Spring 2010 Issue by Carolina Scientific

carolina

sc1ent1fic Undergraduate Magazine

Spring 2010

UNC-Chapel Hill

Volume II, Issue II

Carolina Scientific

Mission Statement: Founded in Spring 2008, Carolina Scientific serves to educate undergraduates by focusing on the exciting innovations in science and current research that are taking place at UNC-CH. Carolina Scientific strives to provide a way for students to discover and express their knowledge of new scientific advances, to encourage students to explore and report on the latest scientific research at UNC-CH, and hopes to educate and inform readers while promoting interest in science and research.

From the Editors To our readers: â&#x20AC;&#x192; We have been with Carolina Scientific since the beginning and as we are nearing our senior years, we will be transitioning to new leadership in the hopes that future generations of Carolina students can take charge and keep Carolina Scientific alive. It has been absolutely amazing to watch Carolina Scientific grow as and to work with other undergraduates who are just as passionate about science and research as we are. We hope you enjoy this last issue of the 2009-2010 school year! ~Adele, Ann, Lenny, and Natalia

Lenny Evans is a junior Physics and Math double major

Spring 2010, Volume II Issue II

Adele Ricciardi is a junior Biochemistry and Biology double major

Natalia Davila is a junior Studio Art major and Chemistry minor

Ann Liu is a junior Biochemistry and Business double major

Carolina Scientific

Contents 4

Stringing Together Two Incompatible Regimes of Physics

Rebecca Holmes

6 8 10

The HIV-VAC: Pre-exposure For HIV May Prevent Transmission

Boys, Soy and Breast Cancer

Microbial Source Tracking: Improving Water Quality One Microbe at a Time

16 18 20 22 24 26 28 30 32 34

Rebecca Searles

How To Fight Back Against Your Own Body Garrick Talmage Exercise: Truly the Best Medicine Mary Morawetz

Helene Kirschke-Schwartz Natalia Stopa

Degradation, Conservation and Appreciation of the American Oyster

Jacob Hill

Vanishing With the Trees: Australia’s Tree Kangaroos Elizabeth Bergen Showy Traits: Why Don’t Human Males Have Them? Kyle Roche Obesity: Tackling A Big Problem With Knockout Mice

Abby Bouchon

Less Is More: Improving Collaborative Genome-Wide Association Studies Keith Funkhouser CLIC Clack: Understanding Chloride Channels

Joshua Thompson

When You’re Your Own Worst Enemy: The Connection Between Genes and Lupus Nephritis

Mary La

Fun In The Sun: The Development of Organic Solar Cells

Lindsay Ross

Undergraduate Research Spotlight Top Ten Questions about Undergraduate Research

Spring 2010, Volume II Issue II

Carolina Scientific

Stringing Together Two Incompatible Regimes of Physics Rebecca Holmes, Staff Writer

NC’s theoretical physicists are explaining the universe on a blackboard. Using the tools of mathematics, theoretical physicists can explain observations, like why excited atoms produce bursts of light only in certain colors. Quantum mechanics demystified this effect, which gives color to neon lights. Theorists can also predict new and strange behavior—for example, black holes appeared in solutions to Einstein’s equations before they were ever observed by astronomers. But the holy grail for theoretical physicists is the “unification” of different areas of physics; that is, showing that different phenomena can be explained by one theory. Theory is powerful in particle physics. Paul Dirac (1902-1984), a pioneer of quantum mechanics, started by modifying a previous quantum mechanical equation— the Schrödinger equation—to make it consistent with Einstein’s theory of special relativity. He noticed that the new equation gave two solutions for an electron: one with positive energy and one with negative energy. A particle with negative energy did not seem possible, but the equation predicted it. Dirac thought the negative energy particle might behave like an electron except with a positive charge. In 1932, Carl Anderson discovered Dirac’s particle and called it the positron. By listening to his

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equation, Dirac had predicted the existence of antimatter [1]. At UNC, researchers are working on the cutting edge of elementary particle physics. Dr. Louise Dolan, postdoctoral associate Dr. Thomas Creutzig, and graduate student John Corn want to explore the connection between two successful areas of physics: quantum field theory and general relativity. Quantum field theory is the foundation of the Standard Model of particle physics, which explains the behavior of electrons and a zoo of other tiny particles. General relativity is Einstein’s description of how things with mass bend space and time—it explains gravity. But the two theories seem disconnected, unaware of each other’s existence.

larger. It predicts the acceleration of gravity on the surface of the Earth, the orbit of the moon, and the attraction between massive clusters of galaxies millions of light-years apart. Quantum field theory describes the interactions of elementary particles on a tiny scale. These particles can diffract and interfere like waves, and they cannot be pinned down to an exact position. They sometimes seem to appear suddenly out of nowhere. Both theories provide an excellent description of their respective regimes, but when physicists try to combine them, contradictions appear. The smooth geometry of Einstein’s spacetime is incompatible with the roiling mess of energy and particles at the smallest length scales. And this is a big problem for both theories. Dr. Dolan’s group is tackling the problem with the tools of string theory. String theory is an alternative to the Standard Model of particle physics which replaces particles with tiny vibrating strings described by general relativity, making it a proposed unification of quantum mechanics and Einstein’s theory. It has been a hot Figure 1. Artist’s conception of space warped around a black hole. topic in contemporary theoretical physics because of its elegance “In theoretical physics,” says as a “theory of everything”—and Creutzig, “different theories have controversial because of its lack of worked in different regimes.” testable predictions. The theory of gravity can deal Graduate student John Corn with objects of everyday size and says that the goals of string theo-

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Figure 2. A Calabi-Yau mainfold, a representation of the “extra” dimensions that string theory predicts.

ry are changing. Popular science writing from ten years ago does not necessarily capture the spirit of string theory today. If physicists are less focused now on the actual strings of the original theory, “we have still gotten a certain benefit out of it,” says Corn. One of those benefits is the so-called anti-deSitter space/conformal field theory (AdS/CFT) correspondence, first proposed by Dr. Juan Maldecena of the Institute for Advanced Study in 1997. AdS/CFT is a relationship between a string theory and a quantum field theory. The string theory describes a universe with gravity, the field theory describes a universe with fewer special dimensions and no gravity—and yet physicists can “translate” between the two. Every important quantity in the string theory with gravity has a corresponding partner in the field theory without gravity [2,3]. The two universes are completely equivalent. No information is lost when a researcher uses mathematics to switch between them—and this can be crucial when calculations turn out to be easier in one of the two worlds. The field theory world,

which has no gravity, exists on the boundary of the string theory world. Imagine a sphere: on the inside, in three dimensions, is a universe where string theory reigns and gravity exists. The surface of the sphere, which is twodimensional, is a purely quantum mechanical universe with no gravity. All the information about the inside of the sphere is encoded in its surface [2]. This is also called the holographic principle—think of a hologram, a two dimensional object which can display information about a three-dimensional object. This is also a key principle in the study of fluids—“If you know how much fluid is flowing out of a surface, you know everything about the fluid inside the surface,” says Creutzig. AdS/CFT works on paper. But can experiments test it? “AdS/ CFT is the crowning achievement [of string theory] in terms of making predictions,” says Corn. The equivalency of results in the two regimes of AdS/CFT has been experimentally verified. [2] Other physicists, both theorists and experimentalists, have been using the “translating” power of the theory to make difficult calculations possible. The mathematics of the theory seem to apply to some realworld physics situations in fields such as condensed matter physics. Many theoretical physicists borrow mathematical concepts as the framework for physical theories. “If you want to do theoretical physics you have to have a patience and understanding for mathematics,” Corn says. Zane Beckwith, another graduate student working in condensed matter physics, adds, “But the math

isn’t the physics. The math helps you do the physics.” Theoretical physicists sometimes use approximations and their intuition instead of the full rigor of the mathematical structure they draw from. This is a distinguishing characteristic between physicists and mathematicians. “Math papers are way easier to read,” says Corn with a laugh. “Every step is there.” Can a theoretical physicist discover something, like the experimentalist in the lab? “A theoretical physics discovery is finding out that two seemingly disparate things are really the same,” says Beckwith. The AdS/CFT correspondence could help to show that gravity fits in with the rest of nature, bringing researchers closer to a “theory of everything”. Theoretical physicists would love to discover that everything in the universe—from an electron lighting up a neon sign to the black hole at the center of our galaxy—is really following the same rules.

~Rebecca Holmes ‘11 is a Physics major

References

1. G. Kane, in Modern Elementary Particle Physics, (Westview Press, 1993). 2. Interview with John Corn, Dr. Thomas Creutzig, and Zane Beckwith. 2/18/10. 3. E. Witten. Adv. Theor. Math. Phys. 1998, 2, 253-291.

Spring 2010, Volume II Issue II

Carolina Scientific

The HIV-VAC: Pre-exposure

treatment for HIV may prevent transmission Rebecca Searles, Staff Writer

Credit: The Center for Disease Control and Prevention’s Public Health Library

fter recent HIV vaccine trials in various countries yielded disappointing results, UNC’s School of Medicine is shedding a new light on HIV prevention with a study on PrEP treatment. Researchers discovered that antiretroviral preexposure prophylaxis (PrEP) treatment protected against intravenous and rectal transmission of HIV-1 in humanized mouse models. By administering antiretrovirals to healthy mice prior to HIV-1 exposure, transmission was prevented almost entirely. The research, published in January, was co-authored by J. Victor Garcia-Martinez, Ph.D., and Paul Denton, Ph.D., of the UNC School of Medicine. Others from the University of Texas and the National Cancer In-

stitute in Maryland also contributed [1]. “These results provide evidence that a universal approach to prevent all forms of HIV transmission in all settings might be possible,” said Garcia-Martinez. “This could greatly facilitate the implementation of a single program capable of targeting virtually all groups of people at high risk of HIV infection [2].” Garcia-Martinez and his colleagues developed a humanized mouse model for their research, called “BLT” mice—mice that have been transplanted with human bone marrow, liver, and thymus cells. The transplant results in a fully functioning human immune system in the mouse’s body. Using the mice, researchers designed an in vivo study to investigate whether HIV-1 transmission can be blocked by administering common HIV-1 medications prior to HIV-1 exposure. The study consisted of two groups of mice, a control group that received no treatment and an experimental group that was administered the antiretroviral drug therapy, Truvada. Both groups were then exposed to HIV, either rectally or intravenously. None of the nine treated mice that Credit: HIV Web Study. Illustration by David Ehlert, MAMS, CMI. were exposed rectalFigure 1. HIV primarily infects vital CD4+ (helper) T cells that support the immune ly became infected, system. An infected host cell reproduces HIV daughter cells that spread to infect other while 12 out of the host cells. After fusing with the host cell membrane, the virus’s DNA becomes integrated 19 control mice bewith the host DNA, producing new viral RNA. The viral RNA codes for proteins that will came HIV positive assemble to form a newly budding HIV cell.

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Credit: Dr. J. Victor Garcia Martinez

Figure 2 a-b) Black spots indicate where HIV-infected RNA is present in a non-treated control mouse versus a mouse that received systemic PrEP. c) When cultured with active HIV cells, treated mice tested negative for the infection in various tissue specimens. d) Using real time PCR analysis, tissues from treated mice tested negative for the presence of HIV-1 DNA.

following rectal exposure [1]. Intravenous exposure is a more difficult transmission route to block, yet 7 of the 8 treated mice were protected against the virus [2]. All six of the intravenously exposed control mice were infected. In a previous study, Garcia-Martinez and his team found the treatment to also be effective at preventing vaginal transmission. In conjunction with his latest findings, Garcia-Martinez has now demonstrated that PrEP treatment can block the spread of HIV through three of the most common modes of transmission, which account for almost 90 percent of the world’s HIV infections [2]. Denton said that the results from the BLT mice cannot be applied directly to humans, but the data demonstrate a great potential for blocking multiple HIV transmission routes in people [2]. Currently, PrEP trials in humans are threatened to cease because of health concerns and a lack of evidence that PrEP treatment works. In humans, a lack of compliance to the strict PrEP regimen can result in increased resistance to the drugs if infection does occur [1]. These drugs can also cause a slew of adverse side effects such as abdominal pain, insomnia, mood swings, nausea, headache, and even liver failure. However, Garcia-Martinez’s research offers more

solid evidence of the treatment’s potential. He and his colleagues hope that their study’s results will encourage the continuation of testing with PrEP clinical drug trials. “Now the head of a clinical trial can take this research to a ministry of health or review board and say, ‘Look, we have positive experimental evidence that if we do this right, it has a chance to work,” Denton said [2].

~Rebecca Searles ‘11 is a Biology and

Psychology double major

References

1. P.W. Denton, et al. Plos ONE. 2010, 5. 2. PrEP treatment prevented HIV transmission in humanized mice. UNC News. 2010.

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HOW TO FIGHT BACK AGAINST YOUR OWN BODY Garrick Talmage, Staff Writer

mmune cells are some of the most complex in the cleotides are essentially randomly added in between human body. They help us fight infections from the V and D regions and the D and J regions, creatpathogens such as bacteria and viruses, and they are ing even more diversity. A combination of these facalso important in other disease states such as can- tors and others allow an enormous variety of immune cer. Immune cells are thought to contribute to either cells to be made. the innate response, which is not dependent on the type of pathogen, or to the adaptive response, which fights an infection with cells that are specialized for specific pathogen. The two main types of adaptive immune cells are T cells and B cells [1]. T cells serve several functions, such as recruiting other immune cells to the site of infection and killing host cells that have been infected with pathogens. The T cell receptor (TCR) is the protein that is specialized for a specific pathogen. B cells, on the other hand, produce Figure 1. The effect of VDJ recombination allows antibodies, the multi-faceted proteins that can bind for T cell and B cell diversity. to pathogens [1]. In order to be prepared for the plethora of patho- However, there is a potential problem with this rangens that could infect the host organism, a large va- dom recombination system. A T cell or B cell could riety of T cells and B cells need to be produced. For potentially target cells or proteins in the organism itexample, approximately 1010 different types of an- self; such cells are called auto-immune cells [1]. Ortibodies can be produced by humans, although each ganisms with immune systems have developed ways person only produces a small percentage of these pos- to prevent such cells from surviving, but some cells sibilities [1]. Encoding for all of those types of genes can potentially escape these control mechanisms and in an organisms genome is not possible because there cause problems throughout the body. These autoare simply too many possibilities. Adaptive immune immune cells are the cause of many diseases such as cells solve this problem with a method called V-(D)- Type I diabetes, rheumatoid arthritis, and lupus [1]. J recombination. Both the TCR and antibodies are Dr. Jeffery Frelinger of the Department of Immusplit into four segments, named the Variable (V), nology and Microbiology at UNC is investigating a Diversity (D), Joining (J), and Constant (C) regions. way to kill these unwanted T cells – without destroyIn the genome of a naïve T cell, there are numerous ing the properly functioning T cells the body needs to variations of the V, D, and J segments in the cell’s protect itself against infections. By specifically killgenome. During the ing only one type maturation process, of T cell, the rest of proteins cleave the the immune system DNA in the cell so can stay intact while that only one variaself-reactive T cells tion of each of the V, are destroyed. To do D, J, and C regions this, other researchare present (Figure ers have proposed Figure 2. The formation of an MHC tetramer. 1). In addition, nuthe use of killer

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Figure 3. MHC tetramers kill target cells because they are taken into the cell. The saporin is released and prevents ribosome function. Credit: Dr. Paul Hess

cells that are designed to induce the cell death of unwanted clonotypes of T cells [2]. Dr. Frelinger thinks he has a better plan: modifying an important immunotechnology, called MHC tetramers, to kill unwanted auto-immune cells. When an infectious agent invades the host, small pieces of proteins, called peptides, of the foreign pathogen are “presented” to the T cells by the Major Histocompatibility Complex (MHC), causing the T cells to perform various functions [1]. MHC tetramers arose when researches wanted to identify antigen-specific T cells in a sample. However, the interaction between a single MHC and a TCR is not very strong. To make a reagent that would bind effectively to a T cell, researchers created a complex of four MHC molecules by attaching one to each end of the tetrameric protein streptavidin (Figure 2) [3]. If a fluorescent tag is attached to the streptavidin and the peptide of interest is presented by the tetramer, cells that respond to that peptide can be readily detected by MHC tetramers. Instead of using MHC tetramers as a detection tool, Dr. Frelinger wondered if replacing the fluorescent tag with a toxin would selectively kill unwanted T cells. To test his hypothesis, tetramers were created that were conjugated to saporin, a very toxic protein that is known to cause cell death by preventing the ribosomes in cells from synthesizing proteins (Figure 3) [4]. An MHC tetramer that was designed for a specific T cell was incubated with T cells. Only the T cells with the proper antigen specificity were killed [5]. Since saporin is only toxic to cells into which it is allowed to enter, only cells that took up the toxic MHC tetramer would be toxic to the cells; T cells of the wrong antigen specificity were safe from the tox-

ic tetramers. The same experiment was done in mice, and it was found that the MHC tetramers were also effective at selective T-cell deletion in vivo without killing other T cells in the mice [5]. Much research needs to be done to determine whether or not this method would be effective at preventing or curing auto-immune diseases [5]. One of the limiting factors of MHC tetramers is that the host will eventually create its own antibodies against the tetramer, a problem that needs be overcome before toxic MHC tetramers could effectively be used in vivo for long periods of time [5]. However, this new biotechnology is promising, and has recently been showing to delay the onset of diabetes in mice [6]. In the future, toxic MHC tetramers could be a new treatment option to fight back against unwanted immune cells in our own bodies.

~Garrick Talmage ‘12 is a Biochemistry major and Math minor

References

1. T. Kindt, et al, in Immunology, (W.H. Freeman and Company, 2007). 2. C. Schütz, et al. Blood. 2008, 7, (3546-3552). 3. JD. Altman, et al. Science. 1996, 274, (94-96). 4. R. Vago, et al. FEBS Journal. 2005, 19, (4963-4995). 5. P. Hess, et al. Blood. 2007, 8, (3300-3307). 6. B. Vincent, et al. J. Immunol., 2010, 184, 4196 - 4204.

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Exercise: Truly the Best Medicine Mary Morawetz, Staff Writer

hy is exercise so important? We know physical activity is part of a healthy life for any individual. Whether it’s going for a jog, riding a bike, or playing a sport, many of us exercise as a way to jump-start our day, manage our weight, maintain our health, or simply to release tension. In addition, physical activity plays an important role in disease prevention. During the past two decades, a convincing body of evidence has emerged suggesting that physical activity helps cancer patients manage treatment-related side effects and perhaps also prevents cancer recurrence. A 2008 study by Irwin and Colleagues reported that cancer patients who participate in routine, moderate-intensity recreational activities are at a lower risk of death [1]. One of the most prevalent and debilitating symptoms of cancer

Claudio Battaglini, Ph.D., Assistant Professor in the Department of Exercise and Sports Science.

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treatment is extreme fatigue. Fatigue exacerbates the physical “de-conditioning” [1] of the body caused by cancer treatment and largely contributes to the psychological distress that many patients experience. Chemotherapy and other treatment methods suppress bone marrow, resulting in blood deficiencies and abnormalities, muscle degeneration, and gastrointestinal distress [2]. These physiological symptoms severely impair a patient’s ability to function, which can lead to depression, decreased self-esteem, and decreased social interaction [1]. The accumulation of these symptoms discourages patients from engaging in physical activity. Consequently, a lack of physical activity has adverse effects on a patient’s health and potential for improvement. This cycle initiates a “downward spiral” [1] that only further encumbers a suffering individual (Figure 3). These side effects of cancer and cancer treatments have led oncologists and researchers to look for a solution that might help to minimize both the physical and mental stress that results from the disease, and many now argue that exercise may be the answer. Dr. Claudio Battaglini, assistant professor at UNC in the department of Exercise and Sport Science, has helped to conduct extensive research on the effects of exercise in cancer

Figure 1. GET REAL & HEEL is a breast cancer exercise treatment program developed by Battaglini.

patients and is currently the principal investigator of the EQUAL Project (research trial involving patients with acute leukemia) and co-director and founder of the Get REAL & HEEL Breast Cancer program developed in collaboration with the UNC-CH Lineberger Comprehensive Cancer Center and UNC-CH Hospitals. Both programs involve integrating a regular exercise plan into the treatment and/or recovery period of acute leukemia and breast cancer patients. Dr. Battaglini’s research involves monitoring the effects of exercise on restoring metabolic, cardiovascular, pulmonary, neurological and musculoskeletal efficiency that is severely compromised by various methods of cancer treatment. Recent findings* show an inverse relationship between the severity of side effects and exercise. For example,

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Cancer Treatment SideEffects  Loss of Appetite  Low blood cell count (anemia)  Loss of lean tissue  Decreased range of motion  Increased cellular debris  Decreased energy metabolism efficiency  Cardiomyopathy  Neuropathy   Decreased psychological well‐being

Benefits of Exercise  Increase appetite  Stimulation of erythrocyte production  Increase in protein synthesis/muscle regeneration  Improve connective tissue integrity, decrease pain  Improve mobilization and removal of cellular metabolites and toxins  Enhancement of energy production and improve energy utilization  Improve cardiovascular efficiency   Improve mobility, reduce pain, improve proprioception   Increase self‐esteem, body self‐perception, and increase social interaction

Figure 2. Side-effects of cancer treatment and the related benefits of exercise.

symptoms of cancer treatment include: loss of appetite, decreased blood cell count (causing anemia and a shortage of immune related blood cells such as neutrophils, thrombocytes and erythrocytes), loss of lean tissue or muscle mass, decreased range of motion and flexibility, increased cellular debris (e.g. toxins), and decreased metabolism. Conversely, exercise is known to increase the appetite, stimulate blood cell production, increase protein synthesis (build muscle mass), improve flexibility, enhance metabolic activity (remove cellular metabolites and toxins), normalize insulin levels and regulate body glucose [1, 3].

Moreover, many researchers highlight the importance of exercise in regulating cytokines (“signaling molecules” secreted by specific cells of the immune system) as a means of preventing future complications with the disease [4]. Finally, physical activity releases endorphins in the body, which serve to enhance mood and provide sustainable energy. Released by the pituitary gland and hypothalamus, endorphins serve as a natural mechanism for combating pain and fatigue [5]. Current strategies used by oncologists to address the side effects of cancer involve the use of exogenous drugs, most of which only provide

temporary relief for various symptoms [1]. Therefore, it is strongly suggested that if the notorious “downward spiral” is combated by a normal exercise routine, then patients will address some of the negative side effects that lead to fatigue in a more effective manner. By helping patients to overcome some of the most debilitating obstacles presented by the disease, a simple exercise regimen has the potential to significantly improve the lives of recovering individuals and prevent cancer recurrence in the future.

~Mary Morawetz ‘12 is an Exercise and Sports Science major

References

Figure 3. Debilitating Fatigue Cycle (DFC) that results from cancer treatment [1].

1. C. L. Battaglini, et al. Medicina Sportiva. 2006, 10(2), 49-57. 2. F. Dimeo. Blood. 1997, 90(9), 32903394. 3. C. Ingram, et al. Seminars in Oncology Nursing. 2007, 23(4), 275-284. 4. N. Young-Moo, et al. Arch Phys Med Rehabilitation. 2000, 81, 777-779. 5. M. Conrad. MedicineNet, 2007.

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Boys, Soy, and Breast Cancer Helene Kirschke-Schwartz, Staff Writer

he reality of breast cancer is fairly [2]. Tumors grow by developing new shocking. Besides lung cancer, blood vessels in a process called anbreast cancer is the most commonly giogenesis. In a process called invadiagnosed cancer in the United States, sion, angiogenesis fuels the cancerkilling more than 40,000 people in ous cells with nutrients that can cause 2009. It is predicted that 1 out of 8 it to expand into other tissues. Cells women in the US will be diagnosed can also travel through the lymphatic with breast cancer in 2010 alone. So system or bloodstream by breaking what really is “breast cancer”? away from the main tumor in a pro Breast cancer is the result of mutacess called metastasis. This is dangertions in the genes that are responsible ous because the cancerous cells will for controlling the growth of cells. appear in a new location and divide Susan McKenney, Clinical Normally cells know when to replenrapidly, thereby creating a tumor in ish themselves in moderation. How- Associate Professor of Surgery another location of the body. Metaever, over time mutations can take at the UNC Cancer Hospital. static breast cancer is most commonly over and tell the body to keep making found in the lungs, liver, bones, and mutated cells, eventually forming a tumor. There are brain [1]. two forms of tumors, benign and malignant. Benign Breast cancer has also been linked to the two genes tumors are common and are not considered cancer- BRCA1 and BRCA2. Usually these are the genes that ous because their growth is more controlled and they encode for cell stability and prevent extensive cell do not invade nearby tissues. Malignant tumors have proliferation. However, mutated versions of these the potential to spread past the original layer of cell, genes have been linked to hereditary breast and ovarthereby becoming a health threat [1]. ian cancer. A woman who has inherited the BRCA1 When the term “breast cancer” is used, it is refer- or BRCA2 gene has an 85% chance of developing ring to a malignant tumor. These tumors normally breast cancer or ovarian cancer as opposed to one begin in the cells of the lobules (the milk produc- without the mutation [4]. The only way to know if ing glands) or the cells of the ducts (the tiny tubes one has inherited this gene is through a BRCA1 and that carry the milk from the lobules to the nipple) BRCA2 mutation test [3]. This gives young women and men an opportunity to prevent cancer in the fuFigure 1. (From left to right) The BRCA-2 gene is located on Chromosome 13 and the BRCA1 gene on Chromosome 17. When the BRCA genes are mutated, the patient has an 85% chance of developing breast cancer.

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Figure 2. Genistein (right), an isoflavone, resembles the female sex-hormone, estradiol (left). Their similar structures enable proteins to accidently bind to genistein instead of estradiol. This can prevent excess tissue growth which is usually instigated by estradiol.

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Figure 3. In needle biopsies, a needle is inserted into the breast lump to extract a tissue sample. The sample is then tested for cancerous cells.

from the estrogen family. Proteins will bind with genistein instead of estradiol, which reduces the biological effects caused by estradiol, including excessive tissue growth. However, soy preventing breast cancer is mostly associated with premenopausal women. Substances rich in isoflavones are usually discouraged for postmenopausal women and women who have or have had breast cancer. With less estrogen available, soy protein isolates can actually stimulate the growth of normal breast cells in the way natural estrogens do. This adds to the risk of breast cancer if progesterone is not present [6]. Myth #3: Biopsies spread cancer.

False. A biopsy is used in order to distinguish between benign and cancerous breast tissue. It involves ture. If a patient carries the gene, they are then fol- removing some cells from the questionable area for lowed carefully so cancer can be detected and treated further testing under a microscope. A biopsy can be done using a needle or through a small surgical early on [4]. It is important that all women get frequent mam- procedure [2]. Many people fear that if the lump is mograms because breast cancer can occur at almost cancerous and tampered with, the cancer will spread any age. Frequent mammograms can reduce breast easily. However, this is untrue. The biopsy is merely cancer mortality by 63% because they detect aggres- to detect cancerous tissue and the chance of it caussive forms of cancer earlier [5]. Mammograms can ing the spread of cancer is extremely slim [4]. be done in the new UNC cancer hospital that opened in September 2009. The hospital features top of the line x-ray equipment and specialized physicians to look for any signs of breast cancer. More information ~Helene Kirschkecan be found at www.unclineberger.org. Credit: Nutrition and Food Science

Schwartz ‘13 is an African Studies major and Chemistry minor

Myth #1: Only women can get breast cancer.

False. Surprisingly, men can also get breast cancer. About 1% of breast cancer cases are male. The cases are usually related to the male carrying the mutated BRCA1 and BRCA2 gene. Breast cancer in men can be overlooked because of how little cases there are. Therefore, less screening and basic awareness is involved with men. Therefore most cases seen are well-advanced because the mass of tissue was detected in its later stage [4]. Myth #2: Soy prevents breast cancer.

Depends. Common food sources of soybeans are edamame, miso, soy sauce, dry roasted soybeans, tofu, and soy milk. Soy contains isoflavones, which molecularly resemble estrogen. Genistein, a specific isoflavone, helps prevent breast cancer by trapping proteins that continue uncontrolled tissue growth. Genistein resembles estradiol, a female sex-hormone

References

1. “What is Breast Cancer?,” 2009, <http://ww5.komen.org/ uploadedFiles/Content_Binaries/806-368a.pdf>. 2. “Breast Cancer,” 2009, <http://www.cancer.org/docroot/ CRI/content/CRI_2_4_1X_What_is_breast_cancer_5.asp>. 3. “BRCA1 and BRCA2: Cancer Risk and Genetic Testing,” 2009, <http://www.cancer.gov/images/documents/abcb7812a132-4e78-a532-f002c92fa9b9/fs3_62.pdf >. 4. Phone Interview with Susan McKenney, (APRN, BC, MSN, OCN). 2/15/10. 5. “Regularly-Scheduled Mammograms Save More Lives,” 2001, <http://www.cancer.org/docroot/NWS/content/ NWS_1_1x_Regularly_Scheduled_Mammograms_Save_ More_Lives.asp>. 6. R. Béliveau, Ph.D, in Foods to Fight Cancer (DK Publishing, 2007).

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Microbial Source Tracking:

Improving Water Quality One Microbe At a Time Natalia Stopa, Staff Writer

ccording to the US Environmental Protection Agency, 13% of surface waters in this country do not meet the criteria for water quality as established through fecal bacteria indicators. In analyzing contaminated water, health authorities do not typically test for pathogenic bacteria that cause disease directly due to the fact that these bacteria are quite variable and usually occur at low concentrations. Instead indicators are used, which are certain species of non-pathogenic bacteria, to detect contamination. Indicators of fecal contamination provide many benefits, such as easy detection, but they are often insufficient in determining water safety on their own because bodies of water are impacted by numerous sources. Another method of monitoring water quality, microbial source tracking, detects non-source points of pollution, which is pollution from diffuse sources such as land runoff, precipitation, drainage, and seepage. This source variability often makes it difficult to fully and accurately assess levels of contamination. â&#x20AC;&#x192; Dr. Jill Stewart at the UNC Gillings School of Global Public Health has been studying and developing microbiological source tracking (MST) techniques to increase understanding of human health risks associated with these water pathogens. Because microbial interactions are so complex and variable, one standard microbial source tracking method cannot be applied across the board. A combination of

rapid, cost effective techniques and accurate and specific identification will reduce human exposure to contaminants and advance the standards by which they are measured. Additionally, Dr. Stewart has evaluated the way human activity, especially development and population growth, has affected these processes. The knowledge gained through such research of microorganisms in surface water will increase the overall effectiveness of management practices by public health and environmental protection officials. â&#x20AC;&#x192; Presently, library-based methods of microbial detection are most commonly used by researchers and scientists. A library is established by creating a database of characteristics, such as genetic fingerprints, antibiotic resistance profiles, etc) of pathogens from known sources. The genotypic and phenotypic characteristics of the isolates (members an inbreeding population that is isolated from similar populations by physiological, behavioral, or geographic barriers) from suspected waters are then compared to this database and a source of contamination is identified [1]. â&#x20AC;&#x192; However, many libraries are not representative because they do not account for enough isolates and do not account for geographical or temporal diversity between watersheds. For example, hydrology, animal migration patterns, and seasonal dietary shifts can all undergo different levels of change between watersheds, thereby decreasing the effectiveness of a li-

Figure 1. A schematic of the flow of water from source water to the consumer. The greatest risk of contamination generally occurs at the source water or collection system.

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Figure 2. Coliform bacteria is used to detect the presence of other pathogenic organisms of fecal origin.

brary [2]. Therefore, there exists an obvious need for MST technique refinement. One proposed method for optimizing the library system is to create a “super library” that could be employed over vast geographical areas and would only need to be updated for population changes over time. The Center for Disease Control has integrated a super library, PulseNet, which is a molecular subtyping (or “fingerprinting”) network for food borne disease surveillance through pulsed-field gel electrophoresis [2]. Recent research has shifted the focus of MST from library-dependent methods to library-independent methods. Library-independent methods allow scientists to look for host-specific characteristics because microbes evolve and adapt to the conditions provided by a particular host and are then unable to persist outside of that specific environment [1]. This approach for microbial tracking tends to be more rapid and less expensive because it is not as financially and time consuming as developing a representative library. In addition, this method marks a specific trait instead of attempting to establish a pattern among a large population and therefore has the potential for high accuracy. Since microbes are constantly changing due to mutation, recombination, migration, selection, drift, time and host diet and antibiotic use, one standardized method or species cannot be used to assess all sources. In fact, one study identified 53 different types of E. coli in 550 isolates from a single human host [2]. Another study of Northeastern marine mammals and birds showed that half of the bacteria sampled from these organism were resistant to at least one antibiotic, and over half of those resistant displayed resistance to four or more antibiotics commonly used in human and animal treatments [3]. With more research, molecular methods (PCR, microarray, nucleotide sequencing amongst others) may help account for the genetic diversity that occurs among bacteria and allow for direct and efficient measurement of these pathogens [2].

These MST techniques can be applied to identify and assess non-point sources of water contamination caused by changes in land use. The southeastern coast of the United States has experienced dramatic urban sprawl. The run-off from these developed areas has become a serious threat to the water supply because low percentages of impervious cover, amount of land that is covered by urban structures, are enough to cause stream degradation. In fact, the EPA states that only 10% of a watershed needs to be transformed to an impervious area to severely alter stream hydrology. Dr. Stewart has participated in studies that reveal the relationships between human growth and development and water quality. One such study compared the water quality in forested, suburban, and urban watersheds using traditional indicator bacteria as well as alternative viral indicators. It was found that as urbanization increased, so did the concentration of bacterial and viral indicators. Furthermore, highest concentrations were found in creek headwaters. This evidence leads to the conclusions that creek headwaters are sentinel habitats for these pathogens and are most predicative of the linear relationship between urbanization and microbe concentration. They should therefore serve as an early warning of at-risk water [4]. Developing new and more efficient technology for sample processing and molecular detection in addition to understanding how humans themselves impact their own health will improve the criteria health authorities use in determining water safety. The formation of a MST toolbox will provide scientists with valuable means for specific identification and realtime response. This toolbox coupled with updated water standards and regularly monitored sentinels will prove indispensible to drastically improving water quality and overall public health [3].

~Natalia Stopa ‘10 is a Biology major

References

1. Interview with Jill R. Stewart, Ph.D. 2/5/10. 2. J.R. Stewart, et al. JWH. 2003, 1.4, 225-301. 3. J. R. Stewart, et al. EH. 2008, 7, 1-14. 4. G.T. DiDonato, et al. Mar. Pollut. Bull. 2009, 58, 97-106.

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Degradation, Conservation, and Appreciation of the American Oyster Jacob Hill, Staff Writer

o matter what seafood restaurant you walk in to, oysters are likely to be a staple on the menu. This marine invertebrate, highly valued for its profits as a fishery and as a delectable food item, has been harvested from the coasts of the eastern United States

benefits of the American oyster (Crassostrea virginica) in temperate coastal ecosystems and developing sustainable methods of harvest (see Figure 2). One of the most important services oysters provide is water filtration because they are filter feeders that constantly remove nutrients and sediment from the water column. When they are prevented from fulfilling this important ecological role, the results can be dramatic. Intense harvesting of oysters in Chesapeake Bay Figure 1. UNC Institute of Marine by mechanical dredging in the Sciences, Morehead City, NC. 1870’s decreased the oyster popuCredit: http://marine.unc.edu lation by over 90% by the early for centuries. But to researchers at 20th century [1]. This removal the UNC Institute of Marine Sci- of the Bay’s natural filtration sysences in Morehead City (see Fig- tem, combined with an increase ure 1), the value of oysters extends in nutrient loading resulting from far beyond the dinner table. These urbanization and industrialization, organisms provide an array of ben- led to an excess of nutrients in the efits to coastal environments such Bay. Such a surplus of nutrients as stabilizing the shoreline, keep- can lead to harmful algal blooms, ing carbon out of the atmosphere by storing it in their shells, and promoting biodiversity by providing habitat. Despite these ecosystem services, oysters have been disappearing from our coasts at an alarming rate, which has prompted research at the Institute of Marine Sciences into ways of effectively restoring these valuable mollusks. Alumni Distinguished Professor Dr. Pete Peterson focuses on this area specifically and is a leading researcher on understanding the

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which often cause depletion of oxygen from the water and can lead to fish kills. The decrease in water quality in Chesapeake Bay led to the ecosystem’s inability to support formerly common large vertebrates like sea turtles, whales, and alligators, and ultimately led to its collapse. The poor water quality and oyster parasites that became increasingly prevalent in the Bay after the decimation of oyster beds have prohibited oyster recovery. Such ecosystem collapse is not limited to Chesapeake Bay, however; human pollution and overexploitation has made temperate estuaries all along the East coast among the most degraded of all marine ecosystems [1]. An understanding of the factors influencing oyster survival is necessary to implementing successful oyster recovery, and is one focus of Dr. Peterson’s research. He created several experimental

Figure 2. American oyster, Crassostrea virginica. Credit: Tony Weeg/ Creative Commons

Carolina Scientific

Figure 3. Hand-tonging for oysters. Credit: Maryland Aquafarmer Online

reefs by dumping mounds of oyster shells into the water and allowing oysters to settle and grow on the mounds for a few years. These reefs were of different heights and were placed at different water depths. Analysis of oyster survival on the experimental reefs showed that flow speed of water over the oysters was the most important factor in determining oyster survival. Since oysters are sedentary filter feeders, they rely on food supplies that are brought to them and the amount of food they receive depends in part on the flow speed. When flow speed is low, a few individuals can deplete resources before those downstream have access to them, but higher flow speed moves food supplies across the reef quickly before these individuals have time to consume resources. Flow speed is higher in the upper regions of the water column, which allows a more equal distribution of food, creating healthier oysters that are less susceptible to mortality from

parasites. The lower flow speed at deeper regions of the reef combined with high sedimentation to yield oysters that were in poor physiological condition and highly vulnerable to parasite mortality. To be effectively restored, reefs need to be high enough to ensure adequate flow speed of water over them and must be harvested in a manner that maintains a height conducive to oyster survival [2]. Sustainable methods of harvesting oysters are another focus of Dr. Petersonâ&#x20AC;&#x2122;s research. Traditional harvesting methods include mechanical dredging, in which a dredge is towed along the seafloor behind a boat, and hand-tonging. The latter method involves a long pair of wooden shafts with metal rakes on the end that are joined together like a pair of scissors. The fisherman opens the tongs, closes them around a clump of oysters, and then pulls them into the boat (see Figure 3). While effective at gathering oysters, these techniques tend to be very destructive by decimating and preventing the recovery of oyster beds. Dr. Peterson compared these techniques to diver harvesting, a proposed alternative method in which a diver swims down to the reef and harvests oysters from it. The results of the experiment showed that although diver harvesting required two fishermen, it produced 25%-32% more oysters per unit time of fishing. Also, diver harvesting only reduced reef height by 6%, while dredging and hand tonging reduced the height of the oyster reef by 34% and 23%, respectively. Thus diver harvesting has the potential to make oyster harvesting more efficient and

sustainable by maintaining reef height, which promotes healthier oyster populations. Additionally, hand-tonging and dredging harvest oysters indiscriminately and often yield oysters that are dead or are below market size (>7cm). Diver harvesting allows fishermen to only collect oysters that can be sold and therefore prevents removal of oysters that are important to reef health, but are not commercially valuable [3]. Dr. Peterson has a number of additional ongoing projects investigating ways in which coastal ecosystems have been degraded by the loss of oysters and efforts that can bring about their recovery. Coastal environments are under constant pressure from burgeoning human development, human overexploitation of resources and the ever increasing threat of sea level rise. The case of the American oyster provides a classic example of how humans can degrade an ecosystem and how proper research, understanding, and management can help to reverse anthropogenic damage.

~Jacob Hill â&#x20AC;&#x2DC;10 is a Biology major

References

1. J. Jackson, et al. Science. 2001, 293, 629-638. 2. H.S. Lenihan, et al. Limnol. Oceanogr. 1999, 44, 910-924. 3. H.S. Lenihan, et al. Fish. Bull. 2004, 102, 298-305

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Vanishing with the trees: Australia’s tree kangaroos

Lizard Bergen, Staff Writer

hink of Australia, and you’ll probably imagine dusty kangaroos bounding through a red desert. But travel northeast to the state of Queensland and you’ll find them engaged in a much different behavior. In the teeming, humid rainforests of the Atherton Tablelands, kangaroos of the genus Dendrolagus are most often spied high above - in the tangled tops of trees. Two species of tree kangaroo exist in Australia and nowhere else: the Bennett’s (D. bennetianus) and Lumholtz’s (D. lumholtzi) tree kangaroos. They are the largest arboreal leaf-eaters on the continent and are highly territorial. Though a male’s range may overlap those of several females, the females’ territories do not overlap[1]. Because of their relatively large size, tree kangaroos have difficulty traveling across smaller tree branches and typically hop on the ground to travel from one tree to the next[2]. Trees serve as a food supply for the kangaroos and provide protection from natural pred-

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ators such as dingoes and pythons. Unfortunately for tree kangaroos, Queensland’s fertile volcanic soils have made the state a productive agricultural region. As farmers have cleared land for cattle and crops, the forest type in which tree kangaroos primarily live has been reduced by more than 60% [3]. The small patches that remain are scattered across the landscape. When tree kangaroos move from one patch to another, they are forced to cross open farmland and roads. Traveling on the ground, without recourse to the shelter of a tree, they may be killed by farmer’s dogs or hit by cars. Most tree kangaroos killed by cars are young males, suggest-

ing that they may travel between patches for the purpose of establishing a territory away from their parents. To devise effective strategies for saving tree kangaroos from the threats accompanying habitat loss, conservationists must have good information about how the animals behave. Research conducted by American students at the School for Field Studies (SFS), a study-abroad program that regularly accepts UNC students[4], aims to improve understanding of the territorial behaviors of the Lumholtz’s tree kangaroo. While students only attend the semester program for about of three and a half months, their individual research projects contribute to a five-year body of knowledge about tree kangaroos that is compiled at the school’s research station in the Atherton Tablelands. One example of how the work of American students has benefitted conservations efforts in Australia is the collaboration during the Spring Figure 1. This Queensland dairy farm is 2009 semester located on cleared rainforest land. between SFS and

Carolina Scientific Australian biologist Dr. Steve Phillips. Students collected data for Dr. Phillips’ publishable research on tree kangaroo distributions and based their own projects off that same data. The research methodology used to collect the data was adapted from Dr. Phillips’ studies of koalas elsewhere in Australia. On a private section of preserved rainforest students ran transects through the tangled rainforest undergrowth; a common technique for assessing wild animal distributions. Running a transect involves marching in a straight line through the forest and, in this case, scanning the treetops a given distance from the line for any sight of a tree kangaroo. Because the rainforest canopy is structurally com-

Figure 2a. Dr. Sigrid Heise-Pavlov shows off improvised storage bags for marsupial fecal pellets collected by students in the field. Figure 2b. This blind female tree kangaroo, perched on the shoulder of Dr. Steve Phillips, is housed at a small, private wildlife rehabilitation location.

plex and tree kangaroos are dull shades of brown and grey, this direct method of spotting them yields few results. In an attempt to improve search efficiency, students under Dr. Phillips’ direction looked at the beginning and end of each transect for signs that tree kangaroos had been in the area recently. Specifically, since the animals live in trees, students looked at the base of trees for kangaroo fecal pellets and on the trunks of trees for scratch marks. Tree kangaroos have large, curved claws on their front feet to help them climb, and when they excrete feces high in the canopy the pellets tend to bounce off branches while falling and land near the base of the tree. These signs could establish the presence of tree kangaroos in an area even when the animals were impossible to see directly. When these signs were found, their locations were noted and entered later into mapping software. The thick rainforest canopy makes GPS equipment unreliable, so the transects were run in a grid pattern and the location of marked trees was noted in relation to transect intersections. The mapped data could then be analyzed for information on tree kangaroo territory density in that area. Students shared their conclusions amongst each other in an informal poster ceremony, and the most significant projects were then presented to the local community. The SFS program trains students in a wide range of ecological field research skills and walks them through the research process from idea formation to presenta-

Figure 3. Wallabies, of which kangaroos are one type, occupy a wide variety of habitats in Australia. This Rock Wallaby lives in a canyon full of granite boulders and bounds up the sides of the massive rocks with apparent ease.

tion of the final project to peers. In the process of training young American ecologists, the program also seeks to give back to the local Australian community by contributing knowledge that may help preserve rare and threatened animals like tree kangaroos.

~ Elizabeth Bergen ‘10 is a Biology major

References

1. G.R. Newell. Wildlife Research. 1999, 26, 129-145. 2. G.R. Newell. Biol. Cons. 1997, 87, 1-12. 3. J. Kanowski, et al. Ecol. Management and Restoration. 2003, 4, 220-221. 4. Email with Kathryn Goforth, UNC Study Abroad advisor. 2/12/10.

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Showy traits:

Why Don’t Human males have them? Kyle Roche, Staff Writer

e live in a world driven by sex. This obser- and visually pleasing, they have their disadvantages. vation is not surprising given the most basic One cost is that elongated feathers require more enconcepts of evolution: organisms, including humans, ergy and materials, resources that could have been have been sculpted for millions of years to be profi- spent elsewhere, such as in gathering food. Another cient at surviving and reproducing. However, some cost is that these feathers most likely interfere with organisms have developed elaborate traits to help its survival ability. The ability to fly is extremely impromote their sexual appeal while others have not. portant to birds: the better a bird can fly, the better it Why is this so? Why do male birds have intricate, is able to collect food, and avoid predators. Although ornate bodies designed to attract this male’s physique contributes to a mates, while male humans look orhigher chance of attracting a female dinary? The answer may be related and mating (a.k.a. higher fitness in to the variation of sex determining terms of sexual selection), its physystems at work between species. sique may also catch the eye of a Before making any guesses as predator, an obvious disadvantage in to why some organisms have determs of being able to mate. veloped showy traits, some basic The fact that females are more atconcepts must be established. First, tracted to males with features that females are generally the “choosy” decrease survival seems contradicsex, and males are the “competitory, but in reality, this fact may cartive” sex. This is not surprising conry sound logic. One possible explasidering the relative investment that nation is that if a male with showy males make with respect to females traits can survive, even with these Figure 1. A bird with showy concerning reproduction. Males evolutionary “handicaps,” then it traits including bright and long in most reproductive systems only may have a genes superior to those plumage. provide genetic material (sperm), of male birds without these handiwhereas females have to invest not only genetic ma- caps [2]. Consider the following example: let’s say terial (eggs), but also time, effort, and resources [1]. that being good at hide and seek is genetically based Because the female’s costs are higher than those paid and increases your chances of survival. You are a feby the male, the female is expected to show more male looking for a male that is also good at hide and preference in mate selection. Since the goal of fe- seek so that your children will also be good at the males is to produce successful offspring, wouldn’t it game so they have a higher chance of living. There make sense that in this scenario, the female would are two potential mates: one wearing all black and select a mate that will give her child the best genome the other wearing a neon jumpsuit. Every time these she can find? This is the basic thought process for two potential mates play, it takes exactly the same why females are the choosy sex. amount of time for you to find each of them. What Next, we must consider why females associate does this mean? It probably means that the potential ornate body plans with better genes. Consider the mate wearing the neon jumpsuit has genes that make bird in Figure 1. It is a beautifully colored male with him very good at hide and seek because he did equalelegantly flowing feathers, surely attractive to any ly as well as the potential mate wearing all black, and female birds looking for a mate. However, this male he was wearing a color that would make him easy to experiences costs for developing and maintaining find. Evolutionarily speaking, this is one line of logic his beautiful physique. First, consider the shape of that makes sense. its feathers. While the long tail feathers are elegant So, we’ve established that females are the choosy

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Figure 2. The relative probablities that a showy trait, labeled as T, will be propagated through a population. The results indicate that that the x-linked system is the least likely of the three to develop a showy trait.

sex, and that males with ornate traits are more likely to have better genes. Returning to our original question: why don’t sexually attractive features evolve in all male populations? These character traits can be inherited via two modes: autosomal mutations or sex chromosome mutations. Autosomal chromosomes encode for more basic developmental processes, while sexual chromosomes encode for the sex dependant developmental processes. The problem with autosomal inheritance is that both sexes express the trait of interest, whereas the only the males would gain the benefits of greater mating success. Conversely, a mutation occurring on a sex-linked chromosome has the ability to express a trait in a sexual dependant manner [3]. In this case, only males would express the showy traits. But since humans have a sex determining system with this type of inheritance, why can’t human males evolve such “showy” traits via mutations on the Y chromosome, their sex determining chromosome? It turns out that different sex determining systems propagate these showy trait alleles with varying success. David W. Pfennig and Hudson Reeve carried out a study in which they demonstrated that the evolution of these traits is more likely in some sex determination systems than in others. They showed that birds with a ZZ/ZW system (representing males and females, respectively) are less likely to lose mutations that promote advantageous sexually attractive structures (showy traits). On the other hand, organisms, like humans, that utilize a XY/XX sex determination system are more likely to lose showy traits. Basically, they found that when the male is the homogametic sex, that is the sex that has two of the sex determining chromosomes, then it is more likely to evolve and propagate showy traits. Because each male has two copies of a showy trait gene, showy traits are harder to be lost randomly. In contrast, within a genetic system where the males are heterozygous at the

sex determining allele (i.e. human males), only one copy of a showy trait allele is present, and it is much easier to lose the novel trait randomly. By utilizing a computer program, Dr. Pfennig and Dr. Reeve were able to simulate allele frequencies for the showy traits within autosomal, as well as sexual modes of inheritance over one hundred generations. As seen in Figure 2, they found that showy trait alleles, T, were present at approximately six times the frequency in Z-linked (homogametic) systems relative to frequencies in X-linked (heterogametic) system [4]. In conclusion, the relative probabilities of whether or not a showy trait would be able to evolve and propagate through a population via computer simulations, were compared, and it was found that populations in which the male was the homogametic sex were the most likely to develop showy traits. So then, why don’t human males have showy traits? It may be due to the fact that male humans have a more alphabetically diverse sex determine chromosome.

~Kyle Roche ‘11 is a Biology major and Chemistry minor

References

1. M, Andersson, in Sexual Selection (Princeton Univ. Press, Princeton 1994). 2. R. Fisher, in The Genetical Theory of Natural Selection (Chicago Press, 1958). 3. C. Darwin. in The Descent of Man and Selection in Relation to Sex (1874). 4. D.W. Pfennig, H.K. Reeve, PNAS. 2003, 100, 1089-1094.

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OBESITY:

Tackling a Big Problem with Knockout Mice

Abby Bouchon, Staff Writer

s of 2008, one-third of the U.S. adult population was classified as obese [1] ; so Dr. Angela Wendel is attacking obesity and a related health consequence, diabetes, with the help of some very chubby friends: obese mice. These obese mice, known as ob/ob mice, possess homologous recessive “ob” alleles, which contain a spontaneous mutation in the gene for leptin. One of the ways leptin works is as a signal to the brain to suppress appetite. Because ob/ob mice lack this signaling, they overeat and consequently, become obese, greatly increasing their amount of adipose (fat) tissue. While adipose tissue stores excess calories, or energy, as triglycerides, too much caloric intake over time can result

better understand the functions of GPAT1 and the effects that decreased triglyceride synthesis has in specific tissues or diseases, Dr. Wendel uses mice that lack the GPAT1 protein, or in other words have GPAT1 knocked-out. “Knocking out” a protein is accomplished by intentionally removing or mutating the DNA needed to make a specific protein. Without that specific protein, researchers like Dr. Wendel can deduce the function of that protein by seeing how the mouse’s phenotype, or characteristics, change. Because Dr. Wendel’s knockout mice lack GPAT1, they synthesize significantly less triglyceride, especially in the liver. However, these mice still have some triglyceride because there are at least three other GPAT enzymes that can also catalyze the synthesis of triglyceride. , Since excessive triglyceride accumulation in the liver is strongly associated with insulin resistance, the GPAT1 knockout mice can therefore serve as an excellent way to investigate whether blocking the synthesis of triglyceride could prevent the body from storing excessive lipid and deFigure 1. Comparison of an ob/ob-GPAT knockout mouse and a lean wildtype mouse. veloping insulin resistance.

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in excessive lipid accumulation in non-adipose tissues like the liver. Excessive triglyceride accumulation in the liver (and increased amounts of adipose tissue) are strongly associated with diabetes and its precursor-- insulin resistance, a condition in which cells do not respond as well to insulin, a hormone that signals for the cells to take up glucose. Thus, ob/ob mice, which are obese and have increased triglyceride accumulation in their livers, serve as a good model for obesity and insulin resistance, as well as research focusing on triglyceride synthesis (see Figure 1). The first step of triglyceride synthesis is catalyzed by the enzyme glycerol-3-phosphate acyltransferase 1 (GPAT1). To help

Carolina Scientific By knocking out GPAT1 in the obese and insulin resistant ob/ ob mice, Dr. Wendel discovered that the absence of GPAT1 in ob/ ob mice resulted in a diminished amount of triglyceride in the liver. This showed that the lack of GPAT1 successfully inhibited the triglyceride synthesis pathway in the liver, thus preventing an excess storage of fat in the liver. However, the ob/ob mice didn’t have an overall reduced body mass, suggesting that while the absence of GPAT1 successfully reduced fat in the liver, it did not reduce fat in the entire mouse (see Figure 2). Furthermore, even though the ob/ ob GPAT knockout mice had decreased lipid accumulation in their livers, they remained insulin resistant, suggesting that lipid accumulation in the liver does not cause insulin resistance. [2]

Figure 3. A close-up of an ob/ob mouse [2].

As incidence rates of obesity, insulin-resistance, and diabetes continue to rise, the necessity for research to combat the epidemic with effective treatment increases.

Figure 2. A comparison of liver cells from Dr. Wendel’s research. The white spheres seen in the ob/ob –GPAT+/+ cells are lipids, illustrating a fatty liver. When GPAT was knocked out in the ob/ob mouse, as symbolized by the double negative symbol, the ob/ob mouse’s liver cells had dramatically less lipid accumulation. Such results suggest that inhibiting GPAT prevents excess storage of fat in the liver.

By studying how tissues synthesize triglyceride and other lipids, researchers like Dr. Wendel can determine how the increases and/ or deregulation of lipid metabolism contribute to the development of obesity and diabetes. This will lay the groundwork for discovering methods that will help prevent or treat these diseases.

~Abby Bouchon‘13 is a Pre-Nutrition major

References

1. K.M Flegal, et al. JAMA. 2010. 303. 235-241. 2. Interview with Angela Wendel, Ph.D. 2/1/10. 3. A Wendel, R Coleman, et al. ADA. 2010. In press.

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LESS IS MORE:

Improving Collaborative Genome-Wide Association Studies Keith Funkhouser, Staff Writer

ntil recently, it has been difficult to associate genetic variations’ contributions to common, complex diseases, such as asthma, cancer, diabetes, heart disease and mental illness. With the development of genome-wide association studies (GWASs), however, researchers have made strides towards solving these puzzles. A GWAS is designed to correlate specific genetic variation with observable traits due to a disease or condition. It is a survey of the entire genome, in which a high-density genotyping platform rapidly scans 1-2 million markers from many people, including af-

fected subjects as well as control subjects. These studies have a high false positive rate, so they require a large sample size (upwards of several thousand subjects) [1]. Once genetic associations are identified, the information can be used by researchers to better develop strategies to detect, treat and prevent disease. These association studies have seen remarkable success in mapDanyu Lin, Ph.D., Dennis Gillings ping genes linked to a number of Distinguished Professor, Department disease traits [2]. In 2005, a small of Biostatistics, Gillings School of scale GWAS showed that age-rePublic Health. lated macular degeneration is associated with variation in a gene regulating protein. More recently, that produces an inflammation- GWASs have identified numerous single nucleotide polymorphisms Recombination rate associated with obesity [3]. One Urate group has published results sugType 2 diabetes Height gesting that asthma and chronic Parkinson’s disesase obstructive pulmonary disease Type 1 diabetes (COPD, a common lung disease) BMI, waist circumference have a common genetic origin and Sphingolipid levels Erythrocyte parameters are due to polymorphism in genes Renal function which regulate lung development Blood pressure [4]. Researchers hypothesize that Bone density GWASs could see even broader Prostate cancer Esophageal cancer use in the future, possibly being Systemic lupus erythematosus used to identify genetic variations Atrial fibrillation contributing to advanced heart Ischemic stroke failure, lung cancer susceptibilCeliac disease Speech perception ity, and depression, among others Pulmonary funct. COPD (e.g. Figure 1). Fibrinogen levels Dr. Danyu Lin, Dennis Gillings Carnitine levels Distinguished Professor of HIV-1 control Biostatistics in the Gillings School of Public Health, is taking the Figure 1. Published genome-wide association studies correlating various lead on sparking advances in the conditions with specific SNP’s on Chromosome 4.

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Carolina Scientific Figure 2. To the left, standard error estimates between the two methods (meta-analysis with summary statistics and mega-analysis with raw data) are compared. The red line indicates where the values on the two axes are equal.

field of GWASs. Throughout his career, Dr. Lin has seen multiple networks and consortia formed in order to share GWAS data on the same disease or related disorders. The method they use to combine these data, he says, is the oldest in the history of statistics: metaanalysis. Meta-analysis is the process by which one combines evidence from multiple studies for the purpose of analysis. It is very commonly utilized in clinical studies, and is often necessary to increase statistical power in order to compensate for the fact that most genetic effects are quite moderate [1]. In the last few years, technology has oftentimes made it possible for these consortia to share raw data. Even still, a number of roadblocks lie in the way of efficient acquisition of raw data. Primarily, the scale of the data is enormous, due to the number of markers scanned and the large sample size. In addition, to protect human subjects, there is strict regulation of data sharing. Some investigators are unwilling or unable to share raw data, and excluding studies that do not contribute raw data can significantly reduce the generalizability of a group’s meta-analysis findings. There is a general percep-

tion that raw data are preferable to summary data since they utilize much more detailed information. Dr. Lin recognized that the costs of obtaining raw data may exceed the benefits [1,5]. To deal with this, Dr. Lin hypothesized that using summary data from multiple studies could be statistically equivalent to using raw data. What he found is that meta-analysis using summary data, when performed properly, is as efficient as mega-analysis (using raw data). Specifically, the estimates of any genetic effect produced by the two methods have approximately the same variance (Figure 2). Furthermore, the conclusions reached via meta-analysis with summary data are the same as those reached via megaanalysis with raw data (Figure 3). By using summary results rather than raw data, an investigator can increase the number of available studies and thus enhance the power of the analysis as well as the generalizability of the results [5]. These findings have significant implications for the future of GWASs. Not only will researchers now have more useful data to work with, but they will be able to cut costs via collaborations. Obtaining raw data slows

Figure 3. The graph on the left compares the combined estimates of odds ratios between meta-analysis and megaanalysis. Both meta- and mega-analysis tend to agree on the conclusions they reach pertaining to certain variations’ effects on phenotype [5].

down research and is oftentimes not possible. These methods can be applied to any other field using meta-analysis as well. While genetics data are current, many other fields may have historical subjects for which original data is not available, and summary statistics are the only option. The GWAS, a recent innovation, will only continue to increase in speed and efficiency, in part thanks to findings such as these.

~Keith Funkhouser ‘13 is a Biostatistics/Mathematics major

References

1. Interview with Danyu Lin, Ph.D. 2/8/10. 2. W.L. Su, et al. Mammalian Genome. 2010, 21. 3. R.G. Walters, et al. Nature. 2010, 7281, 671-675. 4. S.T. Weiss, Am. J. Respir. Crit. Care Med. 2010. 5. D.Y. Lin, et al. Genetic Epidemiology. 2010, 1, 60-66.

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Carolina Scientific

CLIC Clack:

Understanding Chloride Channels Joshua Thompson, Staff Writer

hloride channels have long been known to function as gateways that allow ion transport into and out of almost every cell in the human body. Beyond that, little is known about the physiology of Dr. John Edwards, M.D. most chloride channels due to the difficulty of studyPh.D., is an Associate ing these transmembrane proteins. Transmembrane Professor of Nephrology and proteins, the broad category under which chloride Hypertension at the UNC channels fall, act as gates inserted through the plasma School of Medicine. and intracellular membranes of cells. These specialized proteins allow for active and passive transport of ions in and out of the cell and its smaller interior organelles. Mutations in a variety of genes that code ponents [3]. This observation has led to numerous for chloride channels lead to a plethora of observable questions about the normal physiology of these chandiseases, most notably Cystic Fibrosis and Dent’s nels. How do they work biochemically? How do they Disease [1]. At this time, scientists have identified physically insert into the membrane? What structural four unrelated types of chloride channels: the ClC changes do they undergo in their transition from a family, the ligand-gated family, the Cystic Fibrosis globular, soluble protein to a membrane-inserted Transmembrane Conductance Regulator (CFTR) one, and ultimately what regulates insertion into and the CLIC family [2]. the membrane? These are currently questions being The CLIC family (Chloride Intracellular Chan- studied by the Edwards Lab here at UNC. nel) of proteins consists of 6 proteins all encoded by Laboratory mice are the main tool used to study different genes. Interestingly enough, “chloride in- these proteins. The Edwards lab has developed two tracellular channel” is somewhat of a misnomer as mutant strains of mice with nonfunctional CLIC1 it has not been proved that CLICs actually transport and CLIC4 genes. The knockout mice, designated large amounts of chloride [3]. Some evidence has -/-, do not express the necessary proteins, making obshown that CLICs act as chloride channels in vivo servation and experimentation possible. The CLIC4 (in a living system), while further evidence shows ac- -/- knockouts have a very minor phenotypic abnortivity in vitro (in a conmality, showing little trolled, non living envichange in comparison ronment). Interestingly, to wild type mice. Some CLICs can be found in prenatal death has been two distinct forms; first, observed in the mothas a soluble protein ers who do not express found in the cytoplasm the CLIC4 proteins. The of cells, and second, as CLIC1 -/- mice have a transmembrane (inteno discernable phenogral) protein spanning typic abnormality under the phospholipid biunstressed laboratory Figure 1. Colocalization of an Endothelial cell marker layer of cell membranes CD31 (green) and CLIC4 (red) in a mouse retina. conditions. When bred and other internal com- © American Society for Investigative Pathology (Ulmasov, Bruno, & Edwards) together, however, the

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Carolina Scientific CLIC1 -/- and the CLIC4 ceullar fluid rushes into -/- offspring are nonvithe newly formed pit. able, that is, no offspring The pH of the extraceulare ever born. The prolar fluid (7.5) is higher teins may complement than the cytoplasmic each other; a lack of one pH (7.1). The early enprotein will have no disdosomes are immedicernable side effects, but ately acidified and their survival is not possible if pH falls quickly but the both proteins are absent absence of CLIC4 re[4]. From these experisults in a higher PH for ments, and many others, large endosomes. Esit has been proposed that sentially, without ChloCLICs are important for ride Intracellular Chanangiogenesis, the formanels CLIC4, cells do not tion of blood vessels. In vacuolate as well and vivo, endothelial cells therefore cannot adapt (the cells lining blood to their specialized funcFigure 3. A proposed pathway in which soluble vessels) can line up end tion [4]. CLIC proteins translocate into the plasma to end and create what As understanding membrane of a cell [1]. looks like a column. about CLICs grow, the These cells then accumulate intracellular vesicles, power to use them as a tool for curing disease behollowing out the cell and creating a long tube, a comes more and more of a reality. The idea of a CLIC process known as intracellular tubulogenesis. When inhibitor as a chemotherapeutic regiment comprises stressed, CLIC4 -/- mice show decreased angiogen- an exciting new direction in the study of chloride esis, leading to the conclusion that CLIC4 plays an channels. Some tumors, particularly in breast and important role is this process. kidney cancer, are highly dependent on their blood The best clues about CLIC4s’ involvement in tubu- supply. Tumors cannot grow if they are unable to relogenesis are linked to acidification among intracel- cruit blood vessels which may lead to advances in lular type membranes. During regulated endocytosis, oncological studies. While much remains to be disthe phospholipid bilayer of a cell pinches off, begins covered about these fascinating proteins, one thing to migrate inside the cell and, as it forms, the extra- is certain: CLICs are a burgeoning topic in protein biochemistry.

~Joshua Thompson ‘13 is a Biochemistry and Biology double major

References

1. D. Littler, et al. FEBS. 2010 2. B. Tulk, et al. J Biol Sci. 2000, 35, 26986-26993. 3. J. Edwards, et al. FEBS. 2010 4. Interview with John Edwards, M.D., Ph.D. 2/12/ 2010.

Figure 2. 3D (Tertiary) Structure of CLIC 1 [1].

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Carolina Scientific

When You’re Your Own Worst Enemy: The Connection between Genes and Lupus Nephritis Mary La, Staff Writer

our body depends on its immune system to assist with fighting and, at times preventing, the manifestation of illness and infection. However, serious complications can arise in cases of autoimmune illnesses – when the immune system targets the body’s own tissues. One example of such a disorder is systemic lupus erythematosus. From fatigue and low-grade fever to photosensitivity and organ complications – the wide range of symptoms of lupus makes diagnosing the illness difficult, especially since symptoms depend on which organ(s) have been targeted, and how severe the illness becomes. In one third of lupus cases, patients suffer from glomerulonephritis, the inflammation of the part of the kidney

that filters urine (called the glomerulus as seen in Figure 1) [1]. Lupus nephritis, when glomerulonephritis accompanies lupus, is considered an orphan disease – one with smaller scope when compared to other more common illnesses. Hence there is a lack of FDA-approved treatments specifically for lupus. Instead, treatments that are intended for other diseases are often used to handle the symptoms of lupus. For instance, cyclophosphamide (CYC) is a compound that is not only used to battle cancer, but also in lupus treatment (see Figure 2). CYC must be chemically modified or metabolized in the body to be converted into its active form. Another example is mycophenolate mofetil

Credit: UNC Kidney Center

Figure 1. Cross-sectional diagram of the kidney and the location of the glomerulus, which filters urine.

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Figure 2. Cyclophosphamide.

(MMF), an immunosuppressant often used in post-operation therapies for kidney transplant patients (see Figure 3). Unlike CYC, MMF enters the body in its active form, and is metabolized into its inactive form. Because of the autoimmune nature of lupus, anticancer and immunosuppressive therapies lend themselves well to lupus treatments [2]. However, lupus nephritis patients suffer from poor kidney function. This is often observed with regards to proteins being leaked into the urine, since the glomerulus cannot adequately filter out the urine. The declining kidney function, among other factors, can affect the body’s metabolism of medicines such as CYC and MMF, and hence how well these patients respond to treatment. For MMF treatments in lupus patients, Melanie Joy’s lab at the UNC Kidney Center wanted to better understand the relationship between kidney function, chang-

Carolina Scientific

Figure 3. Mycophenolate mofetil.

es in how these drugs were used by the body (pharmacokinetics), and the status of illness for these patients after treatment (patient outcome). The Joy group investigated the interaction between genetic variation and drug response on a set of lupus patients demonstrating active glomerulonephritis [2]. The genes under consideration were involved in drug metabolism or drug transport, and the aim was to see if the amount of product generated by the transcription of these genes could be correlated to patient outcomes or pharmacokinetic differences. Notably, two UGT genes studied in the MMF part of the study seemed to influence the efficacy of MMF in patients; these genes code for a series of enzymes responsible for

inactivating MMF [3]. Patients with certain variations in these genes might experience differences in the amount of drug tolerated before the drug becomes toxic, as well as the amount of drug needed to remain effective. These UGT genes not only affect how MMF is processed by the body in lupus patients, but also in small vessel vasculitis (inflammation of the blood vessels) patients. Many of these patients had single point mutations in one of these genes, implicating this gene family as critical to drug metabolism. The study has been expanded to a larger subset of small vessel vasculitis patients, to see whether this phenomenon comes from the actual disease, or if it was induced by the drug itself.

Figure 4. Comparison of a normal glomerulus and an inflamed glomerulus (glomerulonephritis). The top images are illustrated diagrams and the bottom images are histopathological sections.

The reason why Dr. Joy became interested in this subject was because of the “very little systematic rational use of drugs in these patient populations, and it was mainly due to the fact that the drugs were never evaluated in these diseases”. By understanding how the body metabolized these medications, as well as how the drug’s efficacy and toxicity varied by patient, administrators of these treatments “could come up with reasonable starting doses for a patient based on certain individualized criteria” [4]. Much work remains to be done in this area, including the continued evaluation of the role that drug transporting or metabolizing genes play in activating/deactivating a drug, which could ultimately determine the course, duration, and efficacy of a patient’s treatment.

Mary La ‘11 is a Chemistry and Computer Science double major and Spanish minor

References

1. “Lupus Foundation of America - Kidney Disease,” 2010, <http:// www.lupus.org/webmodules/webarticlesnet/templates/new_aboutaffects. aspx?a=100&z=17&page=1>. 2. “Genetic - Activity 1 - Glossary, page 5 of 5,” 2010, <http://science.education. nih.gov/supplements/nih1/genetic/other/ glossary/act1-gloss5.htm>. 3. M.S. Joy, et al. Pharmacotherapy. 2009, 29(1), 7-16. 4. Interview with Melanie S. Joy, PharmD, PhD, FCCP, FASN. 2/12/10.

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Carolina Scientific

Fun in the Sun

The Development of Organic Solar Cells Lindsay Ross, Staff Writer

hat could be more important than providing heat for your home, light in the night, or cooked food for your family? All these necessities are provided for by low-cost fossil fuels, which could be gone as early as 2030 [1]. Finding a replacement for fossil fuels is a vital challenge for our scientific community and, Dr. Wei You and his team from the chemistry department have taken a new approach to the problem: organic solar cells. Most of the work on solar cells has been conducted largely with silicon-based inorganic cells. While these types of solar panels have come into production, they have been used only limitedly due to several major problems. First, they are prohibitively costly at about $4 per watt of electricity generated [1]. This is largely due manufacturing costs of the panels which require about ten microns thick (10-5 meters) of ultrapure, light absorbing inorganic material and costly metal casing & other packaging. Additionally, these solar cells are heavy, inflexible, and bulky, making them impractical in many situations. As a post-doc at Stanford, Dr. You noticed these major flaws and started to think about the energy crisis from an organic chemistry perspective [2]. “Organic solar cells would solve the major problems that exist with silicon based cells,” Dr. You told me in an interview. The thickness of the light absorbing compound on the panel is up to 200 nanometers (2×10-7 meters) thick-about 50 times thinner than inorganic-silicon compound films. Additionally, the casing around the organic solar cells could be plastic which is more flexible, durable, and environmentally friendly. These advantages of organic solar cells give them real potential to be mass marketed [1].

Figure 1. Simplified schematic of a solar cell.

Organic solar cells consist of a light absorbing chemical compound (usually an electron donor), an electron acceptor compound, a donor-acceptor interface, electrodes, and an outer casing. When the compound on the cell absorbs light, the sun’s energy is transferred to the compound’s electrons located at highest occupied molecular orbital (i.e., HOMO). This excites electrons to a higher energy level, called the lowest unoccupied molecular orbital (i.e., LUMO). At LUMO sun’s energy is stored as excitons. Excitons are electron-hole bound pairs where the

Figure 2. Series of compounds in solvent created by the You Group for testing with organic solar cell.

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Carolina Scientific

Figure 3. 4,7-Di(thiophen-2-yl) benzothiadiazole (DTBT).

hole is the now-vacancy in the compound molecule’s HOMO energy level created when an electron moves to the LUMO energy level. These excitons travel to the donor-acceptor interface on the cell where an energy difference exists. The energy difference causes holes to go to the donor polymer and electrons to go to the acceptor molecules. Holes and electrons travel through the composite film to respective electrodes on the cell creating electricity [1]. Achieving good current and voltage is vitally important in solar cells to get efficient generation of the electricity. Creating current (the flow of electrons) in organic solar cells favors compounds with low band gaps, smaller energy distances between the HOMO energy level, where energy-absorbing electrons originally reside, and the LUMO energy level. However, generating high voltage (energy per unit of chargeelectrons in this case) requires a large band gap or a big distance between the HOMO and the LUMO energy levels. Thus, to get the best efficiency one must find a band gap balance that allows for sufficient current and voltage at the same time [2]. This is one of the main goals of Dr. You’s research.

In the past few years, the You Group has been creating organic compounds with a balanced band gap and energy levels, that is, compounds that produce both high current and high voltage to maximize electricity output. To do this, the team runs many quantitative analysis tests on various compounds to see which give the best current and voltage [2]. Recently, Dr. You and his team have worked with 4,7-di(thiophen-2-yl) benzothiadiazole (DTBT), to create polymers which had high efficiency (Figure 3). However, DTBT was problematic for actual use on solar cells because its related polymers had a low molecular weight and poor solubility. The lab team fixed this issue by attaching solubilizing chains to DTBT on various places, so as to allow the polymers to better dissolve in the solvent, one key process in fabricating organic solar cells. They found that attaching solubilizing chains at the fourth carbon position on DTBT would not interfere with the intrinsic properties of DTBT related polymers. More importantly, the solubilizing chain also increased molecular weight and gave excellent solubility, leading to a better overall mixture of the organic materials. This discovery significantly increased efficiency in bulk heterojunction photovoltaic cells, one kind of solar cell for which organic materials are being used [3]. Organic solar cells are still limited by current efficiency levels and lifetime, but it is a very fast-improving field. They could be the mass produced solution to the energy crisis and, in the future, perhaps people will be trekking over to Home Depot to pick up a new organic solar cell for their house [2]. No matter what, these leaps in organic solar research are bringing the sun’s potential closer to home.

~Lindsay Ross ‘12 is a Chemistry major and Biology minor

References

1. W.You. Research Overview. 2009. <http://www.chem.unc. edu/people/faculty/you/group/index.html> 2. Interview with Dr. Wei You, Ph.D 2/8/10 3. W. You. Macromolecules. 2010, 43(2), 811–820. 4. Photos by Dan Sears. UNC News Services. Fall 2009.

Sarah Stoneking, a UNC undergraduate student, worked in the You lab to help synthesize efficient organic polymers for solar cells.

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Undergraduate Research Spotlight The Physics Department at UNC has several opportunities for undergraduate students to get involved in research. There are a total of eight research fields: astronomy/astrophysics, condensed matter and materials, high energy physics, string theory, biophysics, gravitational physics, nuclear physics and theoretical physics. For more information,visit: http://www.physics.unc.edu/research/ugrad_research.php.

Name: Lenny Evans, Class of 2011 Major: Physics and Math 1. Why did you want to get involved with research? I did research in high school and I really enjoyed it. As a result, I wanted to continue to do research when I got to college. As for the specific area I’m working on, I think it’s fascinating that we think we know so much about everything, but there’s so much in physics (and any field for that matter) that we don’t know. Sometimes it seems like there are more mysteries behind neutrinos than absolute facts, so I wanted to conduct research in neutrino physics to try to reveal more of these absolute facts. 2. How did you find a lab and what is your research about? I’ve worked with my research group since freshman year, including the summers. I basically just looked on the physics website to see all the professors’ research interests, and emailed the people that did neutrino physics, and got a job. I’m still working with the same group now. Right now I’m building a spark chamber, which is an early type of particle detector. I’ll be going to Switzerland this summer to do some research in particle physics as well. 3. Overall, how has your research experience been? What are some positive aspects? What are some negative aspects? My research experience has been really great. I’ve learned countless things I’d never learn in class, I’ve gone to Raleigh, California, and Hawaii to present my research, and I’ve met and worked with lots of great people. The down sides of research are that I sometimes work on things that I don’t feel I’m really good at. I’m really into data analysis and simulations, so it’s harder for me to do things like building particle detectors, like I’m doing right now. But, from building this detector, I’ve learned so much about electronics and gas systems that I would have never learned otherwise, so it’s still a great experience. 4. Any tips for those who want to get into research? I would suggest just trying to talk to as many people as possible until you can get involved in stuff you want to. From my experience, professors really like to see passionate, capable students. It’s also great just to talk to professors to get to know them and build lasting relations, so even if you don’t get a research job out of them, it’ll still be good that you’ve talked to them.

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Carolina Scientific Name: Ben Ryan, Class of 2012 Major: Physics and English 1. Why did you want to get involved with research? Research interests me because the natural world interests me. It is one thing to read about other people's results after they have diffused into the public realm, but it is quite another to be down in the trenches pushing back the fog that still obscures so much of nature's clockwork. Feynman called nature's imagination "so much greater than man's" and that is pretty much how I feel about it too. The ecstasy of feeling your mind stretch as you learn something new about the universe is a powerful sensation for me, and successful research gives this experience to people all over the world. 2. How did you find a lab and what is your research about? Being new to the workings of academia, I naively assumed that I could just present my resume, such as it was (and is), to the world and that the research opportunities would then come find me. This is not a good strategy. However, I was fortunate in that a job did eventually open up in Dr. Hugon Karwowski's research group, and as I had already traded a few emails with him, he gave it to me. Dr. Karwowski is a nuclear physicist and my work for him has largely been developing and running computer simulations of the interactions between photons and matter, though I also spent a fair part of the previous summer at the Triangle Universities Nuclear Laboratory (TUNL) learning about and completing the odd jobs that keep a nuclear physics lab running. Currently I am working on a project for the Department of Defense, which seeks to develop techniques to successfully, efficiently and noninvasively detect hidden weapons-grade nuclear materials at border checkpoints. 3. Overall, how has your research experience been? What are some positive aspects? What are some negative aspects? My research experience has been absolutely vital, not for the boring reason that graduate schools expect that applicants will have spent some time in a lab, but because I could not have known how much I would enjoy science without actually doing science. Homework and tests are a far cry from the work of real researchers, and I could not have felt comfortable, as I expect I will, going off to graduate school for a research degree in science without having worked in a real lab. So that of course is tremendously positive, as is the excitement of doing real science. Research is inevitably tedious and frustrating at times, but that is the way things are, and, as I have come to believe, hardly reason to flee science. 4. Any tips for those who want to get into research? Let people know who you are. This is I suspect more important to success than a bag full of merit badges from the Boy Scouts or a shockingly high GPA, or even both; undergraduates can rarely offer anything as beginning researchers except tenacity. But that is the main tool of effective scientists, I think. Therefore it helps to pursue positions on research projects that excite you; not only will you be happier, but your enthusiasm will endear you to your PI, and in science personal connections can mean much more than you could think for your career path.

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The Office for Undergraduate Research: Top 10 Questions about Undergraduate Research 1. What is a research university and what are the benefits of attending one? A research university is a complex and interdependent community of individuals who value the intellectual and practical benefits of original inquiry and creative expression. There are also many benefits of contributing to the University’s research mission, including the development of your creative abilities and confidence that you can undertake original work of significance to society. 2. Can any student do undergraduate research? ANY student may choose to do undergraduate research. In fact, students in every major and in every year are ALREADY doing undergraduate research! 3. Why should I consider doing undergraduate research? You will learn to apply what you already know to new issues that interest you, and have the opportunity to influence others. Along the way, you are likely to develop new skills, meet others with similar interests, gain confidence, define your own style, deepen your connections to the Carolina community, and use your experiences to help you choose a future career path. 4. What kinds of research projects have undergraduates done? All kinds! commercial, social, scientific, and artistic entrepreneurship, community-based research… undergraduates from all schools in all majors have undertaken research projects on nearly all continents. To read more about projects conducted by students in particular disciplines, please visit the Past Student Projects section on our website. 5. How can I get involved in doing research at UNC? There are many ways that you might begin. You can enroll in a First Year Seminar or IDST195, “Modes of Inquiry”, which is a seminar designed to introduce you to research in many disciplines. Courses in every major are available to teach particular methodologies and provide opportunities for original investigations. If you like the idea of beginning with a faculty member whom you know and like, you might choose courses with a variety of faculty in your area of interest, read more about what they have done by visiting their websites and finding out more about publications or performances, and then speak to them about your interests. Probably the best place to begin is with students you know who are doing research in an area that interests you. 6. I want to explore my options for research, but I don’t have a specific project in mind. What should I do? Congratulations! It takes courage to try something new, and by deciding to begin, you’ve already accomplished one of the harder steps. Your next steps will involve finding out what is going on at Carolina in your area(s) of interest, and how you can get started. 7. I have a specific idea for a project that I want to do. How can I get started? You will need a faculty advisor, and there are a variety of ways to find one. Start by looking at the OUR database of research opportunities to see if a potential advisor has posted a project description that matches your interests. Talk to peers who have conducted research in this area, graduate student teaching assistants, graduate research consultants, and faculty you know and ask them for recommendations. Faculty research interests are described on their websites, and university librarians can help you identify faculty publications that relate to your interests. 8. Where can I get funding for research? The OUR currently offers three kinds of grants. The first (Undergraduate Research Support) are small awards (up to $750) for those who need essential supplies to go forward with a feasible research project. The second (Undergraduate Travel Awards) are to support those who are presenting their research at professional conferences, or performing at off-campus sites. The third (Summer Undergraduate Research Fellowships) are major awards (at least $3000) for work during the summer. 9. How can I find out more about the research that faculty are doing, especially those who might mentor me? Departmental websites include links to faculty research interests, and are often organized by sub-disciplines. You might want to talk with faculty and graduate students in your courses and ask for suggestions of other faculty who are working in your areas of interest. The OUR maintains a database of research opportunities posted by faculty and an archive of student projects chosen for SURFs together with the faculty advisors of those projects, as well as an archive of abstracts presented at the annual campus Celebration of Undergraduate Research symposium, including the faculty advisors. All of these resources are searchable by discipline and keyword. The majority of faculty on our campus serve as advisors for undergraduate research projects each year, so your chances of finding a suitable advisor are high. However, not all faculty have openings every semester, so if you can be flexible and persistent, you are most likely to find a suitable faculty advisor. 10. How can the Office for Undergraduate Research help me? The resources of the OUR can help to empower you to take the next step that you need in order to engage in undergraduate research. We hope that all students will use these resources in ways appropriate to their situations and feel welcomed into the communities of performance, scholarship and research that comprise the Carolina campus. We look forward to helping you to pursue topics of your greatest intellectual and creative interests, and to communicate the results through campus symposia, publications, and professional meetings.

Adapted from the OUR Website: http://www.unc.edu/depts/our/top10.html

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A Special Thanks To Our: Staff Writers

Production Staff

Abby Bouchon Elizabeth Bergen Keith Funkhouser Jacob Hill Rebecca Holmes Helene Kirschke-Schwartz Mary La Mary Morawetz Kyle Roche Lindsay Ross Rebecca Searles Natalia Stopa Garrick Talmage Joshua Thompson

Elizabeth Bergen Natalia Davila Lenny Evans Carolyn Johnson Ann Liu Rebecca Searles Rohan Shah Kristina Stanson

Production Staff (Left to Right): (Top Row) Carolyn Johnson, Elizabeth Bergen, Kristina Stanson, (Bottom Row) Rohan Shah and Rebecca Searles

For more information, please email us at: carolina_scientific@unc.edu or visit us online at http://studentorgs.unc.edu/uncsci 35

Spring 2010, Volume II Issue II

â&#x20AC;&#x153;Every great advance in science has issued from a new audacity of imaginationâ&#x20AC;? ~John Dewey

Carolina Scientific Spring 2010 Front Cover: Rock wallaby mother and child, Credit: Elizabeth Bergen This publication was funded at least in part by Student Fees which were appropriated and dispersed by the Student Government at UNC-Chapel Hill.