weight more (3). Because none of these viewpoints can provide a definitive answer to the current obesity trend, it is possible that the combination of genetics and self-control determines a person's weight. Regardless of these issues, the dramatic increase of obesity among populations is a warning sign that we are leading unhealthy lives. A more comprehensive understanding of all the issues surrounding obesity will hopefully lead to healthier lives.

References

1)Weight Loss: What is obesity?, an article on WedMD

2)Hunger and Eating Disorders, provides the biological and psychological side of hunger

3)The Great Weight Debate, an article on WedMD

4)Hypothalamic Neuropeptides: Responding to Caloric Challenges

5)Hunger and Eating, provides info about hunger and obesity

6)Prader-Willi Syndrome

7)Why do we eat what we eat: biology of food choice



Full Name:  Kristin Giamanco
Username:  kgiamanc@brynmawr.edu
Title:  Exuberance: The Passion for Life by Kay Redfield Jamison
Date:  2005-04-11 22:12:02
Message Id:  14479
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


"A passion for life is life's ultimate affirmation. To ask the question is to know this to be so; it is to know that exuberance is a god within" ((1), 308).


If you were to stroll down an aisle in your local bookstore, chances are most of the books you would see are geared towards helping an individual with depression, hypochondriasis, and obsessive-compulsive disorders, for example. Very few books discuss individuals who are healthy and happy. However, Kay Redfield Jamison's book discusses and focuses primarily on people who are exuberant and effervescent. Jamison's book serves to separate the notions of happiness and exuberance while explaining how the latter plays a role in creative and scientific explorations. "Exuberance is an abounding, ebullient, effervescent emotion. It is kinetic and unrestrained, joyful, irrepressible. It is not happiness, although they share a border. It is instead, at its core, a more restless, billowing state," ((1), 4).


After reading Jamison's book, I was left with many questions and thoughts for further research that can be done in order to address these issues. This paper focuses on looking at the ubiquitous nature versus nurture topic as well as the positive and negative roles exuberance can play in one's life. Furthermore, I will attempt to address the role of the I-function in monitoring exuberance and use Jamison's ideas to help me on the quest to continue to determine the role between brain and behavior. Lastly, I have examined the transition between childhood and adulthood as well as the transference of exuberance.


Jamison opens her book with an examination of the exuberance (which she later describes as the bubbly effervescent nature of champagne) of John Muir, a naturalist and conservationist and as well as that of Theodore Roosevelt, America's 26th president, possessed. It was their infectious and exuberant natures which drove them to change America with their vision and actions. She also discusses the beauty of nature by chronicling Wilson Bentley's, a New England farmer, obsession with the beauty of each unique snowflake. Another aspect of exuberance Jamison focuses on involves the advantages of playing for animals and young children, discussing the impact of playing on the brain. Perhaps the most interesting chapter of the book comes when Jamison describes A.A. Milne's Tigger and Kenneth Grahame's Toad. These two characters ooze exuberance as Jamison reports and their unbridled enthusiasm, lust for adventure, are compared to the nature of Snoopy and Peter Pan. All of these characters are found within children's books.


Furthermore, Jamison correlates manic depression with exuberance, citing that individuals who experience manic highs are extremely exuberant, animated, and often restless. She also opts to discuss the exuberant nature of falling in love for the first time, the contagious nature of laughter, use of chemicals, such as cocaine and marijuana to help sustain and reinforce exuberance. Another fascinating aspect of this book involves the investigation of exuberance in the role of scientific achievements. Jamison cites that successful scientists are often exuberant at heart and cannot tell the difference between work and play. These individuals are usually driven by their thirst and creativity within the field. Moreover, Jamison believes that great teaching involves exuberance and also involves the spreading of this magic from teacher to student.


The tone of the book changes somewhat towards the end as the author moves to expound upon the exuberance of soldiers engaged in battle and their quest for killing. Jamison concludes with a look at America as a Nation, being exuberant, a country that is world renown for its enthusiasm and infectious happiness as evidenced by the thousands of pioneers, scientists and politicians who have left their footprints on our country.


While I enjoyed this refreshingly optimistic book, I felt that at times, Jamison's focus was lacking as she skipped from example to example within her ten chapters. There was no clear thesis in the book. While she aimed to explain the prevalence and the nature of exuberance, she herself was too restless. She does have a central theme in each chapter, but with the plethora of examples she provides, her argument is often hard to follow (2), (3). However, her writing is captivating and eloquent, so that as a reader, you come to have an intimate appreciation and understanding of exuberance.


Personally, I enjoyed the discussion of the exuberant scientists most and was particularly interested in examining some of Jamison's claims concerning these individuals. Jamison discusses the lives and work of Humphry Davy, Michael Faraday, Richard Feynman, James Watson and Francis Crick, as a few examples. All of these scientists were described as exuberant; they lived for and loved what they did, could not imagine doing anything else in the world and were constantly striving for more. The hunger and thirst for understanding science that these men all possessed allowed them to become extraordinary scientists. Is it true to become a great scientist, you have to fully immerse yourself in all things science? In all of the examples Jamison went through, most of the individuals hardly slept or ate when they were working on their various projects and one scientist even bought shoes without laces so that he would not waste time in the morning on his way to work. Ordinary, less famous scientists greatly outnumber extraordinary famous scientists, which leads me to think that a great scientist is born rather than made. Furthermore, it seems to me that while you can train a scientist to be functional, you cannot train one to be extraordinary. The nature versus nurture question is one that we have been battling with in class and based upon the idea that brain equals behavior as set forth by Emily Dickinson and in the class forum; I firmly believe that nature in this case rules over nurture (4).


A subject that Jamison does not delve into, but one which I think would help in further understanding is the question of whether exuberance within the scientific field is hereditarily transmitted. Perhaps one could accomplish this with a study of scientists and their children. Generally, scientists of all talents and spanning all fields are curious by nature and all possess a degree of passion for their work, therefore, it would be interesting to determine if this enthusiasm is inherited by their children. Will the children inherit this exuberance, but will it be for another field? Is the exuberance inherited or the passion for a particular lifestyle inherited? I feel these future studies would help me to resolve the discussions we have had in class about nature and nurture. Moreover, if you were to place a naturally animated child in a stifling household lacking positive energy, would this child still flourish and pursue their goals?


Another interesting aspect discussed is the difference between exuberance in terms of scientific and creative achievement versus the exuberance a soldier can develop for killing. It seems quite interesting to me that exuberant behavior can be used for both positive and negative actions. What makes the passion a scientist has to cure cancer different from a soldier engaged in war? " 'There is a part of me—maybe it is a part of many of us—that decided at certain moments that I would rather die like this than go back to the routine of life,' " ((1), 259). This quote was taken from a soldier engaged in battle and Jamison is able to document the passion they have for killing, which although startling, has to taken into account since there are so many different ways that exuberance can affect individuals. While it seems that exuberance is only a positive attribute to possess, I began to realize that this passion for life may not always be entirely positive and healthy. Therefore, I found it helpful that Jamison provided stories about the soldiers to help highlight that exuberance is not only channeled into creative, literary or scientific achievements but can also spur on negative activity.


In conjunction with the solider stories, Jamison discusses Andrew Cheng who works at Johns Hopkins Applied Physics Lab and expounds upon how exuberance can negatively impact one's life. While being exuberant affords a scientist with the resilience, passion and drive to explore new ideas and experiments, it can be hard to focus on one task. " '...don't get things done, there are too many projects. You get excited. And you start forgetting meetings and ignoring your other responsibilities. And you start getting other people mad at you,' " ((1), 218). Therefore, it seems that the balance between being successful and responsible is dictated by an individual's exuberant nature. If a scientist is too exuberant, then they will have trouble focusing solely on one project and will put their efforts toward too many tasks at once, thereby spreading themselves too thin. Moreover, if a scientist is not exuberant enough, he/she will most likely lack the passion and drive to accomplish their goals. Perhaps the I-function of each individual serves to monitor their exuberance in the workplace, accounting for why some individuals are able to still accomplish a great deal while keeping focused and others are unable to do so. It would be interesting if Jamison had interviewed the exuberant scientists to see if they were even aware they were skipping out on their other responsibilities or if they were so caught up in their projects they did not even notice. In addition, Jamison could have asked the other scientists to see if they were actively monitoring themselves so that they were more focused, were participating in their meetings, and attending to their other responsibilities.


While we have tackled the role of the I-function in class for much of the semester, we have also looked at the elusive relationship between brain and behavior. Jamison does not directly answer this question but she does offer some theories about the role between brain and behavior by looking at the exuberant nature of animals at play. The act of playing in young animals helps to establish social ties, allowing members of a particular species to bond and communicate. Furthermore, this type of behavior helps to strengthen the immune system and increases the resilience of these animals under stress. Scientists have shown that rats raised in cages with toys and tunnels play more, explore more and in the long run, accrue more new neurons as compared to their counterparts in standard cages. An experiment that I would be interested in looking at entails moving rats from one cage to another and monitoring their brain activity in order to cement the idea that brain does equal behavior. Would the rats raised in standard cages and then moved, develop more neurons and by nature become playful, or are they so conditioned at this point in their maturation that they will not explore in these new cages? While Jamison provides an ample qualitative look at the exuberant nature of playing in young animals and young children, her discussion is lacking any quantitative evidence. She merely asserts that scientists have performed a battery of tests, but there is no real evidence to look at. However, using her discussion and ideas that I expressed in my first paper, thoughts of my classmates established in class and through the online forum, I believe Jamison's writings help me to firmly believe that brain equals behavior (4). Moreover, the experiments I proposed would help to further explore these issues.


Another interesting topic Jamison grapples with is the closing of childhood and the entrance into adulthood. Everyone must make this transition and it seems that some are able to do this more smoothly than others. The successful ones do not abandon their exuberance; rather they channel their passion and love into another venue. While they once enjoyed playing with dolls, building Barbie houses, or running around the neighborhood climbing trees, their childhood hearts and dreams have not been shattered. Rather, these individuals are able to capture their emotions and allow them to be expressed in their work. Most of the scientists Jamison interviews do not even know how many hours a week they work because they do not consider what they do each day actual work. How are some adults able to find careers that allow them to express their exuberance so well, while others are left at jobs that require them to stifle their passions? It seems that the former individuals are not only exuberant, but lucky to have a job that they truly love.


The ideas raised in Jamison's book left me with more unanswered questions than answered questions, but piqued my interest in a variety of topics, some of which we have dedicated class time to studying. The section where she interviews exuberant scientists and discusses their achievements was most interesting to me. Not only does Jamison detail the positive effects of exuberance, but she also describes the almost manic and somewhat scattered nature of these individuals. She juxtaposes the creative, scientific, and literary achievements due to exuberance to the passion that soldiers develop for killing while engaged in battle. These ideas force the reader to realize that exuberance may also play a negative role and there is a sensitive equilibrium that must be maintained within each individual. I propose that the I-function helps to regulate this almost homeostatic process within the brain. The discussion of nature versus nurture and the hereditary transmittance of exuberance also were of interest to me, as we have touched upon this topic in class. Moreover, I also employed Jamison's thoughts in order to come to a more solid conclusion that brain does equal behavior by examining the benefits of play in young animals and children. However, what interested me the most was Jamison's decision to publish a book that was so markedly different than her other work on moods, madness, suicide and manic-depression. It is refreshing to read a book that not only examines the way in which the brain and behavior interact in a negative or malfunctioning light, but also highlights the positive aspects. Her book ends on an optimistic note, instilling hope and exuberance in her readers, which I warmly welcomed.


References

1) Jamison, Kay Redfield. Exuberance: The Passion for Life. New York: Alfred A. Knopf, 2004.

2)Mental Help Net , a review of Jamison's book, published by Christian Perring, PhD.

3)Houston Chronicle website, another review article on Jamison's book published by Diana K. Sugg of the Baltimore Sun.

4)Serendip Home Page, our class website and forum area.



Full Name:  Flicka Michaels
Username:  fmichael@brynmawr.edu
Title:  Lambert-Eaton Myasthenic Syndrome
Date:  2005-04-11 22:44:26
Message Id:  14481
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip



Lambert-Eaton Myasthenic Syndrome (LEMS) is a rare autoimmune disease which affects the neuromuscular junction and interrupts the connection between nerve cells and the muscles.(1) Less than one in every one million people are diagnosed with this disease every year. (5) It was first described in 1953 by Anderson, who examined a 47 year-old man with oat cell lung cancer. In 1966, Lambert, Eaton, and Rooke did an initial study of the disease, and thus it is named after them. (2) LEMS primarily affects middle-aged adults, but cases in children have been found. Cancer is a factor in about 50% of all cases of LEMS; small-cell lung cancer tends to be present in the majority of them. (2) Some researchers suspect that the cancerous cells cause an excess release of a certain protein in nerve cells, which then causes the formation of anti-bodies to this protein. (1) However, one of the most striking aspects of LEMS is that for patients without cancer, the cause of the disease in unknown.

In order for nerve cells to effectively relay signals to muscles so they can contract,they must emit a neurotransmitter called acetylcholine. The emission of acetylcholine from a nerve cell is dependent on a protein called P/Q type voltage-gated calcium channel (VGCC). VGCC allows admission of calcium into nerve cells and therefore the emission of acetylcholine. About 85-90 percent of people with LEMS have been shown to have antibodies for VGCC, therefore preventing the emission of acetylcholine, and associated weakness of muscles. (1)

Symptoms of LEMS are similar to Myasthenia Gravis. They include weakness of upper leg and arm muscles, problems walking, weakness of the facial muscles, problems talking, swallowing or chewing. Other symptoms include dryness of the mouth, eyes, or skin, and droopy eyelids. (3) The progression of symptoms resulting from LEMS tends to move slowly and can often be mistaken for another disease called Myasthenia Gravis. Like Myasthenia Gravis, LEMS primarily affects adults, and is distinguished by weakness of the muscles. However, with Myasthenia Gravis, the body makes antibodies for
acetylcholine receptors, instead of the protein which allows for the emission of the transmitter. Also unlike Myasthenia Gravis, the weakness associated with LEMS tends to improve after exercise. Some doctors think that the repetitive action causes an increase of calcium in the nerve cells, which then increases the amount of acetylcholine released. (1)

The initial diagnosis of LEMS can be made through a physical examination which will demonstrate the patient's muscle weakness. However, in order to distinguish LEMS from Myasthenia Gravis, a blood test is needed to identify the specific autoimmune antibodies that are being produced. In addition, a test can be given, in which a patient is injected with the edrophonium chloride (Tensilon), and if muscles strengthen as a result, the diagnosis is Myasthenia Gravis. (3) The presence of cancer in a patient is also a sign that LEMS is the diagnosis, as opposed to Myasthenia Gravis.

As I mentioned earlier, about 50% of all LEMS cases are associated with some form of cancer. (2) However, Small-Cell Lung Carcinoma (SCLC) is by far the most common. About 60% of people who have LEMS also have SCLC. (6) Research shows that the connection between the two is most likely due to the antigenetic characteristic of SCLC which triggers body's autoimmune response to the cancer and in turn, the production of antibodies to VGCC. (6) Since this process occurs during the very early stages of the tumor, LEMS is usually detected before the cancer. In some cases, the symptoms of LEMS can appear anywhere from 2-5 years before the symptoms of the cancer. (6) However, when symptoms of LEMS are discovered and the disease is diagnosed, the patient should immediately be tested for cancer, SCLC in particular.

For patients with LEMS and cancer, treatment normally centers on treatments to eliminate the cancerous tumors. However for patients without cancer, a process called Plasmapheresis, in which blood plasma is removed from the patient and replaced by
fluid, tends to ameliorate symptoms. (4) One drug, called Pyridostigmine (or Mestinon), is commonly used for patients with Myasthenia Gravis, and may help increase the release of acetylcholine. However, a commonly recommended drug in cases of LEMS is 3,4-Diaminopyridine, which, like Pyridostigmine, increases the emission of acetylcholine from nerve terminals. (6) For patients with more severe or persistent symptoms, immunosuppressant drugs such as Prednisone, Imuran, and Neoral can also help decrease the formation of antibodies.

So why is LEMS so fascinating? Primarily because (in cases where cancer is not a factor) the cause is unknown. It is an autoimmune disease so we know that the body starts creating antibodies to something it would not normally try to suppress. But why? A research study performed in 2001 by the Dr. Andrew Caton at Wistar Institute in Philadelphia showed that the existence of T cells in the body plays a large role in preventing autoimmune responses. T cells are white blood cells that recognize the body's natural proteins, or the 'self'. (7) Dr. Caton explains that in the case of autoimmune diseases, these T cells are altered so that, instead of working towards the destruction of infected cells, they inhibit the usual immune response. He says, "What's interesting about these regulatory T cells is that, although their purpose is to prevent autoimmunity, they themselves react against the 'self'." (7)

Most of the time, we are trying to figure out how the idea of the "self" fits into the nervous system. We never think of the nervous system as an actual "self" because we usually think that our life battles consist of the nervous system (physical) versus
the "self" (mental). However, if part of the nervous system revolts against its normal routine (as with autoimmune diseases like LEMS), does that not mean that we should entertain the idea that a "self" exists within the nervous system? Perhaps if we stop
viewing the nervous system as one entity that always works perfectly, we might be able to better appreciate its partition and complexity.

References

1)Muscular Dystrophy Association, Facts about LEMS

2)eMedicine, Very technical, but in depth article about LEMS by Paul Kleinschmidt, MD

3)Rare Diseases.com, facts about LEMS

4)ADAM encyclopedia on About.com, Health Encyclopedia- Treatment for LEMS

5)Cleveland Clinical Health System, Basic overview of LEMS

6)DLD Diagnostika GMBH, Great article that thoroughly discusses and presents visual images of the voltage-gated calcium channels involved in LEMS.

7)Autoimmune Related Diseases Association, Research study abstract



Full Name:  Elizabeth Rickenbacher
Username:  erickenb@brynmawr.edu
Title:  A New Threshold?
Date:  2005-04-11 23:31:49
Message Id:  14483
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


From childhood and early adolescence, we, members of society, constantly find ourselves bombarded with the idea and understanding of "normal"(1). Throughout school and extracurricular activities, we find ourselves striving to fit in and be included in the accepted and desired way of life. The latest fashion, lingo, and trends are followed in order to achieve the level of normal to not be taunted and discriminated against and maybe even be popular. What determines these standards of normal? Often and sadly the latest fashion and trends capture the interest of most in determining what is normal. Ones behavior and temperament is often a secondary source of information in the order of determination. We are taught early on that discrimination is bad-mannered and wrong, and to embrace the differences in each other, for we all have something to offer to society. However, to enter society, we must act in accordance with its rules and standards of behavior. We are taught that silence is golden and that politely standing in line is the correct thing to do, and if one cannot comply with these rules, medication (20) can assist you in correcting your horrible unacceptable behavior and aid you to reenter society in a fit and normal manner.

Currently, there are 3.3 million Americans (1 in every 83) (3) living with Bipolar Disorder (2) whose struggle to act in accordance with society is a daily battle. Bipolar disorder is an affective disorder in which both manic and depressive episodes occur. Of that 1.7% in the general population, 10% (21) find themselves in a permanent hypomanic state. Hypomania shares symptoms and characteristics with the mania aspect of Bipolar Disorder, but to a lesser degree. The difference between the two is not completely understood or clear (10), however, individuals experiencing hypomania do not experience symptoms that seriously disrupt everyday life, but to the contrary experience a variety of symptoms to the enjoyment of many which elevate energy levels, creativity, enthusiasm, and productivity. Often, individuals experience feelings for less sleep feeling just as rested as having slept eight hours. Individuals often have many ideas and racing thoughts and can easily be distracted moving from one activity to another.

For 10% of the 3.3 million individuals with Bipolar Disorder, this feeling of unwavering energy and productivity is a good thing, almost addicting (14). Things get done quickly and then the next project begins, what's the big deal? Lucky them! It would be great to get one day's worth of work done in two hours! Where does one sign up! It is not that easy. Bipolar Disorder along with a hypomania is a genetically based disorder (6),(7). Individuals with hypomania are often recipients of genes from bipolar family members. Both biological and environmental factors contribute to the onset of Bipolar Disorder (7); however, if criteria are not met for full Bipolar Disorder, derivatives of the disorder such as hypomania are the result. The United States (4) has an extraordinarily large number of hypomanics and individuals living with Bipolar Disorder compared with any other country. John D. Gartner (5), contributes this high occurrence due to the high percentage of immigrants in the United States. The self-selection process of immigration, "those who had the will, optimism, and daring to take the leap into the unknown have passed those traits on to their descendants" (5) has given rise to a population with a greater chance of experiencing an onset of hypomania.

Due to the immense amount of energy and productivity associated with hypomania, many noted individuals have been thought to have hypomania, Henry Ford (18), Emily Dickinson (15), Bill Clinton (19), Christopher Columbus (17), and Benjamin Franklin (16) to name a few. What these individuals have in common is a degree of energy and determination that is contested by few. From a physician's standpoint, symptoms of hypomania can lead to many consequences (22) and even eventual mania, thus the need for medication and therapy. However, 10% (21) of the individuals that experience hypomania do not alter from a depressed or manic mood, but rather experience a permanent hypomania. It would be incredible if we could all experience the positive symptoms (14) of hypomania by taking a simple pill that would alter us from our "normal" (1) behavior to one that allows us to be more productive and creative machines to accomplish our endeavors.

The brain structures and characteristics that differ in hypomanic individuals include the frontal lobe (8). Left frontal cortical activity (9), seen through EEG response, shows an extreme increase in individuals with hypomania. The frontal lobe regions of the brain are associated with the "executive control" of ones behavior such as memory, motivation, cognitive processes, inhibition, and organization. It is no wonder that individuals that are hypomanic process, work, and produce at greater degrees than most.

To be able to be diagnosed with Bipolar Disorder or hypomania, one must be at least eighteen years of age and meet certain criteria used to diagnose the disorders (8). One cannot be diagnosed until the age of eighteen because ones brain is not fully developed well into the teenage years and it is still not fully known what effect experience and maturation have on the brain. Animal studies (8) do not serve as good examples in understanding the frontal lobe development because the development of the human brain is unlike that of any other animal. The frontal lobe is the most developed region in the brain which does not reach a fully developed stage until well into adolescence.

Diagnosing hypomania and Bipolar Disorder is also very controversial (11). Much like the Ritalin debate, which has been under debate for the past two decades, the diagnosis of Bipolar Disorder is becoming more and more common when a diagnosis is sought after. Everyone has their ups and downs, why not call it Bipolar Disorder? The most commonly used reference books used to give standard symptoms for the diagnosis of different conditions, the DSM-IV (13) and ICD-10 (12), often are interpreted differently in both sources. Hypomania is difficult to define because the DSM-IV (13) and ICD-10 (12) do not completely agree on what criteria need to be met in order to be diagnosed with hypomania, or if it is an actual disorder or "disturbance in mood".

We are all different in temperament and behavior and are constantly reminded of this in every day interaction. Routine and stressors plague most of our lives to the point where meaning and enjoyment often escape us. If we all had the energy to be productive and creative on the level of a hypomanic, could we not relieve ourselves of the hardships which we encounter on a daily basis? If one could mimic the chemical balance of a hypomanic and heighten frontal lobe activity in a "normal" (1) individual, we could then work at the threshold of potential and create an entirely new normal standard in which to base our idea of normal! Are the examples hypomanics are providing us with detrimental? If evolution had done its job, why is the threshold at which hypomanics work not the norm? I believe that there is something to be said about rational and careful thought. It would be difficult to be as careful and rational working at a rate unfamiliar.

1) definition of normal

2) bipolar disorder defined

3) prevalence

4) country statistics

5) negative symptoms

6) location on genome

7) gene and brain characteristics

8) development of frontal lobe

9) frontal lobe functions

10) disorders

11) controversy of diagnosing

12) ICD-10

13) DSM-IV

14) positive symptoms

15) Emily Dickinson

16) Benjamin Franklin

17) Christopher Columbus

18) Henry Ford

19) Bill Clinton

20) medications

21) Prevalence percentages

22) consequences



Full Name:  Patrick Wetherille
Username:  pwetheri@haverford.edu
Title:  Remembering Repressed Memories
Date:  2005-04-12 00:25:52
Message Id:  14485
Paper Text:
<mytitle> Biology 202, Spring 2005 Second Web Papers On Serendip

If you've paid any attention to popular media in the United States recently, you're probably familiar with the attention given to adults who report being sexually abused as children. Even famous stars like Rosanne Arnold and former Miss America Marilyn Van Derbur have come forward to discuss their stories of abuse (1). This recognition of such an ugly problem our society faces is certainly a step in the right direction towards eliminating sexual abuse of children. However, what is less discussed is the method that is used to extract evidence that supports claims of sexual abuse. While many cases are well built upon corroborated accounts of the abused individual, some have gone to trial based solely upon "recovered" or "repressed" memories. In recent years, much work has been done to understand the nature of these memories and the processes used to extract them from victims of sexual abuse. We shall investigate repressed memories by looking at how traditional therapy has been criticized in its approach to accessing repressed memories and how these criticisms can be interpreted through a scientific understanding of memory. Before we can begin to answer these questions however, we must first explore what science can tell us about memory.

Modern scientific theory describes the memory as located in the temperal lobe, the diencephalon, and the frontal lobes of the brain (2). Within the temperal lobe, the hippocampus and amygdala are concerned with taking in new information that is part of short-term memory and transferring it to long-term memory. The dichotomy of short and long-term memory was first explored by William James in 1890 and remains a critical part of today's understanding of how memories work (3). The neocortex is used to recall information from the long-term memory (2) for use by a person's "I-function". (NOTE: The I-function is a term to describe one's own conscious stream of thought, without having to go into neurobiological theory of where the consciousness itself exists.) Far from being completely understood, evidence suggests that memories are not located in one particular place, but rather they are broken down as elements and spread out in different regions of the brain.

When a long-term memory is accessed, it is not brought forth to the I-function from one specific location, but rather from several places, compiled of various elements that are relevant to the memory. This process of coordination of various elements is facilitated by the hippocampus (4). The hippocampus, the temperal lobes, and the connected structures of the limbic system all work together in accessing long term memories. Information starts in the hippocampus, flowing to the hypothalamus's mammillary bodies, the anterior thalamic nucleus, the cingulate cortex, and the entorhinal cortex, then travels back to the hippocampus. This circular flow of information is what makes all the elements of long-term memory accessible for use by the I-function of the brain. The 'circuit' that this flow of information makes then has the ability to change the brain itself, making the associations of the relevant elements stronger. This is why repetition allows you to remember things better: the brain is physically linking the elements closer together so that the next time the memory is accessed, it brings the relevant elements together with more ease (4).

Repression is a theme that psychologists have wrestled with for years. Sigmund Freud's famous theory of sublimation of repressed urges is an example of how repression is seen to be part of human behavior in society (5). Traditionally, psychotherapy has encouraged the study of the repressed, often focusing on wants and desires. Hypnosis has been seen as a way to access those repressions, however, as childhood memories of trauma were seen to be the object of repression, attention to the effect hypnosis has on the patient has been overlooked. The idea that any technique to help the patient get their memories out was not seen as problematic and in fact seemed to be a helpful for victims. A doctrine was adopted by some therapists of helping a patient work through their problem by any means necessary, regardless of what it entailed (6). However, based upon what we know about the function of memories in the brain, it seems all too obvious that such an approach endangers the accuracy of the memory if the wrong information is used to fill in the blanks in someone's memory. If a therapist is not careful to remain neutral in their opinion of whether a patient was abused or not, they can create certain presuppositions that can taint the outcome therapy might have on the patient and even implant false memories of abuse when in fact, there were none.

A quick example of this presupposition in dealing with long-term memories (such as memories of childhood abuse) can be seen in Elizabeth Loftus's "Bugs Bunny" experiment. Dr. Loftus interviewed several subjects, asking them about their childhood experiences at Disneyland. She asked not only if they saw a character dressed up, but also if they "hugged his furry body and stroked his velvety ears (7)." By adding the extra information, Dr. Loftus created a presupposition of a furry body and stroking velvety ears in the subject's recollection of the memory. If we think in terms of the physical function of memory, the hippocampus coordinates all of the relevant elements necessary to the memory, even accessing information relevant to the extra information. "Hugging his furry body" and "stroking his velvety ears" seems to have had the effect of accessing an image of Bugs Bunny, not a Disney character, for several individuals, as 36% recalled seeing a cartoon rabbit when asked what the name of the character was that they saw at Disneyland. Bugs Bunny is of course not a Disney character and therefore any memory of hugging him at Disneyland is almost certainly false (unless some random person happened to show up in a Bugs Bunny suit that day at the park). However, since the description matched a bunny and now a mouse or any other Disney character, their memory adapted to the misinformation and created a false memory. This example shows how memory can be tainted by presuppositions of even the smallest kind.

Scientific analysis of long-term memory has been very critical of so-called repressed memories, as suggestibility under therapy can lead to false memories. In 1992, a church counselor provided therapy to a young woman and helped her remember how her father had raped her between the ages of seven and fourteen (8). The suggestive techniques used by her counselor lead her to develop vivid memories of rape as well as memories of being twice impregnated by her father, only to be forced to abort the fetuses. Her father, a minister, was forced to resign. However, subsequent medical examination concluded that the 22 year old not only had never been pregnant, but was also still a virgin. This example of false memory implantation is representative of the misunderstanding many therapists have with the accuracy of long-term memory and the impact suggestibility can have on forming those memories. Hypnosis and other age-regressing techniques that encourage fantasizing, stand the risk of confusing fact for fiction.

It is important to point out that repressed memories can in fact be real. If they can be corroborated with a third party or if the individual has always had some recollection of them (regular access strengthens the association of the elements of a given memory), they are more likely to be true and can support claims of sexual abuse. However, long-term memories can be affected by the aging of the brain, providing an incomplete picture of what really happened. Alzheimer's is this phenomenon in the extreme, but more subtle versions of memory loss could be a function of more subtle changes to the brain. If a memory is not accessed for a very long time, it is unlikely that one will be able to access it as fully as the last time it was accessed. If such a memory is brought forth, it can be hungry to fill in the gaps and any outside influence, be it the media, a therapist, or even a television show, can taint the accuracy of that memory (1).

Hypnosis as a method of retrieving accurate information is not a proven technique, despite its popularity among some therapists. Under controlled circumstances, researchers found that subjects accessing memory through hypnosis do get more questions correct than subjects not under hypnosis. However, they also found that those same subjects get more wrong ones as well (6). This suggests simply that under hypnosis, individuals answer with more confidence in their memory than those who are not under hypnosis. This might explain why hypnosis can have a perverse effect on the memories of people who think they might have been abused as children. Increasing confidence in one's memory does absolutely no good if that confidence is not proportional to an increase in accuracy.

A case in point of this is Dr. Loftus's "shopping mall" experiment, in which she tries to get people to remember a time that they were lost in a shopping mall as a child, when if fact they were not. Specifically, she asks them about how they cried, an elderly woman comforted them, and then they were reunited them with their family. This false story is included with three other true stories for each subject, with information corroborated by close relatives of the subjects who confirmed that individual was never lost in a shopping mall as a child. The subjects knew the stories were written by relatives, but not told that the shopping mall one was false. The true events were remembered by 68% of the test group, while 25% claimed remembering the false one (8). 25% is a significant figure of subjects who remember in detail an event that never happened.

As those 25% tried to remember, the new information was taken in by the hippocampus and amygdala. It remained short-term memory for a little while and the confidence with which the subjects remembered the false story stayed at zero. They denied remembering it for the first interview and some warmed up to it during the second interview. However, it was not until the third interview that 25% reported remembering it with great confidence. For these subjects, the information was stored in the long-term memory and combined with information from other true experiences to make the story real for them. The detail they described in remembering the story was false for the shopping mall context, but much of it was true in the context of other childhood stories. This shows how implantation of a false memory can occur when there is a level of suggestibility involved and how the brain uses other information to make it real to the individual remembering.

If there are gaps in memory, the brain has a way of filling in the missing details (9). Just as a third of individuals in Loftus's experiment recall seeing Bugs Bunny at Disneyland, brains tend to create the fullest picture possible given the information available. However, this information is not always accurate. Hypnosis and other regression techniques can in fact be responsible for the implantation of false memories if therapists are not sensitive to the high suggestibility of persons in a hypnotic state. Presuppositions of sexual abuse can lead an individual's brain to filling in the missing data using whatever tools are available, including images from fantasy or dreams. Encouragement to let one's brain run wild with fantasy can be a mistake if that fantasy can blur the lines between real memories and fantasized ones (6).

In starting this work, I myself was skeptical of those who claim that false memories can easily be implanted in individuals. I had full faith that if a memory was uncovered during therapy, it was in fact "uncovered" and not fabricated. After all, why would those who devote their lives to helping people deal with emotional trauma damage someone's life by implanting a false memory? I've discovered that it's not the intention of therapists to implant such memories. Rather, it is a devotion to the psychiatric methods they have come to know that blinds them to the effect regression techniques can have on memories.

The mind seems to have more control over our experience of reality than anyone would wish to admit. Knowing that memories can easily be confused, twisted, or fabricated by something that is as seemingly harmless as a fantasy is frightening to anyone who believes in free will. While there is more about the mind that needs to be explored, it is important for individuals confronted with the possibility of being a victim of child abuse to remain skeptical of methods of regression that carry presuppositions with it. There seems to be a line to walk in this approach to regression therapy: while it may be necessary for a certain word or image to trigger a memory that has been suppressed, it is dangerous to suggest too much. Understanding how the brain interprets information and draws upon a number of sources when it permits you to remember is a vital step in avoiding drastic conclusions based upon false memories.

References

1) Loftus, Elizabeth & Ketcham, Katherine. The Myth of Repressed Memory. New York: St. Martin's Press, 1994. pp 79-89.

2) Kingshill Research Center, a basic site for the anatomy of memory.

3) Massachusetts Institute of Technology, a lecture by a professor on the history of inquiry into memory.

4) Magill University, a more in depth resource on the function of memory in the brain.

5) Freud, Sigmund. Civilization and Its Discontents. New York: Norton, 1961. pp 51-52

6) Ofshe, Richard & Watters, Ethan. Making Monsters. New York: Scribners, 1994. pp 142-43

7) CNN, Feb 16, 2003, an article on the implanting of false memories.

8) Scientific American, September 1997, an article by Elizabeth Loftus on false memory.

9) Dr. Craig Stark, Johns Hopkins University, NPR interview, February 4, 2005.

10) PBS interactive anatomy of the brain



Full Name:  Sofya Safro
Username:  ssafro@brynmawr.edu
Title:  Shyness vs. Social Phobia: Where do we draw the line?
Date:  2005-04-12 00:43:02
Message Id:  14486
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


I could tell right away that my new friend was a very shy person. Everyone knows what a shy person is like: quiet, hates to be in the limelight, nervous about being in front of groups, etc. However, I didn't realize just how shy my new friend was. It took a long time to get to know her and get her to open up to me, and since then we have actually had many conversations about her shyness. I am an extremely outgoing and loud person, so her timidity, quietness, and embarrassment over so many things just never made sense to me. I attempt all the time to get her to speak up, to be less self-conscious and scared about talking to people, even to me. She says that she can tell when she is "being stupid" (in her words), meaning when she feels like she should be saying something instead of being so quiet and awkward. Yet no matter what, she worries too much about talking to other people and how she is being perceived. With her permission and blessing, she has allowed me to use her as a base for my research, and wants me to come up with some solutions for overcoming her shyness.
So just what is it that makes my darling friend so unbelievably, painfully shy? Was her shyness caused by her genes; because her father is also shy? Is it because of the way she was brought up; in the social environment she was in? Can she change herself and become outgoing if she tries, and what kind of therapy could help her? She has gone to therapy for her shyness when she was younger, because it used to be worse; she could barely speak in front of strangers. She told me that she chose to come to Bryn Mawr College because it was all girls and she would feel more comfortable speaking in classes and that at this point in her life she is the most outgoing she has ever been. To me, she is still the shyest person I have EVER met. However, her mother insisted on accompanying her to therapy, even though my friend wanted to go alone. I thought this was interesting and made me wonder: just how much can parents affect their child by controlling them, or keeping them cut off from the world in attempt to keep them safe? What about children that still become shy even when their parents encourage them to be independent and outgoing? Also, because my friend is shy to the point where it interferes with her life, what are the differences between just being a little shy and quiet, and having chronic shyness or social phobia?
Shyness affects many people, especially teenagers, where they are faced with critical pressures from peers to "fit in" and be liked. It is normal for men and women to feel nervous or uncomfortable when speaking to strangers or being placed in situations where they are not familiar with their surroundings. Shyness is defined as uneasiness and inhibition in interpersonal situations that interferes with pursuing one's interpersonal or professional goals. It entails extreme self focus and obsession with one's reactions, thoughts, and interactions. Shyness is a reaction that can occur in just some of the following situations: when being confronted by authority, interacting with the opposite sex or same sex, meeting strangers, and speaking in front of groups. Shyness can even be a prominent reaction when interacting with friends. There are even physical behaviors attached with shyness, such as averting one's gaze, sweating or shaking, and feeling queasy (1). The consequences of chronic shyness are abundant. It can stem from of form deep psychological issues, such as low self-esteem, anticipation of social failure, dysfunctions in personal and romantic lives, health problems, and the list goes on (2).
Research with babies has proven that differences between "social" infants and "shy" ones are detectable within the first two months after birth. About 20% of newborns may be quiet and reserved in new situations. Shy children show more brain wave movement in the right frontal lobe, unlike standard reactive children who show more left side activity. Introverted people may be genetically predisposed since it has been found that parents who are inhibited have reported more cases of their own children being shy as well. However, I wonder about the word introvert. Introvert means a person who likes to be alone, which could be totally different from a shy person, who does not necessarily like to be alone but is very withdrawn around others. Something else that was very interesting was that blonde hair, blue eyes, and pale skin are more common in families of shy children as well as the most shy college undergraduates! (3) Alas, my friend has dark hair and brown eyes, while I am blonde, blue-eyed, and pale.
Social fear and shyness has been found in the action of the amygdale and hippocampus. The amygdale seems to be connected to distress, while the hypothalamus transmits nervousness to the body. The hypothalamus, in other words, causes those symptoms of shyness (shaking, sweating). Shy people have come, through contextual conditioning, to view general situations like parties, as "fear cues" (3). Biology may play a large role in creating shy people.
Where is the line between being shy and having a social anxiety disorder drawn? Research has shown that in fact only approximately 3% actually have a disorder and treatment is beyond their will power. So how can my friend become less shy? Prescription drugs that were first developed to treat depression or anxiety have been known to reduce the warning signs of social phobia in many victims. The newest and most used are SSRIs, or selective serotonin reuptake inhibitors, which were first developed to treat depression. Paroxetine (Paxil), sertraline (Zoloft) and venlafaxine (Effexor) are the three most effective prescriptions. Psychotherapy is also an effective treatment which may help patients face their shyness and increase their social skills in order to help them feel at ease around people (4).
How big of a factor does society play in bringing up a person to be extremely shy? Self-concept is an interesting term in relation to shyness. It is the opinions an individual holds about themselves, and about the ways others and society regards them. Shy people are constantly assessing other people's opinions: "what does this person think of me? Of what I just said? Did they take it the wrong way? Do they hate me?" My friend has told me that it is not just that she wants everyone to like her, but that she does not want anyone to hate her. This kind of worry may very well play a role in a shy person's analyzing everything they do or say (5).
My friend is by no means a socially awkward or terrible, introverted weirdo. She is very sweet, caring, loves to go out and have fun. We are trying to work on her having the self-confidence to stand up and speak up. Hopefully, with encouragement and a little pushing, my friend may overcome her extreme shyness. Perhaps she is learning something at college, where among women, she feels a little safer for now. Worries about the future, about job interviews are constantly on her mind; will she risk losing a job because she is too shy to really shine on the interview by sending out confident vibes and speaking loudly and affirmatively? Hopefully, the answer will be no.


Bibliography

1. http://www.shyness.com/
2. http://www.sciencedaily.com/releases/2003/12/031217073905.htm

3. http://web4health.info/en/answers/anx-inhib-shyness.htm

4. http://www.sanbenito.k12.tx.us/Hot%20News/030705.html

5. http://www.social-anxiety-shyness-info.com/art/self-concept.htm



Full Name:  Elizabeth Diamond
Username:  ediamond@brynmawr.edu
Title:  A Neurobiological Basis for Art, or How our Mistakes Demonstrate the Workings of the Visual Brain
Date:  2005-04-12 01:02:44
Message Id:  14487
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


A work of art, as we all know from looking at certain modern oeuvres, doesn’t have to accurately reflect life and realism as we know it. But when artists attempt to capture reality in a painting, for example, with a series of lights, shadows, and reflections, a viewer may initially interpret the 2D drawing as a realistic 3D representation of the world. However, examining our perceptions of the devices used in 2D works of art reveals that we aren’t as good at identifying realism as we may have thought. Artists routinely employ illusions that most are not even aware of in order to create a composition that approximates reality while maintaining an artistic deception. What then, are these illusions, and why does it seem so easy to “fool” the brain when looking at such pieces of artwork?

First of all, the illusions evident in many works of art should not be thought of as “optical illusions” in the sense of images that are meant to trick the brain into seeing something that isn’t there. Instead, they should be thought of as what Patrick Cavanagh calls a “simplified physics” employed by our brains to interpret 2D works of art into a 3D image in our minds (1). This simplification of physics is not necessarily a hindrance in our understanding of how the visual brain works, but it should be regarded as a new tool of neuroscience in discovering how humans see the world around them. More importantly, it raises new questions about the nature of art: is it merely an attempt to copy the real world around us or is it a more ambiguous, emotional interpretation of our environment?

Let’s begin with a review on what we learned about ambiguous images and lateral inhibition during the lectures to understand the basis for many of the illusions discussed later in this paper. When looking at a contrast border between two different colors, the retinal output neurons are activated by both the light and dark areas of the light reflected from the image, as in the black and white checkerboard. Where the white and black squares touch, there is a contrast border, where the brightness of each field changes quickly. Signals from neurons picking up on the light from the contrast border are affected, or inhibited, by the signals from adjacent neurons. Approaching the darker border, neurons decrease in signal firing because of inhibition from the brighter border. Approaching the light border, signals increase because they are not completely inhibited by the darker areas (6). This physiology of the neurons in the retina explains several odd phenomena involving the changes in brightness along a contrast border, including the Hermann grid illusion, in which gray spots are seen in the spaces between the black squares of a grid (2). The lateral inhibition phenomenon is also related to the “filling in” of patterns and colors that the blind-spot misses where the retina meets the optic nerve (6).

So how does this relate to how we see artwork? Lateral inhibition is one reason why the brain interprets the stimuli from shadows and contrast borders as recognizable shapes and objects rather than an ambiguous collection of light and dark areas (2). As with the blind spot phenomenon, we tend to fill in fill in the gaps of ambiguous figures to form them into something that we can recognize based on our understanding of the real world. Humans are remarkably good at interpreting ambiguous collections of light and shadow into recognizable forms, particularly faces and bodies. Looking at only an ambiguous dark-red area on a green background in Figure 3 of the Nature article, our brains take the ambiguous stimuli and interpret it as the shadows of a man’s face (1). The lighter red on the same green background is not as readily interpreted as a face, or at least a “shadow cue” that makes the image appear much more 3D and realistic. Figure 9 of the Nature article shows two dancers made up of only isolated patches of color, arranged in such a way to suggest two dancing figures (1). We do not look at such a drawing and see a collection of separate parts, but rather we attempt to put the shapes together to form a whole.

Other conventions and techniques of artists to convey certain illusions also reveal more about how we perceive images in artâ€"perhaps erroneously. One of the simplest and most common conventions in art is the line or contour drawing, usually the first step to creating any 2D piece of art. To create a drawing that is recognizable and discernable from the background of the piece, lines are used to trace a subject and separate it from the rest of the image. But in real life, we do not discern objects by a contour line separating the object from the “ground” or background, but rather our brains interpret brightness and shadow contrasts to allow us to recognize the separation between object and background (3).

The illusion of transparency also requires a form of lines crossing at certain points to create the impression of two layers passing in front of each other. These points where lines cross are called X-junctions, critical points at which the lines intersect to create the appearance of a transparent glass, for example. The X-junctions are all that are needed to create this illusion; in Figure 6 of the Nature article, the painting of the water glass is realistically transparent because of the multiple X-junctions that make up the rim and meniscus of the liquid, but there is no refractory distortion of the lemon slice within the glass as it would appear in real life (1). Yet this does nothing to diminish the illusion of a clear glass, once again indicating the simplified physics of our minds: even when not paying attention to impossible physics, we still perceive these images as transparent, or 3-dimensional, or whatever the illusion would lead us to see. Artwork, then, should not be looked at as simply an attempt to imitate life, for as we have seen with the illusions of contour lines, shadows and light, 2D paintings are not always true to life. Art is the subjective interpretation of the artist of how an object should look while still giving it credence of reality, like the illusion of X-junctions that approach, but do not match, transparency.

Other notable “mistakes” in artwork are not limited to the Renaissance pieces discussed earlier in the Nature article pointing out the inconsistent light and impossible shadows. Through personal observation, so many works of classic art do not follow the normal physics of lighting, yet these “errors” do nothing to detract from the overall perception or even of the piece as a whole. To use an example of one of my personal favorites, I cite Figure 1, a 19th century painting by William Bouguereau called Le Ravissement de Psyche; web-hosted by me (4). In this composition, the light is coming in from two different directions at once, both from behind the two figures as per the sunlight filtering behind them, but also from the front, as if both figures were being lit in a studio setting. This would be fine if the background lighting was consistent with the front lighting, but in the particular setting given, with mountains and a horizon, the figures would normally be in greater shadow if lighted only by the sunlight from behind. This sort of irregularity, however, is not immediately noticeable to the viewer, whose eyes are first attracted to the principal subject of the painting (the well-lit figures) and ignores the impossible lighting in lieu of contemplating the emotions that the painting conveys.

So what are the final implications of studying these “mistakes” and art’s effect on the viewer? Expanding on the previously-mentioned idea of ambiguity, we turn to Impressionism, a style of art that relies on blurred suggestions and patterns that resolve themselves into recognizable shapes and figures. Interestingly, researchers have found certain neural connections in the amygdala and superior colliculus of the brain that respond more strongly to blurred or indistinct images, resulting in stronger emotional responses. For example, more areas of the amygdala are activated when looking at a blurry image of a fearful face, providing strong and quick fear-related emotions (5). The images of Impressionism work in much the same fashion; emotional centers of the brain respond more strongly to indistinct images. Therefore, is artwork simply a reaction to certain visual cues that activate the emotional brain centers? Given all that we know about the brain and consciousness, and after examining the strange ways in which our brains can be “fooled” into believing something is real when it isn’t, I am inclined to agree. Creating artwork is a largely subjective process, and examining the myriad of ways in which art differs from (or imitates) real life can reveal much about the workings of the visual and creative brain.


References

1)Nature, 17 March: The Artist as Neuroscientist by Patrick Cavanagh, the starting point for my paper, provides many visual examples of artistic mistakes and how this relates to neurobiology.

2)The Psychology Papers, an interesting, if simplified, page about optical illusions and ambiguous images.

3)Picture Recognition in Animals and Humans (full article provided in PDF format) by Dalila Bovet and Jacques Vauclair, a very detailed paper about how humans and animals are both able to percieve pictoral images of real objects.

4)Figure 1, Le Ravissement de Psyche by William Bourguereau, simply an image that illustrates the subtle effects of impossible lighting in a painting. Uploaded to my own webhost.

5)Distinct spatial frequency sensitivities for processing faces and emotional expressions, by Patrik Vuilleumier et al., a paper describing the neural connections in the brain's emotional centers that respond most strongly to indistinct or fuzzed-out images.

6)Lateral Inhibition: documents from Serendip, a page from Serendip that clearly explains the process and implications of lateral inhibition in the retina's photoreceptors.



Full Name:  Amanda Davis
Username:  adavis@brynmawr.edu
Title:  Seeing With Our Brains
Date:  2005-04-12 01:09:26
Message Id:  14488
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


It's become clear to me that humans' primary sight organ is our brain. Our retina receives light being reflected from the world around us and transmits information to the brain, but it's up to the brain to interpret that information so we can see. Different parts of the brain see different aspects of the world. There is no "one picture" in the brain. Different kinds of blindness illustrate this. A person with color blindness, which is not due to retinal damage, may have damage to one area of the brain and a person with face blindness would have damage to a different area of the brain. To understand how these different types of blindness affect one's world, one must understand how the brain acts as a sight organ. Additionally, knowing how to see is not innate, one must learn how to decipher the visual world.

How could a man who has seen color all his life suddenly lose all color vision if there was no damage to his retinas? A man named Jonathon I. became achromatically sighted at the age of sixty-five (1). Mr. I. still had all of his cones and they were still transmitting signals to his brain (1). Why then, did he not perceive color? It is because he suffered brain damage (1). He was in a car accident, but it was not clear whether the accident had caused the damage or a minor stroke had caused the damage and the accident (1). An area of Mr. I's brain known as V4 had been damaged (1). The V4 area receives signals from another area termed V1 which responds to wavelength, but not to color (1). Mr. I. could indeed discriminate wavelength – he was shown a color in white light, and then filtered through short-, medium-, and long-wavelength light (1). What he could not discriminate in the white light, he could when it was filtered through different wavelength light (1). But because of the damage, his brain could not translate those signals into color (1). He reported his world as being distorted, even dirty (1). It was not like a color television, which he actually found pleasant (1). This is because he was receiving the information from his cones, which is relayed to V1, then to V4 (1). But Mr. I. was receiving the raw data from V1, which could be described as a "prechromatic sensation" (1). Mr. I. was a painter, and for about a year after the accident, he reported that he still "knew" which colors were right and what was beautiful (1). But after that he became unsure, he had less of a concern with color, and he no longer mourned its loss (1). This is probably because without the input, he forgot color all together; he no longer understood it (1).

Mr. I's experience shows that color is created by the brain. Wavelength is a part of reality, color is not. To think that my brain, as I look outside and see all the colors of the world is almost instantaneously interpreting the wavelengths being reflected from all objects as color is a completely new idea. I had previously known that in the dark I see in shades of grey, but I had thought that I just could not see the true color of objects in darkened environments. For example, if I was in my kitchen without the lights on at night and looked at an apple, I knew it was red even though it looked grey. I thought I knew that in reality it was really red; I just could not perceive its redness in the dark. Now I know that the wavelength the apple reflects in the darkened room changes, thus its "true" color also changes, and my perception of its color also changes.

Far different from colorblindness, there is face-blindness, in which the face is unrecognizable. Recognizing people by their faces is something I imagine most people take for granted, I certainly do. The face does not stand out as a separate unit from the body as normally sighted individuals see it. I was surprised to learn that visual information of faces is sent to the left temporal lobe, while the visual patterns of the rest of the human body are sent to the right side of the brain (2). These messages are split and sent to the different parts of the brain by a "traffic cop" of sorts (2). All incoming sensory goes through the thalamus, so that is the "traffic cop." If the thalamus could send the "face signals" to the same area on the right side of the brain where the rest of the visual patterns for a human go, a face-blind person could be "cured" somewhat (2). The only problem with this is that faces would be as important as hands, shoulders or arms to recognition (2). A face-blind person would, however be able to "see" faces (2). There are several sources of face-blindness (2). One can be born face-blind, or face-blindness can come from damage to the area of the brain that recognizes faces (2). Those born face-blind develop other ways to recognize those around them (2). They learn to recognize people they've seen many times by other visual signals (2). Those who become face-blind cannot recognize any faces, even those of people they've seen frequently, like family members (2).

One thing that is not clear on Bill Choisser's face-blind website is how a face-blind person actually sees a face. Understandably, a face-blind individual would not be able to describe how s/he sees faces in terms a normally sighted person would understand because they have different experiences from birth. I imagine, from what Choisser did describe that faces might look something like a blur.

Another type of selective blindness is motion blindness. This is the absence of the ability to see objects move through space (3). The human retina does not actually detect motion (3). The retina of a frog, however, responds only to movement (3). The more basal the animal, the smarter its retina is (3). The brains of humans and other primates take the job of deciphering the visual world (3). Motion is analyzed by a very specific neural pathway in humans (3). A normally sighted individual's brain gives the perception of motion even when there is none (3). An example of this is a movie, which is a series of still images strung together very quickly so our brain "sees" movement (3). A patient in Munich named Gisela Leibold is unable to make the fusion to see movement – she sees life in a series of still images (3). A part of the visual cortex, called middle temporal area or V5, is not sensitive to color or form, but to movement (4). V5 is directly connected to V1 and both have a similar structure of cells that detect the direction of movement (4). V5 cells do not respond to form or color, but will detect a moving object more quickly if its background's color contrasts with its own color (5). An object moving in the opposite direction of its background will cause the V5 cells to fire more rapidly, and conversely, if the object is moving in the same direction, they will fire more slowly (5). Thus the V5 cells are very good at detecting movement especially if there is contrast in the surrounding environment of the moving object (5). Monkey's whose brains were being stimulated as if they were seeing "up" movement while they were being shown down movement on a screen simultaneously reported seeing only "up" movement (5). This shows that the brain gives the experience of "seeing," not the eyes.

The reverse of these previous conditions, but possibly not any less disabling, is the regaining of sight after forty-five years of almost-complete blindness. Blinded by a triple illness as a child, Virgil had been diagnosed with retinitis pigmentosa, which causes the retina to deteriorate (1). Virgil had thick cataracts also, which a doctor he met later in life thought might be the primary cause of his blindness (1). Virgil had surgery to have the cataracts removed, and he could see, kind of (1). He did not have retinitis pigmentosa, but he did have patchy areas on his retinas that were not functional, but his overall vision was about 20/80 (1). When the bandages were removed from the eye on which surgery was first performed, he could not make sense of what he saw (1). He saw light, movement and color as a blur (1). He realized what a face must be when he heard his surgeon say "Well?" because he knew voices came from faces (1). I wonder if the way Virgil saw faces initially is how face-blind people see them. Sacks does not write further on Virgil's perception of faces. Virgil could recognize letters because in the school for the blind he attended, they felt the alphabet, and even read words that were raised English letters (1). He translated this tactile knowledge to visual cues (1). From the moment we are born, we learn how to see our visual world and what different visual patterns mean. Virgil had no idea about distances because he had not had experience to learn that smaller objects are usually farther away(1). He found walking without his cane "scary" and "confusing" because he had an uncertain judgment of space and distance (1). He could not discriminate his dog from his cat unless he touched them (1). He saw a nose, or a paw, but could not put the different parts together to see a whole animal (1). Virgil had not had the visual experiences to teach him the basic rules sighted people take for granted for how we decipher the messages our retinas send out brain. Virgil enjoyed seeing movement and colors (1).

Seeing movement and color was something Virgil did not have to learn. His brain was wired, so to speak, to see those aspects of the world. This is an interesting contrast to those who were colorblind and motion-blind. It seems that the brain is wired to see different parts of the world in different ways. Recognition of faces goes to one area, the production of color to another, the experience of motion to yet another area of the brain. But one must learn how to see. Perhaps Virgil's experience, and the experience of normally sighted infants is like learning the techniques of drawing, such as overlapping gives the appearance that one object is in front of another, but in three dimensions. I know I can't see without eyes, or without functional retinas. But with functional retinas, damage to certain areas of the brain can affect vision profoundly. Our brains truly are our sight organ. Eyes are just light-receivers.


References

1) Sacks, Oliver. An Anthropologist on Mars. New York: Alfred A. Knopf, 1995. pg 1–41, 108–152.

2)Face Blind by Bill Choisser, Chapter 3: Physical Causes of Face Blindness.

3)"How We See Things that Move: The Strange Symptoms of Blindness to Motion", Montgomery, Geoffrey. Howard Hughes Medical Institute.

4)"How We See Things that Move: A Hot Spot in the Brain's Motion Pathway", Montgomery, Geoffrey. Howard Hughes Medical Institute.

5) "How We See Things that Move: Integrating Information About Movement", Montgomery, Geoffrey. Howard Hughes Medical Institute.



Full Name:  Sae RomLily Yoon
Username:  syoon@brynmawr.edu
Title:  Williams Syndrome: A Blessing and a Curse
Date:  2005-04-12 01:18:23
Message Id:  14489
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Williams Syndrome: A Blessing and a Curse


You are at the park, and a child comes running up to you. You have never met her before, but she displays a familiar friendliness as if she's known you all her life. She's only three years old, but she has an amazing way with words that adds to her remarkable sociability skills and engaging personality. It's not obvious at first, but when you take a closer look at her, you notice distinctive physical traits. When you look into her eyes, she has a star-shaped iris with full periorbital surroundings. Aside from her eyes, she has a full nasal tip and flattened nasal bridge, a wide mouth with full lips and cheeks, a long indentation in the midline of her upper lip, and a small jaw. This child has Williams Syndrome.

People with Williams Syndrome function in the mild range of mental retardation, and they possess IQs averaging about 60.(1) They have a distinctive neuropsychological profile that includes strengths in face perception, affective attunement, short-term auditory memory and select aspects of language, along with weaknesses in visuospatial, motor, visuomotor integration, and arithmetic skills.(1) It is hypothesized that the diverse brain regions and its variations account for different functions within larger networks provide the physiological bases for the specific strengths and weaknesses found in Williams Syndrome. Their display of strengths and weaknesses of uneven cognitive profile and atypical parts of specific areas of the brain is one of the reasons that make the study of Williams Syndrome so interesting for me.

Williams Syndrome is caused by a small genetic deletion on the long arm of chromosome 7, encompassing approximately 25 genes.(2) This deletion codes for four genes that are highly expressed in the brain, FZD9, STXIA, LIMK1, and CYLN2. In addition, the whole brain volume is about fifteen percent smaller than normal, but the superior temporal gyrus, an area that encompasses primary auditory cortex, is of approximately normal volume.(1) Preliminary structural MRI evidence suggests an exaggerated leftward asymmetry of the planum temporal gyrus.(1)

As mentioned briefly before, people with Williams Syndrome possess a heightened interest in music and preserved language abilities. The language of individuals with Williams Syndrome sometimes seems precocious in their use of unusual words and conversational flourishes. (3) These strengths may be due to their neurological traits of the brain structure. Although it is smaller as a whole, a small study using auditory event-related potential found increased amplitude of early endogenous components suggesting hyperexcitability of the primary auditory cortex.(1) And it might be their alterations of the function in this area of the brain that may explain the rate of hyperacusis and language/music perceptual processes. Also, the planum temporale has been linked to hemispheric dominance for language. In musicians with perfect pitch, there appears to be even more pronounced leftward asymmetry of this region, like that of a person with Williams Syndrome.(1)

Despite these strengths, they also have profound visuospatial weaknesses. They have difficulties visualizing the spatial relationships between objects, their distances and overall configuration. They have particular weaknesses in dealing with numerical concepts, spatial cognition and in abstract reasoning.(3) In the mid-1990's, these deficits of visuospatial abilities was linked to the deletion of L1MK1, one of the four brain-expressed genes. However, further studies have shown that deletions involving this gene still displayed an intact spatial ability.(1) This goes to show that there may not be one easy answer to explain a certain deficit or even a strength. It might just be specific combinations.

The functional segregation of visual processes in the brain is split by visual domain into a dorsal stream that connects the occipital cortices and the parietal love and a ventral stream of information flow from the occipital to the temporal cortices.(1) Although this disorder causes spatial deficits, it seems to play a positive role in face perception and recognition. The fusiform gyrus, a region on the underside of the temporal lobes, seems to have a specific role in face perception. Specifically, the presence of the anatomical connection between the fusiform gyrus and limbic areas of the brain may be responsible for many emotional processes that function for face perception.(1)
There may also be a connection with high face perception and social-cognitive skills. It is believed that being able to have keen face perception and understanding the emotional states of others through facial cues may be closely tied to social-cognitive skills and the ability to form and maintain social relationships.(1) This hypothesis is supported by a study with autistic people, who display a lack of interest in social relationships, seem to fail to engage the fusiform gyrus during face perception tasks.(1) While there is no activation of this region for autistic people, individuals with Williams Syndrome seem to have normal use of the fusiform gyrus for face perception. In other words, levels of fusiform gyrus activation can be related to levels of social relatedness. If this is true, in normal brains, can we account for personality differences in sociability to the way our brains, specifically the fusiform gyrus, reacts? And can we say generalize this hypothesis to say that people who are keen at face perception and recognition have higher sociability skills?

This concept of connecting the fusiform gyrus to social relatedness may not work for normal brains and personality traits. In terms of brain studies, it was found that face recognition in healthy adults was associated with scalp voltage waveforms are predominantly localized to the right hemisphere. In contrast, ERP's in adolescents and adults with Williams Syndrome were found to be distributed across both hemispheres and did not distinguish between human faces, monkey faces, and cars.(3) In normal brains, the cortical specialization for face processing observed in normal adults is achieved through gradual experience-driven specialization of an initially more general-purpose visuo-spatial processing system. However, in Williams Syndrome patients, genetic effects during brain development generate initial cortical structures with different neurocomputational biases which yield an overall processing that is poorer but have circuits with greater potential to process isolated features than configurations.(3)
There have been numerous tests to better understand the ways in which individuals with Williams Syndrome display certain weaknesses and strengths, especially in recognizing faces. There seems to be increasing evidence, however, that the ways in which people with this disorder process incoming stimuli may be atypical compared to that of a healthy adult. Then does that mean that it is possible to be good at certain tasks when using abnormal processing mechanisms? This first peek through the window of the mind and brain progression of an individual with Williams Syndrome has revealed that nothing is simple or direct.

1)Journal of the American Academy of Child &Adolescent Psychiatry

2)Stanford Psychiatry:Neuroimaging Laboratory

3)Williams Syndrome: Fractionations all the way down?



Full Name:  Bridget Dolphin
Username:  bdolphin@brynmawr.edu
Title:  My Brother's Corruption
Date:  2005-04-12 01:57:24
Message Id:  14490
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


I don't have a great memory at all. I couldn't even share my "first memory" because my mental timeline is so screwed up I don't know the order in which my recollections occurred. Despite this inaccuracy, I do know that there was never a time during which I was not trying to rebel. I lied regularly to my parents and my friends. I told ridiculous stories to teachers and my friends' parents. I did a lot of things I wasn't supposed to and often made decisions that weren't mine to make. I would kick boys at school, for no reason other than I thought it comical. I don't remember this in the least, but my cousins often show me their scars from my "biting stage" that apparently lasted between the time I got my first tooth and my fifth birthday.

Despite the terror I caused, my parents had another child when I was four and a half. Even then I thought they were brave. Although I tried to coach him to be as rotten as I was, my brother might have been the perfect child. This is not completely unexpected; often second-born children behave and display characteristics that are the exact opposite of the eldest child (4). Sometimes he did misbehave, but he handled it so differently than I did. Of course, I don't recall a lot of specific instances, but I remember watching open-mouthed when he admitted doing something bad the first time he was asked. One time I snuck a box of razor blades out of my dad's toolbox and I was horrified when my mom didn't believe that a saw had come out of the wall and sliced my finger. My brother just gave in. It blew my mind. We would start verbal fights for various stupid reasons, and I was always the first one to make it physical. This lasted for a long time.

One day my parents caught my brother in a lie. I have no idea what it was about, probably something to do with school. He became less consistent in telling my parents where he was going and he started to talk back. I wish I could recall more specifically when I noticed these differences, but I think it happened when he was in fourth or fifth grade. I take full responsibility. I remember a few specific instances of corruption I wish I could just erase from both our memories. I caught him sneaking a piece of candy at church once. I blackmailed him for a while for his allowance and lectured him on how lucky he was that I didn't rat him out. Then I told my mom and he wasn't allowed sweets for a week. I went through a period in middle school during which I decided I wanted my brother's most prominent emotion toward me to be fear, so I yelled at him every chance I got and hit him a lot. I guess it is good I realized that was just dumb after about a day, but it must have been quite shocking to be on the receiving end. The only time I remember him hitting me first I made fun of him for probably about ten minutes. I'm recalling more now... he didn't just hit me, he hit me with a golf club. I deserved it.

This seems like a lot of semi-pointless narration, but I think it's important to preface the main idea of this paper well. My question is this: If I corrupted my little brother, who is responsible for corrupting me? I think I know the reason is internal; I was bad from the beginning. I can't help but wonder, though, if my brother would still be an angel if he had had a different sibling, or if he had been born first. Maybe we both have the "bad kid" gene, his just emerged later in life. Or maybe I ruined him.

There is a lot of research available about birth order. For each article that asserts characteristics of birth order, there are five which contradict it. It is not an exact science, unfortunately, but there are some consistencies. For example, many published articles affirm that first-borns crave the parental attention they once received without competition and they are likely to be more out-going than later-born children. They also tend to do better on standardized tests and be more creative (5). The younger children of any size family are likely to be dreamers and inwardly expressive. Charles Darwin was the fourth of six children and was often scolded by his father and older siblings for being too involved with studying plants and animals. He grew into one of the most rebellious scientific minds in history. Some researchers dare to claim that had he been born earlier in the order, he would not have been so inspired to question theory as he did (6).

From my research, I can conclude that there is any combination of two sources which contributed to my corruption. It was in my genes from birth or I was merely acting out as any normal only and then first-born child would. There are a variety of other contributors to a child's behavior, I understand, but I believe these to be the most key.

The "gene craze" began in the 1990's, when suddenly it was vogue to believe that every aspect of an individual's personality could be traced to his genes. Scientists raced to be the first to find that not only were certain diseases and disorders genetic (alcoholism, depression, etc.), but also every facet of behavior, such as friendliness or criminality (6). Since then the concept seems to have retreated out of the news, though research continues in several prominent institutions. The craze is pretty much over, but someday before I die maybe a doctor will tell me that being a pain when I was a child is imprinted somewhere in my brain and could have been predicted from birth, with no hope of avoiding it.

Even if the "bad kid" genes do exist and are part of my make-up, they cannot be accountable entirely for my behavior. Genes are simply a basis for personality, altered by environment (3). A large part of the environment aspect has to do with birth order, because it constitutes who grows up around a person, and how he or she is affected by them. Before my brother came, I was an only child, so I was probably craving a lot of attention. Sources also state that only children are very strong-willed and enjoy being in control. Slightly understated in my case, I believe, but it is possibly a component of my bad behavior. When I became the eldest of two children, it was hard for me to let go of these tendencies (1), (2), (4), (5), (7). One article asserts that "only children are first-borns in triplicate" (2). So after my brother was born, I became one-third of the terror I was before, but acquired a variety of other delightful attributes including intense competitiveness and unstoppable determination, which was sometimes directed toward accomplishing something constructive (1).

Maybe I wasn't the worst kid who ever lived. I am intentionally not asking my parents for input on the subject. It is comforting to me to know now that according to both genetic and birth order research, it was probably more for internal and environmental reasons that I acted the way I did and less a conscious choice (3). I also learned that I might not be entirely responsible for ruining my little brother. If his behavior pattern is not drawn out in his brain, perhaps it could have been predicted by the intellectuals who study birth order and youngest children. Thomas Hayden would agree, I think. He says "younger siblings often grow into defiant adults" (6). Substitute "pre-teens" for "adults" and the case is solved. Often the youngest child is used to parents and older siblings carrying most of the responsibility; perhaps it took the kid longer to catch on that he could get away with being unaccountable than it takes most last-borns (6). It has also been affirmed that parents tend to be increasingly lenient toward each child born after the first. He might have realized that, too. A final theory is that having been born years later, my brother was in a position figuratively far behind mine. It is natural for him to feel like he needs to catch up, as younger siblings often do (1). Since I wasn't writing novels or running marathons, maybe he presumed the best way to "catch up" was to be as nefarious as I was.

Now not only have I proved that my behavior can be explained by genes and birth order, but so can my brothers. It probably wasn't as much my fault that he went through a difficult phase as I originally imagined. What a relief. Despite the fact that these theories can't really be proved or disproved exactly, at least probably not in my lifetime, I think there has been enough examining done to be confident with the given assertions.


WWW Sources

1)Birth order

2)Personality traits linked to birth order

3)My genes made me do it

4)How birth order affects your child's personality

5)Birth category effects on the Gordon personal profile variables

6)A sense of self

7)Birth order patterns



Full Name:  Sarah Sniezek
Username:  ssniezek@brynmawr.edu
Title:  Why does pain differ in Males and Females?
Date:  2005-04-12 02:00:59
Message Id:  14491
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip



My last paper on people with CIPA brought me to another question, why do people experience pain differently? With people who have CIPA, they have a gene defect that inhibits their nerves from feeling pain, but within regular people there are still different "thresholds" for pain. Are these differences in the sensation of pain based on one's mental ability to deal with pain or is it something more? Women usually are more likely to have a lower tolerance for pain than men and I have always thought that it was just the way emotionally handle things, but it seems to be so much more than that. Below I discuss the differences between the pain felt, and seen within the brain by males and females. I would have never thought that different people are more prone to pain, but in recent studies scientists have shown that one's gender, sex hormones and genes can cause them more pain than others.

Through my extensive research I came to the key question, why is pain different in everybody? An article, Gender Differences in Brain Response to Pain, suggests that the brain difference to pain within males and females goes back to more primitive times because the roles of men and women were clearer. The responses of men and women to the same pain stimuli were different. The women's limbic region, the more emotional area, showed more activity than in males. The male's cognitive regions showed more activity than in females. Since the women's limbic region has the most activity when in pain might be a result of women's nurturer instinct which is more emotional. The male's activity within the cognitive region, when in pain, could be a result of their inherent fight-or-flight reaction (1).

This study gave some insight into the differences of pain between men and women, but just was not convincing enough. The next experiment I discuss seems to give me a clearer and more convincing answer to why men and women feel pain differently.

Scientists have recently posted articles that show that gender, sex hormones, and genes play an important part to how one's body and emotions react to pain (2). It is interesting to me that scientists are finally able to understand how the brain functions through monitoring the chemical activity within the brain while one is in pain. This is done by to monitoring the brain using fMRI and position-emission tomography(PET) while one is in pain.

Many studies have been done, one specifically testing controlled pain in men and women while being monitored. Researches at the University of Michigan have been studying the affects of pain on the brain. Their recent studies suggest that mu-opiod receptors and endorphins are crucial to one's ability to feel pain. Scientists have been studying the mu-opioid receptors which are found through out the brain. The mu-opioid receptors are what needs to be activated by endorphins (natural/synthetic) to help relieve pain. If these receptors do not have anything to activate them to bind then they are unable to block pain. With this information the scientists began their study. (2).

The scientists used and injection of salt-water into the masseter muscle to stimulate pain known as temporomandibular joint pain (TMJ). This pain was sustained and did not have much physical and psychological stress on the person. Throughout the whole process the people were monitored through PET and were also asked to rate their pain. 14 men and 14 women were part of this experiment having the same procedure done to them. (2).

The scientists monitored each person's brain through fMRI and position-emission tomography (PET) while they were in pain. The pain was controlled through injections so that the pain would be constant at all times within each subject. The data showed that the women were more likely to be in more physical and emotional pain than men. This was monitored through the PET which showed that men released more endorphins than the women. The women actually had a reduction of endorphin release. Scientists say this is because all the women being tested were on their menstrual cycle which meant that their estrogen levels were low and an able to release endorphins efficiently. (2).

Another study was done showing that women with high estrogen levels dealt with pain much better than women with low estrogen levels. This experiment was done using the same injection of salt-water to the masseter muscle in women during their menstrual cycle. The women where to wear an estrogen patch, which would increase their estrogen levels towards the end of their menstrual cycle so that they could be monitored with an increase in estrogen, but none of the other hormones changed. Their brain's were studied while in constant pain and the amount of endorphins released while women had high energy levels was significant enough that their responses to the pain was more like the men's responses to pain. This suggests that women are more prone to feeling pain than males, but are able to regulate their pain level with hormones. (2).

The findings suggest that women are more likely to have pain during their monthly menstrual cycle or during pregnancy because of the variations of their estrogen levels. The estrogen levels they are unable to block the feeling of pain. regulate the brain's ability to suppress pain. When the estrogen is high, the brain is more capable of releasing endorphins to help reduce the pain. When the estrogen levels are low, like during one's menstrual cycle/ pregnancy, the brain does not release endorphins efficiently to reduce pain. (2).

This study is interesting because it raises a lot of other questions about women and why we are more susceptible to pain. It gives us a grasp on why we might be experiencing more pain than males and how to go about reducing the pain. Women and men have men differences that set them apart. Will there ever be a way to make males and females equal?

References


1)Pain and the brain:
Sex, hormones & genetics affect brain's pain control system, shaping a person's pain perception, U-M research finds
,

2)Gender Differences In Brain Response To Pain,



Full Name:  Leslie Bentz
Username:  lbentz@brynmawr.edu
Title:  A Lack of Inherent Motor Symphonies in Rett Syndrome Sufferers: Is it plausible?
Date:  2005-04-12 02:45:17
Message Id:  14492
Paper Text:
<mytitle> Biology 202, Spring 2005 Second Web Papers On Serendip

As we discussed the idea of inherent motor symphonies or inherent patterns of activity across motor neurons, I questioned what the exception to the rule might be. Surely not everyone could automatically be so adept as to possess such skills from birth. There had to be an example in which the idea of inherent motor skills, or motor skills that simply needed refining was not such a plausible notion. Surely there had to be some infants who were not inherently born with all the needed internal wiring to understand the feat of walking before they even began to crawl. This idea of innateness in regards to motor skills seemed to be a particularly riveting and a questionable assumption that we had taken to be truth. Since discussing the formations of neurons and each person's variability in this setup, it seemed particularly probable that not everyone is equipped with inherent aptitudes towards performing motor skills. This search for a contradiction led me to Rett Syndrome (RS) with its symptoms of apraxia (inability to perform motor functions) and sudden degeneration that afflict its sufferers.

Initially, RS is very indiscernible in patients and it is only in hindsight that many parents remember the first signs of their infant's health problems. Typically signs of the disorder present themselves early in infancy with the first noticeable indicator being a deceleration of head growth between two and four months of age ((2)). Followed by "a period of developmental stagnation" which quickly, or not so quickly in some cases, develops into regression, these children begin to lose purposeful motor skills. A child's nervous system is not the only affected body system; problems with breathing and digestion are also prevalent ((2)).

The cause of this disorder results from a genetic mutation. RS is a disorder that appears solely on X chromosomes. Thus women are the primary carriers of the mutated gene and are the ones most afflicted by its mutation. Since women are equipped with two X chromosome, one of which randomly is inactivated, patients who possess one mutated MECP2 gene can survive. Although possible for males to posses this altered gene, there have been very few documented cases. It is believed that most male fetuses that embody this genetic mutation die while still developing in the womb ((2)).

"The symptoms and severity of RS may depend on both the percentage of activated defective genes and the type of mutation" ((2)). Once symptoms become visible, genetic testing can be used as a means to diagnose this disorder. This form of testing is the primary means for making an accurate diagnosis but strangely, "as many as 20% of females meeting the full clinical criteria for RS may have no identified [gene] mutation" ((2)).

This gene anomaly leads to a number of affected neurological processes. Firstly, the disruption that this mutation encourages influences crucial parts of nervous system development beyond the initial stages ((8)). This primarily has an effect on the proper development of neural pathways and synapses thus disrupting the genetic processes responsible for controlling the specificity of neuronal connections during the early postnatal period ((4)). These genetic abnormalities create chemical discrepancies in the brain. Due to these chemical idiosyncrasies, excitatory synapses are being overworked, which becomes an essential component in understanding the outward symptoms and seizures that RS patients experience.

These problems involve glutamate, the major excitatory neurotransmitter in the brain. Most neurons possess receptors that respond to glutamate. "Glutamate synapses mediate primary senses such as hearing and vision, activate motor acts such as speaking or walking, and play essential roles in learning and memory" ((3)). Thus glutamate stimulates activity in the brain. Levels of glutamate have been found to be exceptionally high in patients between the ages of 2-8 but are well below average in older women with RS ((3)). It is this drop in glutamate that could account for the stagnate or regressive pattern of development that is witnessed in aspects of behavior and intelligence of RS patients.

More specifically in regards to how motor skills are affected, it is essential to look at how RS has been categorized into four stages of motor skill disorder. The first stage involving developmental arrest is typically noted between the ages of 6-18 months. Babies not stricken with RS typically exhibit attempts at walking during this period but for most RS patients this stage of development is never reached. Next a period of rapid deterioration ensues which is characterized by loss of purposeful hand use as well as seizures. This stage can persist until a patient is ten years old. After the age of ten these women classically do not undergo further deterioration but increasing motor problems do persist. Ultimately, "most patients with RS survive into the fifth or sixth decade of life" but continue to experience severe motor skill impairments ((2)).

Although these are the physical outcomes from internal dysfunctions, it is important to note why this disorder is considered neurological. In classic cases "RS is associated with a significant decrease in cerebral cortex size, cerebella atrophy, and a brain weight that is approximately 70-90% of normal" ((2)). Since expansion of the brain ceases shortly after postnatal development it never reaches full maturity. It is this underdevelopment that is to blame for the permanent motor skill inadequacies. Abnormal motor skills are witnessed in a number of physical outputs. Such manifestations can include, but are not limited to seizures, tensed body postures, and loss of willful hand use. Although devastating, the most intriguing problem one may suffer is the inability to walk.

Although not found in all diagnosed cases, some sufferers have "permanent flexion or extension of affected joints in fixed postures" which is similar to the deterioration that stroke victims fall prey to ((8)). In the case of stroke victims it is the I-function, or will of the person, that is no longer responding. Motor neurons are still reacting which leaves the appendage stiff and unresponsive but the person can not purposefully change the position. I question whether it is a similar phenomenon presenting itself in RS patients. There is no evidence that the nervous system is affected beyond certain aspects of the brain. So then what has limited their motor skills?

As symptoms of RS progress, patients find it increasingly difficult to walk and most are ultimately immobilized. Instances have even presented themselves in which patients never began walking. It was these instances which prompted me specifically to question the notion of inherent motor skills. I am now rather skeptical about the idea of innate motor symphonies which are in place at birth. If it is true that infants are born with the inherent knowledge of how to walk and manipulate their appendages; then it is essential to know the exact point during gestation in which this knowledge or process becomes active. It conceptually seems quite probable that this activation of inherent motor symphonies does not occur until late in the gestation period, thus maybe it is possible to be born without such structures in place.

These women are not paralyzed in the traditional sense. The sensory and motor neurons throughout their bodies appear intact, so why is their mobility impaired? Could simply a lack of will or agency account for this physical shortcoming? Could this be a case in which mind over matter can be attributed? Does this prove that the I-function does in fact play a vital role in central pattern generation? If their central pattern generators have ceased reacting or have never possessed this quality from the start; thus maybe the idea of an inherent motor symphony is not plausible for sufferers of this disorder.

Ultimately there are exceptions to every rule and at the time we discussed inherent motor scores we did not discuss this possibility. We took it as truth and possibly "true reality" but maybe our perceptions and understandings of the working of motor symphonies are not complete. I was forced to reevaluate my perceptions of the world and the controlling of behaviors after thinking about the innateness of motor skills at birth. If motor skills are in fact not intrinsically universal for everyone then a huge reevaluation of how behaviors are learned and perceived to manifest themselves is in store. It is purely my own controversial speculation as to whether or not motor symphonies have to be inherent in everyone at birth but it appears to be plausible that at least in the case of RS patients that our hold on truth might not be such a tight grasp.

References


1) Similar Disabilities information
2) Pervasive Developmental Disorder: Rett Syndrome , Joseph H. Schneider, MD
3) Neurobiology of Rett Syndrome , Michael V. Johnston, MD; Brendan Mullaney, BA; Mary E. Blue, PhD
4) Neurobiology of Rett Syndrome: a genetic disorder of synapse development , Michael V. Johnston, Ok-Hee-Jeon, Jonathan Pevsner, Mary E. Blue, SakkuBai Naidu
5) Child and Brain: The Stages of Development , Gerald Gabriel
6) Syndrome Fact Sheet , National Institute of Neurological Disorders and Stroke
7) Our Rett Syndrome Web Site
8) Rett Syndrome Information for Patients and Caregivers , Joy B. Leffler, NASW, AMIA
9) Rett Syndrome , Huda Y Zoghbi, MD


Full Name:  Imran Siddiqui
Username:  isiddiqu@haverford.edu
Title:  The Function of the Effects of Risk Reward on Dopamine
Date:  2005-04-12 02:49:17
Message Id:  14493
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip



In my previous paper I briefly discussed how risk and reward are related to dopamine functions in the brain. In this paper I will delve deeper into this relationship and ultimately try to answer the question: what function does the risk/reward relationship to dopamine have within the every day function of both humans and animals? In doing so, more questions about risk/reward and dopamine will arise, and I well also attempt o discuss those in further detail.

In the previous paper I discussed a study that monitored dopamine levels in monkeys when they were given rewards to certain stimulus(1). The experiment found that when the monkeys were given a reward randomly, that dopamine levels increased. The study concluded that people worked similarly and showed similar increases in dopamine levels when given a random reward. Ultimately, this was one reason why humans enjoy gambling (1). I was very intrigued by the fact that risk reward causes dopamine release, and wondered why this was a necessary characteristic for humans to have. However, before I researched directly toward this question, I first wanted to do further research on the studies like the example above.

A similar study conducted at Concordia University also used monkeys to detect dopamine fluctuations during risk/reward tasks. The monkeys were put in front of a computer screen which displayed different color visuals (2). During the experiments different color visuals would come up, and a reward (drop of syrup) was associated to a particular visual. During the study the scientists preformed three different types of such experiments. In one experiment the monkey would receive the reward every time the monitor showed reward visual. In the second experiment the monkey would not receive any rewards whether or not the monitor showed the reward visual. In the final experiment the monkey was given reward randomly 50% of the time the monitor presented the reward stimulus (2).

The results showed that in the first experiment dopamine levels rose only the first few times the stimulus showed and a reward was given. After the first few times, the monkey became used to the reward. It expected the reward, and the reward was always given. Therefore, the stimulus would no longer have an effect on dopamine levels (2). The second experiment also showed a similar fluctuation in dopamine levels. At first, the monkey would expect to be given a reward after the monitor presented the reward stimulus. However, after the monkey was not given a reward, and continued to not be given a reward, the dopamine levels were no longer effected (2). The final experiment produced some very interesting results. Because the monkey would be rewarded randomly, the dopamine levels rose every time the monitor displayed the reward stimulus. If the monkey received a reward the monkey's dopamine levels would show a strong outburst. However, even before the monkey received the reward, dopamine levels rose in the monkey's brain. The underlying effect of this experiment was a constant increase in dopamine levels (2).

Now that this study has shown evidence to support the notion that risk/reward increases dopamine levels, I wanted to better understand what role does this function play in human's everyday lives? My initial hypothesis was that humans are creators, and in order to create humans must take risks. For example in order to develop an airplane the Wright brothers had to risk their lives by attempting to fly in machines that probably would not fly. However, the Wright brothers continued to attempt to fly, because the reward of creating a better flying machine made the happy (released dopamine). They did not know if a certain prototype would work, or what the results would be, therefore; the anticipation of the result also caused dopamine release. Without these dopamine releases, the Wright brothers would have had no incentive to try and retry to invent a flying machine.

At first this Hypothesis made sense to me, but later I realized that monkeys were used to replace humans in the experiment, and show the same kinds of dopamine release patterns. However, monkeys do not create as humans do. They do not invent. Therefore, there must be a more general use that this function of dopamine takes, and the incentive to create is only a byproduct of this more general functions within humans. I decided to research more into the actual reason for this dopamine function.

One of the major hypothesis that the literature on this subject proposed was that the dopamine response function to risk/reward acts a s learning mechanism (3). One study found that when dopamine increases, attention increases as well. This makes sense if we relate this back to the initial study. When the reward was given randomly the monkey's dopamine level would increase after the monitor displayed the reward stimulus, but before the reward was given (2). In this situation, it is likely that the dopamine increase functioned to increase the monkey's attention. But why would the monkey's attention need to increase?

Sources state that this increase in attention is used to increase the monkey's ability to learn from what is going on around it (3). Mainly, during the random reward phase of the experiment the monkey is trying to find use cognitive reasoning to find a pattern in the way the reward is being given. Once the monkey figures out the pattern, then the dopamine no longer responds to the stimulus or reward (4). This explains why in the first experiment where the monkey received a reward every time the monitor displayed a reward stimulus the monkey did not show dopamine increases. If dopamine does work this way in risk/reward situations, which there is ample evidence to support, then dopamine release in risk/reward situations is used as a learning tool (4).

This type of learning is called reward dependent learning. Dopamine release pushes animals or humans to not only do things that release dopamine, but also figure out patters for when certain things release dopamine and when they do not. This forces the animal or human to learn more about its environment, and what actions within the environment will produce positive results, and what actions won't. In animals specifically this works to improve choices that the animal makes in terms of finding food, shelter, and safety (4). One experiment conducted took one group of normal rats as the control, and one group of rats that had their dopamine release function blocked. Both rats were put in front of levers that they could push down if they walked over. Out of the group of levers one lever, when pressed, would cause the release of a pellet of food to the rat (4). The results of the experiment concluded that the rats with the dopamine blocked took far longer to learn which lever to press than the normal rats. This experiment supports the notion that dopamine release response to rewards is used to increase the learning capability of the animal. In humans, this would work very similarly (4).

However, how can this be related back to my original hypothesis that dopamine persuades humans to create? In fact, research has developed support for the hypothesis that dopamine is related to creativity. Furthermore, dopamine actually plays a role in how motivated a person is to achieve (5). Studies have proven that people who achieve more actually have more natural dopamine release than those who don't (6). But does this relate to the learning aspect of dopamine, or is this a different function? As I explained in my initial hypothesis earlier, I believe that achievement involves risk reward; therefore, achievement does work similarly to reward dependent learning. I feel that humans are intelligent enough to create and achieve; therefore, do so, and learn from it. However, I am still trying to make a more solid connection between reward dependent leaning and human aspirations towards achievement.

In conclusion, the one of the functions of dopamine reactions towards risk and reward is learning. Humans and animals alike use dopamine level increases to increase attention in order to learn what behavior will cause what effects. However, humans unlike animals have the ability to achieve create, and studies have shown a correlation between dopamine levels and achievement. It makes sense to me that achievement and creation is related to risk reward dopamine release. However, it is still unclear to me how achievement relates to reward dependent learning. I strongly feel that they are connected, because there is support to show that they are both results from dopamine level increases form risk/reward, but it is still unclear how. The research on achievement and dopamine is scarce (5), so hopefully there will be more conclusive results that will lead to more insight on the topic.

References


1)Hijacking the Brain Circuits With a Nickel Slot Machine

2)Gambling on Dophamine

3)Discrete Coding of Reward Probability and Uncertainty by Dophamine Neurons

4)Aneural Substrate of Prediction and Reward

5)Creativity and Addiction

6)The plunge of pleasure



Full Name:  Samantha Thomson
Username:  sthomson@haverford.edu
Title:  "Ultimate Reality and a Closer Look at Magnetoreception"
Date:  2005-04-12 05:26:38
Message Id:  14495
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


It's happened to everyone - when pulling into your driveway after a long car ride home you ask yourself, "how did I get here?" Unfortunately this is a wonderful question with a particularly unsettling answer: LUCK. There are endless speculations about reality, infinite testimonies of "unreal" events that contain no roots to the known, or plausible. "There are two levels of reality, said the Dalai Lama, referring to Buddhism's ordinarily perceived reality and the Ultimate Reality, where the mind stills to such a degree that everything appears in its true nature. Nothing is intrinsically real, he said. Things that appear to be real are so because of our perception, which solidifies them."(1)

It has been suggested that there are two qualities to every object: first, the primary quality is used to classify an object as being able to elicit a particular sensation. The secondary quality, however, is one's reaction to an object. For instance, the roads on which I drove to get back home existed because I assumed that one of their primary qualities included providing a direct route back to my house. There is, however, a problem when describing the secondary qualities of the road-if secondary qualities are defined as a particular reaction to an object (color, shape, size, etc.) then in the case of the roads I took on my drive home, do they retain no secondary qualities since I took no notice of my surroundings? (2) Furthermore, humans only have five common ways of interacting with their environments. So, how does one even begin to speculate about reality if we, as humans, lack particular sensory capabilities? Did the route home actually exist that night, or was it just an assumption I made about previous settings I had once experienced? Many animals, in particular species of birds and fish, display common behaviors in response to the Earth's magnetic field. This "sixth-sense" capability that is inaccessible to humans makes one doubt the reality of the world around us as we know it. Suddenly, given the possible existence of an infinite number of signals, the line distinguishing primary qualities from secondary qualities obtained by sensory organs fades into obscurity.

Extensive research has been conducted on the particular migration patterns of birds. Beginning in 1966 Wolfgang and Roswitha Wiltschko in Frankfurt, Germany designed numerous experiments to determine what effect magnetic fields have on particular species of birds. They conducted the experiments by placing the birds in funnel shaped cages surrounded by signal generator coils which produced oscillating magnetic fields. Then they recorded the side to which the birds migrated. The birds tended to assemble on the southern side of the cage during the fall season regardless of where "true south" was positioned (3)(4). The results were insightful and generated even more questions about physiological mechanisms, neurological integration, and the psychological impact this could have on human perception of "Ultimate Reality".

Scientists, to clarify the physical components of magnetoreception, performed follow-up research. Since the Earth produces an extremely weak magnetic field (only 0.5 Gauss), scientists knew that any proposed magnoreceptors must be capable of responding to miniscule fluctuations in exerted torque. Scientists at the University of California Irvine demonstrated through experimentation that the magnetic compass of birds is in fact light dependent. When test birds were exposed to short wavelengths of blue/green light, normal migration occurred; however, when those same birds were exposed to red light, no North-South orientation was observed (5)(6). This experiment along with many others opened new doors to the possibility of an integration of photo and magnetoreception. One necessary component for this hypothetical sensory receptor is a mechanism present in the nervous system which is able to distinguish ambient light from magnetic force fields; such an integrated mechanism is difficult for science to imagine - but then again I did make it home on a route which may not have existed.

Other experimentation was done to test the link between photo and magnoreception. Scientists attached magnets around the heads of pigeons. Results showed that the birds displayed normal migration on sunny days as the sun served as a guide. On cloudy days, however, the birds were unable to orient themselves (7). Though overwhelming evidence suggests that photoreceptors greatly play into magnoreception in birds, scientists knew that light dependence was not universal because other animals (such as Elasmobranches) are able to accurately migrate completely void of light (8).

By using magnetometers to detect materials within organisms that respond to weak magnetic forces, scientists soon discovered a mineral, F304, which they called "magnetite". Magnetite was first discovered within a particular bacterium that oriented itself in line with the North-South poles; it was then discovered in the heads of birds and Elasmobrachs which are all organisms known for their migratory tendencies (9).

Scientists agree that there are three general methods for detecting magnetic fields. One such way is the biogenetic magnetite complex. Though the magnetite complex's characteristics are consistent among a variety of organisms, little headway has been made with regards to understanding its interactions with a still unknown type of sensory organ for example, hairs, ion channels, etc. (8).

Chemical magnetoreception also serves as a method for detection. This process involves the spin states of molecules and a skewing of possible products to one more common outcome. Though it is thought that chemical magnetoreception is involved with photoreception of the retina, scientists are still skeptical of this method since these types of reactions usually require a much stronger magnetic field to produce any significant skewing of products (3)(8).

The last method of magnetoreception, electromagnetic induction, occurs in sensory structures of Elasmobranchs called the "ampullae of Lorenzini". Electroreceptors at the end of these ampullae detect subtle voltage changes in the current (while taking into account the consequence of their own movement through the water) (8). Though direct evidence of electromagnetic induction in Elasmobranches has yet to be found, it is already speculated that this type of system would be impossible for terrestrial organisms. This type of reception is so natural to the Elasmobranchs because they live in highly conductive salt water. For an induction-based system to exist in terrestrial organisms, a freely rotating internal current loop would be required as well as a specialized transduction organ as least several millimeters in diameter. I've always wondered what that hanging ball in the back of my throat did - maybe now I know!

Dr. Granville Dharmawardena of from The University of Colombo suggests that, "Twentieth century transcended science enables us to scientifically confirm that such concepts as impermanence, rebirth, telepathy and selflessness taught by the Buddha are true phenomena of nature which are beyond three spatial dimensions and therefore beyond classical science." (10) I tend to disagree with Dr. Dharmawardena's assumptions about "classical science". If we only experience the phenomena for which we have sensory receptors, then who's to say that what we experience as humans is "Ultimate Reality"? Classical science includes the phenomena of magnetoreception - a completely foreign reality to humans, yet an accepted type of reception among scientists worldwide. If this type of reception has already been revealed, then what other forms of matter are out there that we will never know about due to our poor diversity of accurate perception. So as an ever-evolving classical scientist I can safely say my home is never more than a short ride away.

References


1) Asia Africa Intelligence Wire, Oct. 7, 2002 "Buddhism's Dialogue with Science" Chopra, Swati
2)Trans4mind.com, public opinions on reality
3)University of Illinois at Urbana - Champaign, "The Magnetic Sense of Animals"
4) Ascribe Newswire, May 12, 2004, Wednesday; "Chemical Reaction in Birds Provides Sense of Direction During Migratory Flights; Study Could Help Identify Mechanism of Magnetoreception in Animals, Humans"
5) Nature, Aug. 5, 1993 v364 n6437 p491 (2)
6)University of California Irvine, a research project on integrated reception in birds
7) Highlights for Children, Oct 1999 v54 i10 p24; "The Magnetic Sense"; Myers, Jack.
8)Duke University, a discussion on magnetoreception
9) Journal of Applied Physics, May 1, 2000 v87 i9 p4653-4658; "Structure, Function and Use of the Magnetic Sense in Animals"; Walker, Michael; Diebel, Carol; Green, Colin.
10)"Buddhism and Modern Science, Buddhist opinion by Dr. Dharmawardena



Full Name:  Liz Bitler
Username:  ebitler@haverford.edu
Title:  Dementia and the Implications of Resulting Altered Neurophysiology on the Concepts of Reality and the Self
Date:  2005-04-12 05:29:32
Message Id:  14496
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Currently, over 20 million people are affected by dementia (1). Dementia occurs in individuals when the activity of brain cells is altered and the brain functions differently. Language ability, memory capabilities, visual-spatial perception, emotional behavior or personality, and/or cognitive skills may be altered as a result of dementia (2). Because dementia results in an altered mind state, it is a topic of much interest in the consideration of neurophysiology and brain function in terms of the I-function. That is to say, what is it about the changes in the brain associated with dementia that result in changes in the mind?

Dementia is associated with several different diseases, many of which have both specific and overlapping physiological sources and symptoms. Generally, it can be stated that dementia is caused by altered levels of neurotransmitters (3), damage to tissues from either vascular (2) or metabolic (4) causes, or damage to neural cells from the entanglement of neurons or intracellular lesions (1). The general symptoms associated with dementia include: memory loss, lack of attention, confusion, decrease in problem-solving skills, decreased judgment capabilities, hallucinations, delusions, altered sensation or perception, agnosia, altered sleep patterns, motor system impairment, disorientation, impaired language ability, and personality changes (such as increased irritability, poor temper control, anxiety, depression, self-centeredness, inappropriate mood, inability to function in social or personal situations, decreased ability to care for oneself) (2).

Alzheimer's Disease (AD)

Alzheimer's disease affects approximately 4 million people (5), and nearly 50% of all people over the age of 85 (6). It is the most common disease associated with dementia. There are several sources of AD in the elderly. Recently, it has been found that there is a strong correlation between high cholesterol (due to the apolipoprotein-E4 allele, which results in increased levels of amyloid beta-peptide) and AD (7). One of the neurological changes frequently observed in patients with AD is neuritis plaques, which occur when protein deposits build up on neurons and prevent them from properly functioning, or destroy them completely (8). Plaque on ACh containing nerve cells (which contain the amyloid protein) are particularly damaging to the proper functions of the brain and result in altered levels of ACh, a neurotransmitter, which may then result in altered levels of awareness and subsequent dementia (9). ACh has been linked to the efficiency of interpreting sensory and cognitive information, as well as for sustaining the sensation of experience and awareness (3). Another particularly interesting cause of AD is the presence of abnormal tau genes. The tau gene (FTDP-17) is linked to chromosome 17, and may become filamentous and result in entangled neurons. The entangled neurons then form masses in the brain and prevent normal functioning (1). AD may also be caused by neuronal and synapse loss (3) or other deficits in the cholinergic system (which is discussed in greater detail below.)

Lewy Body Dementia (LBD)

Lewy Body Dementia is the second most frequent cause of dementia. This disease is marked by the presence of Lewy bodies in various regions of the brain (10). Lewy Bodies are abnormal neural structures that result from the deposit of one of three possible proteins: alpha synuclein, parkin and/or ubiquitin (9). Other noted neurological alterations associated with LBD include changes in the basal ganglia (9), which result in a reduction in the number of cholinergic projections to the thalamic reticular nucleus, which then in turn results in a reduction of the potential cholinergic neurotransmission. Decreased ACh activity has also been observed in patients with LBD, and this may be tied in with the decreased function of cholinergic neurotransmission. Specific to LBD is the correlation between hallucinations and decreased cholinergic function, as well as "absence episodes," during which the individual experiences a lowered level of consciousness while awake. (3)

Vascular Dementia

Vascular dementia accounts for 10-20% of all cases of dementia (5). It occurs when there is a loss of brain function as a result of a stroke or a series of small strokes (2). Multi-infarct dementia (MID) is the most common type of vascular dementia. MID is specifically the resulting damage of multiple regions of the brain from a lack of oxygen (11). A stroke takes place when blood flow is disrupted, causing an inefficient amount of blood to be delivered to the brain to sustain neural activity (5). Because MID is caused by strokes, the causes reflect those of strokes, such as smoking, high blood pressure, and diabetes (2).

Parkinson's Disease (PD)

PD is another disease that is marked by dementia. Deficits in cholinergic neurotransmission are largely responsible for the effects of PD. This may occur in one of various manners. There may be a loss of pedunoculopontine cholinergic neurons (3), which equates to a loss of the neurons that produce important neurotransmitters such as dopamine, norephinephrine, or ACh (9). There may also be other problems in the neurotransmission process, such as an inability for the ACh transporting ions to bind to receptor molecules (3). Similarly to some observed patients with AD, there is also a presence of abnormal tau genes in a sizable proportion of patients with PD (1).

Fronto-temporal Dementia (FTD) aka Pick's Disease and Binswanger's Disease

Little is known about either Pick's Disease or Binswanger's Disease other than a few possible causes, which have been identified because of similar observations in patients with other dementia-causing neurological conditions. Among the proposed causes of Pick's disease are the filamentous tau (1) and resulting neuro-fibrillary tangles (9) and also observed atrophy in the frontal and temporal lobes (12). Cardiovascular lesions have been observed in the white matter of Binswanger's Disease patients, and the dementia has been attributed to that particular neural structure damage. Specific dementia symptoms of Binswanger's Disease patients are memory loss, loss of cognitive function, and notable mood changes. (13)

Cholingelic System

The cholingelic system is of much importance to the study of dementia because it is an extensive neurotransmitter system that has been shown to affect conscious awareness. The system consists of projections throughout the central nervous system, particularly in the cortex and the thalamus. (3) Experimentation results show that altering the cholinergic inputs results in an alteration of cognitive function. More importantly for the discussion of dementia, it has been observed that abnormalities in the regulation of such inputs results in an increased likelihood of acquiring attentional dysfunctions. (14)

Discussion of Possible Implications

Dementia results from altered neurology of and individual, and it provides a clear example for the concept that as the neurology of an individual is altered, their perceptions and cognition of the world around them is altered as well. Because one's concept of reality is tailored to their particular experiences and understanding of the world, each person has a different idea of what is "real." However, it is important to note that there are some underlying facts beyond individual different realities. For example, when presented with a painting, two individuals may perceive the same painting very differently. Yet it remains undisputed by any individual with normal neurological functioning that they perceive the painting in front of them, that is to say that they can see it or reach out and touch it (the argument as to whether or not it is really there should be left to Descartes and Kant.) One of the most devastating results of dementia is the loss of the underlying reality. People with dementia may go beyond perceiving a painting differently to not perceiving it at all, or even to perceiving a painting that doesn't exist. When the topic of dementia is brought up among friends and families of those affected, many say that their loved ones are no longer themselves. They may loose their ability to remember names, places, and events, their behavior may change drastically, and their realities may become completely altered from their previous conceptions. If what makes a person unique and an individual is their I-function and their distinct perceptions and cognitions of the world, then dementia has the ability of killing an individual on a level much greater than the physical death due to associated diseases.


References

1)Tau Protein Pathology in Neurodegenerative Diseases, an article from Trends in Neuroscience

2)Dementia, MedlinePlus Medical Encyclopedia Article

3)Acetylcholine in Mind: a Neurotransmitter Correlate of Consciousness?, an article from Trends in Neurosciences

4)Dementia due to Metabolic Causes, MedlinePlus Medical Encyclopedia Article

5)Multi-Infarct Dementia Fact Sheet, Detailed Information about MID

6)Centenarians Who Avoid Dementia, an article from Trends in Neurosciences

7)A Cholesterol Shuttle and Dementia, an article from Trends in Neuroscience

8)Neuropathology of Dementing Disorders, an article from Trends in Neuroscience

9)Dementia Explained: Parkinson Disease Dementia, Lewy Body Dementia, Alzheimer['s] Disease: Are they the Same? Or Different? Does It Matter?, General Information about Diseases associated with Dementia

10)Dementia with Lewy Bodies Information Page, General Information about LBD

11)Multi-infarct Dementia, MedlinePlus Medical Encyclopedia Article

12)Pick's Disease Information Page, General Information about Pick's Disease

13)Binswanger's Disease Information Page, General Information about Binswanger's Disease

14)Abnormal Regulation of Corticopetal Cholinergic Neurons and Impaired Information Processing in Neuropsychiatric Disorders, an article from Trends in Neuroscience



Full Name:  Lauren Dockery
Username:  ldockery@brynmawr.edu
Title:  Changing Areas of the Brain to Combat Dyslexia
Date:  2005-04-12 06:13:35
Message Id:  14499
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Developmental Dyslexia is the most common neurobehavioral disorder in children (2), and refers to a specific reading disability that affects the reading ability of often otherwise developmentally normal individuals (5). This disorder can prove to be very difficult in highly literate modern societies that rely upon the ability to recognize and equate specific sounds of language to a written word. Reading has become an extremely important skill in the process of educating a child, and much of current knowledge is passed on using written language. This poses a large problem for those who cannot recognize or decode the words as they relate to spoken language. Current research suggests that very specific areas of the brain are responsible for the breakdown of brain activity during reading activities. These areas are malleable and with appropriate therapy such as multisensory teaching and/or phonologically mediated reading intervention the brain can be stimulated to activate in a more normal manner thus improving reading skills.

Both genetic and neurodevelopmental factors play a role in the manifestation of key symptoms of dyslexia in children (1). Adults can develop dyslexia as a result of brain injury later in life, however the true disorder of developmental dyslexia stems from an initial disruption in brain function during development. Key symptoms of dyslexia include reversals, elisions or omissions of letters, slow or hesitant reading, and incorrect order of syllables in word or words in a sentence (4). These symptoms stem from an apparent insufficiency in the phonological component of language; the function of sounds within a language. Dyslexic individuals cannot make the innate connection that specific letters or groups of letters relate to individual sounds of spoken language (2). A person with dyslexia can possess a completely normal and well-developed vocabulary and understand the definition of many words; however their brain cannot perform an important step in the process of reading thereby preventing the connection of a written word with a spoken word from their vocabulary bank.

The process of reading contains two important steps in normally functioning readers; decoding and identification (2). The process of decoding involves recognizing individual phonemes in words and connecting them to the spoken sounds that they represent. Once a word has been decoded a normal individual can then identify the word and connect it to its meaning which is stored in a knowledge "bank". In the case of a dyslexic child, a breakdown occurs in the decoding process therefore no connection can be made between the phonemic pieces of words and their corresponding sounds (2). A deficiency in decoding prevents the identification of a word as a recognizable part of stored language. For example, a dyslexic individual can know the meaning of a certain word, however they will not be able to decode that word as it is written and therefore cannot connect the printed word to his or her definition. Many researchers believe that this breakdown occurs because the process of speech and connecting definitions to the sound of language is natural, while reading is a complex process that must be taught (2).

Phonological processing can be found in the left hemisphere posterior brain system, and it is in this area that a disruption of activity can be found during reading. Recent studies have used functional magnetic resonance imaging to measure changes in blood flow to brain and metabolic activity to map brain function and activity patterns during phonological tasks(2). As predicted the patterns and location of brain activity vary among nonimpaired readers and dyslexic individuals. A positive correlation was found to exist between a child's reading skill and the amount of activation in the left occipito-temporal word form area, while a negative correlation was found to exist between the amount of activation and reading skill in the right occipito-temporal word form region (2). In other words, the more activation present in the right occipito-temporal region while reading the more likely it is that a person possesses poor reading skills and is using other areas of their brain to compensate.

Much research has been conducted to determine whether or not reading intervention or therapy can help dyslexics with word recognition and decoding. The effectiveness of the intervention would thereby prove whether or not the language areas responsible for dyslexia are malleable enough to be altered in order to create more normal activity levels for the improvement of reading. Teaching techniques that focus on phonologically based intervention such as multisensory intervention have been found to produce increased reading ability and also changes in the brain corresponding to the improvement. The International Dyslexia Association purports multisensory intervention which uses visual, auditory, and tactile cues to improve the ability of the brain to trigger memories of specific letters or patterns to their assigned sounds (3). This treatment aims to create more connections and activity in the normal areas of the brain associated with reading, thereby increasing recognition ability. Findings show that not only does phonologically based intervention increase reading proficiency it also increases activity in key areas of the brain. Children not only increase this activity during intervention but are able to maintain it after the fact (2). This leads researchers to believe that these areas of the brain are particularly malleable and can be trained to function in a more desirable manner.

References

1) Hynd, George W. "The Dyslexic Brain." Science 263 (1994): 841-842.

2) Shaywitz, Sally E., Bennet Shaywitz. "Dyslexia (Specific Reading Disability)." Society of Biological Psychiatry 2005.

3)The International Dyslexia Association

4)Dyslexia Online

5) Witelson, Sandra F. "Developmental Dyslexia: Two Right Hemispheres and None Left." Science 195 (1977): 309-311.



Full Name:  Christine Lipuma
Username:  clipuma@brynmawr.edu
Title:  It Makes Me Want to Pull My Hair Out!
Date:  2005-04-12 07:49:19
Message Id:  14500
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Compulsive Hair Pulling, or Trichotillomania (TTM) is a disorder in which the sufferer pulls out their hair, for a variety of reasons which the medical community has recently begun exploring more than they had in the past. The hair can be pulled from any area of the body, usually the scalp, but also the face, arms, legs, and pubic area (8). People use their fingers and tweezers to remove the hair. Once the hair is pulled out, the person will often become fascinated with it in other ways, including examining it, collecting multiple hairs, eating the hair, and running the hair along the lips and mouth for oral stimulation (1). As a person who has been dealing with this disorder since the age of six, I have tried various treatments, none of which have worked as of yet.

TTM is considered to be an Obsessive Compulsive Disorder (OCD) spectrum disorder (2). Obsessions are repetitive, often unwanted thoughts, and compulsions are repeated actions used to cure anxiety and other responses caused by the obsessions (2). For example, a particular OCD sufferer might be obsessed with thinking that she left the stove on, and will compulsively check to see if the stove is on in order to resolve the worry. TTM is in the OCD spectrum rather than being an actual OCD because the "obsessive" component is often not present. Certain types of hair pulling rituals do have an obsessive component, and some clinicians consider there disorders as separate from TTM, while others refer to them as variations within TTM. In the hair pulling variation that is considered to be an OCD, the individual thinks that there are certain hairs which are different or bad (1). This is often because the hair is more coarse or curly than the others, and the individual becomes absorbed in thinking about the unique hair and is not satisfied until it is found and removed. In Body Dysmorphic Disorder, the person becomes convinced that some area of their body is abnormal or unsightly, and when this pertains to hair, the person will compulsively try to remove this area of hair. This is similar to Perfectionism, where the person feels that their hair not as it should be, and so will obsessively pull it out. There have been cases where individuals pluck their eyebrows and eyelashes excessively and end up without hair in these areas (1).

The Habit Disorder form of TTM is where the sufferer feels compelled to pull her hair, often in times of stress (1). This can be either conscious or unconscious, but the patient is usually aware that the behavior is irrational. Many researchers believe that the compulsion happens because TTM is a learned behavior. The person responds to anxiety or discomfort by pulling at the hair and then feels comforted. Since hair pulling brings the reward of relaxation, the behavior is repeated (3). The pathway to pulling that is created is a result of processes in the nervous system. In the nervous system, there are nerve cells (neurons) which have the ability to fire when they are stimulated up to a certain point, and this is known as the creation of an action potential. The signal is transmitted from the axon of the first neuron, which is an outgrowth of the neuron that is sending the signal, to a dendrite of the second neuron, which is an outgrowth that receives signals. The first neuron will send a signal to another neuron, creating a neural pathway. Learning theories have shown when pathways are repeated, it becomes easier to use that pathway. This is summarized in Hebb's Principle (1949), which states that "Whenever an axon of cell A is near enough to excite a cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A's efficiency as one of the cells firing B is increased (4)."

Individuals will also pull when the person's activity level is low, such as while reading or watching television (1). Research has shown that when brain activity is low, levels of the neurotransmitter serotonin are also low (5). A neurotransmitter is a chemical that is released by one neuron and transmitted to another neuron or receptor. At times when serotonin levels are low, the brain is working in a partly unconscious state, and so the hair pulling provides a self-stimulation.

The idea that a decrease in serotonin levels can be a trigger for hair pulling leads to the often prescribed type of medication for this disorder, Selective Serotonin Reuptake Inhibitors (SSRIs). Between the two neurons that are participating in a signaling pathway, there is a space called the synapse. The neurotransmitter leaves from the presynaptic terminal and is taken up at the postsynaptic terminal. Serotonin is transmitted to the postsynaptic terminal, to be taken up again by the presynaptic cell. This reuptake can be a problem because serotonin does not stay in the synapse long enough to be recognized by the recipient neuron (6). This will cause there to be low levels of serotonin in the system. SSRIs block the reuptake of serotonin, thereby increasing serotonin levels in the body, which can in turn increase stimulation during low activity times. SSRIs are used to treat TTM, but there are no definitive answers as to why it works. Although the theory about increasing stimulation in times of low activity is feasible, it is important to note that SSRIs are antidepressants. Since hair pulling is often correlated with an increase in stress, it might just be that SSRIs make people feel better so the trigger for hair pulling is taken away (3).

The hair pulling aspect of TTM is not necessarily the most important part of the ritual for many people. The "grooming" aspect can provide a soothing effect, where the individual receives pleasure from hair stroking, twisting, tweaking, etc (1). The idea that grooming oneself or others can be a positive experience is nothing new, of course, since humans and other animals often partake in this. In mice, grooming has been linked to a certain gene by researchers at the University of Utah, whose results were revealed in 2002. They found that by eliminating the homeobox-containing (Hox) gene Hoxb8, the mice were more prone to pulling out their own hair and the hair of neighboring mice (7). They believe that the Hoxb8 regulates hair pulling in mice, and this could also give explanations for TTM in humans with further research. Other evidence that this disorder has a biological basis is that in twin-studies, 95% of twins both suffer from TTM. It also seems to run in families.

It could be that TTM is genetic in the realm of developing it, but the conditioning is a learned behavior. In my experience, the first time I noticed that there are certain hairs which are curlier than others, I remember thinking, "It is fun to play with these hairs, and I should do it more often." At that time, it was more of a conscious game, but by repeating the behavior, it became a habit. The behavior therapy treatment for this disorder tries to first make the patient aware of what triggers the hair pulling and then try other behaviors to take the place of or to counteract hair pulling (3). Awareness often helps the person to know they are doing it, but attempting to unlearn the behavior is often ineffective. One reason for this might be that the alternative behaviors such as sitting on your hands or squeezing a ball do not give the pleasure that the patient's body has correlated with hair pulling. Because of this, training oneself to perform a new behavior is really just an exercise in obtaining the willpower to stop. Another idea is to put a rubber band on your wrist and flick yourself with it every time you attempt to pull you hair. Having tried this recently, I find myself faced with the decision to either hurt myself or do something that I find pleasurable, and I simply don't have the desire to cause myself the immediate pain brought on by the rubber band.

Although many Americans are thought to suffer from TTM, intense research has only begun fairly recently because the disorder was previously considered to be rare (8). This is in part due to the shame that many people experience and the elaborate mechanisms used to hide the problem instead of seeking help (1). Although the reasons for pulling and methods of pulling are unique to each individual, it is important to note that many people suffer from a variety of methods. This can make curing the disorder even more difficult, since the therapies might only work on certain triggers and responses, even though the individual is afflicted by a variety of complications.

References

1) Hair Pulling, a.k.a., Trichotillomania, Useful website for variations and causes of the disorder

2) Obsessive Compulsive Disorder, Website about OCD and the OCD spectrum

3) Trichotillomania, Information about behavior therapy and the learning theory

4) Synaptic Plasticity, Resource for Hebb's Principle of associated learning

5) FAMILY: Are we producing a generation of hyperactive zombies?, Article which discusses the affects of serotonin on levels of stimulation

6) Selective Serotonin Reuptake Inhibitors, Article that explains the structure and functions of SSRIs

7) Gene Prevents Excessive "Grooming" (at least in mice), Article on gene testing for hair pulling in mice

8) What is Trichotillomania?, Resource on a hair pulling study



Full Name:  MK McGovern
Username:  m2mcgove@brynmawr.edu
Title:  The Effects of Exercise on the Brain
Date:  2005-04-12 08:44:14
Message Id:  14502
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Exercise has been touted to do everything from treat depression to improve memory, with the power to cure a host of problems while preventing even more. In particular, exercise leads to the release of certain neurotransmitters in the brain that alleviate pain, both physical and mental. Additionally, it is one of the few ways scientists have found to generate new neurons. Much of the research done in this area has focused on running, but all types of aerobic exercise provide benefits. Although the exact nature of these benefits is still being determined, enough research has been done to provide even skeptics with a motivation to take up exercise. Exercise exerts its effects on the brain through several mechanisms, including neurogenesis, mood enhancement, and endorphin release. This paper not only examines how these mechanisms improve cognitive functioning and elevate mood states, but also proposes potential directions for future research. Furthermore, it provides an explanation for exercise's generally non-habit forming nature, despite effects on the reward centers of the brain that mimic those of highly addictive drugs like morphine.

One of the most exciting changes that exercise causes is neurogenesis, or the creation of new neurons. The new neurons are created in the hippocampus, the center of learning and memory in the brain (1), however the exact mechanism behind this neurogenesis is still being explored. At a cellular level, it is possible that the mild stress generated by exercise stimulates an influx of calcium, which activates transcription factors in existing hippocampus neurons. The transcription factors initiate the expression of the BDNF (Brain-Derived Neurotrophic Factor) gene, creating BDNF proteins that act to promote neurogenesis (17). Thus the generation of BDNF is a protective response to stress, and BDNF acts not only to generate new neurons, but also to protect existing neurons and to promote synaptic plasticity (the efficiency of signal transmission across the synaptic cleft between neurons, generally considered the basis of learning and memory) (1, 3, 17). However, BDNF's effects are more than protective, they are reparative. For example, in a comparison between sedentary and active mice, scientists found that active mice regenerated more sciatic axons post-injury than sedentary mice. This effect was not observed when the active mice were injected with a neurotrophin-blocking agent, indicating that exercise stimulates injured neurons to regenerate axons via neurotrophin-signaling mechanisms (3).

This reparative effect is particularly relevant to humans because the brain starts to lose nerve tissue beginning at age 30. Aerobic exercise reinforces neural connections by increasing the number of dendrite connections between neurons, creating a denser network, which is then better able to process and store information (4). This suggests possible preventative and therapeutic effects for diseases such as Alzheimer's and Parkinson's that progress via the loss of neurons. Indeed, a correlation between lifestyle and Alzheimer's has already been demonstrated (6). In addition, exercise has been shown to decrease the loss of dopamine-containing neurons in mice with Parkinson's (2).

There is a limit to the positive effects of neurotrophic factors, however. Mice bred to overexercise actually showed an inability to learn. A possible cause for this inability is the disruption of cognitive function by a preoccupation with exercise. The overexercising mice had elevated BDNF and neurogenesis, but the levels reached a plateau that did not increase with more exercise (14). This limitation is further illustrated by a study of exercise effects on a group of 60- to 75-year-olds versus a group of 18- to 24-year-olds. Sedentary 60- to 75-year-olds who began aerobic exercise demonstrated an improvement in executive cognitive functions, e.g. planning, scheduling, and working memory, while the group of 18- 24-year-olds did not. Brain-wave analysis showed a 35-millisecond faster brain response time post-exercise versus pre-exercise in the 18- to 24-year-olds. Essentially, less cognitive function was lost in 18- to 24-year-olds than in 60- to 75-year-olds, so there is less room for improvement, and that improvement will be less obvious (4). Apparently it is not possible to exercise to brilliance.

Fortunately, it may be possible to exercise to happiness. It has been shown that physically active people recover from mild depression more quickly, and physical activity is strongly correlated with good mental health as people age (7). Depression is related to low levels of certain neurotransmitters like serotonin and norepinephrine. Exercise increases concentrations of these neurotransmitters by stimulating the sympathetic nervous system (12). In addition, serotonin has a reciprocal relationship with BDNF, i.e. BDNF boosts serotonin production and serotonergic signaling stimulates BDNF expression (17). Since exercise also increases BDNF production directly, there is a reinforcement of the serotonin-BDNF loop, indicating exercise's significant potential as a mood-enhancer.

In fact, a combination of exercise and antidepressants (which increase BDNF via the serotonin-BDNF loop) has been particularly effective in treating depressive behaviors in rats. The BDNF gene can be expressed in multiple forms, and physical activity increases the expression of two forms: one with fast but short antidepressive effects, and one with slow but longer antidepressive effects. By combining exercise with antidepressants (which increase the expression of the long-lasting form), scientists were able to both increase and accelerate the production of BDNF. The rats showed a decrease in depressive behaviors in two days instead of the two weeks experienced by those given antidepressants alone, indicating a potential therapy for depressed patients that produces almost immediate results (13).

There also seems to be a role for neurogenesis in the treatment of depression. Studies show that the hippocampus of depressed women can be up to 15% smaller than normal. In addition, there is a correlation between the decrease in size and the length of the depression. This damage may be reversed by BDNF-stimulated neurogenesis. Interestingly, the time it took for antidepressants to take effect is equal to the time needed to induce neurogenesis (16). All of these facts seem to point back to BDNF as the key chemical underlying exercise's impact on the brain. Perhaps it is not exercise that has the curative power, but rather BDNF, and exercise is only the trigger.

Another factor to consider is endorphins, the chemicals released by the pituitary gland in response to stress or pain. They bind to opioid receptors in neurons, blocking the release of neurotransmitters and thus interfering with the transmission of pain impulses to the brain (12). Exercise stimulates the release of endorphins within approximately 30 minutes from the start of activity. These endorphins tend to minimize the discomfort of exercise and are even associated with a feeling of euphoria. There is some uncertainty around the cause of this euphoria since it's not clear if endorphins are directly responsible for it, or if they just block pain and allow the pleasure associated with neurotransmitters such as serotonin and dopamine to be more apparent (15). If the latter is true, this would indicate a connection to BDNF via the serotonin-BDNF loop. In this case, BDNF is again the underlying chemical providing the benefits of exercise, and endorphins act in a supporting role by blocking pain and reducing the cost associated with acquiring the benefits of exercise. The release of endorphins has an addictive effect, and more exercise is needed to achieve the same level of euphoria over time. In fact, endorphins attach to the same neuron receptors as opiates such as morphine and heroin (12). Yet, exercise is not nearly as addictive as these opiates; it's not even as addictive as milder substances such as nicotine. It seems strange that an activity as beneficial as exercise, with a built-in mechanism for addiction, is so easy to give up. According to some polls, only about 15% of Americans say they exercise regularly (18).

The key to this seeming contradiction may lie in the delayed gratification experienced during exercise. Exercise differs from other addictions in that there is an initial amount of pain to endure before the euphoric payoff. The approximate 30-minute delay in the release of endorphins requires a certain level of fortitude that has not been cultivated by the American culture of video games, 30-second commercials, and various timesaving devices. In addition, exercising is made up of several tasks— putting on correct clothing, deciding on a form of exercise, maintaining adequate hydration, etc. Though each task may be mundane enough to form a habit, putting all the tasks together requires too much attention for exercise to be experienced entirely as a habit, which associates the reward or pleasure of completing a particular task with the first step of that task. In addition, the subconscious brain may use the feeling of fatigue as a regulated, anticipatory response to exercise in order to preserve homeostasis (8), possibly discouraging the continuance of exercise before the addictive euphoria is attained. If future research could find a way to trigger the release of endorphins at the start of physical activity, exercise might become more popular. Another possibility would be research around the synthesis of BDNF. If it really is the underlying chemical for all of exercise's nervous system benefits, then making it safely and readily accessible could allow people to circumvent exercise altogether, at least in terms of the nervous system.

While exercise is attractive in theory, it can often be rather painful in actuality, and the discomfort of exercise is more immediately felt than its benefits. The delayed release of endorphins creates a lapse between the pain and the pleasure elements of physical activity. The next area for research could be finding ways to make the benefits of exercise more apparent while the exercise is actually occurring, thus satisfying the need for instant gratification and tipping the scales in favor of exercise.


References

Note that starred (*) sources are accessible only to Bryn Mawr, Haverford, and Swarthmore students through Tripod and double-starred (**) sources are informational, but not directly cited resources

1) Modie, Jonathan. (2003). "'Good' Chemical, Neurons in Brain Elevated Among Exercise Addicts." OHSU, online.

2) "Exercise protects brain cells affected by Parkinson's." (2004). Medical Research News, online.

3) "Exercise can help brain healing process." (2004). Medical Research News, online.

4) Chaudhry, Laura. (2004). "Brain Workout." South China Morning Post, online.

5) "Controlling Brain Wiring With the Flick of a Chemical Switch." (2005). AScribe Newswire, online.**

6) Kotulak, Ronald. (2005). "Exercise, education found to supercharge genes, reduce Alzheimer's." Chicago Tribune, online.

7) McKimmie, Marnie. (2005). "Walk away from depression." The West Australian (Perth), online.

8) "Exercise fatigue may be part of a response coordinated in the subconscious brain." (2004). Obesity, Fitness & Wellness Week, online.

9) "Keep Your Noggin Fit With Brain Exercise." (2003). Southern Illinois Healthcare, online.**

10) Francis, Lori. "The Biology of Pleasure." online.**

11) "How to Maintain Brain Power." (2005). Help the Aged, online.**

12) "How Does Exercise Affect Our Mood?" online.

13) Russo-Neustadt, A.A., R.C. Beard, Y.M. Huang, and C.W. Cotman. (2000). "Physical Activity and Antidepressant Treatment Potentiate the Expression of Specific Brain-Derived Neurotrophic Factor Transcripts in the Rat Hippocampus." Neuroscience, 101, 305-312.*

14) Rhodes, Justin S., Susan Jeffrey, Isabelle Girard, Gordon S. Mitchell, Henriette van Praag, Theodore Garland, Jr., and Fred H. Gage. (2003). "Exercise Increases Hippocampal Neurogenesis to High Levels but Does Not Improve Spatial Learning in Mice Bred for Increased Voluntary Wheel Running." Behavioral Neuroscience, 117, 1006-1016.*

15) "The Antidepressive Effects of Exercise." online.

16) Sanders, Jenny. "Brain Physiology." online.

17) Mattson, Mark P., Wenzhen Duan, Ruqian Wan, and Zhihong Guo. (2004). "Prophylactic Activation of Neuroprotective Stress Response Pathways by Dietary and Behavioral Manipulations." NeuroRx, 111-116, online.

18) Farley, Tom, and Deborah Cohen. (2001). "Fixing a Fat Nation." Washington Monthly, online.



Full Name:  Ayumi Hosoda
Username:  ahosoda@brynmawr.edu
Title:  sleep and dreams, important?
Date:  2005-04-12 09:16:05
Message Id:  14504
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Sleeping is an essential activity to everyone. Lack of sleep is something many of us go through and we experience the consequences when we go against our will with sleep: extreme sleepiness and tiredness during day. Sleeping is an inevitable everyday activity, but what is so important about this? The most common thing we all experience during sleep is to dream. Dreaming is a very interesting occurrence, because we often cannot recall what we see in our dreams or we are mystified by the random contents in dreams. What is dreaming? Do they symbolize something? This paper is going to explore the function and importance of sleep and dreams as well as their relations to each other.
Sleep is a repeated cycle of a five stage process. The first four stages are called Non REM (Non Rapid eye movement sleep) when brains are typically in a resting stage. Through stage 1 to stage 4, we get into a deeper sleep. Brain activity is generally very low throughout Non REM sleep. Non REM sleep cycle composes about 80 % of our sleep and usually lasts about 90 minutes. After the first four stages, we go through the fifth stage called REM sleep (Rapid eye movement), when many parts of our bodies are the most active. This was discovered by Eugene Aserinsky and Nathaniel Kleitman in University of Chicago in 1953. Some of the physical changes in REM sleep are the increase in heart rate, breathing, blood pressures and brain activity as well as a body paralysis. REM sleep is usually considered a stage people dream (1).
There are two theories on sleep function; the conservation theory and the restoration theory. The conservation theory proposes that we basically need to sleep in order to preserve our energy for our daytime use. When our use of energy amount is considered in terms of the rate of metabolism, slow wave sleep especially the first four stages spends merely 5 to 25 % of the amount we use during day, and slow wave sleep is strongly "associated with conservation of energy" (2). Another theory, the restoration theory, holds two hypotheses, the whole body restoration and the neurological restoration. The whole body restoration hypothesis suggests that sleep functions as a process of "anabolism" with respect to protein as well as a release of more hormones(2). The neurological restoration hypothesizes that brain is the one that needs to sleep. In addition, each stage is responsible for the partial brain restoration and that is why people need to repeat several Non REM and REM sleep cycles throughout the night (2). Some researchers even hypothesize that these two theories might be both correct, and the sleep function is still a myth.
Why do we sleep in the first place? What triggers to fall asleep is not a single source. For example, it has been said that the hypothalamus, located in the center of the brain, collects messages from certain cells and carry the signal to the pineal gland in the brain. This process causes to produce the "hormone melatonin" which helps the body temperature to go down. Also, another example is raphe nuclei, located in the part of the brain which is in charge of "unconscious activity" such as walking and eating, sends an order to nerve impulses to shut down the brain system. Therefore, falling asleep is not merely a single process but a collective event (3).
As it is stated earlier, REM sleep and dreams have a strong connection, because many dreams take place during the REM cycle. Because of the development of technology, many researches can be done by using fMRI and PET these days. MSNBC.com reports that limbic system, strongly associated with emotions, is the most active area of the brain during REM sleep whereas prefrontal cortex which is responsible of logical thinking is the least active area )(4). This is the reason why dreams sometimes lack clarity in contents and seem very random.
Many researchers have been trying to find out the functions and symbols of dreams. Though there are many theories, researchers have not exactly found out the reasons we dream and whether the contents of dreams have directly something to do with our everyday life. The first theory came up by a psychologist, Sigmund Freud. Freud explained that what is in our dream is the "repressed longing": the suppressed thoughts and desires that we are usually unable to express socially (1). Carl Jung also supports Freudian ideas especially the origin of dreams, but except for one important principle. What Jung sees different is that dreams enable us to see ourselves as well as solve our problems (1). The third theory, "activation-synthesis hypothesis", proposed by Allan Hobson and Robert McCarley in 1970's takes a very different view compared to Freud and Jung. They claim that dream consists of random images which are stored as a memory in our head. These random images, dreams, are created by "nerve signals sent out during REM sleep from a small area called the pons" (4).Though there are many theories to solve the representation of dreams, the recently study in 1997 by Mark Solms using fMRI and PET seem to lean toward Freudian theory. Solms studied people with a brain damage, and concluded that the most active place during sleep was the part which controls emotion regardless of the differences in brain damages (4) . Though many researchers including Solm do not necessarily see Freudian ideas as completely valid, they do believe that unconscious thoughts may be projected on our dreams (4) .
REM sleep and dreams are related, but what is important about them? In the study by William Dement at Stanford University School of Medicine, participants were awaken when they were about to go to REM sleep stage, and Dement concluded that many participants had a psychological problem such as anxiety and irritability (1). According to this theory, REM seems like an essential sleep stage for humans. Jerry Siegel, director of UCLA's center for sleep research explains that "REM sleep may have evolved for physiological reasons" considering that Non REM and REM behave like the automatic temperature change which a lot of animals do. Siegel also see dreams as a kind of "epiphenomenon" of a sleep product (4). The importance and function of sleep and dreams are controversial ; some researchers claim that sleep and dreams are essential for health whereas some claim that they were a necessary development for human.
Although there has been many researches and theories on sleep and dreams, we still have not found why we actually sleep and what exactly the importance of this activity. After all, sleeping can be accepted as a fact that we all have to do everyday in our life regardless of the puzzles in reasoning. Because of the technological advancement, our scientific discovery has been much more rapid. Someday, some research might be able to find out the definite answers for sleep and dreams, but until then, the myth of sleep and dreams remains with us.

Web Sources
(1)1)how dreams work page , how stuff works website

(2) 5)tripod system , Bryn Mawr College Library website

(3) 3)what is insomnia page , yahoo health website

(4)/ 4)what dreams are made of page , on msnbc.com website



Full Name:  Kate Matney
Username:  kmatney@brynmawr.edu
Title:  Acupuncture; A Frontier for Investigating Neurobiology and the Interconnectedness of Body Systems
Date:  2005-04-12 09:21:09
Message Id:  14505
Paper Text:
<mytitle> Biology 202, Spring 2005 Second Web Papers On Serendip

An indefinite understanding of how acupuncture works has largely excluded it from mainstream medicine and, more concretely, health insurance coverage. And yet, despite uncertainties surrounding acupuncture's mechanisms, its robust effectiveness has spurred its Western popularity. More and more practitioners and patient are seeking out the benefits of acupuncture. Reservations that it is merely a placebo-driven trend belonging to a new-age-sub-culture are challenged by its employment for animals. In fact, acupuncture for animals is very common in the most competitive arena for animal owners, horse racing (8.) There are many explanations for the mechanisms behind acupuncture's benefits ranging from the traditional discussion of Qi energy to physiological and biochemical understandings of its effects in the nervous system. With regard to its analgesic effects, advancements in neurobiology have humbled Western attitudes that acupuncture works by placebo. However, there are less clear understandings on how acupuncture treats ailments involving more systems than the nervous system and more symptoms than pain. Thus, acupuncture may serve as a jumping board for better investigating how the nervous system interacts with other systems.

Let us first survey the traditional practice and understanding of acupuncture. Procedurally, acupuncture is the scraping and puncturing of specific points believed to constitute the body's energy network, the Meridian system (6.) A large majority of points in the Meridian system target connective tissue planes, a continuous network enveloping all limb muscles, bones and tendons, surrounding all nerves and blood-vessels, and inserting every organ (3.) The predominance of connective tissue stimulation elucidates the integrative system through which acupuncture works and implies anatomical confirmation for its effects throughout the body. However, if acupuncture is just about stimulating the connective tissue to somehow affect its associated systems, why is it necessary to needle precise points? That is, why is needling not equally effective throughout connective tissue?

In fact, needling at precise Meridian points is shown to produce better results than "sham" acupuncture, which needles at non-acupuncture points. Penetration at sham points tends to share effects with Meridian penetration, but to a lesser degree. For example, a study on acupuncture in treating lower back pain caused by degenerative disk disease found acupuncture more effective than sham-acupuncture in reducing pain (1.) Meridian points might be more powerful penetration points because of two factors: the tissue's ability to create resistance with the needle, and the acupoint's proximity to nerve bundles.

A study comparing acupoints to sham points found that needle grasp of the tissue, measured by the resistance in removing the needle from tissue, was 18% greater in Meridian points (3.) The points' high resistance therefore results in a greater perturbation, which in turn produces an augmented mechanical stimulus. To effect nociception this mechanical stimulation must become sensory nerve input thereby translating into neuron signals. This translation from mechanical perturbation to neuron signaling indicates why acupoints are areas of high electrical conductance.

Experimental support for the higher sensitivity of Meridian points rests in their proximity to sensory nerve endings (10.) Researchers have shown that the nervous system and its signalers (neurotransmitters and endogenous substances) respond to needle stimulation and that a collection of nervous system afferent pathways (including anterolateral tract in the spinal cord, the raphne magnus and the dorsal part of the periaqueductal central gray) are affected by needling (4.) Of the 309 Meridian points traditionally used, 152 of them are directly over nerves, while 73 are within 0.5 cm of a nerve (11.) The precise combination of maximized tissue resistance and nerve proximity gives clues as to why puncturing Meridian points greatly accentuates effects more weakly displayed in sham acupuncture.

Meridian points' nearness to nerve endings fits with a principal hypothesis known as the "gate theory," which proposes that needling stimulates sensory nerves to the point of accommodation (10.) Accommodation essentially means that the strong continuous stimulation of needles activate nociceptors so much that the nerve sensitivity re-establishes equilibrium at a higher threshold, causing a desensitization of nerves. Accommodation of an inflamed or pained area could thus reduce or obliterate pain.

Studies started in the late 1970's provide more neuro-chemically based understandings of acupuncture's pain-reducing mechanisms. In 1977 experiments on rats found that the opioid antagonist naloxone, when microinjected into the periaqueductal gray matter and the hypothalamus, blocks the analgesic affect of acupuncture (4.) This not only demonstrated precise neurological sites of acupuncture analgesia, but also precise biochemical mechanisms involved in acupuncture. In addition to nerve accommodation then, acupuncture could be analgesic by stimulating the release of opioid peptides. Opioid peptides perform their analgesic effects by occupation and in turn, inhibition of sensory receptors whose excitation stimulates the release of proinflammatory neuropeptides. This argument was bolstered when research done a decade later showed that opioid peptides have peripheral as well as central nervous system receptors (7.) Like the gate theory, this evidence explained how acupuncture can have effects acting through afferent pathways to the central nervous system.

Perhaps the most interesting revelation in acupuncture analgesia is recent evidence for its upregulation of nitrous oxide (NO.) What was once considered only harmful (2) is now known to have wide ranging physiological functions including blood vessel dilation. Because of this effect NO is found in heart disease medication, as well as the popular impotence drug, Viagra (13.) A 2002 study on rats showed that hindlimb acupoints needling increases nervous system NO by upregulation of its protein synthesizer, neuronal nitric oxide synthase (nNOS.) NO upregulation is found in the gracile nucleus, an area of the brain which receives somatosensory nociceptive afferents from peripheral tissue where needling is executed (4.)

By providing improved scientific tools and models, such as the expanded role of NO, advancements in neurobiology have generated a greater acceptance for acupuncture as an analgesic therapy. However, there is much experimental evidence that beyond analgesia, acupuncture can treat a vast array of ailments. One interesting example is amenorrhoea, or menstruation loss, generally associated with an imbalance of hormones (8.) Preliminary studies show that acupuncture might in fact be more effective in treating amenorrhoea than hormone supplementation (14.) Because of its involvement with the endocrine system, amenorrhoea's response to acupuncture drives questions of how the endocrine and nervous system work together. Research on acupuncture is beginning to answer such questions and pose fare more. For this reason the cutting edge for acupuncture could also be a vanguard for neurophysiology. By understanding how acupuncture monopolizes on the interconnectedness of our bodies (as it must in treating amenorrhoea) acupuncture can guide the investigation of how body systems work together.

References

1) Goname EA, Craig WF, Whtie PF, et al. Percutaneous electrical nerve stimulation for low back pain: a randomized crossover study. JAMA 1999;281:818-823. (http://www.medicalacupuncture.org/aama_marf/journal/Vol11_1/litreview.html)

2) Kibiuk, Lydia. "Nitric Oxide and Brain Damage" Brain Briefings 1999. (http://apu.sfn.org/content/Publications/BrainBriefings/nitric.oxide.html)

3) Langevin, Helene M., Jason A. Yandow. "Relationship of Acupuncture Points and Meridians to Connective Tissue Planes" The Anatomical Record 269:257-265,2002. (http://www.med.uvm.edu/neurology/downloads/Relationshipofacupuncturepointsandmeridianstoconnectivetissueplanes.pdf)

4) Ma, Sheng-Xing. "Neurobiology of Acupuncture: Toward CAM" Oxford University Press February 2004; 1(1)41-47. (http://ecam.oupjournals.org/cgi/content/abstract/1/1/41)

5) Middlekauff, Holly R., Jun Liang Yu, Kakit Hui. "Acupuncture effects on reflex to mental stress in humans" The American Journal of Physiology- Regulatory and Comparative Physiology 280:1462-1468, 2001. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11294769&dopt=Abstract)

6) Shang, Charles. "The Meridian System and the Mechanism of Acupuncture" 1996. (http://the-tree-of-life.com/acupuncture.htm) 7) Stein, Christoph. "Update on Peripheral Opioid Analgesia" European Society of Anesthesiology homepage (http://www.euroanesthesia.org/education/rc_nice/14rc3.html)

8) The American Academy of Acupuncture and Oriental Medicine homepage; amenorrhoea

9) The American Academy of Veterinary Acupuncture's web site

10)Holistic Online.com— Acupuncture

11)Medical Pain Education homepage; "Channels and Acupoints: An overview."

12) The Skeptics Dictionary; Acupuncture.

13)Society of Neuroscience web page; Brain Briefing; Nitric Oxide and Brain Damage.

14)True Star Health Encyclopedia web page; amenorrhoea.




Full Name:  Catherine Barie
Username:  cbarie@brynmawr.edu
Title:  Levels of Awareness and the Damaged Human Brain
Date:  2005-04-12 10:04:16
Message Id:  14507
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


In recent weeks, the Terri Schiavo case has been at the front of national attention, highlighting the moral issues and legal implications accompanying the advancement of science and medicine. With new technologies comes a greater understanding of disease and injury and their physiological effects, and therefore, an increased capacity for care. But, this greater understanding is both a benefit and a curse: what is considered acceptable treatment and what is not? Where is the dividing line? The Terri Schiavo case thrust this dilemma to the forefront, forcing the nation to reach a decision, both medically and legally. During the legal "right-to-life" battle between her parents and her husband, the pivotal question was whether or not there was any possibility for recovery, or whether or not her life should continue to be sustained artificially. Despite the fact that Terri was biologically alive due to respiration and heartbeat, she was, in essence, cognitively dead because there was no discernable cortical activity.

Schiavo was a 41-year-old woman who suffered brain damage when a potassium deficiency caused heart failure, resulting in a cessation of the flow of oxygen-rich blood to the brain (4). This interruption of blood flow caused extensive brain damage, particularly to her cerebral cortex. Following her collapse, Schiavo lapsed into a coma, a state in which she remained for several weeks, until her eyes opened. This is relatively common for coma victims: "...they almost always emerge from this state in two to three weeks, doctors say, when the eyes open spontaneously. What follows is critical for the person's recovery. Those who are lucky, or who have less severe injuries, gradually awaken... The primitive brain stem, which controls sleep-wake cycles as well as reflexes, asserts itself first, as the eyes open. Ideally, areas of the cerebral cortex...soon follow...But in some cases – Ms. Schiavo's was one of them – the cortical areas fail to engage, and the patient's prognosis becomes dire" (1). Thus, the moments that immediately follow awakening from a coma are crucial; if the cerebral cortex "engages," then the patient will likely recover. But, if the cerebrum does not regain its higher functions, the chances of recovery are significantly reduced.

Following her awakening, Schiavo remained in an unchanging state. She was no longer comatose, but she wasn't conscious either. She exhibited signs of a sleep-wake cycle, and alleged response to stimuli. She was in a state of wakefulness, yet, there was no detectable cognitive awareness of events or conditions occurring in the surrounding environment. Doctors determined that she was in a persistent vegetative state (PVS): "Patients in a persistent vegetative state have severe brain damage and are in a state of 'wakefulness without awareness.' ...[They] are usually considered to be unconscious and unaware. They may experience sleep-wake cycles or be in a state of chronic wakefulness" (3). Schiavo's condition is consistent with that of a PVS. Patients in a PVS rarely improve, and so, after attempting numerous costly but nevertheless futile treatments, Terri's husband, Michael Schiavo, petitioned to have her feeding tube removed.

However, Terri's parents felt that she could possibly still recover. They argued that she was not in a PVS, but rather a minimally conscious state. People in minimally conscious states do eventually recover, in what is described as a slow return to consciousness. Individuals in a minimally conscious state show evidence of higher cognitive function. In 1987, a Texas doctor documented one such case: a teenager suffered brain damage during a car crash. She was in a coma for several weeks, and when she opened her eyes after a few weeks, she was initially unresponsive to external stimuli. After about15 months, the nurses caring for her noticed that she obeyed commands to close her eyes and move her leg. She continued to improve over time, and she eventually even learned to answer multiple-choice questions by blinking her eyes. After three years, she was consistently communicating by blinking her eyes (2). Thus, this patient showed evidence of cognitive function; she was able to answer questions and follow commands. Terri Schiavo, on the other hand, demonstrated no detectable cognitive function. While she did appear to smile and respond to a stimulus, it was not in a pattern consistent with being minimally conscious. These reactions were simply the result of the random firing of neurons. This response was not initiated by the I-function.
Moreover, Schiavo could not have been in a minimally conscious state due to the extensive damage of her brain. One neurologist who examined her in 2001, Dr. Ron Cranford, concluded that: "Schiavo's cerebral cortex had been completely destroyed and replaced by cerebrospinal fluid. The upper brain was about 80 percent destroyed, and there was also damage to the lower brain. The only part of the brain that remained intact was the brain stem, which controls involuntary functions such as breathing and heartbeat—allowing Schiavo to survive (with a feeding tube) even though she no longer had any cognitive function" (3). Thus, Schiavo could not have been in a minimally conscious state; the brain damage was much to extensive. Since her cerebrum was destroyed, she was incapable of higher cognitive function. Moreover, an EEG (electroencephalogram) of her brain showed almost no electrical activity, which would be present if her neurons were firing like those of a minimally conscious person (1).Therefore, Schiavo was in a PVS and not a minimally conscious state.

In conclusion, despite the fact that Terri was biologically alive (respiration and heartbeat), she was, in essence, cognitively dead because there was no discernable cognitive activity; she did not really respond to stimuli, and an EEG showed almost no electrical activity in her brain. The only reason why she wasn't labeled as brain dead was due to her functioning brain stem, which kept her heart beating and allowed her to breathe on her own. Why, then, was her case thrust to the forefront of national attention? This case basically illuminated and personified the moral issues that have accompanied advancements in science and medicine. These advancements have allowed or a greater understanding of illness and injury, and therefore contribute to a greater capacity for treatment. Individuals with conditions that were untreatable 100 years ago are now treated – they live much longer, and some even recover fully. But, this presents moral issues: it can be done, but should it be? Religion and medicine now appear to be locked in this struggle about what is or is not right. Basically, medicine and morality are "evolving" at different rates, so that ethics and morals are sometimes in conflict with medicine. Since the Schiavo case basically personified this struggle, it became the center of national attention. Even though a legal was made, some were unhappy with the decision. But, evolution is a slow and difficult process, and there will probably be more cases like this in the future.


References

1)Inside the Injured Brain, Many Kinds of Awareness

2)Coma, or Reduced Level of Awareness?

3)Terri Schiavo

4)Terri Schiavo Has Died



Full Name:  Amy Venditta
Username:  avenditt@brynmawr.edu
Title:  Deos Selplnig Ralely Mtetar? (Does Spelling Really Matter?)
Date:  2005-04-12 10:29:46
Message Id:  14508
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Correct spelling of words is emphasized at an early age and is something with which even highly-educated adults struggle. Supposedly correct spelling is not only necessary for others to understand the written words, but also for you and your own brain to determine what the word is, what it means, and how it sounds. When children learn to read, they are told to sound out each letter as it comes. Therefore, they are told to pay careful attention to the order of the letters and the sound each makes. The brain then recognizes each letter and corresponding sound to create a word. Why is it tehn taht you are slitl albe to raed tihs sntenece, ditsepe the fcat taht the wodrs are not sleelpd crercloty. Ecah wrod cteniuons to csnsoit of its oinargil leetrts, wtih the frsit and the lsat rnemiinag cstannot, and the mdldie lrttees in a roadnm jmeblud oedrr. This inspires the question of whether the brain takes each letter on its own, or recognizes the word as a whole (specific letters in no specific order). (1)

A more interesting question to me that came from this phenomenon is related to the concept of reality. It seems rather obvious that at times, the physical reality is different than what we perceive it as. The physics of color, for example, promotes many examples of the difference between actual reality and our perceived reality. For example, what color do you think results when you mix red and green? My intuition, resulting from a background slightly stronger in art than theatre, tells me that red and green mixed together result in brown. This is true for paint; however, red and green light mixed together makes yellow light. An interesting fact about this color yellow that we see when red and green light is mixed is that it does not have a pure wavelength. (2)

To expand, the color spectrum consists of red, orange, yellow, green, indigo, blue, and violet. Each of these colors has a specific pure wavelength and frequency associated with it. The color magenta, however, does not have a pure wavelength associated with it. This means that the color magenta is not real according to physics, meaning that our brain has made it up. The yellow that we see when we mix red and green light is another color that our brain has made up. Our brain and color receptors are not able to see the wavelengths of red and green at the same time because this is too complicated, so our brain makes up a color similar to yellow that is associated with the jumbled wavelengths of red and green. The reality of red and green light mixed is the wavelengths and frequencies of red and green mixed together. Our perceived reality is the color yellow. (3)

To relate this to our previous conversation concerning spelling, the rleatiy of the wrdos in tihs scnetnee is taht tehy are sellepd itcronerlcy and are meerly jebumld lretets. Our prieeecvd ritaely is a seetnnce taht mkaes ssnee. It seems that in terms of the previous sentences, 'mind of matter' has prevailed. Just as the nervous system is unable to handle all of the wavelengths and frequencies of red and green at the same time, it may also be unable to handle all the jumbled letters at the same time. In the color situation, your brain makes up for you to see the color yellow (4) , while in the word situation, your brain makes up that it can read all of those words. Maybe your brain recognizes the letters and assumes that these letters make up a known word.

It is harder for your brain to 'read' these words when they are words that you do not know, longer words, or words with repeating letters. (1) This may be because your brain tries to recognize a specific word that it knows has the same letters. For example, what word is this?: vdtitnea. Although you may not know, I can recognize it immediately as my last name: venditta.

It is interesting that in order for these jumbled words to be easily read, the first and last letters must be fixed. Ti si irycludsioul ffctildui ot adre a netcseen ni wchih eht isrtf nda tsla etlters era ont fdxei. (It is ridiculously difficult to read a sentence in which the first and last letters are not fixed.) This may be due to the fact that your brain is able to recognize more than one specific word that is similar to the jumble of words. (5)

For example, try and determine this jumbled word: ngdrea. Need a hint? Think about dirt and flowers. The jumbled word must be 'garden'! Wait, now think about the word caution. The jumble word must be 'danger'! This jumbled word, ngdrea, is both 'garden' and 'danger'. Notice how easy it is to read the same word jumbled differently. Dnegar obviously reads 'danger', and grdaen obviously represents the word 'garden'.

It has been known since 1861 that most language and reading skills originate in the left brain. (6) The occipital cortex of the brain is specifically used for processing visual information, such as distinguishing the words, letters, and characteristics of letters. (7) The frontal lobe is responsible for determining the meanings of the words and relating them to what you already know. (8)

Eevn wehn rnaeidg tsehe jlmebud wrdos, yuor biarn is sitll wrikong the smae way it wulod wtih nmraol wdros, jsut a ltilte hdaerr. So basically, our brains are extremely independent, in the sense that they only need small hints in order to figure things out. More specifically, our brains are able to collect information in a multitude of ways. For example, our brains can recognize a word and its meaning even if the letters within the word are jumbled. Like a detective, our brains take many aspects of the word into account and formulate an educated guess as to what the word may be. In thsee cseas, it is anzaimg how sarmt our bainrs rlaely are, and how lttile seilpnlg rlaely mettras.


References

1) "Read the Mixed-up Words", a Physics forum area.

2) Wikipedia, discussion on physics of color.

3) Wikipedia, discussion on the reproduction of color.

4) Wikipedia, discussion on color.

5) "Language and Reading in the Brain", Martha S. Burns, Ph.D

6) "Oh Say Can You Say", The Brain and Language, Neuroscience for kids.

7) "The Brain and Reading", Sebastian Wren, Ph.D

8) "Understanding the Brain and Reading"


Neuro-Optometric Rehabilitation Association Online, discussion on reading problems and traumatic brain injury.

"Words in the Brain; Reading program spurs neural rewrite in kids", Bruce Bower

"Reading in the Brain", discussion of a person who is only able to read number words.



Jumble your own words!



Full Name:  Amy Johnson
Username:  amjohnso@brynmawr.edu
Title:  Seasonal Depression
Date:  2005-04-12 10:52:40
Message Id:  14509
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Seasonal Depression

Amy Johnson

Why is it that on the first nice spring day every student at this school all of a sudden becomes happy-go-lucky and frolics around campus? Throughout the winter months all everywhere I look I see sad faces and unhappy, tired people trudging along the paths. Yet, the sun comes out, and all the students seem to have forgotten their worries. This is explained by seasonal affective disorder, a depression occurring each year at the same time, starting in the fall and winter and ending in the spring. There is also a lesser version of this, known as the "winter blues ((5))."
Some symptoms of SAD are fatigue, increased need for sleep, weight gain, increase in appetite, and a lack of energy. In general, four to six percent of the US population suffers from SAD ((5)).
The occurrence of SAD increases the further from the equator one travels. More specifically, the higher the latitude of a location the more prevalent SAD is. This is most likely true because the higher the latitude the colder, harsher, and darker the winters are. Changes in the availability of sunlight are one of the main triggers of SAD ((1)). For example, only one percent of the population of Florida suffers from SAD, compared to four in Washington, DC, and nearly ten percent in Alaska ((5)). That is a huge difference and lends support to the idea that it is triggered by a change in sunlight exposure.
In addition, of all the people who suffer from SAD, over seventy percent are young women, which explains the change in mood at Bryn Mawr. One theory as to why women are more likely to suffer is because women with small children are more likely to be isolated during the winter months. And, in general women are more likely to suffer from depression than men ((2)). I believe this could be because when something bothers a man it is socially accepted if he takes out his anger through actions, like punching a punching bag. Women on the other hand, tend to hide their emotions, which is why I believe they may be more likely to suffer from depression. And, supposedly decreased exposure to sunlight affects the biological clock that affects mood, sleep, and hormones making women extremely susceptible ((3)).
Another possible reason for SAD is that neurotransmitters may be altered in SAD sufferers. It is thought that exposure to light can fix this. Which is one reason that the treatment for SAD is, along with mood stabilizers, light therapy. Light therapy requires people to sit in front of a white light for a certain time period each day. They do not need to look at the light and can read or eat or do work in the meantime ((5)).
I find the type of person affected by SAD to be quite interesting, especially since I am close to being in the prime range, young and female. Yet, I never feel like I am overly depressed in the winter months. One of my friends told me that once winter begins I am actually happier, most likely because basketball season (my favorite sport to play and watch) starts. This leads to the conclusion that exercise is a key ingredient, I think, to fighting depression.
Two weeks ago people suffering from SAD would have been still hibernating, yet like all the animals that wake up when spring arrives, so did the SAD sufferers. The young women at Bryn Mawr, who if affected, most likely have the less severe "winter blues" could do as my roommate does in the winter and use a desk lamp that emits sunlight so as to lessen her risk.


References

1) Psychology Information Online: Seasonal Affective Disorder. http://www.psychologyinfo.com/depression/sad.htm

2) Seasonal Affective Disorder and Light Therapy. http://www.ncpamd.com/seasonal.htm

3) Seasonal Affective Disorder (SAD). http://www.healthyplace.com/communities/depression/sad.asp

4) Seasonal Depression (SAD). http://www.emedicinehealth.com/articles/10333-1.asp

5) What is Seasonal Depression? http://www.clevelandclinic.org/health/health-info/docs/2300/2361.asp?index=9293



Full Name:  Erin Deterding
Username:  edeterdi@brynmawr.edu
Title:  Alzheimer's Disease
Date:  2005-04-12 12:16:32
Message Id:  14512
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


One of the most common diseases of aging is Alzheimer's disease. This debilitating disease of neuronal degeneration affects about five million Americans, and is one of the most crippling of age-related illnesses (1). With so many elderly people affected, it's important to understand what Alzheimer's is, what causes it, and what is being done to prevent the effects of this seemingly inescapable sickness.

The classic symptoms of Alzheimer's disease all affect cognitive functioning, but range in their severity (2). For example, those exhibiting early signs of Alzheimer's may find themselves with slight memory loss, while those in the advanced stages have trouble with thinking and perception (3). With such debilitating degeneration to cognitive functioning, Alzheimer's is the leading cause of dementia among the elderly (1).

One of the most interesting aspects of Alzheimer's disease is how the brain is changed throughout the course of the disease. While it is still not completely understood, there are a few key abnormalities that are thought to be the cause of Alzheimer's.

The first of these abnormalities occurs in a specific protein called amyloid precursor protein (2). This protein is found spanning cells in the brain, and is usually spliced so that portions remain inside and outside of the cells. If spliced incorrectly, a protein called beta-amyloid can be formed (4). Beta-amyloid is precursor to the characteristic plaque build-up found in the brains of those suffering from Alzheimer's disease (4). These plaques are comprised of a beta-amyloid core surrounded by clumps of dying axons and dendrites (2). Plaques can ultimately cause swelling of axons, making it impossible for information to be conducted from one neuron to the next, thus causing the deficits in cognitive function (5).

One of the first systems to be affected by Alzheimers is the acetylcholinergic system. These neurons are found in subcorticol areas, such as the nucleus basalis found in the basal forebrain, and in the hippocampus and medial septum (6). Because acetylcholine is an important neurotransmitter for learning and memory, it is thought that the loss of such neurons is the cause for early memory loss in Alzheimer's patients (6).

In addition to plaques, another characteristic change in the brains of patients with Alzheimer's are a build up of neurofibrillary tangles. In these tangles, another protein, tau, hyperphosphorylates fibers inside the cells, causing them to become tangled together. The combination of these extracellular plaques and intracellular tangles is thought to be the leading cause of the neuronal death that leads to Alzheimer's disease (2).

While the causes of Alzheimer's are thought to be partly due to environmental aspects, the biological aspect of the disease is becoming better understood. Research indicates that there may be specific genes that can increase the risk of developing Alzheimer's (7). An understanding of how these genes affect the onset of Alzheimer's may help researchers discover a way to slow down or stop the progression of the disease.

Some recent discoveries in the research of Alzheimer's have shed some light on this intricate disease. One such discovery has shown that cannabinoid brain receptors may play a role in decreasing inflammation in the brain caused by Alzheimer's. Patients with the disease have been shown to have decreased functioning of these receptors, indicating that they do not fully benefit from the protective factors of the cannabinoid receptors (8).

In addition, research has shown that the effects of beta-amyloid on the brain can be reversible due to an anti-amyloid antibody. This discovery points to the persistence of beta-amyloid plaques as a cause of the deficits seen with Alzheimers. However, the study also indicates that this persistence may not be permanent (9).

More and more information concerning Alzheimer's disease seems to be discovered everyday; however, there is still no cure (3). It seems that while the research is continually making sense of more complex issues regarding the onset and progression of the disease, there is still much to be learned. For example, what are the implications of interactions between genes and splicing mutation of amyloid precursor protein? Is the splicing error an isolated incident, or do the genes associated with Alzheimer's control for those errors? Another important question is what are all the structures in the brain that are affected by the disease? While ultimate result of Alzheimer's is shrinking of the brain, does that mean that all parts of the brain are directly involved in the disease, or is the entire brain affected as a secondary side effect (2)? These questions may some day be answered, but for now, they remain a mystery.

References

1)Alzheimer's Disease: Understanding Alzheimer's, The Alzheimer's Information Site.

2)Meyer, J.S. and Quenzer, L.F. Psychopharmacology: Drugs, The Brain, and Behavior. Massachusetts: Sinauer Associates, Inc, 2005. 148-149.

3)Treatment, The Alzheimer's Information Site.

4)About Drugs Targeting Beta-amyloid, and the "amyloid hypothesis", Alzheimer's Association Website.

5)Nerve 'Traffic Jam' Marks Early Alzheimer's, The Alzheimer's Information Site.

6)Carlson, N.R. Physiology of Behavior, 7th Edition. Boston: Allyn and Bacon,2001. 448.

7)Doctors Identify Possible New 'Alzheimer's Gene, The Alzheimer's Information Site.

8)Marijuana-like Ingredient Could Slow Alzheimer's, MSN Health & Fitness Website.

9)Antibody Helps Reverse Alzheimer's Nerve Damage, MSN Health and Fitness Website.



Full Name:  Alfredo Sklar
Username:  asklar@haverford.edu
Title:  Obesity: Science and Society
Date:  2005-04-12 13:25:03
Message Id:  14514
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Over the past few years, obesity has become one of science's hot topics. Not a week goes by without hearing about the latest warnings from the top scientific researchers about how an alarming percentage of the population is clinically obese and how things will likely only get worse. Or if not a warning it is controversy and complaints by those being called obese (last month it was professional athletes) about the new measure of testing for obesity: the BMI. However, this obesity buzz is not unfounded. It is estimated that over 300 million people worldwide are considered to be obese, earning it the title of an epidemic (2). And as opposed to popular belief, it is affecting developing countries as well as industrialized countries, sometimes even at a higher rate. It has also been shown that obese people are at a higher risk for cardiovascular disease, hypertension, type II diabetes, and chronic sickness in general (2). But what causes obesity and why have we seen it proliferate to such an extent in resent years? Is it genetics, society, both? By taking a neurobiological perspective and realizing that eating behaviors have some influence on the topic, we would think that at least part of the answer lies in the function of some brain region. But if so, what region? As we shall see, although much information has been gathered, this is still one area of science that requires much research and effort.

In coming up with some reasons as to why an individual might be obese or even just overweight, a lack of will power or a large appetite are often mentioned. Using this as a starting point, if we know what area of the brain is responsible for controlling our appetite throughout the day we can discover a possible cause for obesity. In general, the hypothalamus is thought to be the control center for all homeostatic functioning, including hunger. It is currently believed that the hypothalamus achieves homeostasis by regulating bodily functions to adhere to various set points (3). For our current investigation, we will concern ourselves with the weight set point. What the concept of a weight set point means is that our hypothalamus will adjust for variations in our body weight above or bellow our set point by making us experience either hunger or satiation.

To discover how the hypothalamus is able to accomplish this, researchers preformed a series of brain lesions on different areas of a mouse's hypothalamus. From these experiments, they were able to deduce that the ventromedial hypothalamus is responsible for inhibiting an organism's experience of hunger (3). Damage to this area of the mouse's brain caused it eat whenever food was available regardless of how much it had already eaten. Conversely, when the lateral hypothalamus is damaged, the mouse would not eat and eventually starve itself to death no matter how much food was available (3). This made researchers believe that this portion of the brain was responsible for the hunger response. There are some flaws with this rather simplistic view of appetite and obesity. Firstly, how do we know that this pattern of anatomical responsibility is the same in humans as it is in mice? Teitelbaum provided more evidence against the dual center theory (stated above) in his experiment on a rat's motivation to eat (8). In this study, a normal rat's motivation to eat was compared to that of a rat with a lesion in the ventromedial hypothalamus by having them push on a lever to get food. At the beginning, when they only had to push the lever once or twice to receive food, the rats with the damaged brains show more of a motivation (were quicker to push the lever). But as the experiment progressed and they had to push the lever several more times in order to receive food, sometimes upwards of 200 times, the rats with the brain lesion showed significantly less motivation than the normal rats (8).

Besides there just being neuronal control over appetite exerted by the hypothalamus, there is also an endocrine control system that takes place largely at the same brain regions. In a series of studies conducted less than a decade ago, it was discovered that a relationship, similar to that between the ventromedial and lateral hypothalamus, exists between the hormone leptin and the neuropeptide NPY. Leptin is a hormone that is released by fat cells into the body's circulatory system (1). Once in our blood supply, leptin travels to the hypothalamus where it with two groups of receptor cells known as "anoretic" and "orexigenic". These cells are located in the ventromedial and lateral hypothalamus respectively. When leptin activates the "anoretic" cells, it causes them to release various appetite-suppressing neuropeptides (this is not surprising knowing the role of the ventromedial hypothalamus in appetite control). However, when leptin interacts with the "orexigenic" cells, it inhibits the release of NPY which regulates the hunger response in the lateral hypothalamus (1). It is believed that the ratio of leptin to NPY plays a large role in determining body weight. Normally, when fat levels are high they release a lot of leptin which helps decrease hunger levels. In obese individuals, although concentration of both leptin and NPY are relatively high, the receptors for leptin in the hypothalamus are desensitized, allowing the hunger reflex to go unregulated (4).

Another hormone which is thought to be very much involved with the onset of obesity and especially type II diabetes is insulin. Although it is not yet clear whether high insulin levels cause obesity or what the nature of the relationship between the two is, studies have been able to show that increased insulin levels in the blood can lead to an increased storage of fat in our bodies, hypertension, and atherosclerosis (5). Scientists have also been able to determine the function of insulin in our bodies. In response to an increase in blood glucose levels, the pancreas will release insulin into our circulatory system in order to aid in the absorption of glucose to the inside of the cell from the bloodstream (5). If insulin is not present in normal levels inside the body or if it is not able to function normally, as is the case with type II diabetes, glucose cannot be absorbed by our cells, leading to high blood-glucose levels (5).

Although scientists have had little success in identifying a "fat gene" responsible for weight gain in humans, it is still believed that much of the processes mentioned above have a genetic basis. For example, the rate of the genetic expression of several neuropeptides, such as NPY, is thought to have an effect on weight gain. However, there has been strong evidence supporting the idea that expression of certain genes can indirectly fight against obesity. An experiment preformed by Ron Evans and several members of the Salk Institute showed that the over expression of the PPARS gene in mice resulted in the conversion of fast oxidative muscle fibers to slow-oxidative muscle type (the type formed by regular aerobic exercise) (6). The results also showed that these mice burned more calories at rest than then normal mice, leading the researchers to believe that the expression of these gene helps fight against obesity (6). These finding lead us into a discussion of the social factors that play a role in obesity and its rapid increase to epidemic proportions in our population.

As mentioned in the analysis of the above experiment, the conversion to the slow-oxidative muscle type which helps fight against obesity can be achieved through regular exercise. This brings in a completely non-biological, will-based aspect to the cause and sharp rise in obesity rates: a lack of physical activity. This is what Frank Booth and Darrell Neufer point to as the cause of the obesity epidemic. In there article, they disprove the commonly held notion that the rise in obesity rates is the result a significant increase in our appetite and food consumption by pointing out that our caloric intake has actually decreased from hunter-gatherer times (7). Instead, they blame the cause of the epidemic on the increase of the ratio of caloric intake to expenditure from 3:1 in hunter-gatherer times to 8:1 in the present day (7). This means that we are using up a much smaller amount of the calories we take in daily through physical activity. And as for the cause of this decrease in activity? Booth and Neufer put the blame on such social influences as the Industrial Revolution and computer age (7). They contend that these "advances" in society have nearly eliminated the need for any physical activity in our daily chores such as transportation, agricultural practices, etc. Simply put, because we are doing less, we are gaining more

References

1. 1)How leptin may influence hypothalamus, appetite, and weight,

2. 2)Obesity and overwight,

3. 3)Appetite control system and brain, obesity,

4. 4)Obesity,

5. 5)Insulin, obesity and insulin-resistance syndrome,

6. 6) Evans, Ronald et al. (2004) Regulation of muscle fiber type and running endurance by PPARS. PLoS Biol 2(10):e294

7. 7) Booth- Frank, Neufer- Darrell. Exercise Controls Gene Expression

8. 8)PSY337: The neural control of feeding,



Full Name:  Jasmine Shafagh
Username:  Jshafagh@brynmawr.edu
Title:  The Importance of Engaging in Active Learning
Date:  2005-04-12 13:46:47
Message Id:  14515
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Transitioning to the college educational approach is a difficult task for most freshman to grasp, let alone rising juniors and seniors. As a freshman at Bryn Mawr College, I found it difficult to shift my learning style from the high school method to the more active learning approach that is required and necessary in any college. After reflecting upon the forthcoming completion of my first year here, I have realized that although lecture and classroom times have been drastically decreased since high school, I have learned much more in these past few months than during any time of my high school career. To understand the reason for this peculiar happening, I realized that my learning style has shifted to accommodate the college's educational approach; this year, I have become more of an active learner, whereas in high school, I was more passive. Although I was still an active learner in high school, I believe high schools in general foster the passive learning styles (where teachers write out all the notes that will be on tests so students memorize them), whereas college professors teach in a manner that fosters the implementation of active learning on the part of the students (i.e. lectures are only there to supplement the learning and reading you do or research on your own). So I am curious as to what constitutes active learning and how it plays such a significant role in making education more beneficial and valuable than passive learning methods. I would also like to know what the neurobiological basis for this notion is – and if it even has any validity at all. After all, isn't learning something that is quite subjective according to the individual's personal style? And can one particular learning approach bring about more prevalent changes in the brain that cultivate long-term and better learning?

According to many psychiatrists and education specialists, there are about twelve different theories on how people learn. Among those is active learning, also known as brain-based learning, (the concept that the structure and functions of brains are always existent, and what determines how much we learn or what we learn is the extent to which we actively utilize our brains) (1). Although learning is achieved through a general combination of the twelve processes, fairly recent neurobiological studies accredit active learning with being the most effective method of all. The idea behind active learning is that each individual is born with a brain that functions, and as long as it isn't prohibited from working normally, it can learn based on what the individual wants or on how the individual uses it. For active learning to be most effective, individuals must be in an environment that immerges them into the educational realm, the individuals must be relaxed and must eliminate their fears to be challenged, and the individuals must be able to "internalize information by actively processing it," (1). For example, college students must do the reading, writing, discussing and analyzing themselves (instead of professors giving it to them) so that they engage in higher-order thinking tasks, (3).

An important principal behind active learning is that it must involve both an experience (through the act of doing or observing) and a dialogue (either with the self or with others). Let's examine the dialogue component first. To learn, an individual reflectively thinks about any topic, examining what they think of it, what they were taught to think of it or what they should think about it. In this way, the individual not only thinks about what they are being told, but he/she also examines what it is, if he/she agrees or disagrees with it and if he/she wants to question or test it (7). Dialogue with others also helps us learn because we learn what other people's perspectives are and compare theirs with our own to reach a consensus; others might also help us look at something in a completely different way. Furthermore, the experience portion can be done through doing and observing. Doing is important because an individual gets direct contact and experience with something. Observing is equally as essential because the individual sees a direct action through the hands of someone else (possibly someone experienced who can teach the individual something new!) (4). As Henry David Thoreau once said, "Experiences themselves are educative only if the students actively clarify, internalize, and reflect on them," (2). In addition, research shows that just after two weeks, individuals remember 90 % of what they did, what experiences they had, the discussions they had, and the things they said (all active experiences!) However, they only remember about 20% of what they heard (on television, for example), 10 % of what they read, and 30 % of pictures they saw (all passive exercises) (5). Thus, the actions that condone active learning, such as experiencing something and engaging in dialogues, help us retain more information and become better learners.

So what is the neurobiological basis for the notion that an active learning approach is actually better than a passive one? To understand this, we must first comprehend how learning affects the human brain and its structures. There is an important region of the brain called the neocortex, which contains a full set of nerve cells that were developed at an individual's birth. The dendrites, the receptive branches and extensions of the nerve cells, are responsible for a majority of the postneocortical growth. The significance of the dendrites in the neocortex is that their neural networks are the basis of human intelligence. Dendrites receive and process inputs from other nerves, and based on what that input is, they either create new neural networks or follow the path of pre-existing ones to carry out the output. According to research, these dendrites increase with use and decrease with disuse (9). So, to understand what this means in the larger scheme of things, we must employ the common cliché: "use it or lose it," (referring to the human brain). Because there is no limit to the human's capacities to learn more, neurons are continuing to make new connections on a day to day basis throughout our lifetime (7). So, if we are learning passively, the dendrites won't create enough neural networks for enhanced learning. Active learning (or the continual use of the brain in experimentation and dialogues) on the other hand, is essential because our brains will create new neural networks that override pre-existing ones to help us make more connections, become more intelligent, and process more information (9).

Researchers at Howard Hughes Medical Institute have also undergone experiments to understand how different learning experiences rewire the brain. They have developed a new microscopy method that lets them see how the brains of active mice are rewired as they learn to adapt to different experiences. According to their studies, rewiring the brain (through the dendrites' activities) involves the creation and elimination of synapses (the connections between the neurons). Researchers at Hughes wanted to know whether learning could cultivate the restructuring of brain and neural circuitry. To do this, they used transgenic mice that were created to produce a green fluorescent protein inside the neurons of a specific part of the brain that processed the tactile sensory inputs from their whiskers. Scientists made a two-photon laser scanning microscope (with infrared lasers) to excite the green protein in the neurons through a small glass window put in the mouse's skull. Over time, researchers were able to conclude that through the active learning process, dendrites were constantly created and destroyed on a day to day basis. What's rather interesting is that these scientists changed the traditional view that the formation of synapses ceases as we get older; because of the stable density of these neural networks and synapses, we used to believe there were no new synapses created. However, "the stable density only indicated a balanced rate of birth and death of new synapses," (8). On any particular day, about twenty percent of the networks rearranged themselves in the brain. Researchers were also intrigued by the fact that certain axons and spines persisted for months while others consistently changed.

Hughes researchers also wanted to see how the mice would respond to different types of experiences (some active, some passive). They decided to cut off the mice's whiskers to see how they would respond to external stimuli. Researchers concluded that the mice employed new learning techniques to generate tactile stimulus, and as a result, new synapses were created and destroyed on a daily basis. "This finding indicates that there's a pronounced rewiring of the synaptic circuitry with the formation of new synapses and the elimination of other synapses," (8). However, while these researchers only experimented with tactile sensory changes, there was no evidence that other stimulations, such as visual ones, would create the same amount of neural turnover. In an article published in Nature magazine, researchers from New York School of Medicine found that there was almost no increase in the synaptic cell production in the visual cortex of the mice. According to Karel Svoboda, a researcher at Hughes, the result of these findings may be that the brain responds to different inputs in different ways. This theory supports the argument that active learning is more beneficial than passive learning; the active learning employed in mice through new sensory and tactile experiences created new synapses, while the passive visual experiences in the mice did not. Svoboda and other researchers conclude that certain neural connections are more favorable and are brought about by different types of experiences (8). Thus, from a neurobiological approach, active learning does seem to be more beneficial for enhanced learning.

In conclusion, based on neurobiological understandings and much research, it is evident that active learning has a more beneficial effect than passive learning on individuals because it creates new neural networks and synapses. Although learning is something that is quite subjective and comes from many different methods and external stimuli, it is proven that employing active learning with any particular style or method can increase brain power and intelligence. Active learning brings about many prevalent changes in the brain (such as new neural networks and synapses) that cultivate more and better learning!

The results of this research have helped me make more connections with the lecture material presented in class. Before taking this class, I did not fully grasp the input/output processing of signals in neural networking. I was always curious as to why certain individuals seemed to process things better, or how individuals are able to learn in general. I also wondered if individuals were able to change their brain wiring to consolidate for certain losses. Now I understand how these rewiring networks work, and the power and capability we have to use our brains in the more effective and active manners to be better learners. As professor Grobstein once said in a lecture about learning: "Have experiences, think about them, make up your own stories about them and test those stories" in order to be active learners (6). Indeed, the more we experience and actively think and reflect upon those experiences, the more we will learn and get out of our college and life experiences!

References


1)Funderstanding Website, information about different types of learning.

2) Bickman, Martin. Minding American Education: Reclaiming The Tradition of Active Learning. New York: Teacher's College Press, 2003.

3) National Teaching and Learning Forum , information about active learning.

4) Honolulu Community College Intranet , information about active learning.

5) Online Effective Teaching Workshop , information about active learning.

6)Serendip Website, information on becoming a better learner.

7) New Horizons for Learning - Online Journal , information about mind and Brain Learning Principles.

8) New Horizons for Learning - Online Journal , information on rewiring the brain.

9) New Horizons for Learning - Online Journal , information about the brain: use it or lose it.



Full Name:  Katherine Cheng
Username:  kcheng@haverford.edu
Title:  Confessions of a Teenage Mind
Date:  2005-04-12 13:52:55
Message Id:  14516
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Statistics provided by the National Center for Statistics and Analysis show that though adolescents aged 15-20 year old constitute only 6.4% of 194.3 million licensed drivers in the United States, they are involved in 14% of vehicular accident-related fatalities. In 2003 alone, 7,884 adolescent drivers were involved in fatal crashes, almost half (3,657) of which were caused by the teenage drivers. With such high accident rates, car collisions constitute the number one killer of Americans aged 15-20 years. 1)National Highway Traffic Safety Administration, NHTSA Traffic Facts: 2003. Traditionally, the frequency of adolescent automobile accidents has been attributed to factors such as alcohol intoxication, drowsiness and inexperience. While such explanations remain legitimate concerns, recent scientific research suggests that a significant component of the answer may in fact lie in the very structure of the teenage brain.

Until fairly recently, researchers and medical practitioners presumed that a brain's course of development corresponded to its physical growth, so that by the time the brain grew to 95% of its adult size around age six, it would be impervious to change. Earlier studies had determined that during gestation in the womb and the first 18 months of life, a child's brain undergoes a stage referred to as "overproduction," during which the brain produces an excessive amount of cells and neural connections. Those that are not used are "pruned," or removed, a process that scientists once believed to signal the end of the brain's development. 2)Frontline: Inside the Teen Brain, Interview with neuroscientist Jay Giedd. A longitudinal study conducted by Dr. Judith Rapoport of the National Institute of Mental Health, however, revealed evidence to the contrary. Utilizing MRI (magnetic resonance imaging) to scan the brains of 149 children and adolescents at two year intervals, Rapoport found that brains continue to develop well into adolescence, engaging in a second stage of overproduction characterized by a thickening of the brain's grey matter, the nervous tissue responsible for information processing. 3)National Institute of Mental Health, "Teen Brain: A work in progress." The frontal lobes, a division of the cerebral cortex that manages emotions, personality, impulses and reasoning, undergo particularly significant growth, but by puberty, the second stage of overproduction beings to wane. 4) Talukder, Gargi, "Decision-making is Still a Work in Progress
for Teenagers." From this point on, the grey matter thins as it prunes away cells and synapses that have not been used and trained in the learning of new skills, such as violin playing. 2)Frontline: Inside the Teen Brain, Interview with neuroscientist Jay Giedd.

Significantly, the frontal lobes, which inhibit behavior, are one of the last divisions of the brain to finish developing. Researchers now speculate that this division of the brain responsible for making "executive decisions" based on methodical rational thinking and planning continues to develop throughout a person's early 20's. Thus, while the frontal lobes develop, other parts of the brain help process emotional information normally handled by fully-developed frontal lobes. A 1999 study conducted by Deborah Yurgelun-Todd, Director of Neuro-psychology and Cognitive Neuro-imaging at McLean Hospital in Belmont, Massachusetts, demonstrates as much. Expanding upon the research initiated by Rapoport, Yurgelun-Todd and colleagues showed adult and teenage subjects photographs of various facial expressions and asked them to articulate the illustrated emotion. While they deliberated, Yurgelun-Todd and colleagues employed MRI to scan the subjects' brains. Interestingly, they discovered that half of the teenage subjects incorrectly identified expressions of fear as sadness or shock, while every adult subject correctly identified the emotion of fear. Close inspection of the MRI revealed that the teenage and adult brains employed different parts of the brain to process the emotional information. 5)Frontline: Inside the Teen Brain, Interview with director of neuropsychology and cognitive neuroimaging Deborah Yurgelun-Todd. Compared to the teenagers, the adult subjects experienced heightened activity in their frontal lobes and lesser activity in the amygdale, the part of the brain involved with emotional and 'gut' responses. 4) Talukder, Gargi, "Decision-making is Still a Work in Progress
for Teenagers." This finding implies that teenage brains, by virtue of their immature frontal lobes, are not completely equipped to think through their behaviors and responses using the cognitive reasoning processes matured and available in normal adult brains. Until their frontal lobes have fully developed, adolescents and teenagers react to and interpret the external clues provided by the world through a lens significantly colored by emotional and "gut feeling" reactions, oftentimes relying on impulse rather than cool-headed critical analysis of a situation and potential consequences.

This insight into the developing structure of the teenage brain sheds new light on the sometimes seemingly perplexing and unnecessarily risky behavior of teenagers and adolescents, particularly when placed within the context of driving. Due to frequency of exposure and inevitability of interaction, it is reasonable to speculate that teenagers are frequently involved in car collisions because they misinterpret the behaviors of other drivers as threatening and therefore drive more aggressively, or perhaps some drive more recklessly because they do not fully think through the consequences of their decisions, particularly in high-stress driving conditions. But all of this is not to say that teenagers are incapable of processing situations and weighing the possible positive and negative outcomes of certain behaviors. Instead, it clearly makes evident that well beyond the age societal standards consider the start of adulthood, young brains interpret the world in ways markedly different from brains in which matured frontal lobes privilege rational judgment and behavior control over emotion-inspired impulsivity. This information must be taken into consideration when dealing with teenagers and adolescents in both personal and social capacities and guiding the development of their brains. During this crucial period of development, adolescents and teenagers should be encouraged to participate in the learning of various skills and activities. Never again will grey matter be more abundant, the brain more fruitful and plastic to change and development.

Moreover, these findings give rise to some interesting ethical questions. If scientific research demonstrates that in general, people do not maintain full possession of their cognitive faculties until their mid-twenties, these studies conceivably justify movements to enforce stricter guidelines on the behavior and rights of adolescents and young adults. In 1984, President Ronald Reagan signed into law the national 21 minimum drinking age legislation, since which alcohol-related car collisions and associated fatalities have decreased. 7) Mothers Against Drunk Driving, "On 20th Anniversary Of 21 Minimum Drinking Age Law." At the very least, these recent findings provide scientific evidence verifying the logic of this law, but for proponents of a higher drinking and/or driving age, this research stands as support for tighter regulations of teenage drivers. In the past few years, many states have already passed legislation limiting the use of cellular phones while driving and restricting the number of passengers a teenage driver may have in the car at one time.

Applying the same vein of thinking to a different context, opponents of the military draft can use this research to argue against the recruitment of individuals under the age of 25 for two reasons, the most obvious being that young men and women are simply too cognitively underdeveloped to function well in such situations in which they'd be forced to make decisions that would very literally be matters of life or death. If injuries and fatalities caused by car collisions are already a significant concern, one can only imagine the repercussions of arming a squad of young soldiers with machine guns and the authority to shoot. Secondly, the teenage and young adult years are the most formative of a person's life. If conditioned to observe and participate regularly in the systematic violence of military life, beliefs, norms and behaviors integral to this lifestyle will indubitably become ingrained within the young men and women, possibly replicating themselves once the individual returns to civilian life. Likewise, but to a different effect, the discovery that the brain maintains a significant degree of plasticity throughout adolescence gives rise to the hope that during this crucial period, individuals experience behavioral problems can change relatively easily. Regardless, the research discussed here verified, at the very least, that we have barely grazed the surface of the amazingly complex organ that is the human brain.

Web Sources

1) http://www-nrd.nhtsa.dot.gov/pdf/nrd-30/NCSA/TSF2003/809774.pdf


2) http://www.pbs.org/wgbh/pages/frontline/shows/teenbrain/interviews/giedd.html


3) http://www.nimh.nih.gov/publicat/teenbrain.cfm#readNow


4) http://www.brainconnection.com/topics/?main=news-in-rev/teen-frontal


5) http://www.pbs.org/wgbh/pages/frontline/shows/teenbrain/interviews/todd.html


6) http://www.brainconnection.com/topics/?main=news-in-rev/teen-frontal


7) http://www.madd.org/news/1,1056,8582,00.html




Full Name:  Beverly Burgess
Username:  bburgess@brynmawr.edu
Title:  Language Acquisition and Retention
Date:  2005-04-12 14:11:45
Message Id:  14518
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Language and our ability to communicate through language is something that the vast majority of the human world takes for granted. It has the power to organize, shape and control mankind whether it is used in parent-child interactions, television and radio advertising, or the U.S. Constitution. Our ability to recognize and reproduce the sounds and symbols that represent our thoughts and ideas is crucial to our participation in society. Even though all of the nations of the world do not share the exact same language, it is apparent that humankind does share the ability to harness their creativity and to facilitate their livelihood through the innate capacity for language acquisition. If we consider the neurological factors involved in language learning, we reveal that limitations to language acquisition and retention can and do exist.


The evolution of language has been a subject of debate for many years, but most participants in the discussion can generally agree that the brain as the central location for the formation of language. Three areas in the left hemisphere of the brain participate in the complex activities that comprise language generation and understanding. Wernicke's area is associated with spoken language comprehension, while Broca's area is tied to language production. These two regions are linked by Geschwind's territory which has recently been found to play an important role in the acquisition of language during childhood. Somewhere between the fifth and seventh years of life this area matures, culminating in the development reading and writing skills (3), (4).


The development of language is believed to begin very early in our lives. At birth, we are all endowed with more neurons then we will ever need in our lifetime. As
we age, these neurons undergo a process of connecting and pruning in relation to that which we encounter in our environment via a process often referred to as "neural
Darwinism" (7). Only those synaptic connections that are regularly stimulated and used will remain active while those that are unused will deteriorate. It is for this reason that many believe in the critical period hypothesis of language learning. The critical period hypothesis suggests that the ability to learn a language is restricted to the years before puberty. If language acquisition is attempted after this period has passed, considerable difficulty is encountered due to neurological changes in the brain (2).

For example, there are case studies of children who were neglected or abandoned during the early years of their lives and robbed of the essential human interaction that is critical for the formation of those areas of the brain related to language. One such example is the "savage" or "Wild Boy of Aveyron". The young boy was captured in the winter of 1800 in a small village in the south of France. Estimated to be around 11-12 years old, the boy appeared mysteriously from the woods and was captured by a villager. Devoid of clothing, speech or manners, it was estimated that the boy had been abandoned and spent five or six years surviving alone in the forest. His style of self expression was limited to using facial expressions and a few gestures, skills that were well below what one would expect of a child of his age. In this boy's case, even if he had gained some language ability prior to being abandoned, the isolation that he experienced may have contributed to a process of atrophy of neural connections in his brain. Even with continued effort to bring about the ability to speak and write, the boy failed to ever truly gain a fully functional ability to communicate broad ranging and sophisticated ideas verbally or in writing (6).


In the event that primary language acquisition proceeds normally, second language acquisition may be achieved; however studies suggest that the optimal period
for learning a second language falls within the range of the critical period. A second language may be learned with some difficulty later in life depending on the method of instruction, the similarity between the first and second language, and the individual's general aptitude for learning (8).


After language has been acquired and mastered, there exists the possibility for loss of language skills due to a condition known as aphasia. Aphasia can affect anyone at any age, but most cases are found among the elderly and are typically associated with a stroke. Other possible causes include tumors within or physical injury to the brain with loss of function typically corresponding with damage to one or more of the brain's language regions. Symptoms of this disorder can be mild to severe resulting in the loss of memory of a few words to the inability to construct or comprehend complex sentences. Global aphasia spans all language centers of the brain and affects the entire range of communication skills, while Broca's aphasia affects the frontal lobe and reduces speech output, as the centers for vocabulary retrieval and fluency are affected. Persons with Broca's aphasia retain the ability to understand spoken and written language but tend to drop small words such as "the", "it" and "and" from their communications thus producing sentences with vague meaning. A decline in language understanding occurs in the temporal lobe as Wernicke's aphasia diminishes the comprehension of written and spoken words. These individuals often construct meaningless sentences by making up
words and/or putting words in the wrong order. Currently there is no cure for aphasia; however depending on the level of brain damage, speech therapy may be an effective treatment. In some cases language skills may only be lost for a few hours or days, as in the case of people who suffer very a very mild stroke (1), (5).


It is apparent that nature and nurture both play critical roles in language acquisition and retention. The development of language centers in the brain relies heavily on external stimuli while the retention of language depends on the continuous integrity of brain structure. It is through the study of exceptions to the norm that we may gain a firmer understanding of where and how language forms in our minds.



References

1)Aphasia Fact Sheet, National Aphasia Association website


2) The Impact of Abuse and Neglect on Neurological Development , Feral Children website


3) Brain imaging reveals new language circuits , Medical News Today website


4) Finding Geschwind's Territory , Mind Hacks website


5) Aphasia , National Institute on Deafness and Other Communication Disorders website


6) Shattuk, Roger. The Forbidden Experiment. New York: Farrar Straus Giruox, 1980.


7) Shreeve, James. "Beyond the Brain" National Geographic 2005: 2-31


8) A Critical Period for Second Language Acquisition?, Stanford University website



Full Name:  Emily Trinh
Username:  tmai@brynmawr.edu
Title:  Gene Therapy and Brain Tumor
Date:  2005-04-13 00:41:25
Message Id:  14535
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


According to the American Cancer Society, it is estimated that about 19,000 people will be diagnosed with malignant tumors of the brain or spinal cord during the year 2005 and that approximately 13,000 people will die because of this cancer (1). The 5-year relative survival rate for all people with brain tumor varies with age, type of cancer, and kind of treatment. For instance, the percentage of 45 to 64 year old patients who survive at least 5 years after they were first diagnosed with brain cancer is 16% (2). Since brain cancer is so diverse, and the survival rate for patients is so slim, many new treatments were developed over the years to target this disease. Treatments include performing a biopsy, radiation therapy, chemotherapy, and immunotherapy (1). One exciting new treatment that has a potential for altering the method in which brain tumors are treated is gene therapy. Even though gene therapy has been shown to work on diminishing tumors in rat brain, the medical field is still uncertain whether gene therapy is a feasible treatment for human with brain tumors.

In order to understand how gene therapy is considered a possible treatment for brain tumors, it is important to gain some insight into the causes and the symptoms of this cancer. Brain tumors are produced by abnormal cells that exhibit uncontrolled growth in the brain that can then spread to new places. These abnormal cells can be derived from neurons, glial cells, epithelial cells, or myelin producing cells (3). Genetic factors like abnormal or missing genes are usually the main causes of brain tumors. Patients with brain tumors might have inherited the genetic defect from their parents. They could also have acquired the genetic abnormalities through environment factors such as pollution or ionizing radiation that can affect the genetic materials in the cells.

Tumors that are found in the brain are either classified as benign or malignant. Some of the benign tumors are pituitary adenoma and acoustic neuroma. Benign tumors are non-cancerous because they do not spread or invade surrounding tissues. These tumors, however, can be life-threatening when they are located in vital areas where they can exert pressure on nerve tissue in the brain (2). Malignant tumors, on the other hands, are glioma and metastasis like breast cancer. Malignant tumors are cancerous, and they are further classified as primary or secondary tumors. A primary brain tumor is one that originates in the brain. The tumor is named after the cell type from which it originates or the location in which the cancer develops. Secondary brain tumors are caused by cancer cells that spread to the brain from a primary cancer that is found in another area of the body. They occur more frequently than primary brain tumors. These tumors travel to the brain by blood vessel because the brain has no lymphatic drainage system (4).

Depending upon the size and the location of the tumor in the brain, the symptoms that result from the tumor are very diverse. Some of the common biological symptoms include brain edema, increased pressure in the skull, and inflammation around the tumor mass. Furthermore, the tumors can cause focal neurologic symptoms by damaging local tissue. The patients might experience difficult in speaking, hemihypoesthesai, aphasia, hemiparesis, or ataxia (3). They also suffer headaches, seizures, nausea, vomiting, vision, and hearing problems. Some of the behavioral and cognitive problems include loss of recent memory, inability to concentrate, loss of inhibitions, loss of consciousness, intellectual decline and a decrease in tolerance and patience (5).

Since most of the brain tumors are caused by damaged or missing genes that produce cells with uncontrolled growth, researchers believe that introducing a specific genetic material (DNA or RNA) into the cells will help the cells function normally again. The concept is that the incorporated genetic material will restore a missing function or provide the cells with a different set of functions. There are several ways in which researchers are using gene therapy to treat cancer cells. In one approach, researchers add healthy functioning genes to cells that have damage or missing genes in order to substitute the bad non-working copy of the gene with a better copy of the working gene (6). In other studies, scientists inject tumor cells with genes that make them more vulnerable to chemotherapy and radiation therapy. Researchers can also inject genes into cancer cells so that they can be easily detected and destroyed by the immune system or use gene therapy to increase and stimulate the body's ability to fight off cancer cells. Other research is aimed toward finding a gene that can be inserted into the cancer cell and prevent the tumor cells from forming new blood vessels (angiogenesis), so that the blood supply of the tumors will be cut off and stop the tumors from growing (6). One of the most radical treatments of gene therapy is to inject the cancer cell with genes that can destroy the cells. For instance, suicide genes are inserted into the tumor cells. A pro-drug or an inactive form of a toxic drug is administered to the patients, and this drug will kill off any cancer cells with the suicide genes in them.

In order to treat patients with gene therapy, however, it is important for the researchers to know what gene is altered or missing, and how to incorporate these new functioning genes into the cells. One method that is commonly used in lab is the in-vivo techniques. Virus or a plasmid is absolutely necessary because gene cannot be directly inserted into a cell. The gene is inserted into the person's cell by using a vector. A vector acts as a bacteriophage or a plasmid (circular, small pieces of DNA) that can transfer genes from one cell to another. Vectors from the viruses' adenoviruses are often used for gene therapy because viruses reproduce by inserting their genetic material into the cells they infect. In addition, viruses can be directed to attack specific types of tumor cells. In the lab, researchers insert the wanted gene into the virus, and inactivate or remove certain genes that can cause disease (7). The virus is injected into the patient to infect the cancer cell and the new gene will then pass on to these cancer cells.

Scientists can also transfer genetic materials into cancer cells by using ex-vivo techniques. Cancer cells are taken out of the body from the patient's blood or bone marrow, and the necessary genes are added to them in the lab (6). The cells are later placed back into the patient by injection into a vein. This process is used to get the body's immune system to attack the cancer cells that look like the new incorporate cells in the body by making the cancer cell more easily detected by the immune system. On the other hand, immune cells (dendritic cells) can also be removed from the body and altered to make them stronger and more likely to go after cancer cells once they are placed back into the body (7).

Gene therapy, thus, has some potential toward treating brain cancer, but scientists are still very skeptical about it because they have discovered many risks and flaws with the treatment. First of all, gene therapy is not suitable for all patients with brain tumors, and it is not guaranteed to work for all types of brain cancer. Thus, patients who show an interest in gene therapy must undergo a rigorous screening process to determine their eligibility. Some screenings include the Karnofsky assessment, a neurologic examination, as well as physical examinations to test overall health. Patients who are qualified for this treatment are those that have recurrent malignant gliomas or who have just been diagnosed with malignant gliomas (8). Furthermore, their tumors must also be accessible by surgery and have proven not to respond well to standard treatments like mediation and radiation. Gene therapy should only be considered as a possible treatment for people who are suffering from malignant tumors such as glioblastoma mutliforme, and only for cases in which all conventional therapies have failed.

There are also many risks that are associated with gene therapy and many feel that gene therapy is still lacking in its ability to fight brain tumors. In order to inject gene cells into the specific region of the brain, doctors are required to performed stereotactic brain surgery. Some risks from the surgery might include hemorrhaging or deterioration of functions in the nervous system. After the genes are injected into the region, there is the possibility that the viral vectors that are used to transfer the genetic material into the cell might infect healthy cells as well as cancer cells (9). The new gene might also insert into the wrong location in the DNA, thus leading to harmful mutations of the DNA and triggering unwanted reaction by the immune system. The transferred genes can also be overexpressed by producing a lot of missing proteins. Finally, inflammation of the lining of the brain or infection can occur after the treatment (8).

One of the biggest problem facing gene therapy is the possibility that if this treatment is effective in curing brain tumors, people will allow scientists to use gene therapy to target germ cells and let the inserted gene be passed on to the future generation. The positive side of this germline gene therapy is that future generations in the family with this genetic disease (brain tumor) can be saved from it (7). The negative side, on the other hand, is that the gene therapy will affect the development of the fetus in many unexpected ways like causing long-term illness or other side effects. The human gene pool can also be permanently affected by these gene alterations.

With all the risks and ethical issues that are involved with gene therapy, this treatment is only currently available in research settings. As a result, there is a very slim chance that gene therapy can become a common technique for treating brain tumors. However, if researchers are able to overcome some of the problems that result from gene therapy, there is still a possibility that it can be used to help save million of people that are suffering from cancer. For instance, scientists should find more efficient ways to inject genes into the cell, like creating vectors that specifically focus on the target cells. Researchers can also try to manipulate and control the body's physiologic signals and pathway in order to achieve a greater precision of transplanting the genes to specific locations in the patient's DNA. Even though there is a huge risk with gene therapy, one must be willing to take that risk to survive.

WWW Sources

1)Cancer Facts and Figures 2005, Publication summarize the current scientific information about cancer in 2005

2) Brain and Spinal Cord Tumors in Adults, A description to the causes, symptoms, and treatments for brain tumors.

3)Brain Tumors: Primary, A publication about primary brain tumors in 2001.

4)Brain Tumors, A free encyclopedia (Wikipedia) that has article on brain tumor.

5)Clinical Trials and Noteworthy Treatments for Brain Tumors, This website main focus is toward brain tumor symptoms.

6)Making Treatment Decisions, This article talks about gene therapy treatment.

7)Cancer Facts, Gene Therapy for Cancers: Questions and Answers.

8)National Brain Tumor Foundation, Gene Therapy: A New Experimental Treatment for Brain Tumors

9)Gene therapy of brain tumors: problems presented by physiological barriers, The article is about gene having problem crossing the blood brain barrier.



Full Name:  Yinnette Sano
Username:  ysano@brynmawr.edu
Title:  Memory Loss and Memento
Date:  2005-04-15 01:50:51
Message Id:  14580
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Memento is a contemporary movie which brings to the forefront a moderately
popular Hollywood subject, amnesia, or in this case more specifically, short term
memory loss. The movie is both quite fascinating as well as confusing as it puts one in
the shoes of the main character, Leonard, who suffers from a neurological impairment as
a result of an accident. Leonard is out to get revenge for his wife's rape and murder, but his condition makes this task almost impossible. The viewer is made to look at the movie as the main character sees the world; through snippets of information gathered by him on post it notes, tattoos on his body, as well as through Polaroid shots he takes of people and places so as to "remember" who they are. This movie presents Leo as person who is not
able to retain any short memories whatsoever. He is, however, able to remember his past
very vividly and believes that he can survive only on the basis of instinct and if he
conditions himself. After viewing the movie I decided to do some web research to see
how accurate the film was in terms of describing Leonard's condition and if there had in
fact been some scientific investigations in this particular area.

Memento actually does perpetuate some of the myths about amnesia and short
term memory loss. The character repeatedly states to everyone he meets that he knows
who he is because he does not have amnesia, and this is an incorrect usage of the term,
since the word "amnesia" means loss of memory not loss of identity (1). .There are many
types of amnesia because memory formation and brain function are complex. For
example, memory can be divided into: Immediate — recalling information for a few
seconds after learning it; Short-term — recently learned information that can be recalled minutes or more after presentation; and, Long-term—remote memory of events occurring long months or years ago. One's identity however, is among the most durable long-term memories, therefore, forgetting who you are is rare, especially without other significant neurological and/or psychiatric illness(2). . Leonard suffers from what is known as anterograde amnesia. Anterograde amnesia is a selective memory deficit resulting from brain injury in which the individual is severely impaired in learning new information. Memories for events that occurred before the injury may be largely spared, but events that occurred since the injury may be lost (1).. This fact is clearly depicted in the movie as he forgets conversations and people he has encountered, sometimes doing something and then forgetting mid-way why he is doing it. This disorder can come as a result of damage to parts of the brain such as the hippocampus and the areas which are connected with it in the medial temporal lobes. This damage can arise from numerous things that affect thousands of people. Things such as strokes, brain aneurysms, epilepsy, encephalitis, hypoxia, Alzheimer's disease, and various other complications may have an effect on this area of the brain and can leave the person who has suffered any of these with Anterograde amnesia. In the movie Leonard is able to remember the incident that caused his condition. In reality, the person seldom remembers the incident that actually put him/her into that situation1.

In terms of actual research done on people with this disorder, there is a well known case of a patient known as HM in the late 1950's. This man suffered from difficult epileptic seizures which originated in the medial temporal lobes of his brain. In order to stop these seizures doctors opted to remove the parts of his medial temporal lobes where the seizures were originating. Inthe process HM lost almost two thirds of his hippocampus which, as stated above, are critical in the formation of new memories. However, one form of memory left intact in both Patient HM and Leonard in the movie is the ability to learn skills. Called procedural memory, it is what allows us to learn how to do things such as ride a bike or play an instrument. "By performing sets of actions (procedures), the brain forms a kind of unconscious memory of the skills that you 'just know how to do 1(2). '" The areas of the brain outside the medial-temporal lobes are involved in procedural memory, which is why an injury that results in anterograde amnesia doesn't affect procedural memory (3). . Procedural memory is central to a subplot in Memento.As the movie progresses Leonard has flash backs to when he himself was an insurance investigator and was carrying out a case on a man claiming amnesia. Leonard wanted to make sure the man was not "faking" his memory disorder so as to claim benefits from the insurance company. In the movie the man, Sammy, undergoes a test several times in which he receives a small electrical shock when he picks up a block of a certain shape. In the film, Sammy again and again picks up the electrified block, so as to tell us that his mind does not respond to what Leonard calls "conditioning", something which he thinks he has mastered (2). . However regardless of Sammy being unable to recreate short memories of the past testing he should be able to not pick up the electrified shape based upon some
instinct within him some feeling that is generated from within that has nothing to do with the hippocampus or that part of the brain.

The people who make up our society in many ways look to the media as their
source of accurate knowledge. In this particular case Hollywood was able to get it "less
wrong" as far as portraying the very real and very serious condition of complete short
term memory loss. I think that movie also did a pretty good job in portraying a different
reality, one that comes along with living without a short term memory and how
confusing, frustrating, and just sad it can be. However, it did fail to acknowledge the fact
that although a part of our brain may not be functioning "correctly" for whatever reason;
there are other systems within us that may allow us to make the everyday distinctions so
as to be able to continue living. I think that many times we tend to forget how important
our instincts and inherent human characteristics are especially when the body/brain has to
make up for the lack of a function. The past couple of classes have dealt with perceptions
of reality and how what we "see is not always not what you get", in this case not seeing,
or forgetting, in a sense equals a different perception of reality.


Websites used:
1)
http://www.intelihealth.com/IH/ihtIH/WSIHW000/35320/35323/345689.html?d=dmt
HMSContent
2) http://www.rashmisinha.com/archives/04_06/memento-memory.html

3) http://www.memorylossonline.com/spring2002/memlossatmovies.htm

4) http://www.neuroanatomy.wisc.edu/coursebook/neuro6(2).pdf


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Full Name:  Amelia Jordan
Username:  ajordan@brynmawr,edu
Title:  Insomnia
Date:  2005-04-16 21:38:56
Message Id:  14622
Paper Text:
<mytitle> Biology 202, Spring 2005 Second Web Papers On Serendip

Sleep. For the majority of us it serves as an escape from the perpetual stress and reality of the surrounding world. It is often a few coveted hours that one looks forward to after a long day of work or school. Unfortunately, a lot of people do not receive an adequate amount of sleep on a regular basis, which is a characteristic of insomnia. But if it is so desired, why do so many people have such a massive sleep deficit? Why does it even matter in the first place if you get enough sleep? What happens when you don't sleep enough? Technically, sleep occurs when the body's supply of adenosine breaks down. Adenosine is used by cells in a process called hydrolysis. Once an ATP (adenosine triphosphate) molecule is formed, the third phosphate group can be removed by hydrolysis. After this has occurred, free energy is released, which the body uses to function (1). So, when there is less adenosine in the body, fatigue sets in. Many attempt to combat exhaustion with high-energy substances, such as caffeine; however, ultimately, nothing can substitute for real rest. Health is at risk when one does not sleep enough. It has been shown that the immune system uses energy to rebuild itself when a person rests, but when his or her body is too active, there is not enough energy to fight illness and maintain alertness simultaneously. The result is prolonged or worsened sickness. Day to day tasks are also much more difficult when a person does not get sufficient sleep. Driving a car, studying for a test, and sitting through class, are all undertakings that prove to be a great deal harder when one is sleep deprived. General concentration and well-being are greatly affected by sleep disorders, which is why it is so important that patients with insomnia (and other sleep-related problems) be treated quickly and effectively A night like the following is quite typical of an insomniac: You have been lying awake in bed for hours staring at the bright green numbers on your digital clock. The time is passing quickly and every time you roll over to check the time you cannot help but think about how frustrating it is that you are unable to get to sleep. You also know that you have an eventful day ahead and will not be rested enough to get through it all with a satisfactory amount of energy. Now it's five in the morning and the alarm on that little machine that directs your life's schedule is going to go off in a few hours. The worst part is that the harder you try to make yourself fall asleep, the more difficult the task seems to be. Many of us have been there at least once, if not more. The term insomnia is not defined simply by how many hours of sleep one gets every night. However, the dictionary defines it as "prolonged and usually abnormal inability to obtain adequate sleep." People with insomnia seem to agree to that difficulty falling asleep, waking up too early in the morning, waking up many times throughout the night with difficulty falling back asleep, and an un-refreshing sleep are all symptoms of the disorder (2). It is diagnosed through various evaluations of sleep and medical histories. The sleep history can come from a sleep diary or journal that the patient keeps (3). Special cases are sometimes referred to sleep specialists for specific testing (2). Insomnia can be classified in three different ways. There is transient or acute (short term), intermittent (on and off), and chronic (long term) insomnia (3). Acute insomnia usually lasts from a single night to a few weeks. The causes of acute and intermittent insomnia often include: physical discomfort, emotional distress, environmental factors, or simple factors such as jet lag (2). Chronic insomnia generally lasts for more than a month and often has to do with mental disorders, primarily depression and anxiety (3). This type of insomnia can be categorized in two ways: primary and secondary. "Primary" is when the disorder is not caused by any medical or health condition (4). "Secondary" insomnia is just the opposite; it is based on a health factor (e.g. cancer, asthma, arthritis, alcoholism) (2). After insomnia has been diagnosed (chronic particularly), it can be treated in a number of different ways. There are three behavioral methods that are frequently used by doctors and counselors. One is called "Relaxation Therapy" and its objective is to make the patient's mind stop "racing" so that his or her muscles can loosen up, and reduce anxiety. "Sleep Restriction" is implemented when the patient spends too much time in bed trying to fall asleep. It gradually integrates more hours sleep into one's night, in order that a more normal sleep cycle is established. The third is "Reconditioning," which is supposed to help the patient associate the bed with sleep only. The patient is told to use his or her bed solely for sleep and sex, and to only lie down if tired. If the patient cannot fall asleep, he/she is instructed to get up and return to bed when she feels tired again. This method tells the patients not to nap, and to wake up/go to sleep at the same time every day (5). Sleeping pills are generally a last resort, as they can cause dependence and various side effects such as morning sedation and headaches (4). Clearly, getting enough sleep is an issue that one must conquer on his or her own. However, it can be done if one actually provides the effort necessary. WWW SOURCES 1) http://users.rch.com/jkimball.ma.u/tranet/biology pages1A/ATP.hml 2) www.4woman.gov 3) http://.nhlbi.nih.gov/health/public/sleep/insomnia.txt 4) http://sleepfoundation.org/hottopics/index.php?secid=6&id+216 5) http://www.nhlbi.nih.gov/health/public/sleep/insomnia.htm


Full Name:  Nadia Khan
Username:  nkhan@haverford.edu
Title:  Hallucinations: What happened to external stimuli?
Date:  2005-04-17 18:48:35
Message Id:  14651
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Hallucinations: What happened to external stimuli?

"...suddenly became strangely inebriated. The external world became changed as in a dream. Objects appeared to gain in relief; they assumed unusual dimensions; and colors became more glowing. Even self-perception and the sense of time were changed. When the eyes were closed, colored pictures flashed past in a quickly changing kaleidoscope. After a few hours, the not unpleasant inebriation, which had been experienced whilst I was fully conscious, disappeared. what had caused this condition?"
Albert Hofmann- - Laboratory Notes (1943)
This was how Albert Hofmann sought to describe his experience taking lysergic acid diethylamide, commonly known as LSD or acid, for the first time. The hallucination is a phenomenon often solely associated with recreational drug use. It is described as a 'false and distorted sensory perceptions that appear to be real perceptions' (1). . These perceptions are mentally generated in the absence of a real external stimulus. Hallucinations feel like reality and can be felt, seen, tasted and even smelt.
Besides recreational drugs like mescaline, LSD and PCP (angel dust), hallucinations can stem from everyday experiences such as extreme sleep deprivation, prolonged stress and tension. In addition meditation can also cause hallucination by drawing on a memory of a past experience, lacking a physical stimulus. Neuro-electrical activity with a sensation involving touch, known as 'aura' can appear hallucinatory in the onset of a migraine and often as a warning of one. Individuals suffering from mental illnesses such as schizophrenia and bi-polar disorder also experience hallucinations as do patients of brain damage.
Besides aura, there are other mild hallucinations that we experience everyday including hypogognic hallucinations which are the sensation of falling just before going to sleep. Similarly, there are hypopompic hallucinations that occur as a person is just waking up from a state of sleeping.
Hallucinations do not have to be as severe in nature as a drug induced vision or someone suffering from paranoia hearing voices. There are some hallucinations that linked to the olfactory system. When surrounded by very strong smells such as burning rubber, melting sugar and feces, the nervous system creates the sensation of taste.
When we close our eyes and gently press out finger tips to the eyelids, we can experience a mild hallucination, reminiscent of those imagined during a drug induced perceptionary state. We see small illuminated geometric patterns like exploding stars, honey combs and spirals. Additionally, flickering lights can also cause mild hallucinations. This range of hallucinations has a mathematical pattern that can be examined and regulated by experts.
"Physiology and the way that images are mapped onto the brain's visual cortex play large roles in hallucinatory patterns, to be sure, but mathematics helps explain how instabilities in the brain arise and contribute to these patterns." (2).

It is unconfirmed as to whether the patterns arise as a result of the pressure exerted on the eyeball interfering with the retina's connection with the brain and visual images on the cortex, but when visual stimuli is completely cut off, the brain tries to compensate by creating perceptions based on experience.
In a sense, humans are constantly hallucinating when our vision compensates for the blind spot. We don't see the world with a gaping hole in it, but that is what out technical vision is. Instead we compensate for the gap but filling it in neurologically.
In the case of hallucinogenic drugs, hallucinations are created as a result of slowing down of inhibitory cells. Schizophrenic patients are hypothesized to see hallucination as a result of neurological confusion between 'external and internal stimulus source' (3). . They have also been attributed to the high levels of serotonin in patients of this disease. Schizophrenic visual hallucinations often occur in conjunction with auditory and olfactory hallucinations. It has also been hypothesized that a reduction in the size of frontal lobes could also be responsible for this occurrence. Patients of Charles Bonnet disease are in the process of becoming visually impaired and often completely blind. They are recognized by their strange content which shows hyper-imagination in the form of extremely vivid colors and pronounced images. Researchers wonder how patients who are lacking in sight can have hallucinations when they are obviously lacking in external visual stimuli but Dr. Pascual –Leone and his associates ran a test experiment blindfolding seeing individuals and found that after an extended period of time, these test subjects also started to experience hallucinations similar to those of patients of Charles-Bonnet disease. (4).
Hallucinations, as I said earlier, are a very complex phenomenon, largely because they are experienced in an altered state of normalcy. Therefore, studies and research is affected by this variable and scientists struggle to find a stable environment in which to study the neurobiology behind hallucinations. To a large extent, this reasoning is hypothetical because there are still no concrete linkage between changes in the brain and the imagining of external stimuli. However, there are some extremely viable theories behind the different types of hallucinations that we either hear about regularly or experience ourselves daily.



References:
1. Transcranial Magnetic Stimulation Reduces Auditory Hallucinations by Kenneth J. Bender, Pharm.D., M.A. Psychiatric Times July 2000 Vol. XVII Issue 7
2. The roots of visual awareness :a festschrift in honour of Alan Cowey. Alan Cowey; Charles A Heywood; A D Milner; Colin Blakemore 2004 1st ed.
3. Voices in the Brain: The Cognitive Neuropsychiatry of Auditory Verbal Hallucinations Spence, Sean; David, Anthony S.
4. Pitt mathematician tracks origin of hallucinations Monday, August 02, 1999 By Byron Spice, Science Editor, Post-Gazette http://www.postgazette.com/healthscience/19990802lsd1.asp
5. http://serendipstudio.org/bb/neuro/neuro01/web3/Cohen.html
6. Anti-angiogenesis Drug Improves Response to Radiation Therapy http://focus.hms.harvard.edu/2005/Jan14_2005/research_briefs.html



Full Name:  Anna Tomasulo
Username:  atomasul@brynmawr.edu
Title:  The Validity of Repressed Memory and Sexual Abuse
Date:  2005-04-18 19:47:22
Message Id:  14698
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip



As we discussed in class, every person's understanding of reality is slightly different. We all have different experiences and different perceptions of the same experience or event. Therefore, we must also have different memories of the same events. I decided to further research memory and how it affects individual people. In doing so, it has come to my attention that a specific area of the human memory has been given a lot of attention in the past few decades: recovered memory. Recovered, or repressed, memory is "a traumatic event unconsciously retained in the mind, where it is said to adversely affect conscious thought, desire, and action" (1) . Many sexual abuse trials have dealt with recovered memory. Often people will experience something that will trigger a spontaneous memory. Sometimes this memory will be of traumatic events such as sexual abuse. In this case, some have sought therapy to recover more of these memories and have then taken their sexual abuse cases to court. However, the concept and validity of recovered memory is not supported by all. There are those that support the recovered memory movement, and those that propose an alternative response to these spontaneous memories. These people believe in false memories and the False Memory movement. In this essay I will examine arguments from both sides with the hope of determining which argument I agree with, and hopefully sharing some valuable information about our memory, how it functions and its weaknesses.

Repressed memory was first examined by Sigmund Freud in the late 1890's while he was studying the unconscious (2). He performed case studies on women who were victims of sexual abuse and concluded that when we experience trauma, a mechanism in the brain unconsciously represses this trauma from our awareness. It is a way for us to protect ourselves from these haunting experiences (3). The Recovered Memory movement began in between the mid 1980's and lasted until the late 1990's, encouraged by Freud's studies and the book The Courage to Heal by Laura Davis (4). This book influenced women who were suffering from either physical or mental difficulties to visit therapists because there was a good chance that their suffering was due to repressed memories of abuse from childhood. The idea was to uncover these repressed memories in therapy and to heal them, also healing the troubles the person was currently suffering from (5). Thus started the craze of recovered memory therapy.

Lenore Terr, Linda Meyer Williams and Dr. Judith Lewis Herman support the beliefs put forward by the Recovered Memory movement. Psychologist Lenore Terr suggests that there are two types of traumatic events, Type I, which is a single traumatic event and Type II, which is a repeated traumatic event (6). Terr argues that repeated traumatic events are those that are repressed unconsciously(1) . Williams conducted a study on 129 women who had been sexually abused in the 1970's. Almost two decades after the sexual abuse of these women, in the mid 1990's, Williams questioned these women. The answers varied; 38% of the women did not remember being admitted into the hospital, 12% do not remember the actual abuse, and 16% claimed that for a period of time they did not remember the abuse, however they recalled the memory at a later date (6). These answers support the idea that traumatic events can cause memory loss and perhaps an unconscious repression of the event itself. Dr. Judith Lewis Herman conducted a study similar to that of Williams on women who had been sexually abused. She found that two thirds of the sexual abuse victims suffered from memory loss (7). There are also individual cases of recovered memory that have proven to be true. For example, college professor Ross Cheiter woke from a dream one night about a former camp counselor molesting him. After research and therapy, he found the camp counselor who admitted to molesting young boys(6). Clearly there is support for this movement and reason to look further into repressed memories and their validity.

It is a reasonable desire to search for understanding of our dreams and our current psychological troubles. However, as pointed out by critics of the Recovered Memory movement, this theory and these case studies have their flaws. For example, in reference to Lenore Terr's argument, there is evidence that repetition increases the ability to remember something. According to memory expert, Daniel Schacter, "hundreds of studies have shown that repetition of information leads to improved memory, not loss of memory, for that information" (1) . So how is it possible that a repeated traumatic event can be unconsciously repressed? Further, in the studies by Williams and Herman the ages of the women who had been sexually abused were not stated. Victims could have been infants who would not remember the events because the brain of an infant is not developed like that of an adult therefore it has little capacity to remember such things(6). Critics of the Recovered Memory movement also suggest the flaws with recovered memory therapy. In Daniel Schacter's book The Seven Sins of Memory: How the Mind Forgets and Remembers, he identifies memory's weaknesses: transience, absent-mindedness, blocking, suggestibility, bias, persistence, and misattribution (8). Critics of the Recovered Memory movement, such as Schacter, aruge that therapists are largely responsible for "sins" such as suggestibility (8). It is argued that therapists practice ask questions and offer suggestions that influence our memories. For example, the child psychologist Jean Piaget was convinced that he was kidnapped at the age of two, and was able to give details of the kidnapping such as the description of the police officer chasing his kidnapper. This story was confirmed by his babysitter and his parents. However it is doubtful that a child of such a young age would be able to vividly remember such an event. Years after the "occurrence" the baby sitter admitted to making up the entire story. Because of the suggestions by the baby sitter, Piaget created his own detailed memory of the event(9).

What Schacter and fellow critics of this movement suggest as an alternative to the Recovered Memory movement is the False Memory movement(7). This movement supports that our brains are able to consciously suppress or block memories of traumatic events, but there is no known mechanism that enables us to unconsciously repress these memories(1) . The movement also suggests that due to weaknesses of the memory, such as the seven "sins" identified by Schacter, our minds can create false memories. Several false memories have been identified such as that of Jean Piaget. Another example of a false memory occurred when a woman accused a doctor of raping her. She had been preparing for a live interview with the doctor when the rape occurred. According to Schacter, she confused the memory of the rape with that of the interview and accused the wrong man of raping her(9). Failures of the memory and false memories are dangerous to those experiencing them as well as to others. This is another reason why the Recovered Memory movement has so many opponents. Because the validity of these memories is so weak and because not enough is known in this area to really determine their truth, many families have been destroyed by false accusations of sexual abuse(9).

Another alternative suggested by Schacter is that these traumatic events have not been repressed, but dissociated. Schacter refers to a dissociative order as a disorder that prevents individuals from integrating specific aspects of an experience in our brains thus making it difficult to remember(6). Personally, I agree with Schacter. In the case of a traumatic event such as sexual abuse, I believe that the victim would not want to think about or remember the event at all. This means that the victim would most likely refuse to analyze the sequence of events that made of the traumatic experience. Further, this means that there is no repetition of information, which also increases the memory of an event or experience.

The debate continues today and there is much to be learned about our brains and the complex function of memory. This essay does not provide a solid answer with proof to the absolute validity to of either the Recovered or False Memory movement, however, to me, it seems that there is more logical evidence supporting the idea that memories can be consciously suppressed or "lost" by dissociation. Further, I believe that therapy patients with claims of recovered memories of sexual abuse should be more thourougly investigated. This does not mean that I discredit them; sexual abuse is an extremely serious affair and should be dealt with in a severe and efficient manner. However, false accusations can be equally as traumatizing for those suffering the accusations. What is also worrisome to me is the realization that our memories are not as reliable as I believed them to be. As implied by Daniel Schacter, they are quite easily manipulated. The question that next comes to mind is if our memories are so easily manipulated, what about our life experiences and what we view as our past? Are we truly aware of all that we have lived and experienced? Once again, questions for another essay.

Web References:

1)The Skeptic's Dictionary , "Repressed Memory"

2)Sigmund Freud, "Sigmund Freud"

3)A Guide to Psychology, "Repressed Memories"

4) Recovered Memory Therapy and False Memories, "Psychologists Educating Students to Think Skeptically"

5)Repressed Memory , "Imaginary Crimes"

6) Debate of Memory Repression of Childhood Sexual Abuse, "Greendoor Resolutions P.L.L.C."

7) Fletcher, Camille L. Journal of Law and Policy. Vol. 13:335 "Repressed Memories: Do Triggering Methods Contribute to Witness Testimony Reliability?" 2003.

8) APA Online, "Seven Sins of Memory"

9) The Skeptic's Dictionary , "False Memory"



Full Name:  Sophia Louis
Username:  slouis@haverford.edu
Title:  Interrupted Nerve Fibers and Multiple Sclerosis
Date:  2005-04-18 23:21:51
Message Id:  14713
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Interrupted Nerve Fibers and Multiple Sclerosis
I am interested in what happens in extreme cases of nerve damage. More specifically, what happens when electrical impulses between nerve fibers are interrupted? The nervous system is a network of specialized tissue that controls actions and reactions of the body and its adjustment to the environment. The nervous system has two main divisions, the central and the peripheral nervous system. I am most concerned with the central nervous system. The central nervous system (CNS) consists of the brain and the spinal cord. Many analogies have been made and my favorite reads "the brain might be compared to a computer and its memory banks, the spinal cord to the conducting cable for the computer's input and output, and the nerves to a circuit supplying input information to the cable and transmitting the output to muscles and organs"(1). But, what happens if there is a malfunction in the transmission of messages? What happens if the cable is damaged?
When the cell body of a neuron is chemically stimulated, it generates an impulse that passes from the axon of one neuron to the dendrite of another through the synapse. Electrical impulses may pass directly from axon to axon, axon to dendrite, or from dendrite to dendrite. So-called white matter in the central nervous system consists primarily of axons coated with light-colored myelin produced by certain neuroglial cells. Myelin is a fatty substance, which protects the nerve fibers in the CNS and helps to conduct electrical impulses (2). Myelin is considered fatty because it is rich in protein and lipids, it forms layers around the nerve fibers and acts as insulation. Referring back to analogies, the nerve can be compared to an electrical cable, the axon (nerve fiber that transmits the nerve impulse) is like the wire, and the myelin sheath is like the insulation around the wire, protecting the flow of electrical impulses along the line. Nerve cell bodies that are not coated with white matter are known as gray matter. There are regular intervals along peripheral axons where the myelin sheath is interrupted. These areas, called nodes of Ranvier, are the points between which nerve impulses, in myelinated fibers, jump, rather than pass, continuously along the fiber (as is the case in unmyelinated fibers). Transmission of impulses is faster in myelinated nerves, varying from about 3 to 300 ft (1–91 m) per sec (3).
When extensive damage is suffered by myelin, a condition called Multiple Sclerosis occurs (MS). About 200 people are diagnosed every week. Worldwide, MS may affect 2.5 million individuals. Most people are diagnosed between the ages of 20 and 50 and two to three times as many women as men have MS. Multiple sclerosis (MS) is an autoimmune disease of the myelin in the central nervous system (CNS) that is clinically characterized by episodes of neurologic dysfunction separated by time and space (4). In MS, myelin is lost in multiple areas, leaving scar tissue called sclerosis. These damaged areas are also known as plaques or lesions (5). Sometimes the nerve fiber itself is damaged or broken.
In MS, an immune system reaction causes a breakdown in the myelin layer, or sheath. When any part of the myelin sheath is destroyed, nerve impulses to and from the brain are distorted or interrupted. These "shorts" in the system may impair bodily functions such as movement, speech, or sight, depending on where in the central nervous system they occur. The name itself explains this: "Multiple" because many areas of the brain and spinal cord are affected and "Sclerosis" because scleroses, or hardened patches of scar tissue, may form over the damaged myelin. Some people remember this more easily by thinking that MS is short for "many scars" (6, 7). It was long believed that no nerve damage accompanied damage to the myelin sheath in MS. Recent studies have, however, drawn this belief into question.
To answer my initial, one must have a deeper understanding of the function of myelin. Myelin not only protects nerve fibers, but also makes their job possible. When myelin or the nerve fiber is destroyed or damaged, the ability of the nerves to conduct electrical impulses to and from the brain is disrupted, and this produces the various symptoms of MS. Symptoms of MS are unpredictable and do vary from person to person and from time to time in the same person. For example, one person may experience abnormal fatigue, while another might have severe vision problems. A person with MS could have loss of balance and muscle coordination making walking difficult; another person with MS could have slurred speech, tremors, stiffness, and bladder problems. While some symptoms will come and go over the course of the disease, others may be more lasting (8). Recent studies suggest that the MS disease process starts long before symptoms begin, and by the time symptoms appear, there are already signs of brain and spinal cord atrophy. The cause of MS is unknown, and it cannot be prevented or cured. A test called the Expanded Disability Status Scale (EDSS) is used to rate the severity of symptoms. It is also used after a diagnosis to gauge the status of the disease, and score the effectiveness of treatments. The scale ranges from zero to ten with higher scores indicating more severe symptoms. There is no single test that can accurately diagnose MS and for this reason several laboratory procedures are necessary before a diagnosis can be made. These procedures usually include: an Analysis of Cerebrospinal Fluid (CFS); an Evoked Potential (EP) Test; and Magnetic Resonance Imaging (MRI) (10).
While there is no cure for MS, research is being done towards the future of myelin repair. There are efforts being made to reverse the damage caused by MS and restore "normal" function in people suffering from the disease. This is not the only treatment to consider though, because MS is an autoimmune disease, the body destroys its own myelin. So researchers need to find a say to stop the immune system from fighting and damaging its own CNS tissue. In 2003 several hundred researchers from around the world participated in an intensive three-day workshop organized by the National MS Society. They realized that the first step to repair and treatment is stopping the underlying immune attack from perpetuating damage to repaired tissue, which is why ongoing research to find better immune-modulating treatments for MS is vital (International Workshop). Advancements from that weekend show that the body can repair myelin by stimulating neighboring oligodendrocytes (the cells that make myelin) or by recruiting immature "progenitor" cells that move to the lesion and replace damaged myelin. Some participants noted that this natural repair process might actually be stimulated by the inflammation that occurs during MS attacks.
I mentioned before that women are more prone to getting MS than men.
Apparently, there are genetic difference between men and women, which could be the reason why MS strikes more women than men, says Dr. Brian Weinshenker from the Mayo Clinic. The online edition of "Genes and Immunity" explains that genes and environment are probably both involved in the development of MS. Doctors from the Mayo Clinic studied the genes of MS patients in the U.S, and at gene patterns in people from Northern Ireland and Belgium (1). Women with MS were more likely to have a variation of a gene that produces high levels of a protein called interferon gamma. Interferon gamma can aggravate MS by promoting inflammation and tissue damage (1).In the U.S. and Northern Ireland, men with the gene variation were more susceptible to MS. That was also true for Belgian men, but the effect wasn't significant there. The gene variation was less common among men. "That might explain why men are generally protected more from MS," says Weinshenker in a news release.
I think there is a bright future for patients suffering from MS. New advancements are on a steady rise. Scientists have discovered the ability to use potential cells found in skin and bone marrow to transform into brain cells. These cells can be used as a source of replacement cells useful in viable new tissue. Possible sources also include: skin derived cells, bone marrow, and umbilical cord blood cells, fetal cells, and Schwann cells from the PNS. This will be promising if the immune attack can be stopped. Then new ways to repair the nerve damage and restore nerve function will arise.

Why more women get MS
International Workshop
MS information
What is Multiple Sclerosis,
Multiple Sclerosis: Overview,
Personal Stories
General Information,
Multiple Sclerosis,
Detection of Neuroimmunologic Disorders

Myelin function-overview
Nervous System: Anatomy and Function



Full Name:  Sophia Louis
Username:  slouis@haverford.edu
Title:  Interrupted Nerve Fibers and Multiple Sclerosis
Date:  2005-04-18 23:28:25
Message Id:  14715
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Interrupted Nerve Fibers and Multiple Sclerosis
I am interested in what happens in extreme cases of nerve damage. More specifically, what happens when electrical impulses between nerve fibers are interrupted? The nervous system is a network of specialized tissue that controls actions and reactions of the body and its adjustment to the environment. The nervous system has two main divisions, the central and the peripheral nervous system. I am most concerned with the central nervous system. The central nervous system (CNS) consists of the brain and the spinal cord. Many analogies have been made and my favorite reads "the brain might be compared to a computer and its memory banks, the spinal cord to the conducting cable for the computer's input and output, and the nerves to a circuit supplying input information to the cable and transmitting the output to muscles and organs"(1). But, what happens if there is a malfunction in the transmission of messages? What happens if the cable is damaged?
When the cell body of a neuron is chemically stimulated, it generates an impulse that passes from the axon of one neuron to the dendrite of another through the synapse. Electrical impulses may pass directly from axon to axon, axon to dendrite, or from dendrite to dendrite. So-called white matter in the central nervous system consists primarily of axons coated with light-colored myelin produced by certain neuroglial cells. Myelin is a fatty substance, which protects the nerve fibers in the CNS and helps to conduct electrical impulses (2). Myelin is considered fatty because it is rich in protein and lipids, it forms layers around the nerve fibers and acts as insulation. Referring back to analogies, the nerve can be compared to an electrical cable, the axon (nerve fiber that transmits the nerve impulse) is like the wire, and the myelin sheath is like the insulation around the wire, protecting the flow of electrical impulses along the line. Nerve cell bodies that are not coated with white matter are known as gray matter. There are regular intervals along peripheral axons where the myelin sheath is interrupted. These areas, called nodes of Ranvier, are the points between which nerve impulses, in myelinated fibers, jump, rather than pass, continuously along the fiber (as is the case in unmyelinated fibers). Transmission of impulses is faster in myelinated nerves, varying from about 3 to 300 ft (1–91 m) per sec (3).
When extensive damage is suffered by myelin, a condition called Multiple Sclerosis occurs (MS). About 200 people are diagnosed every week. Worldwide, MS may affect 2.5 million individuals. Most people are diagnosed between the ages of 20 and 50 and two to three times as many women as men have MS. Multiple sclerosis (MS) is an autoimmune disease of the myelin in the central nervous system (CNS) that is clinically characterized by episodes of neurologic dysfunction separated by time and space (4). In MS, myelin is lost in multiple areas, leaving scar tissue called sclerosis. These damaged areas are also known as plaques or lesions (5). Sometimes the nerve fiber itself is damaged or broken.
In MS, an immune system reaction causes a breakdown in the myelin layer, or sheath. When any part of the myelin sheath is destroyed, nerve impulses to and from the brain are distorted or interrupted. These "shorts" in the system may impair bodily functions such as movement, speech, or sight, depending on where in the central nervous system they occur. The name itself explains this: "Multiple" because many areas of the brain and spinal cord are affected and "Sclerosis" because scleroses, or hardened patches of scar tissue, may form over the damaged myelin. Some people remember this more easily by thinking that MS is short for "many scars" (6, 7). It was long believed that no nerve damage accompanied damage to the myelin sheath in MS. Recent studies have, however, drawn this belief into question.
To answer my initial, one must have a deeper understanding of the function of myelin. Myelin not only protects nerve fibers, but also makes their job possible. When myelin or the nerve fiber is destroyed or damaged, the ability of the nerves to conduct electrical impulses to and from the brain is disrupted, and this produces the various symptoms of MS. Symptoms of MS are unpredictable and do vary from person to person and from time to time in the same person. For example, one person may experience abnormal fatigue, while another might have severe vision problems. A person with MS could have loss of balance and muscle coordination making walking difficult; another person with MS could have slurred speech, tremors, stiffness, and bladder problems. While some symptoms will come and go over the course of the disease, others may be more lasting (8). Recent studies suggest that the MS disease process starts long before symptoms begin, and by the time symptoms appear, there are already signs of brain and spinal cord atrophy. The cause of MS is unknown, and it cannot be prevented or cured. A test called the Expanded Disability Status Scale (EDSS) is used to rate the severity of symptoms. It is also used after a diagnosis to gauge the status of the disease, and score the effectiveness of treatments. The scale ranges from zero to ten with higher scores indicating more severe symptoms. There is no single test that can accurately diagnose MS and for this reason several laboratory procedures are necessary before a diagnosis can be made. These procedures usually include: an Analysis of Cerebrospinal Fluid (CFS); an Evoked Potential (EP) Test; and Magnetic Resonance Imaging (MRI) (10).
While there is no cure for MS, research is being done towards the future of myelin repair. There are efforts being made to reverse the damage caused by MS and restore "normal" function in people suffering from the disease. This is not the only treatment to consider though, because MS is an autoimmune disease, the body destroys its own myelin. So researchers need to find a say to stop the immune system from fighting and damaging its own CNS tissue. In 2003 several hundred researchers from around the world participated in an intensive three-day workshop organized by the National MS Society. They realized that the first step to repair and treatment is stopping the underlying immune attack from perpetuating damage to repaired tissue, which is why ongoing research to find better immune-modulating treatments for MS is vital (International Workshop). Advancements from that weekend show that the body can repair myelin by stimulating neighboring oligodendrocytes (the cells that make myelin) or by recruiting immature "progenitor" cells that move to the lesion and replace damaged myelin. Some participants noted that this natural repair process might actually be stimulated by the inflammation that occurs during MS attacks.
I mentioned before that women are more prone to getting MS than men.
Apparently, there are genetic difference between men and women, which could be the reason why MS strikes more women than men, says Dr. Brian Weinshenker from the Mayo Clinic. The online edition of "Genes and Immunity" explains that genes and environment are probably both involved in the development of MS. Doctors from the Mayo Clinic studied the genes of MS patients in the U.S, and at gene patterns in people from Northern Ireland and Belgium (1). Women with MS were more likely to have a variation of a gene that produces high levels of a protein called interferon gamma. Interferon gamma can aggravate MS by promoting inflammation and tissue damage (1).In the U.S. and Northern Ireland, men with the gene variation were more susceptible to MS. That was also true for Belgian men, but the effect wasn't significant there. The gene variation was less common among men. "That might explain why men are generally protected more from MS," says Weinshenker in a news release.
I think there is a bright future for patients suffering from MS. New advancements are on a steady rise. Scientists have discovered the ability to use potential cells found in skin and bone marrow to transform into brain cells. These cells can be used as a source of replacement cells useful in viable new tissue. Possible sources also include: skin derived cells, bone marrow, and umbilical cord blood cells, fetal cells, and Schwann cells from the PNS. This will be promising if the immune attack can be stopped. Then new ways to repair the nerve damage and restore nerve function will arise.

Why more women get MS
International Workshop
MS information
What is Multiple Sclerosis,
Multiple Sclerosis: Overview,
Personal Stories
General Information,
Multiple Sclerosis,
Detection of Neuroimmunologic Disorders

Myelin function-overview
Nervous System: Anatomy and Function



Full Name:  Student Contributor
Username:  
Title:  The Mad Gene: Creativity and Mental Illness
Date:  2005-04-19 10:21:45
Message Id:  14730
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


One could argue that if there was anything cliché about Ron Howard's film A Beautiful Mind, it was the recycled theme of the "mad genius." Russell Crow played John Nash, the brilliant, asocial mathematician who won the Nobel Prize in Economics in 1994. It's hard to critique the novel as cliché, however, because the concept of the "mad genius" wasn't cultivated – Nash, indeed, suffered from serious mental illness. Nash wasn't the only creative thinker to contribute to the "mad genius" phenomenon; twentieth century American poet Sylvia Plath, who was believed to have suffered from severe bipolar disorder, committed suicide in 1963. Nineteenth century painter, Vincent Van Gogh, spent the later years of his life at the St. Remy Asylum after his infamous act of mutilating his ear. The list goes on. The observation that there exists a link between creativity and mental illness is not a recent one; Aristotle once wrote that eminent philosophers, politicians, poets, and artists all have tendencies toward "melancholia" (1).

There have been numerous studies in the past century examining the "mad genius" phenomenon, the most impressive of these studies conducted in 1987 by Nancy C. Andreasen (6). Conducting her studies at the infamous center for creative writing, The University of Iowa Workshops, Andreasen examined 30 writers and found that 80% had experienced at least one episode of major depression, hypomania, or mania. Andreasen also examined 30 controls and found that 0% had experienced some form of mental disorder (6). It was also found that there was a higher prevalence of mental disorder and creativity in the writer's first degree relatives compared to that of the control, suggesting that "mad genius" might be a genetically heritably trait (6).

It appears that the most common mental disorder amongst creative thinkers is bipolar disorder. This illness is characterized by four stages: major depressive, mixed, hypomanic, and manic episodes (5). During major depressive and mixed, the patient usually suffers from apathy, lack of energy, hopelessness, sleep disturbance, and slowed thinking (3). In the episodes of hypomania and mania, the mood is generally elevated, activity and energy levels increase, the need for sleep decreases, and speech is often rapid and excitable.

These observations led to some interesting questions: Does creativity cause bipolar disorder? Does the type of creativity matter? Psychiatrist Albert Rothenberg argues that there isn't a link and, in fact, because mental illness disrupts the cognitive and emotional processes necessary for creative thinking, highly creative people do better when they are treated for their mental illnesses (1). In direct opposition to this argument is HimaBindu Krishna's assertion that drug treatment often subjugates the creativity in the patient (5). Andreasen's conclusion regarding her observations of the University of Iowa writers supports Rothenberg's argument; she has found that most writers write when their mood is "normal," neither elevated nor depressed (6). In fact, when writers claim to suffer from severe depressive episodes, their writing usually suffers.

Does the type of creativity matter? Not really. Bipolar disorder affects a high percentage of people in artistic professions, including but not limited to, writers, poets, artists, and musicians (1). Interestingly, in a more recent study carried out by psychologist James Kaufman, it was found that female poets were more likely than fiction writers to have signs of mental illness, such as suicide attempts or hospitalizations, a phenomenon Kaufman has dubbed "the Sylvia Plath effect" (4).

The recent discussions in Neurobiology 202 provide some interesting insight into these above observations. If the neocortex and the rest of the nervous system are intimately connected through a series of pathways, and so inevitably leave traces of each other long after communication has ceased (if it ever does cease), it is not unbelievable that ailments of the "unconscious" can effect the "storyteller." Or to put it more simply, if the unconscious causes an individual to suffer from serious depressive illness, it is likely that the changes made to the nervous system following the disorder may cause some changes in the neocortex. Nothing in the body exists as an isolated system. Of course, the changes made do not necessarily have to translate into the ability to have creative impulses. But it shouldn't come as a surprise that a serious physical ailment of the body will probably have an effect on another seemingly unrelated part of the body.

It is important to note that there has been some speculation suggesting that the rise of mental illness in creative communities is due to the fact that there is much more toleration of mental illness than there is in the rest of society, and not an innate occurrence (1). Artists feel safe in a community that, to some respects, seems to value mental disorder in its members. But the nature of the creative profession is also not conducive to healthy living; there are very few jobs that have a higher rejection rate, that demand a serious removal of both mental and physical faculties to allow for serious speculation, and often writers find themselves absorbed in uncommonly shared symbols that can leave one feeling misunderstood.

While the above assertions are valid, it is hard to define the high occurrence of mental illness in writers as nothing more than a coincidence. Interesting questions to further explore would be why individuals decide to become writers in the first place. Does creativity run in the family, and if so, does a history of mental illness also run in the family? Is there such a thing as the creativity gene? Was it the feeling of alienation that led to the need to write, or did writing lead to the feeling of alienation? These are question that are well worth exploring to help shed light on the phenomenon of the "mad genius."


References

1) Bailey, Deborah Smith. "The Sylvia Plath Effect."

2) Davis, Laurie. "Mental illness meets creativity in new journal of literary arts." Chicago Chronicle. 2002. 21:11

3) Jamison, Kay Redfield. "Suicide and manic-depressive illness in artist and writers." National Forum. Wntr 1993. 73: 28

4) Kaufman, James C. "The Cost of the Muse: Poets Dies Young." Death Studies. 27: 813-821.

5) Krishna, HimaBindu. "Bipolar Disorder and the Creative Genius."

6)"Virginia Woolf's Psychiatric History: Creativity and Psychiatric Disorder."



Full Name:  Georgia Griffin
Username:  ggriffin@brynmawr.edu
Title:  Dissociative Fugue and the Conscious/Unconscious Chasm
Date:  2005-04-21 01:02:33
Message Id:  14761
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Automatisme Ambulatoire, also known as hysterical fugue, dissociative fugue or simply fugue, is a mental disorder wherein the afflicted individual is prone to taking unexpected trips in a state of unconsciousness such that she is unable to recall where she has been, or how she ended up in a particular place. These individuals, sometimes called "fuguers," are able to travel great distances unaware of their actions, and yet function in such a way that people they encounter never suspect their mental state. This separation of the self from the actions of the body characterizes fugue as a dissociative disorder, meaning that it entails the separation of certain mental and physical actions from a conscious awareness of those actions. In other words, dissociation "is defined as disruption in the integrated function of consciousness, memory and perception,"(1) which is what allows a fuguer to behave normally without the "knowledge" of the conscious self. This description closely resembles that of another disrupted consciousness type behavior, namely, somnambulism, better known as "sleepwalking". The similarities between the two provoke the question of what, if any, the implications of their resemblance might be. That is to say, do the phenomenon of hysterical fugue and somnambulism challenge the distinction between being awake and being asleep?

Eyewitnesses report that someone in the midst of a dissociative fugue appears to behave normally "apart from [an] inability to recall their past or personal information".(2) However, when a fuguer "comes to" he often behaves as though he has just been awoken from a deep sleep, that is, he appears dazed and disoriented. In addition, such an individual is unable to recall how she arrived at her destination, or why. "His brother found him in a nearby town helping a traveling umbrella salesman. Tapped on the shoulder, he acted as if he were awaking from a deep sleep, groggy and confused, astonished to find himself where he was, carting umbrellas."(3) This is very similar to the reports given by sleepwalkers and those who observe them in the act. An individual who is sleepwalking appears at first glance to be conscious, however when she awakens she has no recollection of her unconscious wanderings. Moreover, witnesses to both phenomenon report that fuguers and sleepwalkers both exhibit what is described as a "blank facial expression".(4) In other words, although both fuguers and sleepwalkers are able to perform a variety of complex functions, including mobility and verbal communication to some extent, it is still apparent that their "minds" are elsewhere during an episode. This is evident in their inability to recollect their actions upon "awakening". Therefore, from the perspective of an outside observer it would appear as though these two conditions, automatisme ambulatoire and somnambulism, look like the same thing. Is somnambulism a dissociative disorder? Are fuguers asleep? And if the answer to either of these questions is yes, then what is the difference between being awake and being asleep?

One method that scientists use to distinguish between the states of sleep and wakefulness is monitoring neurobiological status. That is, the patterns of brain functioning associated with being awake are different than the patterns associated with being asleep. For example, an electroencephalogram (EEG)-which monitors electrical activity in the brain-of an individual who is awake alternates between two patterns of activity. "One is low voltage (about 10-30 microvolts) fast (16-25 Hz or cps; cycles per second) activity, often called an "activation" or desynchronized pattern. The other is a sinusoidal 8-12 Hz pattern (most often 8 or 12 Hz in college students) of about 20-40 microvolts which is called "alpha" activity."(5) In contrast the patterns of brain activity in an individual who is asleep cycle between five different stages. The first four are the stages of NREM (non rapid eye movement) sleep and the last stage is REM (rapid eye movement) sleep. Although the first four stages are distinct, they are generally more similar and are characterized by a presence of slower, higher amplitude waves known as "delta" waves, which correlates to the increase in synchronicity of brain activity. REM sleep, however, exhibits a mix of frequencies (i.e. it is desynchronized) and appears similar to both the awakened state and Stage 1 of sleep.(6)

Sleepwalking is generally associated with the early stages of sleep and would therefore consist of high voltage low frequency brain activity patterns, similar to the "activated" state of wakefulness (10-30 microvolts, 16-25 Hz).(7) Not surprisingly, the brain activity of someone in the midst of a dissociative disorder like fugue is slightly slower than normal awake activity (approximately 8-13 Hz).(8) However, when we compare this to the brain activity of a sleepwalker, this is surprising. On the basis of brain activity alone it appears as though sleepwalking is a more "activated" state than fugue, which is a wakeful, albeit unaware, state. This seems to imply that despite the fact that fuguers are awake and are more functional than sleepwalkers (in that they are able to communicate clearly and to travel great distances), their conscious is actually less involved.

So what does this all mean? At most this has serious implications for the belief that sleep is distinct from wakefulness and that we are able to tell the difference. That is, fuguers, who are not asleep, are to the outside observer almost identical to sleepwalkers, and both conditions are rather difficult to distinguish from an awakened, fully conscious state. Moreover, the neurological activity of individuals who suffer from these two conditions would seem to produce a conclusion about the respective "awareness" of fuguers and sleepwalkers that is the opposite of the one we now hold. To conclude, however, that this means we cannot actually differentiate between wakefulness and sleep is perhaps a bit hasty. At the very least though, this poses an interesting challenge to our categorization of automatisme ambulatoire and somnambulism.

References

1), The National Society for Epilepsy. Dedicated to providing information and support for people with epilepsy.

2), Genesis Health System, a healthcare provider and information source for health related issues.

3) Hacking, Ian. Mad Travelers: Reflections on the Reality of Transient Mental Illnesses. University Press of Virginia. Charlottesville, VA. 1998 (p21)

4), Medicine Plus, a Service of the U.S. National Library of Medicine and the National Institutes of Health.

5), Basics of Sleep Behavior. A rich guide to information on a broad range of topics related to sleep.

6), Basics of Sleep Behavior. A rich guide to information on a broad range of topics related to sleep.

7), Basics of Sleep Behavior. A rich guide to information on a broad range of topics related to sleep.

8), EEG Research. A collection of research papers on the topics of EEG Biofeedback and Neurofeedback.



Full Name:  Courtney Black
Username:  cblack@brynmawr.edu
Title:  Monogamy or Polygamy? Human Preference and Human Action
Date:  2005-04-29 17:25:12
Message Id:  14995
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Throughout our lifetimes we have encountered people whose parents are married, divorced, never married, or entirely unknown to them. While these various combinations may seem like natural occurrences to us, much of our grandparents' generation would argue that children should not exist outside of marriage, and that there has been a general decline in respect for this institution during their lifetimes. But, in this case, what both generations are failing to realize is that marriage, or more appropriately, monogamy, is in itself an evolution. Just has human beings did not arrive on this earth as Homo sapiens; they did not arrive as monogamous creatures. This paper will explore the evolution of human preference from polygamy to monogamy, while also discussing the semi-regular reversions of individuals to the former.

Amongst humans sex has always existed. What has changed overtime have been the circumstances within which it is preformed. As humans developed from quadrapeds into bipeds, their bodies shifted and adjusted to life on two feet. Many changes in body structure occurred in both men and women in response to this change. In relation to this paper, the most important of these adaptations are those that occurred in the female body. Among them are the narrowing of the space between the legs, a decrease in the size of the birth canal, and the forward tilting of the vagina (1).

The narrowing of the space between the legs occurred in conjunction with a widening of the pelvis. This served both to stabilize walking and to provide greater support for the heavy torso. However, as the legs grew closer together and the pelvis changed its shape, females developed shorter and narrower birth canals. With this decrease in birth canal size, females also saw a decrease in the gestation period and an increase in premature births (2). While this may at first seem like a negative change, it is actually a positive adaptation that greatly increased the chances for survival of both mother and child. Because they were born prematurely, infants now had smaller heads which made the actual process of birth easier (3).

In addition to these changes, the birth canal also saw one more adjustment that would play a major role in the adoption of monogamy: the forward tilting of the vagina. Originally, like all of our primate cousins, humans had engaged in sex from behind, however, over time, this would change, first within a small minority and finally amongst the majority. The evolution of a forward tilting vagina had two effects that encouraged monogamy. The first of these was its encouragement of face-to-face copulation which in turn fostered the development of close relationships between two people engaging in sex. By having sex face-to-face, humans were able to see each other's face during the act, a fact that strengthened the bond between partners by encouraging communication (4). The second positive result of the forward tilting vagina was that it enabled a male's public region to massage the female's clitoris during sex. This opened the door for female pleasure during sex, the possibility of which, like pleasure in males, encouraged females to have sex.

Returning to the notion of premature births, we realize that while this is a positive in that is increases the survival odds of mother and child, it is also a negative in that a younger infant requires a greater amount of its mother's energy if it is to survive infancy (5). Whereas a mother had previously been able to return to her role within the social group relatively soon after giving birth, the shorter gestation period meant that she could no longer quickly return to group activities because her more vulnerable child needed increased care and protection. Because of this increase in time commitment it became harder for females to catch their own food, and more and more often they, and their young, were forced to go hungry (6).

It is at this point that female pleasure from sex became important. Because of this possibility for pleasure, in conjunction with the notions of female sex drive and ability to copulate at any point during their monthly cycle discussed in my first paper, females were now able and potentially willing to have sex at any time. This ability/interest coupled with difficulty in finding food led females to seek male assistance in supporting and protecting their young. To achieve male assistance females would effectively trade sex for meat, engaging in regular sex with males in exchange for a portion of his catch which he would share with her and her young. Over time, as the potential gains from these relationships became more and more apparent, the cooperation between males and females evolved from casual flings to full-fledged relationships (7). This evolution was further bolstered by face-to-face sex which helped to encourage communication between partners and solidify relationships. As males became increasingly connected to individual females, they also developed attachments to her young – many of whom they had sired during the course of their relationship. Thus, monogamy was born (8).

However, the evolution of monogamy was not this simple. Prior to settling into monogamous relationships, humans had chosen their partners according to the traits and preferences that they wished to see passed on to their young (9). While monogamy did offer the support of a family in raising young, giving them a better chance of survival, it did not offer the unrestricted access to the gene pool that humans were accustomed to, and required to ensure that their young would be endowed with the best genes available. So while humans generally adopted monogamy, it was by no means unheard of for them to engage in sex with another partner to increase the odds of creating the fittest young (10).

As discussed in the introduction, this meandering between monogamy and non-monogamy, or polygamy, still occurs today. While some people believe that it occurs due to a lack of values or respect for existing institutions, in truth, it appears to be genetically programmed into each of us at birth. That's not to say that the philandering that occurs in one out of five marriages is acceptable or even excusable, it's simply to point out that maybe there is some biological reason underlying infidelity (11).?

Returning to the differences in understanding of proper parentage between our generation and our grandparents' generation, it is true that we have seen a decrease in the percentage of the population that is married, as well as increases in divorce rate and single parent families over the past 50 years (12). These changes raise questions as to the importance of monogamy for human survival. As we move forward into the future, it seems that the need for monogamy and the support of a two parent family is continually decreasing. Gone are the days when it was necessary for people to hunt for their families and protect them from wild animals. Today it is quite common for a single parent to work, buy food, enroll their children in school or a daycare program, and be easily assured that their child will survive until adulthood.

So where does this leave us? Well, it certainly says nothing about the benefits of having both a mother and a father who are active in their children's lives, but it does suggest that single parenting has become increasingly easy over the past 50 years. As technology continues to improve, it is probably a fair assumption to say that raising children alone will only get easier in the future. If so, then what happens? Without monogamy being a reproductive necessity, do we revert to polygamy? In many ways it seems that we have already started in this direction, so what's there to prevent us from returning to it fulltime? Well, for one, there's always the evolved understanding of the benefits of having both parents, but again, this is something that can still be achieved in divorced households. In truth, it seems that the one factor that will continue to encourage human monogamy is perhaps also the least stable of the factors that encouraged it in the first place: the development of close relationships, and subsequently, love. In my opinion that's a lot of pressure riding on a little word.

References

1) Fisher, Helen E.. The Sex Contract: The Evolution of Human Behavior. New York: Quill, 1983. p. 95

2)"Sex, Reproduction, Parenting in the Evolution of Primates.",

3) Fisher. 1983. pp. 82-83

4) Ibid. 1983. p. 95

5)"Sex, Reproduction, Parenting in the Evolution of Primates.", (2005?).

6) Fisher. 1983. pp. 80-83

7)"Sexual Paradox: Complementarity, Reproductive Conflict and Human Emergence: Humanity's Evolutionary Heritage.", (2005?).

8) Blum, Deborah. Sex on the Brain: The Biological Difference between Men + Women. New York: Penguin Books, 1997. pp. 107-110

9) Baker, Robin. Sperm Wars: The Science of Sex. Great Britain: Basic Books, 1996. pp. 135-137

10) Ibid. 1996. pp. 134-137

11)"Cheating Wives: Women and Infidelity.", Davis, Jeanie Lerche. 2004.

12)"US Divorce Statistics.", Divorcemagazine.com. 2005.



Full Name:  Courtney Black
Username:  cblack@brynmawr.edu
Title:  Sexual Selection and the Evolution of Physical Traits
Date:  2005-04-29 18:05:46
Message Id:  14996
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


In 1871 Charles Darwin introduced the theory of sexual selection (1). This theory concerns the advantages that a given individual has over other individuals in the competition for mates. In the battle for a mate there are typically two deciding mechanisms that control who is selected and why. The first of these mechanisms is mate competition between individuals for access to other individuals, usually of the opposite sex, which has lead to the development of elaborate traits designed to give the bearer an advantage over their competition. The second of these mechanisms is mate choice which allows the individuals for whom competition ensues to choose one potential mate over another based on their evolved sexual traits. While each mechanism applies to both sexes, competition occurs most commonly between males, whereas choosiness is mostly associated with females. Across species this phenomenon has lead to the evolution of many sophisticated physical and sexual traits. Examples of these traits include the colorful tails of peacocks, the trunks of elephant seals, the horns of antelopes, and the bright plumage of many birds (2). This paper will discuss the various physical traits which humans have developed as a response to sexual selection and the role of these traits in influencing human mate choice.

Perhaps the most obvious example of physical evolution that has occurred in humans as a result of sexual selection is the size dimorphism between males and females. On average human males are 20 percent larger than human females (3). This distinction has arisen out of overt female preference of physically larger males because of the idea that they are stronger and better equipped to hunt food and to offer protection from predators and other males. Likewise, a preference for men with defined musculature and androgenized male faces with large chins and cheek-bones has also arisen (4). These features are a result of an abundance of the male hormone testosterone at puberty; when combined they illustrate overall health, the potential for economic successes (hunting, protection), and provide the bearer with an advantage when fighting with other males for mating rights (5). In addition to the visible effects of testosterone female choice also favors symmetry in both body and face. Like size, symmetry demonstrates health, whereas asymmetry suggests that the male may suffer from parasites, disease, or have been unsuccessful at obtaining food.

A final and perhaps less obvious, male evolution is gonad size. When compared to our primate cousins the human male has exceptionally large testicles. Though this evolution may not be immediately apparent to nor understood by choosy females, it can be vital to a maleˇŻs reproductive success. Large testicles allow a male to produce a larger amount of sperm which in turn provides them with better odds of fertilizing any female they may copulate with. This is particularly important in the event that a female has had more than one partner in a short span of time (6).

As seen in males, female symmetry is also a key indicator of general health. Yet while males focus their developmental energies on characteristics that emphasize their size and strength, females direct their efforts towards the development of features that suggest fertility. Examples of these characteristics include narrow waists and hips, estrogenized faces with small chins, and a limited amount of body hair (7). Across cultures and throughout history, the preferred female waist-to-hip ratio has shown to be around 0.7. Regardless of whether a female is thin or fat, if she posses this optimal waist-to-hip ratio, she is generally considered to be attractive. This male preference for women with waists that are significantly narrower than their hips reflects a good hormone balance, resistance to disease, and demonstrates her fertility by proving that she is not already pregnant (8). In addition to health, most men prefer women with hairless, child-like faces. Aside from distinguishing them from their male peers, estrogenized faces resemble the youthful faces of children in their smoothness and soft features. This youthfulness further suggests fertility by illustrating that a woman is within child-bearing age. Further carrying on the notion of youth, the lack of obvious hair over most of the female body both distinguishes it from the male body while at the same time allowing the child-like smoothness of their skin to be visible. At the same time, the presence of obvious body hair in the pubic region and under the arms is evidence that the bearer has reached sexual maturity and is capable of reproducing (9).

I have left the most obvious examples of female sexual traits for the end of my discussion because of the uniqueness of the circumstances surrounding their evolution. Contrary to popular belief, female breasts have no function beyond serving as a sexual stimulant. Ignoring the nipple and mammary glands which are in theory necessary for reproduction, the excess fatty tissue that makes up the breasts is entirely unnecessary for the function of producing and distributing milk. Instead, breasts seem to have developed both as a means of pleasurable stimulation for the female and as a way to encourage face-to-face copulation which in turn fosters the growth of close relationships. I will save the discussion of male and female relationships for a later paper, however the encouragement of face-to-face copulation is important to note. Before humans were bipedal copulation occurred from behind where the male view would have been of a femaleˇŻs fleshy buttocks rather than her face. But as humans began to walk on two feet, and as the development of close relationships became essential to survival, the vaginal canal shortened and titled slightly forward making frontal copulation the preferred method. Despite their lack of physiological function, it has been suggested that females breasts evolved as a way of mimicking the fleshy buttocks males were accustomed to seeing during copulation and as an agent of physical stimulation. Eventually those females with soft, rounded breasts spawned more offspring than those without, and breasts became the accepted norm (10).

Accepting that these traits are in fact the product of evolution, how then do we know that they are the result of human choice? Perhaps the easiest way to test human preference is by evaluating our own societyˇŻs ideals. The sources used in this paper stressed that female choice tends towards males who are physically able to demonstrate their health, vitality, and potential for economic success. A survey complied by People Magazine in their annual ˇ°50 Most Beautiful Peopleˇ± edition clearly demonstrates this theory. According to People, the ten most beautiful men of 2005 are (10-1): Jude Law, Usher, David Beckham, Johnny Depp, Clive Owen, Jamie Foxx, Matthew McConaughey, Colombian singer Juanes, Orlando Bloom, and Brad Pitt (11).

Physically, each of these males fit the characteristics suggested by our authors; symmetrical faces and bodies, defined musculature, and masculine bodies that demonstrate strength. The only questionable characteristic amongst this group of men is the female preference towards androgenized faces (*). Owen, Foxx, McConaughey, and Pitt all posses definitively masculine faces, whereas those of Law, Depp, and Bloom actually appear to be more feminine, while the faces of Usher, Beckham, and Juanes seem to be both simultaneously. During an informal discussion on this topic one female student suggested that Beckham may actually have a feminine face, but because he is associated with sports, he also comes across as being decidedly masculine. In either event, it is important to remember that the argument of our authors is that these traits evolved as a response to preference, and that for every preference which exists, there is almost certainly an opposing opinion. Therefore, while many women may prefer masculine faces, there are also those that would more likely choose a male with more feminine features. No single preference can be expected to be representative of society as a whole, but rather illustrative of a trend in taste.

The second set of characteristics preferred by women in sexual selection are those dealing with a manˇŻs potential for economic success. This category proved to be even more interesting than the first, especially when comparing it to male choice as we will see later on. As stressed by our sources, female choice is strongly centered on a manˇŻs ability to provide and protect. No where was this more apparent than the PeopleˇŻs description of the qualities that made these ten men desirable. Rather than focus solely on the description of idealized physical features, People utilized most of their caption space to discuss the charitable efforts and family-oriented nature of these men. In fact, DeppˇŻs most attractive quality was specifically listed as ˇ°his commitment to his familyˇ± (12). It was also pointed out that Pitt had topped this list twice before in 1995 and 2000 (13). These examples serve to illustrate two things: first, that women prefer men who are committed to their families because they are more likely to be invested in providing for and protecting their mates and the mateˇŻs children; and second, that sexual selection is not arbitrary. Trends and preferences do exist and are shared within cultures.

To keep this comparison as balanced as possible, my examples of male preference are also derived from a ranked list. According to Askmen.comˇŻs annual list of the ˇ°Top 99 Most Desirable Womenˇ±, the ten most preferred women of 2005 are (10-1): Halle Berry, Angelina Jolie, Beyonce Knowles, model Elsa Benitez, Brooke Burke, Heidi Klum, model Josie Maran, Charlize Theron, Monica Belluci, and model Adriana Lima (14). Again, each of these women fit the characteristics established by our authors. With waists that are significantly narrower than their hips and generous breasts, these women are identified as healthy and fertile. However, with the women, as with the men, we again run into the problem of facial preferences. Knowles, Benitez, Burke, Maran, Theron, and Lima all have feminine facial features. On the other hand, the faces of Jolie and Belluci have larger, more masculine features, whereas it is thought that BerryˇŻs face could go either way. As stated in my discussion of female preferences amongst male faces, it is important to remember that preferences are guidelines rather than rules.

Where these two lists differed significantly was is their use of caption space. While this may be in part due to a difference of sources, it is also probably a response to the difference in audience. Just as the list of men focused on the female preference for strength and stability, the list of women is oriented towards the male preference of female beauty over other traits. Therefore, while People used their captions to describe appealing personality traits of the men, Askmen.com focused on the physical beauty of the women. Examples of this can clearly be seen in their description of Knowles:


SheˇŻs a phenomenal creature, with a heart-stopping face, impossible curves, and the confidence and savvy to flaunt them both in clingy shirts and mini skirts. SheˇŻs got perfectly smooth skin, mesmerizing eyes, and the kind of moves that can make any man weak in the knees (15).


As well as in their description of Burke:


As the ˇ°beautiful bodyˇ± in the Bally Total Fitness commercials, BrookeˇŻs physique was famous well before her face or name ever were. And that speaks volumes to us. The fact that she has a pretty face as well easily cinched Brooke the No. 6 slot on AskMen.comˇŻs list for the third consecutive year, but let's face it: itˇŻs really all about that body. A perfectly contoured stomach, toned legs and a more than ample chest should secure Brooke a spot on this list for years to come (16).


Only briefly, in their comments on Klum, did Askmen.com center a caption on the womanˇŻs personality. And even then it was only to say that she was amicable; lending further support to the notion that males rank beauty first among attractants.

Overall, I agree with Darwin. Though they cannot be representative of society as a whole, and are certainly not representative of all of humanity, I believe that these lists are evidence enough to support the notion of specific sexual traits as an evolutionary response to human choice. Combined, they demonstrate that it is possible for certain individuals to posses characteristics which make them more sexually appealing, and subsequently more sexually and reproductively successful than their competition. Likewise, if a particular preference exists within a population (ex. the men and women who complied the lists discussed in this paper) than it is quite possible that these traits would become more prolific in future generations. However, these lists also illustrate that there is variance in taste; even within fairly predictable populations (ex. the anticipated readership of the two magazines used). While this possibility for difference in choice must be acknowledged, this comparison remains a valid demonstration of the presence of carefully selected physical traits within a given population.

References

1)ˇ°A Review of Sexual Selection and Human Evolution: How Mate Choice shaped Human Nature.ˇ±, Miller, G.F (1998).

2)ˇ°Sexual Selection and the Biology of Beauty.ˇ±, M©Şller, Anders Pape (1997).

3) Fisher, Helen E.. The Sex Contract: The Evolution of Human Behavior. New York: Quill, 1983. p. 96.

4)ˇ°Sexual Selection and the Biology of Beauty.ˇ±, M©Şller, Anders Pape (1997).

5)ˇ°Why Are Boys Prettier Than Girls? A Discussion of Sexual Selection.ˇ±, Hickman, Crystal (2003).

6. Baker, Robin. Sperm Wars: The Science of Sex. Great Britain: Basic Books, 1996. pp. 291-295.

7)ˇ°Sexual Selection and the Biology of Beauty.ˇ±, M©Şller, Anders Pape (1997).

8) Baker, Robin. 1996. p. 126.

9) Fisher, Helen E.. 1983. p. 98.

10) Fisher, Helen E.. 1983. pp. 95-96.

11)ˇ°50 Most Beautiful People.ˇ±, People Magazine (2005).

12)ˇ°50 Most Beautiful People.ˇ±, People Magazine (2005).

13)ˇ°50 Most Beautiful People.ˇ±, People Magazine (2005).

14)ˇ°Top 99 Most Desirable Women of 2005.ˇ±, Askmen.com (2005).

15)ˇ°Top 99 Most Desirable Women of 2005.ˇ±, Askmen.com (2005).

16)ˇ°Top 99 Most Desirable Women of 2005.ˇ±, Askmen.com (2005).

*) In my evaluation of both male and female faces I consulted with a group of four other female students to determine which sex we thought the celebrity facial features were most closely aligned with.



Full Name:  Courtney Black
Username:  cblack@brynmawr.edu
Title:  Why Sex?
Date:  2005-04-29 18:34:14
Message Id:  14997
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


What is it about the human mind that compels the body to engage in the bizarre activity of sex? Of course, thereˇŻs always the obvious answer: to procreate. But this answer ignores the real oddity of the sexual act: why do people crave sex even when they think that they do not want children? To get to the bottom of this problem, it is necessary to understand what it is that drives males and females to actually get together and engage in sex. It has sometimes been suggested that this is a learned behavior, and while to some extent that may be true, throughout history, humanity has successfully managed to have sex somewhere in excess of 6,511,859,430 times - and thatˇŻs only enough times to populate the world once over, today (1). With a figure like this, itˇŻs probably safe to say that sex is largely the product of instinct. This paper will explore the factors that drive men and women to have sex and discuss what role these factors play in our daily lives.

Sexually, the human male is significantly less complicated than the female. Because it is nearly impossible to pinpoint exactly when a woman is fertile (a point that will be discussed later) reproductively, it is in a manˇŻs best interest to keep his sperm inside his partnerˇŻs body at all times. As a result of this, at any point of any year, month, or day, the human male is theoretically physically able to engage in sex. In response to this almost constant readiness, males have developed highly sensitive penisˇŻ which enables them to derive great pleasure from intercourse. This pleasure is key to a manˇŻs reproductive success. Hormonal urges coupled with the potential for extreme pleasure both subconsciously and consciously drive males to attempt to copulate as often as possible, whether it is with a single partner or different partners (2).

The seeming simplicity of the male sex drive is a necessary response to the complexity of the female sex drive. The primary obstacle in a femaleˇŻs sexual motivation is her fertility. As mentioned previously, a man must essentially be prepared to have sex at any time because of the difficultly in detecting female fertility. Unlike many of our primate cousins, the human female hides rather than advertises her fertility. This probably occurs as a result of the human preference for monogamy (3). Despite this preference, humans are driven to exploit the gene pool and at times may have more than one partner in search of the best genes to pass onto their young. Naturally, this occurrence is unfavorable to the male who knowingly or unknowingly is left to raise another maleˇŻs young (4). However, if her mate is unable to discern when a woman is fertile than he isnˇŻt able to guard her as closely from other males, thereby giving her the opportunity to have other partners.

Unlike many primates that actively advertise their readiness to potential mates through various swellings, increased interest in sex, and even occasional changes in color, the human female does nothing of the sort (5). Having long ago lost this period of ˇ°estrusˇ±, the female body instead ˇ°creates an environment in which conception is relatively easy but only if the timing is absolutely right,ˇ± while at the same time doing nothing to advertise the appropriate timing to either herself or her mate (6). Females achieve this state by possessing fluctuating levels of interest in sex and irregular ovulation cycles. In this way not only does a woman hide her fertility from her partner, but she also hides it from herself. While both of these fluctuations are controlled by hormones, neither can be reliably predicted, nor does the presence of one necessarily indicate the presence of the other. That is to say, just because a woman is inclined to have sex, it does not mean that she is fertile, nor does her fertility imply that she will be interested in sex (7). As mentioned before, this unpredictability probably occurs as a means to facilitate a femaleˇŻs philandering, thereby giving her a choice in which maleˇŻs genes she selects, while also making it difficult for her mate to know that she has engaged in intercourse with another male (8).

No discussion of female sex drive is complete however, with out addressing the female capacity for pleasure. Like males, females too are capable of deriving immense physical pleasure from the act of sex. In fact, just as the penis is covered with nerve endings designed to receive and transmit pleasurable signals, the female is equally as gifted by the presence of a clitoris; the sole function of which is pleasure (9). The reason this feature was not mentioned previously, or in any major capacity, is because female pleasure, unlike male pleasure, is not necessary for sex to end in reproduction. However, the possibility of pleasure does encourage females to engage in sex.

I chose to write this paper as means of understanding why sex occurs. Recognizing the proliferation of sex and the sexually themed within our society, it is obvious that there must be some greater cause for interest in sex beyond reproduction. Or is there? While my brief study of this topic has demonstrated that to some capacity most sex does occur with reproduction at least subconsciously in mind, it also demonstrates that not all sex is intended to end in conception. In fact, most sex isnˇŻt. But if reproduction at some point is the ultimate goal, why then, is sex such an issue? Surely the continuation of our species is something that most people would find beneficial? Unfortunately, the presence of sexual taboos, particularly those in regards to religion and sex outside of marriage, has raised many questions about sexual practices (10).

Despite these taboos, the twentieth and twenty-first centuries have seen an extreme relaxation in the rules surrounding the accepted practicing of sex in the United States. Among the more revolutionary developments of this relaxation are: interest in female sexual satisfaction, the commercialization of sex, and an increase in the percentage of people engaging in premarital sex (11). Much of this liberalization has been in response to advancements made in the scientific study of sex, such as the work of Alfred Kinsey, which have allowed people to better understand why people engage in the act (12).

Why then, does sex remain a taboo? According to Robin Baker in his book ˇ°Sperm Warsˇ±: ˇ°Confusion over what is biological and what is cultural often arises because it is misunderstood exactly how much of our behavior actually has a biological baseˇ± (13). Yet in truth, as this paper has attempted to demonstrate, the desire for routine sex is a biological response programmed into all men and women - ultimately to prepare them for conception (14).

References

1)World Population Clock. Accessed: February 22, 2005 ~ 4:39 am.

2) Baker, Robin. Sperm Wars: The Science of Sex. Great Britain: Basic Books, 1996. pp. 8-13

3) Ibid. 1996. p. 10

4) Fisher, Helen E.. The Sex Contract: The Evolution of Human Behavior. New York: Quill, 1983. pp. 98-101.

5) Ibid. 1983. p. 88.

6) Baker, Robin. 1996. p. 10

7) Fisher, Helen E. 1983. pp. 88-89

8) Blum, Deborah. Sex on the Brain: The Biological Difference between Men + Women. New York: Penguin Books, 1997. pp. 110-112

9)ˇ°Amazing Facts About Sex.ˇ±, Bodyteen.com (2005).

10)ˇ°Basic Sexological Premises.ˇ± Weiss, David L. (2005?).

11)ˇ°Basic Sexological Premises.ˇ± Weiss, David L. (2005?).

12)ˇ°50s Sexuality Research Still Causing a Stir.ˇ± Mann, Denise (2004).

13) Baker, Robin. 1996. p. xviii

14) Ibid. 1996. p. 9



Full Name:  Elizabeth Rickenbacher
Username:  erickenb@brynmawr.edu
Title:  Sexual Dimorphism
Date:  2005-05-02 23:49:40
Message Id:  15022
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


The term sexual dimorphism (1) refers to the difference in form between individuals of different sex in the same species. Dimorphism in nature is easily observed; in many mammals the male is quite a bit larger than the female such as the case in humans. In birds (2), the male usually has vividly colored feathers in contrast with the female coloring. The presence of body parts such as horns or antlers that are used in quest for dominance are present in males are excellent examples of dimorphism that occur. Dimorphism transpires from the highest order mammal to the small worm order Osedax (3), which live on whale falls. The females feed on whale bones while the males inside the female. The males do not develop past their larval stage except to produce large amounts of sperm.
Through evolution (4) the struggle for reproductive success has yielded separate evolutionary paths for males and females leading to the sexual dimorphism observed today. Natural selection (5) has rendered dimorphism in species that do not seem advantageous, due to energy consumption and lack camouflage, however, biological reasons ensure that the reproductive success (6) of an organism is more important than long term survival. The innate yearning to protect ones young is to pass on genetic information to the next generation. Animals will take precautions and risk their own lives to ensure this. Prairie dogs (7) risk their own lives by giving warning signals to those around them to ensure the lives of those close to them genetically to ensure that genetic information will be passed on. When a prairie dog gives the warning signal, the signal sacrifices their location to the predator.
Genetic polymorphisms(8) are controlled by genes on sexual chromosomes(9). Humans have 46 different chromosomes. The X and Y(9) chromosomes on the human genome determine sex. Chromosomal abnormalities concerning the X and Y chromosomes can lead to disorders. Klinefelters syndrome (XXXY)(10), Turner's syndrome (X instead of XX or XY) (11), XYY syndrome (12), and Triple-X syndrome (13) are all disorders associated with chromosomal abnormalities. Diversity in behavior and orientation are not a function of abnormality in the human genome alone. Diversity and sexual orientation describe the gendeR (14) one is primarily oriented toward. Different sexual preferences such as Heterosexuality (15), Homosexuality (16), Bisexuality (17), and Asexuality (18) are and have been subject to immense scrutiny. The cause of varied sexual preference is still under debate. Both biological and environmental theories have been employed to further understand determining factors in sexual orientation.
Sexual orientation (19) refers to how individuals create feelings with regards to another individual. A persons sexual identity (20) may not necessarily reflect the sexual orientation which they are representing. The debate over what causes sexual orientation has long been under debate. According to Dr. Alfred Kinsey (21), almost any human under extreme circumstances, will interact sexually with any human. According to Kinsey, a minority of humans, about five to ten percent, can be considered fully heterosexual or homosexual. The rest of the population resides on a continuum and depending on external and predetermining factors will move between heterosexual and homosexual means (22).
Unlike most species, humans invest energy and means in different ways to ensure the passing of genetic information. Generally, a human female will give birth to 2-4 children in her lifetime. The gestation period of a human embryo to adulthood is about 18 years, much longer than any other animal. To ensure the maturation of the offspring, the mother must invest and take precautions to make certain the offspring will survive. The nature vs. nurture debate (23) has questioned the importance of ones upbringing in determining ones behavioral traits. The term nurture is no longer allocated in defining ones upbringing, but also ones genetic influence and upbringing. Environmental determinants of sexual orientation including birth order, social pressure, stressors, upbringing, and personal choices (such as religion) all play important roles in influencing sexual orientation choices. The choice hypothesis (24) concerning sexual orientation suggests that orientation is a matter of conscious choice. If this were true, then external influences certainly provoke thought and therefore choice. If we all are on a continuum as suggested by Alfred Kinsey (22), then external influences simply drive us to one side or the other.
Twin studies have been done to determine the prevalence of homosexuality and sexual preference concerning genetic makeup. Both monozygotic and dizygotic (25) twins have been compared. The first large scale twin study concerning homosexuality was done by Kallman in 1952 (26). In his study, 100% concordance was found between monozygotic twins and 12%-46% concordances between dizygotic twins. In 1991, J. Michael Bailey and Richard Pillard (27) estimated that the heritability of homosexuality is between 31%-74%. These studies provide examples that genes are not the only factor involved in determining sexual orientation, but definitely increase occurrences along with other external factors.
According to Dr. Eric Vilain (28), "Sexual identity is rooted in every person's biology before birth and springs from a variation in our individual genome". According to a study conducted at UCLA, Vilain and his team attempted to determine whether genetic influences could explain variations between female and male brains. They compared the production of genes in male and female brains in mice embryos that had not developed the sex organs which control hormone (29) production. Until this study was carried out, the view on sexual differentiation and behavior was reliant on gonadal steroid hormones (30) which acted directly to promote sex differences in neural and behavior development. Evidence found by Vilain et al indicates that even though gonadal hormones have significant effect on sex differences, they are not solely responsible. Genes, by directly inducing sexually dimorphic patterns of neural development, can influence the sexual differences between male and female brains. From his study he found that the identification of genes differentially expressed between male and female brains prior to gonadal formation proposes that genetic factors may have roles in influencing brain sexual differentiation (31).
In a study performed at the Maryland School of Medicine, a discovery was made that in adult males, sexual behavior in rats is determined by the actions of signaling molecules called prostaglandins (32) that "wire" the developing brain for sexual behavior. According to Margaret M. McCarthy (33), "if you stop the production of prostaglandins just before birth and just after birth, you erase adult male sexual behavior. Without prostaglandins during brain development, male rats do not develop the brain wiring necessary to respond to testosterone as adults." In this study, the researchers used non-steroidal anti-inflammatory medications like aspirin to interfere with prostaglandins during brain development. This study raises the question to whether non-steroidal anti-inflammatory drugs should be taken during pregnancy, and if taken they might affect sex differences in the brain of humans. According to this study, prostaglandin also organizes neural structures that control male sexual behavior. The newborn male rats treated directly with potent anti-inflammatory drugs after pregnancy, were completely asexual during adulthood.
Stress (34) and the repercussions that follow during pregnancy can also alter hormone (35) levels. Prenatal stress in rats has been found to change the sexual dimorphism of brain structures and the sexual behavior of male offspring. During the prenatal period, stress can lead to drastic impaired masculinization (36) of the brain. In order for the brain to masculinize properly, the brain depends on three elements: adequate levels of testosterone, aromatase activity (37), and brain estrogen receptor (38) density Henry C. et al. (39). If these requirements are not met, appropriate masculinization of the individual is unable to occur.
According to past evidence collected, sexual dimorphism in both the structure of the brain and in function relies heavily on the actions of the gonadal hormones. In recent studies however, evidence suggests that genetic mechanisms controlling sex specific neuronal characteristics do not occur separately, but together or in parallel with hormonal effects. Carrer H et al. (40) postulates that the shaping of the sex-specific neural circuits is subject both to the influences of the genome and to epigenetic influences of gonadal secretions, mainly testosterone and estrogen (41). The genomic determinants are not limited to the differentiation of the respective gonads but are also expressed directly in the brain, shaping sex-specific characteristics of neuronal and glial cells (42), including their sex-specific responses to estrogen. Sex-specific synaptic connections (43) and functional characteristics are influenced by steroids such as estrogen available to particular cells at different times during development. Different levels of such steroids effect growth and sexual differentiation in the individual.
Perinatal hormones (44) occupy a substantial role in organizing sexual dimorphism in the brain. Differentiation in behavior and chemical balance can effect and render great consequences in hormone organization if an environment is not ideal for a specific organization. Sexual preference and feeling female and male has to do with hormonal levels and reactions starting with perinatal hormones. Differentiation in hormonal levels can lead to a more masculine or feminine being. Adhering to these internal feelings and environmental factors determine our sexual preferences and will move us up and down the continuum we are located on. Future research conducted will provide further explanation and understanding in whether by choice or predetermined factors sexual orientation is determined. The social stigmas which surround this debate, will never completely subside, for we will never all be identical in behavior or orientation due to evolution.

1)Sexual Dimorphism
2)Birds
3)Osedax
4)Evolution
5)Natural Selection
6)Reproductive Success
7)Prairie Dogs
8)Genetic polymorphisms
9)Sexual Chromosomes
10)Klinefelters Syndrome
11)Turner's Syndrome
12)XYY Syndrome
13)Triple-X Syndrome
14)Gender
15)Heterosexuality
16)Homosexuality
17)Bisexuality
18)Asexuality
19)Sexual orientation
20)Sexual Identity
21)Dr. Alfred Kinsey
22)Kinsey means
23)Nature vs. Nurture Debate
24)choice hypothesis, Environmental determinants of sexual orientation
25)Monozygotic, Dizygotic
26)Kallman
27)Michael Bailey and Richard Pillard
28)Dr. Eric Vilain
29)Sex Organs which control Hormone
30)Gonadal Steroid Hormones
31)Brain Sexual Differentiation
32)Prostaglandins
33)Margaret M. McCarthy
34)Stress
35)Hormone
36)Masculinization
37)Aromatase Activity
38)Brain Estrogen Receptor
39)Henry C. et al
40)Carrer H et al
41)Testosterone and Estrogen
42)Glial Cells
43)Sex-specific Synaptic Connections
44)Perinatal Hormones



Full Name:  Sonnet Loftus
Username:  sloftus@brynmawr.edu
Title:  Regret on the Brain...
Date:  2005-05-03 00:42:15
Message Id:  15023
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Regret is one of the most unpleasant feelings. It is daunting to think, 'what if'. A mind can be thoroughly exhausted when a series of such "what ifs" runs through it. The possibility of acting on something and then be less than content with the outcome is discouraging. So I wonder, what makes regret weigh so heavily on the brain and is it possible to lessen the degree of regret?

I find that regret is something that is attributed solely to humans. If a dog knocks over his water bowl he will not think twice about it, unless of course he is scolded by his owner and made to take notice of what he has done. The dog does not care if the floor is wet—he does not have to clean it up, he can instead simply walk around it. If a human does something as simple as knocking their water glass over at a fancy restaurant, they immediately recognize the consequence of their action. They do not only have to ask for extra napkins, but they also have to succumb to the embarrassment of having everyone around them witness the commotion, which ultimately makes them regret that they had not been more careful.

Regret arises from a feeling of disappointment. When we regret, we are contrasting the outcome of our specific action to an outcome that we imagine, or more specifically, an outcome that our counterfactual thinking dreams up (1). This alternate outcome is presumably the more favorable option. Counterfactual thinking is a cognitive process that mediates emotions (2). This mediation of emotions involves the orbitofrontal cortex.

The orbitofrontal cortex is part of the cerebral cortex and is located at the front of the brain. The orbitofrontal cortex plays a significant role in emotional behavior by receiving inputs and sending outputs to several brain regions which include the cingulate cortex, hippocampal formation, temporal cortex, lateral hypothalamus, and amygdala (3). The amygdala, a component of the limbic system, is particularly important in that it organizes emotional responses. The amygdala is a set of subcortical nuclei that allows us to have emotional feelings and behaviors. The output of the orbitofrontal cortex has a direct effect on behaviors and physiological responses which include the emotional responses such as regret that are organized by the amygdala (3).

In determining what causes regret to weigh heavily on the brain, I wonder about the relationship that exists between regret and counterfactual thinking. The distinction is made that regrets are feelings and counterfactuals are thoughts (4). If we can control our thinking, then can we control our feelings? This leads me to wonder what role age plays in regret. It is much more relevant for an older being to regret than a child, as a child would often carry on their way after wrongdoing until an adult calls their attention to a specific action. In this case a child would act similarly to an animal knocking over their water bowl. It therefore seems logical that regret increases as the human brain matures. An adult has more complex thoughts. As thoughts become more complex regrets become more probable. An adult has more to think about—they have more obligations, more responsibilities, and most importantly, more to worry about because they are more likely to be held liable for their actions. I wonder however if rationalization has an effect on the degree to which one regrets. Is it possible for an adult to form a defense mechanism in order to make irrational acts or feelings appear rational to oneself?

Adults are theoretically better rationalizers. It is certainly the case that experience has a lot to do with this because adults learn from situations. This makes me think about the I-function. It is with experience in rationalization that I see a relevant role for the I-function. It is suggested that functions of the central nervous system control personality, with the I-function being the particular part that controls what we refer to as "self" (5). If the I-function is specifically related to the brain, then I think that the I-function has some control over the nervous system. If an individual, regardless of age is able to focus and suppress any negative thoughts that are running through their head, then they win the battle--they observe the situation and work things through. If this is possible, then it seems as though the feeling of regret can be lessened. Regret is focused around one's own actions and involves the thought of what could have been (4). I think that this notion of 'self' in regret largely encompasses the role of the I-function.

The I-function allows us to sort out the truths from the false realities. Perhaps this has an effect on regret. If the ability to rationalize and the ability to think things through more clearly is assisted with age and experience, then it seems logical that a more comfortable view of one's own view of 'self' would have an effect on how an individual portrays their repent. If the comfort level of one's view of self is expected to strengthen as one gets older, I wonder if it is possible for an individual to have a strong feeling of regret, but to conceal it well enough in their mind to get to the point where they deny its existence. The answer to this question I am unsure of, but I tend to think that concealing the feelings involved with regret would only exacerbate the situation by further creating false realities.

An experiment was conducted in order to examine emotional reactions of normal subjects against those who had damaged orbitofrontal cortices (6). In this gambling experiment, it was found that normal subjects were regretful of gambling decisions when they lost while the subjects who suffered from brain damage showed no regret (6). It was further found that normal subjects consistently made decisions that allowed them to minimize future regret, whereas the brain damaged subjects did not make such decisions, causing them to lose more often. I think that this illustrates the influence of rational behavior. The normal, healthy subjects recognized problems and were able to change their strategies.

Regret strongly forces an individual to cling onto the past. If we attach ourselves to the past in the form of regret, then we are theoretically denying our current presence (7). I think that the human brain is charged to hold onto the past. It seems logical that the emotional responses produced from the output of the orbitofrontal cortex will remain unchanged until the I-function steps in. I am a firm believer in the concept that you get out what you put in. Therefore the degree to which an individual moves into the present depends on how much they are willing to let go of past regret. A release of the past detaches an individual from self-pity and powerlessness that causes an individual to be mentally or psychologically absent (7).

This is worrisome to me because I am unclear if it is realistic to assume that an individual chooses absence of the current moment as a conscious attempt to avoid a present discomfort or if absence of the current moment is itself regret and recognition of present discomfort. If the mind-psyche is not in the present, then it makes sense that that the counterfactual thinking associated with regret causes the brain to dream up alternative outcomes that are more favorable, hence preventing the brain from accepting the current outcome which is an indication of the disappointment associated with wishing things could have been different. It is the act of wishing different outcomes that makes me believe that with regret, the brain is not avoiding discomfort, but instead recognizing the discomfort and pondering how things could have turned out.

Neurotechnology is currently providing new tools to influence human emotion, cognition, and sensory systems. It is perceived that neurotechnology will have profound consequences for how people identify social, political, and cultural problems (9). A theory has been postulated that identifies a chain reaction that begins once an emotion triggers a feeling (9). More specifically, this theory recognizes a change in body state as a response to an external stimulus. It is therefore hoped that by influencing the neurochemistry of the central nervous system via sensoceuticals, we can influence the conception and the self-reflection that our minds have of ourselves and the environment (9).

Regret is directly related to mental health. With the usage of sensoceuticals, a pleasure gradient is thought to alter the image that our mind has come up with of ourselves (8). This theory of neurotechnology suggests a neurocompetitive advantage, a form of competitive advantage that goes beyond what information technology can provide (8). By targeting multiple sub-receptors in specific neural circuits in the human brain, it is thought to be possible to eventually create a dynamic intracellular regulation of an individual's neurochemistry (10).

I wonder if it is truly possible to break the constraint of one's own neurochemistry and improve mental health with the usage of sensoceuticals. Sensoceuticals are something of the future. Neurotechnology has not yet advanced to the point where sensoceuticals are something of today's psycho pharmaceuticals (10). In order for sensoceuticals to be possible, it is necessary to break the brain imaging bottleneck and develop biochips for DNA, RNA, and protein analysis (8). Furthermore, I worry that the re-growth of damaged sensory tissues will be done correctly. More specifically, what if there are complications and the sensory tissues are not restored to their original condition that further effect mental health? I just think it is too risky to play with one's neurochemistry. I do not think that the function of neurons should be influenced by neuro-active drugs. I would rather see a mental state improved by improving one's self-image without the use of drugs. Drugs are often the easy way out. It seems to me that with respect to regret, neuro-active drugs would simply mask the emotion and inhibit an individual from growing from their unsatisfying experience. If an individual is not learning to cope, then they will most likely never be able to break the cycle of dissatisfaction of their self-image.

In conclusion, I think that although regret is an unpleasant emotion, it does serve a purpose. Regret helps to keep the brain functioning. If there was no way to gage how we personally feel about ourselves and our actions, then there would most likely be no way to maintain responsible behavior. Regret and the learning process it involves maintains mental health. I think that it is possible to lessen the degree of regret an individual will feel by learning from past situations, but I do not think that is possible or wise to use sensoceuticals to alter the image that our mind has come up with of ourselves.

References

WWW Sources
1) http://www.scifidimensions.com/Jul04/regret.htm; An online science fiction magazine that showcases research on evolutionary biology.
2) http://www.corante.com/brainwaves/archives/2004/06/01/forget_regret.php; The world's first blog media company that is an unbiased source on technology, science, and business.
3) http://www.driesen.com/glossary_o-t.htm; A site dedicated to neuropsychology, medical psychology, and psychology resources.
4) http://www.psych.uiuc.edu/~roese/cf/; A counterfactual research news site maintained by Dr. Neal Roese, Department of Psychology, University of Illinois.
5) Grobstein, Paul. Lecture-Neurobiology and Behavior. Bryn Mawr College. February 1, 2005.
6) http://www.betterhumans.com/News/news.aspx?articleID=2004-05-20-1; A site dedicated to information, analysis, and opinion on the impact of advancing science and technology.
7) http://www.fullyalivecoaching.com/insidenews.html; An inspirational site devoted to transforming lives for the better.
8) http://www.globalcoordinate.com/items/243755.aspx; A site to share a variety of technological stories around the globe.
9) http://www.corante.com/brainwaves/archives/000316.html; The world's first blog media company that is an unbiased source on technology, science, and business.
10) http://www.abc.net.au/rn/science/mind/stories/s1082012.htm; A site featuring the current news in science.



Full Name:  Sarah Malaya Sniezek
Username:  ssniezek@brynmawr.edu
Title:  Ways to Relieve Pain
Date:  2005-05-03 10:51:38
Message Id:  15028
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


The last two papers I had written were related to pain. I have always have wanted to know what are the best ways to relieve pain. My father being a physician, specializing in Pain management and Rehabilitation, and a devout Catholic has always shown me different techniques of relieving pain. I truly want to know what the best ways to relieve pain are.

Do these different types of relieving pain change your brain or is it all mental? I was beginning to feel that ways of relieving pain is mental. I have always had some sort of thought that it is all mental. Playing many sports, and being able to some how play during the game and not know I am injured is unbelievable. But why is it later on, one realizes they are in pain? There are even days that I know I am in pain, but I choose to ignore it. Am I really in pain, or have I put my pain aside? I cannot even really tell because I do not even know I am in pain until I really throw my back out. What is the best way to relieve pain, and why is that?

I have heard many different ways people try to relieve pain. The most interesting way for relieving pain that I have heard is through spirituality. My father truly believes in using many different techniques to help ones pain and spirituality is one way. Studies have shown that when one believes that there is some higher being, God, their pain tends to go down. They are calmer and have less stress upon themselves. The people that also have this spirituality tend to get rid of chronic pain if they truly believe. How does this work? There have not been many studies to show how and why this works, but many believe that pain, in some way is a way of thinking. If you are able to calmly relax and think about things other than your pain and leave your pain to some higher being than pain is relieved. Studies show that patients who even believe that they are taking some sort of medicine that will help them, even though it is not proven to, it changes their brain states and they begin to feel better. This is also unexplainable, but I do feel it goes under the relaxation techniques of relieving pain.

There are many healing scripture that people read while in pain that tend to help them put themselves in to perspective. This best helps people relieve their chronic pain. Many people have been known to have cancer and have only a little time to live. There have been stories that people where "saved", relieved of their pain or illnesses because of their belief in a higher being. I wonder how much of it is true, or is just when one has so much faith, there is a chemical change within their brains.

Another way people tend to relieve pain is through relaxation. These relaxation techniques reduce the tension in the muscles and keep the pain from getting worse and can relieve some of the pain. The relaxation varies from person to person and situation to situation. It is often difficult to relax when there is just too much on your mind. When able to relax the technique are very helpful to relieving pain, helping with sleep, gives you more energy, and reduces stress and anxiety. Many feel though that pain medicine and/or using cold/hot packs work faster to relieve pain because it relaxes one quickly. If one really is in pain there are natural inflammatories that can help to loosen your body so that one is capable of performing these tasks to relieve pain.

There are basic rules one must know when beginning the relaxation techniques. Fist off, one must understand that the relaxation process takes a couple of weeks of process before one can begin to feel the results. Even with this said, your ability to relax is different each day, so one must be patient. There are numerous different ways to relax, and not one way is best for everyone. Try many different way and use the best one for yourself.

The another way to relieve pain is through acupuncture. Many believe that acupuncture is worthless, and then there are many who live by it. Acupuncture has been around for centuries and began as a kind of anesthetic in China. Today it has expanded its use to relieved many different types of pain- acute and/or chronic. In acupuncture, tiny needles, about the size of one of your arm hairs, are inserted in different points on your body. There are different combinations of points on one's body that are useful in helping relieve certain types of pains.

Most acute conditions improve within first 4 to 6 sessions. Usually a block of 10 to 15 sessions is required before assessment of effectiveness is determined. In more chronic conditions, more sessions may be indicated. Again, reassessments are performed every two to three weeks to determine the need for further treatment. Once condition is improved, then acupuncture treatment can be tapered off accordingly. The frequency of visits is a function of the condition and health of individual and will be determined by the patient and physician. (1)


There are some useful dietary modifications that are known to help with pain and inflammation. These on should try before using medication, but if these do not work then, fast pain relief can be gotten from medication.

"Dietary modifications
Eliminate polyunsaturated and artificially saturated fats and increase intake of omega-3 fatty acids in any form.

Supplementation
The B-vitamin niacinamide can be very helpful for osteoarthritis. Start with 500 milligrams twice a day, increased by 500 milligrams at three-week intervals if necessary to a maximum daily dose of 2,000 milligrams. Other supplements that support an anti-inflammatory state include a multivitamin, magnesium (400-1000 mg/day), EPA/DHA (1-2 g/day), and coenzyme Q10 (100 mg/day).


Herbal treatments
Ginger, especially in dried form, and the Ayurvedic herb Boswellia, or the extract made from it, boswellin. Health food stores sell it; follow dosage recommendations on the products. Ginger and boswellin may provide relief in fibromyalgia.

For extensive bruises and hematomas resulting from trauma, an excellent treatment is bromellain, the pineapple enzyme you can find in capsules at health food stores. Take 200 to 400 milligrams three times a day on an empty stomach. Bromelain promotes healing of tissue injuries, but occassional individuals may develop an allergic rash from it; discontinue it if you develop any itching." (1)

These examples of relieving pain are very interesting because they are alternatives to taking drugs. I think that using all three of these ways to relieve pain is the best. They all do rely on relaxation. I think that even believing in a higher being and acupuncture is just another form of relaxation. As for these three different alternatives to relieving pain, I am surprised in how well they work.

For the last three weeks, I have been trying these three techniques in pain relief. I have chronic back pain, headaches, and other joint pain. The aspect on believing in some higher being, is something I already practice, but I tried to take more down time to pray and reflect. I usually combined this praying with my other relaxation techniques. I did not like much of the intense stretching to relax, but I did like taking deep breaths, reflecting on my injuries, imagining my body floating, etc. I was in shock how my body began to relax quickly and then I was able to stretch my muscles.

I would combine relaxation through prayer, breathing, and stretching. And I tried Acupuncture treatments. When getting treated for my pain, when I did not relax before and during I found it less affective. When I was able to relax before getting treated and while getting treated the pain relief was a lot more.

There was though, a day when I was unable to move because of my back. Relaxation and acupuncture were unable to help me loosens my muscles. This is when most people tend to take medicines to help their muscles loosen up. The medicine here is crucial to ones recovery and helps to speed up the process and minimize the pain. There is though an affective way of relieving pain through natural herbs and are better than going straight for the medicine. I have taken many supplements and changes my diet to give my body more support in fighting my pain.

Using all of these techniques, with a combination of your own, do speed up ones process for pain relief. Trying new things is important if ones pain is crucial. Something that did not work for someone else could be the key to your pain relief. Your body changes everyday and there are many different reasons why you might be experiencing pain, but just be prepared with many different ways of relieving pain for your certain injuries. Remember though, that if the pain is not to intense, the best way of healing it is through a natural way.

I find pain relief is very important, but wheat is the key to it? Is it all about your mental states, or is it truly something one takes in? I guess we will just have to wait and see till there is more information about pain.

References


1)Advanced Medical Rehab and Pain Center

2)How to Relieve Pain without Medication



Full Name:  Amy Venditta
Username:  avenditt@brynmawr.edu
Title:  Tick, Tock; The Wonder of Our Internal Clocks
Date:  2005-05-03 18:45:02
Message Id:  15029
Paper Text:
<mytitle>

Biology 202, Spring 2005
Second Web Papers
On Serendip


Today is a Saturday, and I woke up at 7:30am. Despite my numerous attempts to fall back to sleep on one of the only days that I will be able to sleep in before the school year is over, I was wide awake at 7:30am, at least three hours before I had intended. After leaving my disgruntled roommate and going on an early morning run, I realized two things: one; I was hungry, and two; I had a dream that I was pregnant and surrounded by adorable babies.

All three of these things, waking up at 7:30am despite my attempts to sleep, being hungry, and dreaming about babies, occurred because of my internal biological clock, located in the hypothalamus of my brain. Scientists have determined that all living things have some sort of internal clock; although it is only in some mammals that this clock is located in the brain. These internal clocks have been evolved to help adapt to the Circadian rhythm of life. Circadian rhythms (derived from Latin words 'circa', meaning 'about', and 'diem' meaning 'day') are necessary for living things to adapt to night and day, temperature changes, hunger, and even mood. Internal biological clocks have many purposes and influence much of living beings' activity. The biological clock is composed of an environmental input receiver, genes, and an actual timekeeper.

The environmental input receiver includes both the light and temperature detectors. These are significant because it is the light detector that controls sleep patterns as well as moods. The genes within the internal clock are there because they have the ability to make sure that other genes throughout the body are influenced and controlled by the clock. These genes act as transporters of specific instructions (from the internal clock) that produce proteins. It is the levels of these proteins that fit into rhythmic patterns, producing oscillating biochemical signals. Finally, the actual clock within the internal biological clock is composed of a timekeeping mechanism made of chemicals. (1)

Our internal clock, hoarding the ability to regulate our bodies with the time of day and the seasons of the year, is located in a small cluster of nerve cells within the hypothalamus of our brains. The hypothalamus itself is responsible for regulating hormone levels and influencing emotions. (2) This cluster of nerve cells, located right above the optic nerve, is called the suprachiasmatic nucleus, more simply known as SCN. When the SCN is destroyed in normal living being, all rhythms, such as sleeping and eating, are gone. Although these activities remain, they are done randomly, since there is nothing to tell the body when it is appropriate to eat and/or sleep. There is a specific protein, released in the brain, that is responsible for telling cells when to grow and when to rest, and is associated with the internal clock. Research has determined that although biological clocks cannot be slowed down or sped up, using this protein, they can be reset. These results provide future help to those with jet lag and/or other sleeping disorders. (3)

Internal biological clocks are able to communicate specific methods of timing and timing signals to the rest of the body by use of chemicals and proteins. It is also assumed that lesser internal clocks reside in each individual cell. It is the SNC that is responsible for the synchronization of all the individual cell-clocks, mainly through use of transporter hormones. For example, when daylight hits the light receptor in the hypothalamus (notice that it is not the same light receptor as that within the optic nerve), the SNC sends signals throughout the body telling the individual clocks in the cells that it is time to wake up. Our circadian rhythm, despite the earth's rotation which gives us exactly a twenty-four hour day, is approximately twenty-four hours and ten or twenty minutes. Thus, sunlight is able to reset our biological clocks everyday so that our circadian rhythm is in sync with a normal twenty-four hour day.(3)

So this tiny cluster of nerve cells located in a sliver of the brain essentially directs all of our actions. I can comfortably say that my brain directs me; although I am sure that many would argue with this. 'What about your heart?', one may say, 'how do you explain doing things when you don't seem to have a purpose?'. These are questions that I have considered, and questions which I have left unanswered. Although I believe that my brain directs me, sometimes it directs me in many different directions at once. How is it possible for me to have so many conflicted thoughts and feelings, all originating from the same brain? Emily Dickenson's description of the brain helps me to clarify my thoughts, and hopefully get everything less wrong.

'The Brain - is wider than the Sky -
For - put them side by side -
The one the other will contain
With ease - and You – beside-'

Emily says that 'you' are contained in the brain. I believe that 'I' am a bunch of conflicting randomness, which gets information through use of my five senses, and soaks it all in. My brain is responsible for sorting through and making sense out of the conflicting randomness that is me. Thus my best definition for my brain at this moment is the director and organizer of me. In this way, my brain is somewhat its own separate entity since 'I' am merely something that is included within it. What I bring to my brain is jumbled information, and what my brain does is organize it and tell me what to do with it. Therefore, I believe that there are many thoughts and things that my brain tells me that I do not control.

The internal clock is one of these things that the brain does without us knowing. It gets the information from sight, hearing, and feeling and determines when the body should sleep, when it should eat, and how it should feel. Between 6am and 8am, our internal clock signals to our cells that it is time to wake-up. Our internal clock sends out information and produces proteins that tell our metabolic rate, blood pressure, and glucose levels to increase, getting our body ready for the day. Around 11am to midday, we are able to concentrate the best, since our internal clock gets our body ready to do the things that we need to do. At dinner time, approximately 7pm, our internal clocks send messages and proteins to our digestive system and liver to get them ready for an evening meal. In these ways, it becomes obvious that our internal clock directs our many of our activities throughout our day. (4)

Just like with any other part of the brain, in order for the internal clock to make things happen in the body, there needs to be some sort of input and output (whether the input and output originate within the brain or never leave the brain is irrelevant). Most inputs to the internal clock come from the environment rather than originating in the brain. It is up to these environmental inputs to set and reset the internal clock. For example, in the spring, we lose an hour of sleep because we spring forward. Although since our body is on a specific schedule and we may take a few days to get used to the time change, the sunlight in the morning still acts as an input and reset to your internal clock, telling it to produce proteins to wake your body up and get it ready for activity. The internal clock takes the inputs and organizes them into a time frame. The outputs are then bodily actions occurring in the timeframe that the internal clock has organized. The following figure shows this relationship between inputs, outputs, and the internal clock. (5)

The internal clock keeps the time and maintains the Circadian rhythms throughout the body. Thus, it directs more than just sleep and eating patterns; it also controls things like body temperature, blood pressure, oxygen consumption, alertness, hormone secretion, and heart activity. Looking at all of these things that the internal clock has the ability to direct, it is easy to see how important the internal clock really is. When the internal clock is disrupted in some way, whether by time change or lack of sunlight, the body reacts in undesirable ways. For example, when you travel to and from different time zones, you experience 'jet-lag'. This is due to the fact that your circadian rhythms and internal clock are not in sync with the environment. The more scientists learn about our internal clocks and the proteins that they produce, the more information they will have about treating 'jet-lag' and other sleeping disorders. (1)

Many people feel more tired, upset, or depressed in the winter time, when they are exposed to a lesser amount of sunlight. This has become popular to the point in which it has been named a disorder: seasonal affective disorder (SAD). This disorder occurs because the Circadian rhythms are not as strongly synchronized due to the lack of sunlight. Therefore, the internal clock is not as easily able to synchronize with the environment, and thus is not able to send the correct proteins at the correct times. This leaves the person tired and depressed. As the SCN gets the signal of light, it prepares the body for activity by producing proteins. In order to be 'prepared for activity', your body needs to have adequate energy and alertness, since without these things, one will feel tired and depressed. Scientists and doctors believe that light therapy synchronized with an individual's internal clock will result in increased mood and energy. (1)

So far, I have explained why I woke up at 7:30am on a Saturday, even though I had wanted to sleep until 10:30am. This proves my point in a way that my brain is separate from me, and I am just in my brain. I wanted to sleep in for at least three more hours. My body, however, and my internal clock knew that it was light outside, and that I had been waking up at 7:30am for the previous few days. Despite my desire to sleep in, my internal clock directed my actions and I was awake. But what does my internal clock have to do with me being hungry? Since the internal clock also directs metabolism, this makes sense. My internal clock told my body to get ready for activity, and to do that, my body needed fuel; hence, my hunger.

The remaining mystery is what my internal clock has to do with my dream about babies. Women talk about their internal biological clock ticking. Our eggs are limited and they are only in prime condition for a short time. But can our internal clock really tell us when we should put these eggs to use and procreate? The answer is yes. This is because one of the many aspects of the body that the internal clock directs is hormone secretion. Menstruation is a process that requires timing and occurs in a rhythm. The hormone released that control menstruation need to be released at the appropriate times in the appropriate Circadian rhythms. Menopause is the end of menstruation. It is between the beginning of menstruation and menopause that a woman has the capability to bear children. Although menopause results as the ovaries age, it also results as the internal clock ages. As we age, our internal clock goes faster. This explains why older people tend to wake up earlier, become more tired than they used to, and take naps throughout the day. (6)

The internal clock, therefore, can also be a timekeeper for the amount of time before menopause: the amount of time a woman has to procreate. As the internal clock ages and becomes slightly out of sync with the environment by going faster, the release of hormones will be faster. This is why during pre-menopause and menopause, hormones are so out of control for many women. Studies have been done that show that the menstruation hormone release in young women is very rhythmic and predictable, and as women age, the release of these hormones becomes more erratic. The internal clock knows when a woman is most fertile, and knows how much time of fertility she has left. (7)

Although I am only 22 years old, my hormone secretion from my internal clock will become increasingly erratic as I age, and I will soon lose the ability to conceive. My internal clock knows this, and is attempting to direct to take advantage. I believe this is what all of my baby dreams mean. My internal clock is indeed ticking and my time is limited. Therefore, my SCN and hypothalamus are directing me to make some babies while I still can. They are doing this through my hormone release, which is getting amplified in my dreams.

So, my theory about my brain and my internal clock is hopefully a little closer to the reality, and thus a little less wrong. As shown by my internal clock, my brain is separate from me. Yes, I am in my brain, but my brain controls things and does this that I am unaware of and even things that I disapprove of. My internal clock controls and directs my body, my mood, and even some of my dreams, whether I want it to or not.

References

1) The Genetic Science Learning Center, "The Time of our Lives"

2) SFN Brain Briefings

3) Biological Clocks

4) Health.telegraph, "Losing an Hour Could be Bad for Your Health", 03-23-05

5) Ask A Scientist, General Biology

6) Science Daily, "Internal Clocks Keep Everything From Humans to Algae Ticking"

7) Phyllis M. Wise, Ph.D., Scientific American, Women's Medical Issues, Women's Health, "Brain as a Clock for Menopause"

8) SFN Brain Briefings

9) The Tummy Clock

10) Biological Clocks

11) Dr. Michael E. Geusz, Current Research Projects