Student Profiles Archive - URSP 2013-2014
Here you will find information about past and present students funded through scholarships administered by the Undergraduate Research Center - Sciences. We are proud of the achievements of our research scholars.
Please click on the program year to get information about the supported students, their mentors and their research projects.
| Wai Man Yu
Ms. Wai Man Yu
Mentor: Dr. Yi Tang
Funding: Gottlieb Endowment
Title: Towards the synthesis of strictosidine, a precursor of Vinblastine
Wai Man is currently a fourth year Biochemistry (B.S.) major. She has specific interests in pharmaceutical related topic, which led her to conduct research in Dr. Yi Tang’s laboratory. The Tang research group is aimed to study natural product biosynthesis and biocatalysis. The group is centered on elucidating biosynthetic pathways of polyketides, nonribosomal peptides and related compounds through genetic and enzymatic methods and studying enzymes that are involved in the synthesis of compounds that have medicinal bioactivity.
The goal of this research project is to engineer the biosynthetic pathway in yeast to make strictosidine, a precursor of vinblastine and other plant vindoline alkaloids. Vinblastine is one of the front-line anti-cancer drugs approved by FDA; however, its complicated isolation process and low production in plants makes it one of the most costly drugs. Producing the metabolites needed for vinblastine using yeast as a host is a desirable solution due to its rapid growth advantage. Therefore, Wai Man’s first short term goal is to produce 10-hydroxygeraniol, a building block of iridoids, and increase the titer of geraniol, an important starting material of the pathway, through engineering of the yeast strain. A new yeast strain, BY4741 will be used instead of WAT11 because of its more availability of selective markers and more accurate integration process. Cytochrome P450 reductase (CPR) will be introduced into the BY4741 strain to activate cytochrome P450 enzymes. Integration process, such as homologous recombination, will be done to introduce the mutant erg 20 into the yeast genome to produce a higher yield of geraniol. Wai Man’s second goal is to make iridodial, the precursors of secologanin and strictosidine, through integration process to introduce genes such as geraniol synthase(GS), geraniol 10-hydroxylase (G10H), alcohol dehydrogenases (ADH), iridodial cyclase (CYC) into yeast strain. The overall goal is to construct the biosynthetic pathway to make strictosidine from secologanin and tryptamine in yeast.
Wai Man would like to thank her mentor, Dr. Tang, for his invaluable support, and also her supervisors, Ralph Adrian Cacho and Anthony DeNicola, for their continued guidance on this research. She would also like to express enormous gratitude for the Gottlieb family for their generous endorsement, and the Undergraduate Research Scholars Program for the support of her scientific endeavors. Upon graduation, she hopes to pursue a career in the pharmaceutical field.
| Paulina Young
Ms. Paulina Young
Mentor: Peter Narins
Paulina Young is a fourth year undergraduate at UCLA majoring in Physiological Science. This is her second year working in the Narins Lab under the Integrative Biology and Physiology Department. Her current research involves investigating nonlinearities in the frequencies of tree frog vocalizations, placing special emphasis on biphonated elements within individual calls.
Land-dwelling vertebrates employ one of two possible organs for the production of sound. Birds possess a syrinx that functions in vocalization, while amphibians, reptiles, and mammals use a larynx to achieve the same purpose. As a result of its two-unit organization, the syrinx is capable of simultaneously producing distinct sound components from each part. It so follows that several examples of separate yet overlapping frequencies, called biphonation, are common in avian calls. It was widely believed that the larynx, due to its singular structure, is not capable of producing more than one sound at a time. However, calls recorded and analyzed by the Narins lab have shown that several species of tree frog also display biphonated vocalizations. Two particular species of current interest are the Cascade tree frog, Littoria pearsoniana, and the southern ornate nursery frog, Cophixalus australis. Paulina’s research will focus on examining the recorded vocalizations of both frog species and documenting biphonations and other nonlinearities present in each call. Computer analysis of the calls will eventually progress to anatomical studies that will explore the possibility of a second sound source outside of the larynx.
After graduation, Paulina plans to pursue a career as an MD. She would like to thank Dr. Peter Narins for being the most wonderful mentor and friend as well as the Wasserman Family for their generous support.
| Allison Yip
Ms. Allison Yip
Mentor: Dr. Daniel Kamei
Title: Novel Block Copolypeptide Vesicles as Carriers for Targeted Chemotherapy
Allison Yip is a fourth year bioengineering student and has been performing research in Dr. Daniel Kamei’s lab since the spring of her sophomore year. The Kamei Lab focuses on engineering drug delivery vehicles for the treatment of cancer as well as developing diagnostic tools for the improved detection of biomolecules. Specifically, Allison’s project focuses on using a novel block copolypeptide vesicle for the enhanced delivery of chemotherapeutic drugs.
Cancer is the second leading cause of death worldwide. Although chemotherapy remains one of the most common cancer treatment options, current chemotherapeutic drugs are nonspecific, eliciting negative side effects by killing healthy cells along with cancer cells. The development of nanoscale drug delivery vehicles is exciting, because of their potential to encapsulate and protect the drug as it circulates throughout the body. Additionally, these carriers can be directed and targeted to tumors by decorating them with proteins that bind preferentially to the surfaces of cancer cells. The Kamei Lab has been investigating a novel class of nanoparticles composed of amino acids, known as polypeptide vesicles. In particular, the lab has been studying a negatively charged vesicle comprised of the block copolypeptide called poly(L-glutamate)60-poly(L-leucine)20. These drug carriers have been found to be nontoxic, and can be prepared to all have approximately the same size. These vesicles can also be loaded with the common chemotherapeutic known as doxorubicin, decorated with a polymer called polyethylene glycol to improve its stability within the body, and attached to a targeting protein known as transferrin. Allison’s research aims to characterize these vesicles and to optimize the experimental conditions in order to design vesicles that are efficient at killing cancer cells.
After graduation, Allison plans to pursue an M.D. degree and to continue to conduct biomedical research. Allison would like to thank Dr. Kamei and her other laboratory mentors for their continued guidance and support. Finally, she would like to thank the Lau family for their generous funding to aid her research endeavors.
| Esther Yang
Pictured (left to right):Cindy Fast, Esther Yang, Dr. Aaron Blaisdell
Ms. Esther Yang
Mentor: Dr. Aaron Blaisdell
Title: Neural Mechanisms Mediating Inferential Reasoning in Rats
Esther Yang is a fourth year Psychobiology major pursuing a career in animal behavior. She has worked in Dr. Aaron Blaisdell’s psychology lab since July 2012 and is currently working under graduate student Cindy Fast to investigate rodent neural mechanisms involved in reasoning about ambiguous situations.
Patients suffering from neurodegenerative disorders, such as Alzheimer’s Disease, often suffer from cognitive deficits, particularly in regards to inferential reasoning and implied information. This phenomenon is not well understood, yet essential to understanding, delaying and potentially reversing the loss of neurocognitive function in patients. The purpose of this study is to examine the expression pattern of an early gene indicator of neural activity, c-fos, in various brain regions of reasoning and non-reasoning rats. The goal of Esther’s research is to further elucidate the physiological mechanisms by which mammals exhibit inferential learning and thinking.
Esther would like to thank Dr. Aaron Blaisdell and Cindy Fast for their commitment to mentoring her. She also thanks the URC-Sciences and the Boyer Foundation for their support of her research and pursuit of a rigorous academic education.
| Joshua Weinreb
Mr. Joshua Weinreb
Mentor: Dr. John Colicelli
Title: Identifying Small Molecule Activators of GDP Bound RAB5
Joshua Weinreb is a fourth year student in the department of Molecular, Cell, and Developmental Biology major with a minor in Biomedical Research. He has been part of the Colicelli lab since the summer going into his junior year. The Colicelli lab focuses on analyzing the role of RAS signaling pathway within normal and transformed cells.
RAS is a GTPase and also one of the first oncogenes identified. The human genome encodes more than 170 RAS-related GTPases that participate in virtually all cell functions. When bound to GTP, these proteins adopt an “active” conformation with high affinity for downstream effector molecules. Upon GTP hydrolysis, GTPases convert to an “inactive” conformation with low affinity for downstream effectors. We hypothesize that some small molecules can activate a GDP-bound GTPase, not by releasing GDP but by allosterically inducing a conformational change that mimics the high affinity for downstream effectors normally associated only with a GTP-bound GTPase. I am testing this hypothesis by developing an assay to identify small molecule activators of RAB5, a GTPase that regulates receptor endocytosis in mammalian cells. Constitutively activated RAB5 may lead to increased degradation of receptor tyrosine kinases (RTKs) and thereby reduce RAS activity, which could be therapeutic for solid tumors of epithelial origin.
Josh would like to thank Dr. John Colicelli and the members of the Colicelli lab for their continued guidance and the incredible opportunity to conduct undergraduate research. He would also like to thank the Wasserman family and the Undergraduate Research Scholars Program for their support of his scientific endeavors. Upon graduation, Josh hopes to pursue a combined MD/PhD degree and pursue a career in both clinical medicine and basic science research.
| Jane Wang
Pictured left to right: Dr. Ren Sun, Jane Wang, Dr. Jiaying Feng
Ms. Jane Wang
Mentor: Dr. Ren Sun
Title: Murine Gammaherpesvirus 68 Open Reading Frames 40 and M1 Aid in Modulation of the Unfolded Protein Response
Jane Wang is a fourth-year student in the department of Molecular, Cell, and Developmental Biology. Under the guidance of her postdoctorate mentor Dr. Jiaying Feng and faculty mentor Dr. Ren Sun, Jane has been characterizing the Murine Gammaherpesvirus 68 Open Reading Frames 40 and M1 expression kinetics and their relation to viral modulation of the Unfolded Protein Response.
The Gammaherpesvirinae subfamily of Herpesviridae is known for its inclusion of the cancer-implicated Epstein-Barr virus (EBV) and Kaposi’s sarcoma-associated herpesvirus (KSHV). EBV and KSHV are characterized by their abilities to establish lifelong latent infection, evade host immune responses, and spontaneously transition to the lyric replication cycle in compromised host immune systems. Regulation of late gene expression is not yet fully understood in this herpesvirus subfamily. Late gene protein products are primarily involved in capsid formation and contribute to the production of infectious viral progeny. Though much remains to be elucidated, previous studies conducted in the murine gammaherpesvirus 68 (MHV-68), a mouse model of the human oncoviruses EBV and KSHV, indicate that particular viral protein products may be involved in late gene regulation, one of which includes the open reading frame 31 (ORF31). Jane seeks to determine the nature of KSHV’s reliance on ORF31 in the hope of paving the way to the development of novel therapeutic antiviral treatments for this virus.
Jane would like to thank Dr. Ren Sun, Dr, Jiaying Feng, and the members of the Sun lab for their continued guidance and the incredible opportunity to conduct undergraduate research. She would also like to thank the Hilton family and the Undergraduate Research Scholars Program for their support of her scientific endeavors. Upon graduation, she hopes to pursue a career in the medical and public health fields.
| Christine Sutanto
Ms. Christine Sutanto
Mentor: Dr. Julian Martinez-Agosto
Funding: Mac Dowell
Title: Mes-4 gene regulates growth in Drosophila Melanogaster
Christine Sutanto is a senior at UCLA, majoring in Molecular, Cell, and Developmental Biology with a minor in Biomedical Research. She has been working in the Martinez-Agosto laboratory, in the department of Human Genetics, since September 2012. Her current project aims to understand the molecular mechanism through which Mes-4, the Drosophila homologue of NSD1, regulates development and growth. Mutations of the mammalian NSD1 results in Sotos syndrome, an overgrowth condition that is characterized by macrocephaly, mental retardation and cancer predisposition while genomic duplications of the NSD1 gene have been proposed to cause a reciprocal phenotype associated with undergrowth, short stature, microcephaly, delayed bone age and intellectual disability.
Growth signaling pathways are controlled by a plethora of genes and regulatory elements that eventually determine the overall growth of an organism. A slight change in any of the regulatory elements could have dire consequences and lead to diseases and irregularities in the growth pattern of an organism. With the genetic tools and research techniques we now possess, we are able to manipulate the expression of specific genes in order to obtain a better understanding of the roles of specific molecules in a growth signaling pathways, to expand our knowledge of cancer pathogenesis and identify the genetic defects in human overgrowth conditions.
Using the Drosophila Melanogaster as the model organism, Christine’s project seeks to study the Drosophila Mes-4 to dissect the molecular mechanism by which NSD1 deletion causes tissue overgrowth. Mes-4 is a methyl transferase that plays a role in the addition of methyl groups to histone tails; specifically lysine 36 of histone H3 (H3K36). H3K36 methylations are highly enriched in the transcriptionally active euchromatic regions of the nucleus. Through performing immunohistochemical analyses and epistatic experiments, important growth regulatory pathways will be manipulated in the background of Mes-4 overexpression and downregulation to better understand the key players in the mTOR and InR signaling pathway that is causing overgrowth.
Christine would like to thank Dr. Julian Martinez-Agosto for his constant guidance and advice in the laboratory and the Mac Dowell foundation for their generosity and their support in her research endeavors at UCLA. She would also like to thank the Biomedical Research Faculty and URC for their unwavering support and guidance.
| Amit Sumal
Mr. Amit Sumal
Mentor: Dr. Benhur Lee
Title: Examining the Differences in CD4 and CCR5 Usage Efficiency As a Selective Factor in Perinatally Transmitted Human Immunodeficiency Virus Isolates
Amit Sumal is a 4th year Microbiology, Immunology, and Molecular Genetics major. With the help of his mentor, Kelechi Chikere (Ph.D.), he has performed research in Dr. Benhur Lee’s laboratory since his sophomore year. The Lee Lab investigates the viral envelopes of HIV and Nipah Virus with a focus on viral entry and cell surface receptor interactions.
Specifically, Amit’s research studies the perinatal transmission of HIV. HIV infects cells through the engagement of its envelope glycoprotein with CD4 and the coreceptor CCR5. Thus, a virus’s relative usage of the CD4 and CCR5 receptors during infection can elucidate its means of viral pathogenesis. Making use of a GGR Affinofile cell line that can simultaneously and independently induce CD4 and CCR5 at up to 48 different combinations, Amit will be able to able to quantitatively determine the relative efficiencies that maternal and infant HIV envelopes use CD4 and CCR5 during infection. Using this system, Amit hopes to provide insight on the perinatal transmission of HIV with respects to the means of viral pathogenesis of maternal and infant HIV envelopes, the selective pressures behind perinatal HIV transmission, the differences between transmitter/founder and chronic envelopes, and lastly, therapies and vaccines that prevent HIV entry.
In the future, Amit plans to graduate in the Spring of 2014 and subsequently, become a doctor specializing in infectious diseases. He would like to thank Kelechi for his guidance and assistance over the past year, as well as Dr. Benhur Lee for the unique opportunity to work in his laboratory. He would also like to thank the Gottlieb family for their contribution and support.
| Naomi So
Ms. Naomi So
Mentor: Dr. Edward Lee
Naomi So is a 3rd year Physiological Science major. She is involved in both clinical and translational research here at UCLA. As a part of Emergency Medicine Research Associates at the Ronald Reagan Hospital, Naomi helps collect clinical data for the Nexus CT Head study, among other studies, in validating the current criteria used to assess whether or not patients with blunt head trauma need a CT scan.
For her research in the translational field, she focuses predominantly on Irreversible Electroporation (IRE), specifically on the pancreas. With the ongoing development of cancer therapy research, many new methods have been proposed regarding the treatment of pancreatic cancer. Irreversible Electroporation (IRE) is a minimally invasive treatment that causes cell death via apoptosis by using high frequency electrical currents to a target tissue. IRE has been shown to have the potential of preserving vital structures in a clearly delineated manner and can be monitored with real-time imaging in tissues such as the liver. Currently, Naomi is evaluating the effects of IRE on pancreatic tissue, monitoring its effects on peri-pancreatic vessels and bile ducts on a swine model by correlating and analyzing immunohistological and CT data. With the recent collection of data, she is now also focusing on the pancreatitis associated with IRE ablations as well as specific parameters for IRE on human pancreatic cancer cells. These methods are crucial steps in translating this technique to a clinically applicable method for human pancreatic cancer.
Naomi plans to pursue a career in the medical field and perhaps even academic medicine. She would like to thank the Wasserman family for supporting her research endeavors and providing her with the opportunity to delve into research topics of her personal interests in the translational field of medicine. She is truly privileged to have the opportunity to conduct research at UCLA and have the wonderful support of the Wasserman family in order to so.
| Sampat Sindhar
Mentor: Dr. Frank Laski
Title: Understanding Retinal Degeneration in Drosophila melanogaster
Sampat Sindhar is a fourth year majoring in Molecular, Cell, and Developmental Biology, with a minor in Biomedical Research. She has been conducting research in the Laski lab since October 2012. The Laski lab is interested in identifying genes that are involved in light-dependent retinal degeneration and understanding the RNA expression patterns underlying light-dependent retinal degeneration in white-eyed flies.
Retinal Degeneration, a leading cause of blindness and retinitis pigmentosa in humans, is marked by photoreceptor cell death. To better understand retinal degeneration, the lab is conducting an RNAi screen in Drosophila melanogaster to identify genes that are involved in maintaining photoreceptor organization. Additionally, the lab has observed that harmful amounts of bright light cause damage to the rhabdomeres of wild-type white-eyed Drosophila eyes. Sampat’s project has focused on understanding the changes in RNA expression under light conditions in white-eyed Drosophila and determining whether the damage induces transcription of repair proteins in photoreceptor cells’ nuclei. Through understanding the changes in gene expression, the lab hopes to understand the pathway by which exposure to light leads to retinal degeneration.
Sampat would like to thank Dr. Frank Laski, Tiffany Mao, Alexander Tonthat, the Undergraduate Research Scholars Program, and the Boyer fund for their generous support and continual guidance.
| Sara Shu
Ms. Sara Shu
Mentor: Dr. Ting-Ting Wu
Title: Characterization of the Interaction of Kaposi’s Sarcoma-associated Herpesvirus Open Reading Frame 54 and Ubiquitin-Associated Protein 1
Sara Shu is a third year undergraduate majoring in Biochemistry with a minor in Biomedical Research. She has been pursuing undergraduate research with Dr. Ting-Ting Wu in the Molecular and Medical Pharmacology department since October 2012.
Sara’s research focuses on characterizing the interaction of Kaposi’s Sarcoma-associated herpesvirus open reading frame 54 (ORF54) and ubiquitin-associated protein 1 (UBAP1).
The human gamma herpesvirus, including Epstein-Barr virus and Kaposi’s Sarcoma-associated herpesvirus, has oncogenic potential, especially in immune-compromised patients and is known for establishing lifelong persistent infections. Understanding viral inhibition on the interferon immune response mechanism is crucial for improving the efficacy of interferon therapy. ORF54 is of particular interest because it is known to inhibit this response, thereby assisting to establish persistent infection. Previous studies identified UBAP1 as one interacting protein candidate of ORF54. Sara wishes to identify the functional significance of the ORF54 interaction with UBAP1 in down-regulating the immune response by mapping residues on ORF54 involved in the interaction and determining the effects of abolishing the interactions through mutating these binding residues. Successful confirmation and characterization of this interaction will be crucial for identifying a key target for increasing the interferon efficacy.
Sara would like to thank Dr. Ting-Ting Wu, Dr. Ren Sun, and the members of the Sun Lab for their continued guidance, mentorship and support, enriching her undergraduate education with the experience and opportunity to conduct such exciting and pioneering research. Sara would also like to express her deepest gratitude to the Wasserman family and the Undergraduate Research Scholars Program for their generous support.
| Vivian Shi
Ms. Vivian Shi,
PI: Dr. Ren Sun
Direct Mentor: Dr. Laith Al-Mawsawi
Vivian is a fourth year Molecular Cell and Developmental Biology major working in the virology lab of Dr. Ren Sun under the mentorship of Dr. Laith Al-Mawsawi.
Vivian's project involves using a large-scale co-immunoprecipitation (Co-IP) screen to identify interactions between HIV-1 and putative cellular cofactors, which will provide both an insight into HIV-1 pathogenesis as well as afford an avenue for pharmacological advancements. The research program in Vivian’s lab has long aimed to uncover the interplay between viral pathogens and the innate immune response.
Newly identified direct protein-protein interactions between the HIV-1 virus and host cell proteins critical for viral replication are attractive targets for drug research as they represent unexploited stages of the HIV-1 life cycle for inhibition. In a literature search of small interfering RNA (siRNA) screens, a number of cellular proteins have been implicated in assisting the progression of HIV-1 infection. These putative cofactors encompass a multitude of cellular processes to provide a global analysis of HIV-1 interactions. Direct protein-protein interactions between HIV-1 and the host cell found to be critical for viral replication are extremely attractive targets for further drug design to add to the current cocktail of highly active anti-retroviral therapy (HAART).
Vivian would like to thank her PI, Dr. Ren Sun, for his valuable input and continuous support as well as her mentor, Dr. Laith Q. Al-Mawsawi, for his limitless patience and careful guidance. Vivian would also like to thank the Hilton Scholarship for their generous funding of her research.
| Steven Shen
Mr. Steven Shen
Mentor: Dr. Kang Ting
Steven Shen is a 4th year UCLA student majoring in English with a Pre-medical focus. He has cultivated a versatility in his studies that assists in gaining insight a multitude of fields. In addition to his volunteering at the Cedar Sinai medical center and the tutelage he provides on behalf of CityLab, his research at the Ronald McDonald Research Laboratory has been a cornerstone to his college career since the beginning of the winter quarter of his 3rd year.
Working under the mentorship of Dr. Kang Ting, Steven has devoted his time in lab studying the potency of a specific growth factor, NELL-1 on cartilage and bone formation within the body. In the past, his studies reaffirmed that chondrogenesis, the process by which cartilage and bone is formed, is promoted when NELL-1 is present with another protein, BMP2, but is inhibited when NELL-1 is administered alone. Expanding upon his findings, Steven plans on more closely examining the pathway by which NELL-1 functions, specifically focusing on one of its primary response genes, a nuclear factor of activated T Cells (Nfatc2), whose siRNA knockdown has been shown to significantly reverse the inhibitory properties of NELL-1 supplementation. By focusing on the inhibitory pathway of NELL-1 supplementation, Steven hopes to gain a better understanding of NELL-1’s specific effects on chondrogenesis and to reinforce its potential in future therapeutic approaches for cartilage regeneration.
Steven plans on graduating in the spring of 2014 to pursue a MD and would like to thank Dr. Kang Ting and the members of the Ting lab for their guidance and patient tutelage. Additionally, he would also like to thank the Ehrisman foundation for their generous support.
| Philip Shamash
Name: Philip Shamash
Mentor: Dr. Felix Schweizer
Title: Vestibular and Neuroendocrine Vesicle Release Patterns
Philip Shamash is a 3rd –year Neuroscience major and French minor. He has been working in the Schweizer lab since Winter quarter of 2012. This lab uses electrophysiology, imaging, and biochemical methods to investigate synaptic vesicle release, its diversity among different secretory systems, and its plasticity.
The vestibular system is our ‘sixth sense’ that measures head motion in order to maintain balance and orientation. In his project, Philip will examine the utricle, a vestibular structure in the inner ear that uses hair cells to sense linear acceleration. Its synapses frequently show morphological specializations, yet we know very little about how they work. The project’s goal is to begin to decode the utricle’s signals to the central nervous system. He is starting by studying the electrophysiology of neuroendocrine cells, an excitable cell type that is interesting in itself but can also be used as a standard with which to compare vestibular electrophysiology. Then, in the utricle, he will use optogenetics to stimulate particular hair-cell types and regions. With whole-cell patch-clamping, he will track the resulting ionic currents and synaptic vesicle release in these hair cells and in the neurons to which they report. Elucidating this cellular electrophysiology is the first step toward understanding how we manage to stay balanced and how to repair this function as it degrades with age and disease.
Philip would like to thank Dr. Schweizer and Kathy Myers for their continual mentorship and guidance, as well as the MacDowell Trust for their generous support.
| Saumya Shah
Ms. Saumya Shah
Mentor: Dr. Denis Evseenko
Title: Identification and Functional Characterization of Opioid Kappa Receptor (OPRK) in Human Chondrocytes
Saumya Shah is currently a third year Biology major. With the help of her mentor, Dr. Denis Evseenko, she has conducted research at the Evseenko laboratory since the winter quarter of her freshman year. The Evseenko lab focuses on investigating the generation of cartilage committed progenitors from human pluripotent and mesenchymal stem cells with an ultimate goal to develop therapeutic strategies in patients with osteoarthritis.
Specifically, Saumya’s research project deals with the functional characterization of the opioid kappa receptor (OPRK) within fetal and adult chondrocytes. Previous studies within the Evseenko laboratory have shown that primitive chondrocytes in cartilaginous bone rudiments highly expressed opioid receptor kappa (OPRK) at 6-8 weeks of human development. OPRK is one of the three main classes of opioid peptide receptors most commonly known for its effects in the central nervous system (CNS) with large influences over many functions including pain control and regulation of vascular development. However, its presence and function during muscle-skeleton development has not been reported previously, especially, its functional role in chondrogenesis remains elusive. Saumya is currently running multiple studies and experiments to understand the role of the OPRK in chondrocyte differentiation.
Saumya plans to graduate with her Bachelor’s Degree in the Spring of 2015 and hopes to attend medical school and pursue a career in medicine subsequently. She would like to thank Dr. Evseenko for his daily committed and dedicated mentorship and the opportunity to conduct research and gain this incredible learning experience in his lab. She would also like to thank Ling Wu for his patience and guidance and to her family for their unwavering, strong support in all of her endeavors and ambitions. Finally, she would like to express her gratitude to the Oppenheimer family for their generous financial support.
| Maxwell Roth
Mr. Maxwell Roth
Mentor: Dr. Christopher J. Evans
Maxwell Roth is a fourth-year Neuroscience major at UCLA. Working under Dr. Christopher Evans in the Hatos Research Center for Neuropharmacology, Maxwell studies how chronic opiates alter the functional connectivity of reward circuitry in the brain.
Chronic opiate exposure has been shown to alter the dendritic processes and possibly the synaptic connections between neurons involved in motivation and reward. Similar drug-induced changes in connectivity have been found in heroin addicts as well. These studies suggest that a reorganization of the neural networks involved in reward contribute in part to dependence and the reinforcement of habitual drug use. Yet, there have been no such studies regarding the effect of chronic opiates, such as morphine, on the partial connectome of D1 and D2 receptor enriched medium spiny neurons (MSNs) in the ventral striatum. By studying how the gross structure of the reward circuitry changes in response to chronic opiate use, Maxwell hopes to broaden the understanding of how the brain may be implicated in human health and disease, specifically addiction.
Maxwell is extremely thankful for the support of Dr. Evans and Dr. Walwyn. Their guidance and daily encouragement have been instrumental in motivating Maxwell to excel within this field. Maxwell also follows an interest in biomedical ethics and will be teaching a seminar on the biomedical ethics of technology in the spring. After graduation, Maxwell plans to pursue a career as a physician-scientist. Maxwell would also like to sincerely thank the Gottlieb Foundation for their generous funding, recognition, and support of his research.
| Marci Rosenberg
Mentor: Dr. Alvaro Sagasti
Title: Temporal analysis of the appearance of adherens junction markers during sensory axon ensheathment in zebrafish
Marci Rosenberg, a third year Neuroscience major and Biomedical Research minor, has been conducting research in the Sagasti lab since March 2013. Under the guidance of post-doctoral scholar Jeff Rasmussen, Marci is studying the process by which sensory axons are ensheathed by skin cells in embryonic zebrafish.
The epidermis is innervated by the axons of peripheral sensory neurons. These neurons play a key role in sensory processing by mediating touch sensation. Glial cells, which have long been considered the characteristic support cells of the nervous system, are not found in the epidermis. Emerging research in the Sagasti lab has led us to believe that skin cells may handle some of the crucial functions of glial cells. For example, early in zebrafish development, peripheral sensory axons are ensheathed by skin cells, similar to the way peripheral glia sometimes ensheath axons. Neither the mechanism nor function of skin ensheathment is known, although similar ensheathment channels are seen in the skin of a wide variety of other organisms. Previous work by the Sagasti lab has led us to propose a model of ensheathment involving 1) cellular signaling to indicate the presence of sensory axons, 2) deformation of the underlying cell membrane around the axon, and 3) formation of adherens junctions to close the membrane cup that has formed around the axon. The goal of Marci’s project is to test this model of ensheathment, first by determining the time points at which different proteins associated with adherens junctions and cellular remodeling can first be visualized co-localizing with sensory axons, using confocal microscopy. Next, Marci will use molecular methods to prevent zebrafish from developing sensory axons and determine how this affects the appearance of adherens junction and cytoskeleton markers. Finally, Marci will begin investigating the identity of the elusive initiating signal of this ensheathment process.
After graduation, Marci intends to take a year off to immerse herself in lab work fulltime while applying to MD/PhD programs. She is very grateful to the Helga K. and Walter Oppeneheimer Educational Trust for their immense generosity. In addition, she would like to acknowledge the excellent opportunities and instruction provided by the Biomedical Research minor, and would especially like to thank the very kind Dr. Ira Clark and Dr. Rafael Romero. Finally, she would like to deeply thank Dr. Sagasti, Jeff Rasmussen, and the rest of the Sagasti lab for creating a driven, exciting, and fun lab environment where questions are always encouraged.
| Darshan Randhawa
Mr. Darshan Randhawa
Mentor: Dr. Ram Raj Singh
My name is Darshan Randhawa and I am a 4th year MCDB major at UCLA. I have been studying the role of innate immune responses in the onset of autoimmune diseases for the past three and a half years in Dr. Singh's Lab of Tolerance and Autoimmunity.
Systemic lupus erythematous (SLE) is a chronic autoimmune disease characterized by inflammation in almost every organ system. There is no specific treatment for this disease. In SLE the body’s own immune system turns against antigens within the body’s own cells. This process is called the breakdown of tolerance, which results in the production of antibodies against self proteins by B cells. These antibodies, called ‘auto-antibodies’, bind various antigens including nuclear antigens such as self-derived ribonucleoprotein (RNP) and DNA released by dying cells. It is believed that complexes of these autoantibodies and their respective antigens, called immune complex, deposit in various organs, which triggers local inflammation, eventually resulting in organ damage.
A known key early event in the onset of SLE is the activation of a subset of dendritic cells (DC) called plasmacytoid DC (pDC). DCs are a major class of immune cells that play a role in the initiation of immune responses. In addition, pDCs secrete type I interferon (IFNs) that are known to cause an unabated differentiation of monocytes to DCs, which then stimulate B and T-cells while also lowering the threshold of activation of B cells. Activated B cells in SLE produce auto-antibodies.
Another immune cell called neutrophil is also suspected to play a role in SLE. Neutrophils are the most abundant innate immune cell in circulation in humans at any point in time. Upon infection, neutrophils may undergo a form of cell death known as NETosis resulting in the formation NETs. [Apoptosis is another, well-studied, form of programmed cell death.] NETs are a web-like structure released by dying neutrophils, which are composed of chromatin backbones and granular molecules. This process is well controlled, as the NETs are normally degraded within hours of their formation. This process of NET degradation may be impaired in patients with SLE, likely mediated via anti-RNP autoantibody.
Taking cues from the above observations, I propose that the impaired NET formation/degradation is important in the activation of pDCs in patients with SLE. Specifically, I propose to examine the correlation of SLE NETs and the amplification of pDCs resulting in production of IFN-alpha.
My aspirations are to become a physician - scientist by continuing my formal training is a MSTP program. I aspire to one day to become a scientist studying translational medicine while simultaneously practicing medicine. In addition, I would like to thank the Wasserman family for their generous support in funding my research endeavors.
| Vishwajith Ramesh
Mr. Vishwajith Ramesh
Mentor:Dr. Harley Kornblum
Title: Sustained Local Delivery of the Chemotherapeutic Taxol to Treat Glioblastoma via Tunable, Amphiphilic Diblock Copolypeptide Hydrogels
Vishwajith Ramesh is a third year undergraduate student working towards a B.S. in Bioengineering at UCLA, with a minor in Biomedical Research. Vish has been conducting scientific research in the Kornblum lab since the beginning of his second year at UCLA. The Kornblum lab focuses on studying the processes behind neurodevelopment, neural repair, and brain tumor formation. In keeping with this, and in collaboration with the Deming lab, Vish tests the therapeutic applications of diblock copolypeptide hydrogels (DCH), particularly to deliver chemotherapeutics to treat glioblastoma brain cancer.
Gliomas are highly infiltrative brain tumors without clear margins, making complete surgical removal nearly impossible and radiation therapy ineffective. Systemic chemotherapy could theoretically better target diffuse gliomas, but the blood-brain barrier hinders drug diffusion into the brain. DCH are biocompatible, biodegradable substances that integrate well with central nervous system tissue, can carry a variety of molecules, and display no toxicity or inflammatory reactions in vivo. Because of their unique properties, Vish tests the ability of DCH to deliver a lethal dose of the chemotherapeutic taxol to U87 glioblastoma cells either suspended in media (in vitro) or implanted into immune-deficient mice (in vivo). With initial tests giving encouraging results, the ultimate goal of the project is to show that DCH is a promising replacement for the current therapies for glioblastoma.
Vish would like to thank his research mentors for helping him develop the skills necessary to solve major biomedical challenges. He would also like to thank the Oppenheimer family for their recognition and generous support of his work. After graduation, Vish plans to pursue a Ph.D. in Bioengineering, and hopes to eventually break into the biotechnology industry.
| Navneet Ramesh
Mr. Navneet Ramesh
Mentor: Julian Martinez-Agosto
Title: The Role Of Endocytosis In Tissue Growth Maintenance In Drosophila Melanogaster
Navneet is a third year undergraduate majoring in Molecular, Cell, and Developmental Biology and minoring in Biomedical Research. Since September 2012, he has been working in Dr. Julian Martinez-Agosto’s laboratory. Navneet is currently researching how mutations in a specific endocytic protein can cause abnormal growth in Drosophila melanogaster.
Endocytosis is a fundamental cellular process by which molecules are taken up and internalized by cells through vesicles. This process is key to providing nutrients to cells, as well as degrading pathogens or dead tissue cells. Endocytosis has also been implicated in the regulation of growth. Accordingly, disruptions in endocytic pathways can lead to the loss of regulation of key signaling pathways, which can often lead to cancer.
Navneet’s current project seeks to characterize the role of a specific endocytic protein that has been shown to cause abnormal growth when mutated. Interestingly, the same protein appears to be found at high levels in human cancers. Navneet aims to identify which signaling pathways the mutated protein affects and develop strategies to genetically rescue the abnormal growth. Furthermore, he would like to reconcile how both mutations and overexpression of the gene causes cancer in different model systems.
Navneet would like to thank Dr. Julian Martinez-Agosto for his continued guidance and support in the laboratory. He would also like to sincerely thank the Oppenheimer Foundation for their generous contribution towards his research.
| Bill Quach
Mr. Bill Quach
Mentor: Dr. Hong Wu
Funding: Van Trees
Title: A direct role for EMT in prostate cancer metastasis
Bill Quach is a fourth year Molecular, Cell, and Developmental Biology major and is pursuing a Biomedical Research minor. He joined the Wu Lab in January of 2012 under the mentorship of Marcus Ruscetti (Ph.D candidate) and continues to work with Marcus. The Wu lab studies the role of the tumor suppressor gene PTEN in a number of malignancies including prostate cancer. Bill's research project currently focuses on characterizing mesenchymal, epithelial and EMT-like tumor populations and their role in the metastatic process of prostate cancer.
Prostate cancer is the second leading cause of death in American men, with the majority of these deaths due to metastases. The epithelial-mesenchymal transition (EMT) is one explanation for the development of metastatic disease and proposes that epithelial tumor cells undergo a morphological alteration and become more motile in order to invade the surrounding tumor microenvironment, travel through blood vessels, and seed metastases at distant sites. During this process, tumor cells display a loss of epithelial markers such as E-Cadherin, and gain of mesenchymal markers such as Vimentin. In agreement with this model, recent studies have demonstrated that circulating tumor cells (CTCs) isolated from the blood of men with metastatic prostate cancer express Vimentin and have lost Epcam expression. However, a direct role for EMT in prostate tumor progression, dissemination of CTCs into the blood stream, and seeding at distant sites remains unclear due to the lack of a sufficient in vivo model. In order to develop a better understanding of the metastatic process, the Wu lab has recently developed a murine model that recapitulates metastatic human prostate cancer and exhibits an EMT phenotype at the primary tumor site by conditionally deleting the Pten tumor suppressor gene and activating the Kras oncogene. To investigate the role of EMT-like tumor cells in tumor progression and metastasis, our lab has generated a Cre+;PtenL/L;KrasG12D;Vim-GFP (CPTKV) model. By using GFP as a mesenchymal marker and Epcam as an epithelial marker, we are able to FACS sort and characterize epithelial (Epcam+GFP-), mesenchymal (Epcam-GFP+), and EMT-like (Epcam+GFP+) tumor cells from the prostates of CPTKV mice. If EMT contributes to the metastatic process, then Vimentin may be used as a biomarker and potential therapeutic target for metastatic prostate cancer.
Bill hopes to pursue a medical degree after graduating from UCLA in Spring of 2014. He would like to thank the Van Tree Foundation for their generous donation, Dr. Wu for the opportunity to be a member of her prestigious lab and the Wu Lab prostate cancer group for their continuing support and guidance.
| Monish Patel
Mr. Monish Patel
Mentor: Dr. Jay Jiang
PI: Dr. Kang Ting
Funding: Mac Dowell
Title: Temporospatial Expression of Nell-1 in Developing Murine Cartilaginous Tissue
Monish Patel is a third year Molecular, Cellular, Developmental Biology major and a Biomedical Research minor. He has worked in the Gordon & Virginia McDonald Medical Research Laboratories for Dr. Kang’s lab in the department of orthopedic surgery since the spring of his freshman year. Dr. Ting’s laboratory has studied Nell-1, a secreted molecule that participates in bone and cartilage development and repair, for more than 15 years. Nell-1 deficient mice have abnormal skeletal growth and are neonatal lethal due to malformation of the spine and ribcage. Monish’s project focuses on the mechanistic role of Nell-1.
Nell-1 has been used to treat cartilage defect in an animal model, but the process of determining the mechanism of Nell-1 in cartilage development and its exact stage- and tissue- specific effects still needs to be figured out. To elucidate these mechanistic roles, Monish is performing a systemic and dynamic evaluation of Nell-1 in developing cartilaginous tissues of wild type mice to elucidate its mechanistic roles. His project can be broken down into two specific goals. The first goal deals with characterizing the expression of Nell-1 in the developing limbs from 11.5dpc to skeletal maturity (16 week of age). The second goal is to determine the regulating role of Nell-1 in chondrogenic differentiation through each of these stages. Observations will be made about how the presence or absence of Nell-1 affects levels of early chondrogenesis genes (Sox9, Col-II, ACAN) and cartilage hypertrophy genes (RunX2, Col-X, VEGFa and OPN) throughout normal development.
After graduating in the spring of 2015, Monish plans on pursing a degree in MD/PhD to prepare for a career as a physician-scientist. He wants to thank Dr. Ting for his support and for giving him the opportunity to conduct his own research project using the lab’s facilities. He would also like to extend his gratitude to Jay Jiang for his continued support and guidance throughout his years in the lab. And finally, he thanks the McDowell and the staff members of the URC Sciences for aiding undergraduate researchers academically and financially.
| Katie Pannell
Ms. Katie Pannell
Mentor: Dr. Jerome Zack
Katie Pannell is a third-year Microbiology, Immunology, and Molecular Genetics major with a minor in Biomedical Research. She recently joined the laboratory of Dr. Jerome Zack, which specializes in innovating new model systems for the study of HIV and AIDS. She currently works with her mentor, Dr. Deirdre Scripture-Adams, on a project aimed at optimizing T-cell differentiation from human embryonic stem cells for projects with clinical relevance to HIV and cancer.
T cell based Stem cell therapies for HIV and cancer are in development in multiple laboratories, but the process of making T cells from hESC is still very difficult and inefficient, and very few labs have successfully been able to generate T cells in vitro from hESC. Better in vitro and in vivo model systems are therefore needed to answer basic research questions regarding the generation of T cells from hESCs, and for more in depth pre-clinical studies. Alongside her mentor, Katie is manipulating existing in vitro model systems, and helping to develop new systems for hematopoietic precursor formation, and T development.
Katie hopes to continue her education in immunology with a PhD program after completion of her undergraduate degree. She would like to thank Dr. Scripture-Adams for the incredible education and support, as well as both the Undergraduate Research Scholars Program and the Oppenheimer Fund for the opportunity to further her passion for research.
| Trenton Otto
Mr. Trenton Otto
Mentor: Dr. Louis-Serge Bouchard
Title: Operando Spectroscopy of Microreactions Catalyzed by Multivariate Metal-Organic Frameworks
Trenton is a fourth year chemical engineering undergraduate and chemistry research fellow at UCLA. As a freshman, he joined the Louis Bouchard lab in the department of Physical Chemistry, and has continued to conduct research there since. Trenton's research projects concentrate on the characterization of novel catalytic species, as well as the development of models and analytic methods to investigate gas-solid heterogeneous reactions. His past projects include the formulation of a spectroscopic method to measure gas temperature profiles in a catalytic reactor, which has resulted in the publication of a Nature letter on the topic.
His most recent work focuses on in-situ studies of Metal-Organic Framework (MOF) materials in heterogeneous reactions. A relatively new class of compounds, MOFs have strong potential as a novel generation of heterogeneous catalysts due to their characteristically large specific surface areas and the wide variety of MOF structures that are possible: which may allow tuning of the structure for enhanced selectivity. His work has helped establish the dependence of catalytic turnover on structure in palladium-based MOFs, and gleaned insights into the adsorption-diffusion behavior of reactant gases into MOF crystallites.
Following graduation from UCLA, Trenton hopes to continue his work on catalysis and reaction engineering as a graduate student in chemical engineering.
I am deeply grateful to my PI, Professor Louis Bouchard, for rigorously introducing me to the world of research. Professor Bouchard gave me a chance to begin my research career when I was only a college freshman, and his guidance over the years has been instrumental in my development as a scientist. I would also like to thank Mrs. Gottlieb for financing my research. Her contributions have made much of my work possible, and have strongly enhanced my prospects as a researcher.
| Jose Ortiz
Mr. Jose Ortiz
Mentor: Dr. Martha Blum Lewis
Title: Genetic Analysis of Acute HIV infection and Latent HIV Reservoirs
Jose Ortiz is a senior at UCLA majoring in Molecular, Cellular, and Developmental Biology. He has been training in the laboratory of Dr. Martha Blum Lewis since September 2012. The Lewis lab focuses on studying the pathogenesis and evolution of chronic viral infections.
HIV infects CD4+ T lymphocytes and integrates itself into the host DNA, which makes it very difficult to eradicate. During acute HIV infection large amounts of virus are being produced in the body at an exponential rate with a sharp drop in CD4+ T cells. After this period, CD4+ T cells return to “near-normal” levels and the virus load drops dramatically. This is called the asymptomatic or latent period, when the patient does not exhibit any major symptoms of disease. Antiretroviral (ARV) therapy inhibits HIV replication, which help patients reach undetectable levels of virus in the blood and live a prolonged live. Latent infection is not blocked by ARV treatment because long-lived resting CD4+ T reservoir cells contain HIV proviruses capable of replicating Therefore, Jose seeks to understand the persistence of virus reservoirs during ARV treatment. The results of the project could reveal valuable information in understanding the time point HIV reservoir cells develop during ARV treatment.
In the future, Jose plans to graduate in the spring of 2015 and hopes to pursue a MD/PhD. He would like to thank Dr. Lewis for her incredible patience and excellent guidance in his project. Also, he would like to thank everyone in the Lewis laboratory for all their wonderful help in the lab. Jose would also like to thank the Wasserman family for their contribution and support.
| Alexander Zai
Mr. Alex Zai
Mentor: Dr. Jamie Deusner
Alex is a fifth year student majoring in Chemical Engineering, Biochemistry, and History with a minor in Biomedical Research. Since Winter 2012, he has been involved with the Feusner team discerning structural differences and eye-tracking patterns in Anorexia Nervosa and Body Dysmorphic Disorder patients.
The Feusner lab investigates the neuropathology of psychiatric disorders such as Anorexia Nervosa, Body Dysmorphic Disorder, and Obsessive Compulsive Disorder. Body Dysmorphic disorder is a body-image disorder that affects around 1-2% of the population, which causes those afflicted significant suffering and functional impairment. The findings from these studies may assist in identifying salient regions for further investigation of the pathophysiology underlying the clinical symptoms, and potentially could be used to help identify those at risk for BDD, and/or predict treatment response.
He wishes to thank the Gottlieb Endowment foundation, his mentor Dr. Jamie Feusner, his graduate advisors, and the faculty of the Biomedical Research Department for their unending support.
| Tianna Wilson
In Photo from Left to Right: Jason Ear, Tianna Wilson, Dr. Shuo Lin
Ms. Tianna Wilson
PI: Dr. Shuo Lin
Mentor: Jason Ear
Title: The Role of Activin Signaling in Diamond Blackfan Anemia
Tianna Wilson is a senior undergraduate researcher majoring in Molecular, Cell, and Developmental Biology and minoring in Biomedical Research. She has been working for three years under the guidance of Ph.D. student Jason Ear in the laboratory of Dr. Shuo Lin.
The Lin Lab is currently studying the molecular mechanisms of vasculogenesis and hematopoiesis using zebrafish as a model organism. Tianna’s project focuses on understanding the pathology of a blood disorder called Diamond Blackfan Anemia (DBA). Although the definitive cause of DBA is not yet known, it is widely accepted that malfunctioning ribosomal proteins cause blood progenitor cells to undergo premature apoptosis. Tianna is studying the role of p53 and Smad downstream of Activin signaling during ribosomal stress in order to elucidate the mechanisms of this disease. We hope to inspire the development of novel treatments and an effective cure for DBA in the future.
Tianna is grateful to the members of the Lin Lab, especially Anne Lindgren and Matt Veldman for their mentorship and guidance. She would also like to thank USRP and the Wasserman Family for their funding and support.
| Cynthia Wang
Name: Cynthia Wang
Mentor: Dr. Anthony Aldave
Title: Gene Expression in Loci Associated with Endothelial Corneal Dystrophies
Cynthia Wang is a fourth-year student in the Microbiology, Immunology, & Molecular Genetics department at UCLA, with minors in English and Japanese. She began her undergraduate research career with Dr. Anthony Aldave in the department of Ophthalmology towards the end of her second year. Her research focuses on corneal genetics, particularly with regards to endothelial corneal dystrophies.
The corneal endothelium, a monolayer of cells lining the posterior surface of the cornea, plays a vital role in maintaining corneal clarity. These cells transcribe genes that are important to sustaining homeostatic levels of hydration, pH and metal ions within the corneal stroma. Defining the normal corneal endothelial cell transcriptome will refine the understanding of the functional roles that the endothelium plays in normal cornea. Thus, the Aldave Lab aims to identify the transcriptionally active genes present in the chromosomal loci associated with the endothelial corneal dystrophies. They also hope to determine the impact of Fuchs endothelial corneal dystrophy (FECD) on the expression of age-dependent genes and genes associated with FECD, the most common indication for corneal transplant in the United States. Because specific gene expression profiles underlie particular cellular microenvironments, the gene expression profile of a cell changes rapidly during development, leading to cell differentiation. Understanding these changes may provide insights into the molecular mechanisms that set the foundation for the development of endothelial corneal dystrophies. Cynthia hopes to identify genetic differences between healthy and FECD tissues, and to identify the genetic factors that lead to the promotion of endothelial corneal dystrophies.
Cynthia would like to thank Dr. Anthony Aldave, Ricardo Frausto, Dr. Doug Chung, and all the members of the Aldave Lab for their ongoing support and mentorship, as well as for creating both a friendly and highly educational environment in which to learn and conduct research. Additionally, she would like to thank the Gottlieb Foundation for their generous support of her research. After graduation, Cynthia plans to pursue an MD/PhD joint degree.
| Stephanie Wang
Ms. Stephanie Wang
Mentor: Dr. Daniel T. Kamei
Stephanie Wang is a fourth year Bioengineering major at UCLA. Since March 2012, she has worked as an undergraduate researcher in the laboratory of Dr. Daniel T. Kamei. Her project focuses on enhancing the drug delivery efficacy of nanoparticles by conjugating them to a transferrin (Tf) variant possessing a lowered iron release rate.
Current chemotherapies are effective at killing cancer cells, but also demonstrate similar toxicity towards healthy cells, resulting in severe side effects for patients. To address this issue, the Kamei lab has investigated Tf-conjugated nanoparticles, which can exhibit both passive and active targeting towards tumor microenvironments. The lab has performed mathematical modeling using the principles of mass action kinetics to describe the cellular trafficking pathway of these Tf-conjugated nanoparticles. The model predicted that lowering Tf’s iron release rate could translate into increased cellular association and greater drug potency when such Tf variant molecules are conjugated to nanoparticle surfaces. To test these predictions, Stephanie is now investigating poly(lactide-co-glycolide) nanoparticles coated with polyethylene glycol and conjugated to a Tf variant possessing a slower iron release rate for the targeted delivery of doxorubicin, a common chemotherapeutic. Overall, the aim of her study is to compare the in vitro cytotoxicity of Tf variant nanoparticles versus their wild-type Tf counterparts in experiments with cultured human prostate (PC3) and lung (A549) cancer cells.
Stephanie would like to thank Dr. Kamei and all the members of the Kamei lab for their continued mentorship, guidance, and maintenance of a family-like atmosphere within the lab. She would also like to extend her gratitude to the Gottlieb Foundation and URC-Sciences for their support of her undergraduate research endeavors.
| Timothy Voros
Mr. Tim Voros
PI: Dr. Benhur Lee
Mentor: Dr. Mickey Pentecost
Funding: Van Trees
Title: Elucidating the Molecular Regulation of Paramyxovirus Matrix Protein Function through Comparative Proteomics
Now a fourth year undergraduate in the department of Microbiology, Immunology, and Molecular Genetics, Tim has been working in Dr. Benhur Lee’s Lab for the past year under the direct oversight of Postdoctoral Fellow Dr. Mickey Pentecost. Tim’s project involves using comparative proteomics to understand novel pathogen-host interactions associated with paramyxovirus matrix proteins.
The Paramyxoviridae family consists of pathogens of medical and agricultural importance including viruses that infect humans (e.g. Measles and Mumps), agricultural animals (e.g. Rinderpest and Newcastle Disease Virus), and newly emergent, highly lethal viruses for which there are currently no vaccines or licensed therapeutics (e.g. Nipah and Hendra). Matrix is the primary structural protein shared by all paramyxoviruses and is known to play a role in viral assembly and budding. Tim’s project is focused on understanding the previously unappreciated non-structural roles of matrix during infection. In collaboration with Dr. James Wohlschlegel’s lab in the Biochemistry department, Tim has conducted a comparative proteomic screen of the interactomes of matrix proteins from five paramyxoviruses. Results from this screen preliminarily suggest that paramyxovirus matrix proteins interact with host mRNA export machinery during infection to inhibit host gene expression for more efficient viral replication. Tim is currently working to determine whether mRNA export is inhibited during paramyxovirus infection. Tim is hopeful that this project will provide important insight into how paramyxoviruses co-opt the cell and may ultimately identify novel drug targets broadly applicable to many paramyxoviruses.
Tim would like to thank Dr. Benhur Lee, Dr. Ira Clark, and Dr. Olson for their support and commitment to him as an undergraduate student and researcher. Additionally Tim would like to thank his mentor Dr. Mickey Pentecost of his daily mentorship, support, and commitment. Tim is also very grateful to Van Trees fund and the Undergraduate Research Scholars Program for enabling him to pursue his scientific endeavors in biomedical research. Upon graduation Tim seeks to apply his background in microbiology to the field of environmental science.
| Melissa Truong
Ms. Melissa Truong
Mentor: Dr. Leanne Jones
Melissa Truong is a junior at UCLA studying Microbiology, Immunology and Molecular Genetics. She has been working in the laboratory of Dr. Leanne Jones since June 2012, both at UCLA and at the Salk Institute in San Diego.
The Jones lab uses the fruit fly Drosophila melanogaster as an in vivo model to study the dynamic interactions between the niche and adult stem cells in the adult germline and intestine. Stem cells reside within specialized microenvironments that are known as the stem cell “niches”, comprised of the chemical and physical elements and interactions that control stem cell behavior. Previous studies have shown that interactions between adult stem cells and their niches change in order to maintain homeostasis and in response to stress or aging.
Melissa’s project will revolve around headcase, a Drosophila gene whose molecular function is still unknown. Previous work in the lab identified headcase as a factor required to prevent cell death within certain types of cells in the testis niche. In the intestine, headcase is required for the maintenance of intestinal stem and progenitor cells within the posterior midgut of the adult fly. Future studies this year will focus on characterizing and quantifying headcase expression as a function of age, as well as in the context of tissue-specific challenges.
After graduation, Melissa plans to pursue a Ph.D. in stem cell biology. She would like to thank Dr. Jones for her ongoing mentorship and guidance, Dr. Pedro Resende for his initial work with headcase in the testis, and the rest of the Jones lab for their incredible advice and support. She would also like to thank the Oppenheimer Foundation for its generous support in her research.
| Tam Tran
Ms. Tam Tran
Mentor: Dr. Michael S. Fanselow
Tam Tran is a fourth-year undergraduate student majoring in Neuroscience and minoring in Art History at UCLA. She has been conducting research in the laboratory of Dr. Michael S. Fanselow in the Department of Psychology since January 2013. Her project, “New Neurons’ Role in Learning and Recall,” explores the involvement of the hippocampus and amygdala in learning and memory.
Based on previous studies, it is known that the hippocampus and amygdala are important for contextual fear conditioning: the hippocampus is involved in the spatial recognition of an environmental context, while the amygdala establishes emotional connections between contextual stimuli in the environment and unconditioned stimuli like pain sensation. However, the role of newborn neurons, present only in the hippocampus, is unknown. To investigate this, mice will be trained to distinguish between two distinct contexts, after which brain tissue sections from the hippocampus and amygdala will be probed for markers indicating their activity and age. It is expected that activity of new neurons will impair context discrimination, for new neurons are characterized as being hyperexcitable when compared to older, more mature neurons. Understanding the role of new neurons in the hippocampus will lead to greater insight into the mechanisms and development of generalized anxiety disorders, including PTSD.
Tam Tran is currently applying to neuroscience graduate programs across the nation, with the intention of beginning graduate work in Fall 2014 and earning a Ph.D. in neuroscience. Afterwards, she plans to pursue a postdoctoral fellowship and ultimately either begin her own lab, teach at the university and college level, or both. She would like to thank the Wasserman Family for their generous contribution to URSP as well as their support of her research at UCLA.
| Michelle Tibbs
Ms. Michelle (Shelley) Tibbs
Mentor: Dr. Carrie Miceli
Funding: Van Trees
Shelley is a San Diego native who is in her senior year at UCLA as a psychobiology major. In her junior year she discovered an interest in her current immunology project as well as translational medicine (Duchenne muscular dystrophy) through her research work in the Miceli lab.
The immune system relies on the ability of the T cell receptor, expressed on the surface of T cells, to recognize and respond properly to antigens. In the case of CD8+ cytotoxic T lymphocytes (CTLs), TCR engagement with an antigen leads to the release of cytotoxins and proinflammatory cytokines. Cytotoxins are released by CTLs in order to kill infected cells through apoptosis. Proinflammatory cytokines are released in order to communicate the presence of an infection to other cells and to coordinate a system wide response; cytokine concentrations need to be kept in a specific range in order for an organism to respond properly to infection.
The protein Discs large homolog 1 (Dlgh1) plays a role in both proinflammatory cytokine production and granule-dependent cytotoxicity. Dlgh1 has been recently shown by Shelley's lab to be alternatively spliced into two main protein variants within T cells: Dlgh1 AB and Dlgh1 B. Both variants are able to promote the release of cytotoxic granules through a p38-independent pathway, but only Dlgh1 AB is able to induce proinflammatory cytokine (IFNg and TNFa) gene transcription. Ultimately, she will be quantifying expression levels of Dlgh1 using qPCR in order to elucidate the splice variant’s ability to mediate T cell responses after stimulation.
Shelley would like to thank Dr. Carrie Miceli, mentor Jillian Crocetti, members of the Miceli lab, and her family for their support and guidance. She is especially thankful for the scholarship provided by Ms. Knapp through the Van Trees Scholarship, which has allowed her to continue research while being a full time student.
| Justin Ondry
Mr. Justin Ondry
Faculty Mentor: Dr. Sarah Tolbert
Justin is a third year Chemistry/Materials Science major at UCLA. Justin works under the guidance of Professor Sarah Tolbert in the Department of Chemistry and Biochemistry. His current project examines how nanoscale architecture affects device performance in photovoltaic devices.
Quantum dots are attractive light absorbers for photovoltaic devices because of their tunable band gaps and facile solution phase processing. Lead sulfide quantum dots are attractive light absorbers in photovoltaic devices because of their tunable band gap, strong absorption in the visible part of the spectrum and their relative air stability. Recently there have been several reports of lead sulfide quantum dot heterojunction solar cells using titania as an electron acceptor that have achieved good efficiencies. Little work has been done to explore now nanoscale architecture affects device performance.
The goal of Justin’s project is to fabricate a quantum dot heterojunction solar cell using mesoporous lead sulfide nanocrystal thin films as the light absorber. He will use block copolymer templating of nanocrystals to create the mesoporous thin films of lead sulfide quantum dots. Atomic layer deposition will be utilized to deposit the titania on the nanocrystal films. The device will be characterized using X-ray diffraction, scanning electron microscopy, energy dispersive spectroscopy, porosimetry, and various solar cell measurements.
In his free time Justin enjoys skiing, sailing and the outdoors.
Justin would like to thank the MacDowell Award for their generous support.
| Brandon Nguyen
Mr. Brandon Nguyen
Mentor: Dr. Eric Ley
Title: Prevention of Toxic Neuronal Calcium Influx After Traumatic Injury Through Adrenergic Receptor Inhibition
Brandon Nguyen is a third-year Physiological Science major and Classics minor conducting research in the lab of Eric Ley in the Department of Surgery. He currently focuses on how neurons and astrocytes respond to after traumatic injury and hopes to show that inhibition of adrenergic receptors will prevent the toxic neuronal calcium influx that initiates apoptosis in stretch injured cells. After graduation Brandon hopes to pursue an M.D./Ph.D and ultimately a career as a pediatric trauma surgeon.
Traumatic brain injury initiates a prolonged cascade of neurotoxic biochemical changes in the brain, yet there are no treatments available to address this post injury dysregulation. Injured brain cells exhibit a characteristic increase of cytoxolic calcium derived from extracellular and intracellular stores. By using a stretch-plate model, Brandon hopes to show that inhibition of beta adrenergic receptors results in reduced calcium enzyme activity, as shown by a reduction i reduction in cleaved spectrin fragments. Cells treated with beta adrenergic receptor inhibitors should also demonstrate a reduced fraction of apoptotic cells, with an increased fraction of surviving cells. Understanding the in vitro effects of adrenergic inhibitors on injured cells will inform the design of future studies and suggest a means of measuring the efficacy of drug delivery and activity in vivo.
Brandon would like to thank Dr. Ali Salim, Dr. Eric Ley, the Undergraduate Research Scholars Program, and the Boyer Scholarship for their generous support and continual guidance.
| HuyTram Nguyen
Pictured, left to right: Dr. Albert Lai, HuyTram Nguyen
Ms. Huytram Nguyen
PI: Dr. Albert Lai
Direct Mentor: Dr. Arthur Chou
Funding: Van Trees
HuyTram Nguyen is a fourth year undergraduate majoring in Neuroscience and minoring in Cognitive Science. She has been working in Dr. Albert Lai’s laboratory under the mentorship of Dr. Arthur Chou since her sophomore year in 2012. Dr. Albert Lai’s laboratory is working toward improving the care of patients suffering from malignant brain tumors. Currently, HuyTram is working on a retrospective study investigating the efficacy of isotretinoin, a retinoic acid, in treating patients with gliomas.
Gliomas represent the most common malignant primary brain tumors and may affect up to 25,000 patients in the United States every year. Despite the new treatment combining maximal surgical resection, radiation and chemotherapy, prognosis of malignant glioma patients remains poor. A mutation in the isocitrate dehydrogenase 1 (IDH1) and isocitrate dehydrogenase 2 (IDH2) genes were recently found in about 80% of low grade gliomas and secondary glioblastoma that has progressed from low grade gliomas. IDH1/IDH2 mutations might represent the early event of gliomagenesis; however, the role of these genetic alterations in glioma formation has not been well understood. Isotretinoin, 13-cis-retinoic acid, is a synthetic analog of retinoic acid, which has been shown to be effective in treating several types of cancer. Retinoic acid shows inhibitory activity toward cellular differentiation and induces cellular apoptosis. Several studies have also shown modest effect of isotretinoin in delaying recurrence time of malignant gliomas; however, the efficacy of isotretinoin in prolonging glioma patient survival still remains controversial. From these observations, HuyTram aims to evaluate the effects of isotretinoin in treating patient with gliomas. Through a retrospective review of patients who were treated with isotretinoin at UCLA, she hopes to examine if isotretinoin treatment provides therapeutic benefit to glioma patients, especially patients carrying IDH1 mutations.
HuyTram plans to graduate in the Spring of 2014 and pursue a medical degree in the future. She would like to express her deepest gratitude to Dr. Arthur Chou and Dr. Albert Lai for the invaluable opportunity to conduct this clinical study. Their guidance and encouragement have been instrumental to her educational experience. She would also like to thank all members in the laboratory for their ongoing support over the past years. Finally, HuyTram would like to sincerely thank the Van Trees family for their generous funding and recognition of her research.
| Peter Nauka
Pictured left to right: Peter Nauka, Juneyoung Lee, and Dr. Heather Maynard
Mr. Peter Nauka
Mentor: Dr. Heather Maynard
Title: Exploring Linker Length as a Way to Increase Polymer-Protein Conjugation Yield
Peter Nauka is a 4th year Chemical Engineering student. He has been working in Dr. Heather Maynard’s laboratory for over two years alongside Juneyoung Lee (Ph.D. Candidate). The Maynard lab specifically works on protein-polymer conjugates and how they can be used to stabilize various interesting therapeutic proteins.
Many therapeutic proteins suffer from limitations, including, short half-life in vivo, poor solubility, high immunogenicity and short shelf-life. Polymer conjugates can be used to correct some of these deficiencies. In particular, poly-ethylene glycol polymers and various derivatives have become increasingly popular, and there are currently numerous polymer-drugs on the market. However, it has been observed that some polymers are relatively low or none yielding upon conjugation with a therapeutic. Peter is working on a way to improve the yield of polymer-protein conjugation by varying the linker length between the protein reactive end group and the polymer backbone. Specifically, he is synthesizing various linker sizes between the end group and backbone and then using reversible addition-fragmentation chain transfer (RAFT) to create poly(poly(ethylene glycol methyl ether) acrylate) (pPEGA). pPEGA-protein conjugation has been targeted in the past, but the modification is relatively low yielding. It is believed that a long linker length will reduce steric hindrance between the protein and bulky branched pPEGA polymer. Peter hopes that this research will help increase understanding in why certain polymer can only be conjugated onto proteins with difficulty, and what steps can be undertaken to rectify this problem.
Peter plans to graduate in 2014. He would like to thank Dr. Maynard for her support and invaluable guidance over the past year and Juneyoung for his mentorship in the subject matter. He would also like to express his immense gratitude to Ehrisman for funding his research.
| Marcos Munoz
Mr. Marcos Munoz
Mentors: Dr. Robert Modlin and Dr. Dennis Montoya
Marcos Munoz is a fourth year Biology major at UCLA. Marcos is in his third year working Dr. Robert Modlin’s lab immunology lab which focuses on identifying novel mechanisms in diseases such as Leprosy and Tuberculosis, by which the innate and adaptive immune system combat microbial pathogens. Tuberculosis, a bacterial infection of the lungs, is caused by Mycobacterium tuberculosis invasion of human macrophages. Marcos currently focuses on elucidating the vitamin D response pathway required in host defense against M. tuberculosis.
The vitamin D response pathway can be induced by immunomodulatory cytokines, interleukin 15 (IL -15),interferon gamma (IFN-γ) or can be triggered upon bacterial recognition from toll-like receptors (TLR). Subsequently, the required transcription factor vitamin D receptor (VDR) and the enzyme CYP27B1 are induced. CYP27B1 catalyzes the conversion of the inactive form of 25-hydroxyvitamin D3 (25D3) to the active vitamin D prohormone (1,25D). This conversion activates the expression of the antimicrobial peptides cathelicidin (CATH) and human beta defensin 2 gene (DEFB4), which leads to direct antimicrobial activity against mycobacterium. Microarray gene expression analysis of IL -15 stimulated monocytes demonstrated induction of interleukin 32 (IL-32), known to play a role in hose defense against mycobacteria.. We therefore investigated the role of IL-32 in the vitamin D-mediated antimicrobial pathway. Preliminary data indicate IL-32 is sufficient to induce expression of CYP27B1, CATH and DEFB4 in human peripheral blood monocytes. Thus, the goal of this project is to define the role of IL-32 in the immune response. We hypothesize that IL-32 will be sufficient to induce the IL-15 and IFN-γ induced vitamin D program and that induction of antimicrobial activity will also be dependent on IL-32.
Marcos plans to graduate in Spring 2014 and pursue an M.D degree. He would like to thank Dr. Dennis Montoya and Dr. Robert Modlin for the support and opportunity to conduct research. He would also like to express his appreciation to Boyer Scholarship.
| Faye Mendoza
Pictured (left to right): Woytek Bartkowski, Nicholas Webb, Faye Mendoza, Dr. Benhur Lee
Ms. Faye Mendoza
Mentor: Dr. Benhur Lee
Title: Examining HIV Entry Across an In Vitro Model of the Blood-Brain Barrier
Faye Mendoza is a fourth year Neuroscience major and Classics minor. Since the summer of 2012, she has been conducting research at the lab of Dr. Benhur Lee in the Department of Microbiology, Immunology, and Molecular Genetics. Dr. Lee’s lab investigates molecular viral- host interactions, specifically enveloped virus entry and budding mechanisms, with a special emphasis on pathogens that cause emerging infectious diseases. Under the mentorship of postdoctoral fellow Woytek Bartkowski and graduate student Nicholas Webb, Faye’s current project focuses on establishing an in vitro model of the blood-brain barrier, in order to study HIV entry across this dynamic interface.
NeuroAIDS, a complication of HIV infection, is characterized by a series of neurodegenerative symptoms such as motor impairment, sensory loss, dementia, and an increased susceptibility to opportunistic infections in the central nervous system (CNS). These symptoms are believed to be linked to disruptions in the blood-brain barrier (BBB), a highly selective permeable division between the body’s circulatory system and the CNS. The BBB consists of brain microvascular endothelial cells on the “blood side” and stabilizing astrocytes and pericytes on the “brain side.” HIV is able to breach this tight barrier and infiltrate the brain. By co-culturing stem-cell derived endothelia with astrocytes, the BBB can be simulated to examine the mechanism of HIV entry across the barrier. Transendothelial electrical resistance (TEER) will serve as a measurement of well-organized tight junctions, while immunohistochemistry will validate the expression and localization of BBB markers GLUT-1 and PECAM-1. The successful establishment of this in vitro model is crucial to identifying brain-penetrating molecules and exploring the disease pathway of HIV in the brain.
Faye’s other research interests include virus evolution and neuroplasticity. After graduation, she plans to attend medical school to pursue a career in pediatric infectious diseases or pediatric neurosurgery. Faye would like to express her gratitude to Dr. Benhur Lee for his constant enthusiasm and guidance, Woytek Bartkowski and Nicholas Webb for their daily mentorship and unwavering support, as well as the Lee Lab family for encouraging an atmosphere of scientific excellence. In addition, Faye would like to thank URC-Sciences for providing undergraduate students with enriching opportunities, and above all, Mr. Lau for his gracious contribution to her research.
| Rebecca McGillivary
Ms. Rebecca McGillivary
Faculty Mentor: Dr. Margot Quinlan
Rebecca McGillivary is a third year student majoring in Molecular, Cell, and Developmental Biology with a minor in Biomedical Research. She has worked in Dr. Margot Quinlan’s Lab in the department of Chemistry and Biochemistry since October 2012.
Rebecca is studying mutant versions of a protein, metavinculin (MV), that are associated with dilated cardiomyopathy. This is a genetic disease affecting the heart muscle; patients with this disease develop enlarged and weakened ventricles. The heart’s ability to pump blood is impaired, increasing the risk of heart failure. The only treatment for severe cardiomyopathy is a heart transplant.
MV and Vinculin ensure proper force transmission between adjacent heart muscle cells by anchoring actin filaments to intercalated discs. MV is a larger splice variant of Vinculin, a protein that anchors actin filaments to cell membranes in all cell types. MV is expressed mainly in smooth and cardiac muscle cells. MV is known to sever actin filaments and create fine actin meshworks, while vinculin bundles actin filaments. In the heart, both vinculin and MV help anchor actin filaments to intercalated discs, the main site of force transmission between cardiomyocytes.
Individuals with mutations in MV have abnormal intercalated discs and show symptoms of dilated cardiomyopathy. Rebecca is investigating how these different mutations organize actin filaments compared to wild type MV. Rebecca is using bulk assays and single molecule imaging techniques to see how tightly the MV mutants bind to actin filaments, to what extent the mutants bundle actin filaments, and how much the mutants sever actin filaments. These assays include high and low-speed co-sedimentation, measuring light scattering, and total internal reflection fluorescence microscopy. Understanding how these MV mutants organize actin filaments will help further the understanding of dilated cardiomyopathy at the molecular level.
Rebecca would like to thank the Oppenheimer Foundation, the Undergraduate Research Scholars Program, and the members of the Quinlan and Reisler Labs for their support. Rebecca plans to graduate in the Spring of 2015 and hopes to pursue a Ph.D.
| Zoë MacDowell Kaswan
Ms. Zoë MacDowell Kaswan
Mentor: Dr. Christopher Colwell
Zoë MacDowell Kaswan is a fourth year neuroscience major, and has been a part of the Colwell lab since she transferred to UCLA in Fall 2012. The Colwell lab studies circadian rhythm dysfunction and rescue in several mouse models of neurological diseases and disorders. Specifically, Zoë’s project will involve using immunohistochemical and stereological methods to analyze the suprachiasmatic nuclei of the BACHD Huntington’s disease mouse model for cell loss and other anatomical changes.
Circadian rhythms are physiological and behavioral rhythms that take place on an approximately 24 hour cycle, synchronizing the body to the solar day. This is controlled, in mammals, by a small bilaterally paired portion of the anterior hypothalamus known as the suprachiasmatic nuclei (SCN) which receives direct photic input from the retina in order to coordinate intrinsic cellular rhythms with the outside environment. There are two main neuronal subtypes in the SCN – vasoactive intestinal peptide (VIP) and arginine vasopressin (AVP) – as well as a large population of supporting astrocytes. The proper functioning of this circadian system is disrupted in many neurodegenerative diseases, as evidenced by the insomnia and other sleep disturbances reported by many patients and confirmed by studies on the SCN of deceased patients. This circadian disruption often precedes other symptom onsets by years if not decades, lowers quality of life for both patients and caregivers, and may exacerbate disease progression in ways not currently understood. One such disease is the dominant genetic neurodegenerative disease Huntington’s disease (HD), the symptomology of which has been well recapitulated in the mouse model BACHD. Zoë will stain the SCN of BACHD mice at the age of symptom onset (symptoms including behavioral and physiological circadian deficits) for VIP and AVP to quantify these two cell populations. She will also stain astrocytes and examine them for an increase in surface area as another indicator of damage. By gaining a better understanding of the mechanisms through which the circadian system is disrupted in HD, more useful therapies can be developed with the aim of eventually increasing patient well-being.
After graduating in Spring 2014, Zoë plans to attend graduate school for a PhD in neuroscience and continue doing anatomic research in the circadian rhythms field. Zoë would like to thank her mentor, Chris Colwell, for his support and guidance. She would also like to thank her graduate student mentor, Dika Kuljis, for her assistance and advice, and all other members of the Colwell lab for their enthusiasm and encouragement. Lastly, Zoë would like to thank the Waingrow endowment for their support.
| Harding Luan
Mr. Harding Luan
Mentor: Dr. Ting-Ting Wu
Title: Characterizing the Interaction of Murine gamma-herpesvirus 68 Open Reading Frame 34 and RNA Polymerase II
Harding is a fourth-year student majoring in Molecular, Cell, and Developmental Biology with a minor in Biomedical Research. He began his undergraduate research with Dr. Ting-Ting Wu in the Molecular and Medical Pharmacology department early in his first year. Currently, his research focuses on characterizing the interaction of Murine gamma-herpesvirus 68 Open Reading Frame 34 and RNA Polymerase II.
The two human gamma-herpesviruses, Kaposi’s Sarcoma-associated herpesvirus and Epstein-Barr virus are associated with several cancers totaling more than 200,000 cases per year. Like all other herpesviruses, progression of gene expression during lytic infection is highly regulated. The subset of genes known as viral late genes are defined by the dependence of their expression on viral DNA replication and are responsible for structure, packaging, and egress. Little is known about how the expression of this subset of genes is regulated, except that five viral open reading frames (ORFs) – 18, 24, 30, 31, and 34 – are essential for late gene expression. Using murine gamma-herpesvirus 68 (MHV-68) as a model, Harding is studying a novel interaction between ORF34 and RNA polymerase II, the primary player in transcription. He is currently using site-directed mutagenesis methods to map critical residues on ORF34 for this interaction. Mutants will then be tested to demonstrate the essential nature of this specific interaction during the gamma-herpesvirus life cycle.
Harding would like to thank Dr. Ting-Ting Wu, Dr. Ren Sun, and all the members of the Sun Lab for their ongoing mentorship and for creating an environment that is both fun and highly educational. Harding would also like to extend his sincerest gratitude to the Gottlieb Foundation for their generous support of his research and to URC – sciences for promoting scientific discovery in the undergraduate community.
| Tiffany Lin
Ms. Tiffany Lin
Mentor: Dr. Zhefeng Guo
Tiffany Lin is a third-year Microbiology, Immunology, and Molecular Genetics major. She has been working under the guidance of faculty mentor Dr. Zhefeng Guo since Spring 2012. Currently, her research is focused on determining the structure of the fibrils formed by yeast prion Ure2.
Prions are infectious proteins that underlie fatal neurodegenerative disorders called prion diseases, such as Creutzfeldt-Jakob disease in humans and mad cow disease in cattle. Prion protein forms amyloids, long unbranched protein fibrils. Amyloid formation is involved in many neurodegenerative diseases, including Alzheimer’s and Parkinson’s. The structure of fibrils is critical to understand prion biology and to develop effective treatments. Yeast prions share many features with human prions, and thus, are excellent models for study. Tiffany aims to determine the fibril structure formed by yeast prion protein Ure2, using analytical techniques to gather structural constraints that will be used to obtain a high-resolution structural model of Ure2 fibrils.
Tiffany would like to thank Dr. Zhefeng Guo for his guidance and mentorship, as well as the Wasserman family for their generosity and support of undergraduate research.
| Benjamin Lee
Mentor: Dr. Chentao Lin
Title: Luciferase Assisted Proteome Detection Platform for Plant Systems Biology
Benjamin Lee is a fourth year Biophysics student who has been working under Dr. Chentao Lin since winter quarter of freshman year. Over the years, Benjamin has developed a deep, newfound respect for plants and their potential utility.
The plant is a biological system, not a biological pathway. Thus, to achieve a new level of knowledge, we move into systems biology using the Arabidopsis thaliana. In plant biology to date, there is no scientific methodology that allows for inexpensive, highly sensitive, in vivo, and real-time kinetic analyses of proteomic behavior. Though mass-spectrometry based proteomic studies have been done, mass-spectrometry is not a suitable platform to systematically study individual proteins and determine their biological functions. Thus, we have undertaken the effort to develop the Luciferase Assisted Proteome Detection (LAPD) library, a transgenic A. thaliana population individually over expressing gene-regulating proteins of the A. thaliana proteome. The DNA constructs that are inserted into the A. thaliana genome contain a luciferase tag and an affinity tag fused in frame with the coding sequence of a gene of interest from the Arabidopsis with a constitutive promoter upstream. The luciferase tag allows for in vivo real-time kinetic analyses of a target protein because luciferase signal intensity correlates to fusion protein abundance. The affinity tag allows for immunoprecipitation of target protein to study protein-protein, protein-DNA, and protein-RNA interaction at the systems level. Furthermore, a library of transgenic plants with over expression of an individual target protein allows for systematic identification of its biological function.
In short, the LAPD library will serve as a tool to systematically study the A. thaliana and allow for study of in vivo proteomic behavior under varying conditions.
Benjamin plans to graduate in the coming spring 2014. He intends to obtain a joint MD/MBA degree and work at the institutional level in healthcare to combat the cycle of poverty. Benjamin thanks Dr. Chentao Lin and his many other mentors and sponsors for their support over the years. Lastly, Benjamin Lee expresses gratitude to the Andy Lau Foundation for their generosity that encourages him to continue to strive for everything he believes in.
| Jessica Lee
Ms. Jessica Lee
Mentor: Dr. Peipei Ping
Title: Characterizing the Connection between Chromosome Origin and Mitochondrial Proteins in Relation to Function and Disease
Jessica Lee is a third year at UCLA majoring in Microbiology, Immunology, and Molecular Genetics. She joined the Ping lab during the summer of 2012 and is currently researching the connection between genomic and proteomic characteristics of mitochondrial function and disease.
Mitochondria are immensely vital in the operation of life, responsible for essential processes such as energy production, metabolic and signaling regulations, and apoptotic initiation. Being so intricately woven into cellular life, mitochondrial dysfunction has been implicated in numerous complex disease phenotypes in humans, ranging from neurodegenerative disorders, such as Alzheimer’s and Parkinson’s diseases, to various cancers and cardiomyopathies. The drive to unravel the complexity of these diseases and identify therapeutic targets led to extensive studies of the mitochondrial proteome. However, disease phenotypes often manifest at multiple levels of expression and regulation, making an integrative, multi-omic approach imperative to fully understanding mitochondrial involvement in complex diseases. By combining proteomic and genomic perspectives, Jessica aims to characterize the correlations between the genetic origins, biological functions, and disease associations of the mitochondrial proteome.
After graduation, Jessica plans to pursue an M.D./Ph.D. dual degree and continue research in genetics and pathogenesis. She would like to thank Dr. Peipei Ping for the invaluable experience of conducting research in her lab, and she would like to thank the members of the Ping lab for their continued support. Finally, she would like to thank the MacDowell Foundation for their generous funding to support her research.
| Danh Le
Pictured left to right: Dr. Analyne Schroeder, Danh Le, and Dr. Christopher Colwell
Mr. Danh Le
Mentor: Dr. Christopher Colwell
Title: Oxidative Stress and Inflammation in Mice with Disrupted Daily Activity Levels
Danh Le is currently a fourth-year undergraduate student majoring in Physiological Sciences with minors in Biomedical Research and Education Studies. He has been conducing research in the Laboratory of Circadian Rhythm and Sleep Medicine with Dr. Colwell since June 2012 in the Department of Psychiatry and Biobehavioral Sciences. Under the guidance of Dr. Analyne Schroeder, Danh is currently studying the impact of disruptive daily activity levels on the circadian system and the resulting effects on inflammation and oxidative stress pathways.
The circadian system drives daily rhythms in biological and behavioral processes including locomotor activity. At the same time activity is able to feed back to the circadian system and alter its output. This study aims to determine whether scheduling of activity at the wrong time of day will disrupt the circadian system that leads to oxidative stress and pathology. C57B6 mice under 12:12 light/dark conditions, will be provided either no wheels or daily running wheel access during the first 6 hours of the light period (ZT0-6), a time when mice are normally asleep. Studies suggest that mice utilize the wheel during this time, leading to disruptions in daily rhythms of HR, body temperature and activity. The hypothesis is that disruption of circadian rhythms as a result of improperly scheduled wheel access will induce inflammation and oxidative stress in the heart and hippocampus as well as cause abnormal physiology. Over a 15-week period of scheduled wheel access, weight and blood pressure will be monitored. At the end of the study, mRNA levels of inflammatory and oxidative stress genes will be measured using real-time PCR, whereby an altered level in expression is expected. These studies will determine whether improperly timed activity can alter processes of inflammation and oxidation that may lead to abnormal physiology.
Danh would like to thank Dr. Colwell, Dr. Schroeder, and all the members of his lab for their guidance and support. He would also like to thank Dr, Lau for his generous contributions to the Undergraduate Research Scholars Program and the URC - Sciences office for working so hard to provide students with unique opportunities and programs to further their research endeavors.
| Chae Yoon Kim
Pictured, left to right:Dr. Stephanie White, Chae Kim, Dr. Nancy Day
Ms. Chae Kim
Mentor: Stephanie White
Title: Effects of Overexpression of FoxP2 in Area X on Male Zebra Finch Song
Chae Kim is a third year psychobiology major and began conducting research in Dr. Stephanie White’s lab in January 2013. Chae is working under the guidance of Dr. Nancy Day to study how overexpression of FoxP2 in Area X (a song-dedicated brain region of the basal ganglia) affects song in male zebra finches.
A mutation in the gene FoxP2, a transcription factor, results in severe speech and language deficits in humans. Songbirds, including zebra finches, learn their songs in a manner similar to how humans acquire speech. Therefore the lab studies how FoxP2 affects singing behavior to investigate genes that are critical for human speech. FoxP2 expression is greatest in Area X, a basal ganglia brain region dedicated to singing. The expression pattern changes based on whether the bird is singing by himself or if he is singing to a female. Chae’s project examines how FoxP2 supports song maintenance in adulthood in different behavioral contexts and how these songs are altered after constitutive overexpression of FoxP2 in Area x.
Chae would like to thank Dr. White and Dr. Day for their help, guidance, and continued support. She would also like to express her gratitude for the MacDowell endowment.
| Jason Kerr
Mr. Jason Kerr
Mentor: Dr. Andrea Kasko
Jason Kerr is a fourth year biochemistry major at UCLA working in the bioengineering department under Professor Andrea M. Kasko. His interests in research started during the summer of sophomore year to delve into the world of tissue engineering and biomaterials. Currently, Jason is developing azo-modified linkers that will thermally degrade within a hydrogel.
Hydrogels are commonly used as scaffolds due to their similarity to the body's natural extracellular matrix (ECM), which aids in the healing process. The ECM is often remodeled as tissues evolve; therefore, dynamically active artificial materials are desirable. Modification of hydrogels is usually achieved through degradation. Finding a means to control degradation both spatially and temporally is a goal in tissue engineering.
One type of degradation is thermally breaking covalent bonds in the crosslinked network in a hydrogel. While thermal degradation of materials is well-cited, little research have been reported on thermal degradation in hydrogels. Of the few temperature systems that have been reported, a solubility change of a non-covalently crosslinked hydrogel is involved and require extreme temperatures. To combat this issue, Jason will be designing an azo-linker that degrades at relatively low temperatures in the crosslinked network of a hydrogel.
Jason plans to pursue graduate school in biomedical engineering for a doctorate degree. Afterwards, he intends to continue the advancement of tissue engineering in either an academic or industrial setting. Jason would like to express his deepest gratitude to the Gottlieb endowment for their generous donation.
| Jennifer Kadowaki
Ms. Jennifer Kadowaki
Mentor: Dr. Matthew Malkan
Jennifer Kadowaki is a fourth year Physics major. She has been working with Professor Matthew Malkan in the Department of Physics and Astronomy since January 2012. Professor Malkan's research group studies Flat Spectrum Radio Quasars (FSRQ), a subclass of active galactic nuclei with aligned relativistic jets.
Although FSRQ’s brightness and rapid variability are caused by non-thermal jet radiation, the role of accretion disks in jet variability of gamma-ray loud quasars are unclear. The group observed 15 gamma-ray emitting FSRQs with big blue bumps and redshifts of z=1 by monitoring their flux changes over 15 nights in BVRI-bands and 20 nights in JHK-bands in a 12 month period using NASA's Fermi Gamma-ray Space Telescope, Lick Observatory's Nickel Telescope, and Kitt Peak National Observatory's 2.1 meter Telescope. Differential photometry is used to obtain photometric measurements with 1-2% level precision. Preliminary results based on the light curves of a few targeted FSRQs have shown significant variation in quasars' brightness over the 12 month monitoring period, with varying levels of fluctuation for each observed wavelength and some correlations between gamma-ray and optical bands.
Jennifer will be graduating in Spring 2014 and intends to pursue a PhD in Astrophysics. She would like to thank Professor Matthew Malkan for his continual mentorship and guidance. She also thanks Ms. Evers-Manly for her generous contribution and support for her project and for undergraduate research.
| Eric Jung
Mr. Eric Jung
Mentor: Dr. Carrie Bearden
Eric Jung is currently a 4th year Neuroscience major. He joined Dr. Carrie Bearden's neurogenetics laboratory during the summer after his first year. The Bearden lab’s research aims to understand genetic, cognitive and neurobiological risk factors for the development of adolescent-onset neuropsychiatric disorders. The lab examines these questions through two complementary lines of research: the investigation of intermediate neuroanatomic and cognitive traits associated with the development of psychosis and mood disorder; and the study of neurobehavioral manifestations of syndromes with an identified genetic origin.
Eric's research focuses specifically on one neurogenetic disorder, 22q11.2 Deletion Syndrome (22qDS). Among other cognitive and physiological anomalies, a marked deficit in visuospatial ability is exhibited in 22qDS. Specifically, Eric is investigating the neuroanatomic substrates involved in the visuospatial information-processing deficit characteristic of 22qDS. His most recent project found increased cortical thickness in many regions involved in the visual circuits of the brain, and that this cortical thickness was negatively correlated to visuospatial performance. Using further neuroimaging techniques such as structural MRI and DTI analysis, he is examining the specific developmental effects of this syndrome as well as the potentially affected visuospatial pathways in the brain. Many genes deleted in the 22q locus are known to be essential for neuronal migration and brain development, and this study could add to our knowledge of the intricate gene-brain-behavior relationship, as well as possible areas for clinical focus.
Eric plans to attend medical school upon graduation this coming Spring. He is fascinated by the brain and hopes to continue involvement in neuroscience in his future research endeavors and career. Eric would like to express his gratitude to Dr. Bearden for being an tremendously supportive mentor. He would also like to thank Nicole Enrique, Carolyn Chow, and the entire Bearden lab for the incredible guidance throughout his years as an undergraduate student. Finally, Eric would like to thank the Boyer foundation for its generous scholarship, and the URC for supporting undergraduate research.
| Erik Jue
Mr. Erik Jue
Mentor: Dr. Daniel Kamei
Title: Rapid Extraction from Aqueous Two-Phase Systems for the Enhanced Detection of Viruses and Proteins Using the Lateral-Flow Immunoassay
Erik Jue is a fourth-year bioengineering major and has been conducting research in Dr. Daniel T. Kamei’s Lab since March 2012. His current project focuses on using rapid aqueous two-phase systems to improve the sensitivity of the lateral-flow immunoassay. After graduating from UCLA, Erik plans to pursue a PhD in bioengineering.
Point-of-care detection of viruses and proteins is crucial for disease diagnosis in resource-poor settings. The lateral-flow immunoassay (LFA) is a potential detection method for this application due to its low cost, rapid time to result, portability, and minimal power requirements. LFA consists of a small nitrocellulose strip that absorbs a sample through capillary flow and is able to detect the presence of a target biomolecule through a specific antibody bound to a colorimetric indicator. However, the sensitivity of LFA is lower than its lab-based counterparts such as ELISA and RT-PCR. Therefore, Erik’s project focuses on the pre-concentration of the target biomolecule using aqueous two-phase systems (ATPSs). Unlike typical oil-water solvents, ATPSs provide a mild environment for the biomolecules during the liquid-liquid extraction step, since both phases are composed primarily of water. ATPSs are also easy to use and inexpensive making them desirable as a pre-concentration step for LFA. The Kamei Lab has previously investigated the combination of ATPSs and LFA, but the concentration step took hours to complete. Erik’s research revolves around reducing the time of the concentration step. This includes the investigation of rapid polymer/salt systems and early extraction from the system before equilibrium is achieved. However, due to the high salt concentration in these systems, an additional modification must be made to the LFA colorimetric indicator for additional stability. Specifically, Erik has been conjugating polyethylene glycol to sterically stabilize these particles from aggregating in solution. Furthermore, Erik has been developing a method to quantify the signal intensities from LFA.
Erik sincerely thanks Dr. Kamei and all members of the Kamei Lab for their continued mentorship, support, and guidance. He would also like to thank the Gottlieb Scholarship and the URC-Sciences for their generous sponsorship.
| Sunjong Ji
Mr. Sunjong Ji
Mentor: Utpal Banerjee
Title: In vivo cultures of Drosophila lymph glands via whole-organ transplantation
Sunjong Ji is a 4th year Molecular, Cell and Developmental Biology major and Biomedical Research minor currently working in Dr. Utpal Banerjee’s laboratory. His research focuses on adult hematopoiesis in Drosophila and the terminal fate of the lymph gland.
Hematopoiesis in Drosophila occurs in a specialized organ called the lymph gland, which consists of primary lobes and several secondary lobes. The primary lobes contain three areas of interest including a medullary zone consisting of quiescent prohemocytes, a cortical zone consisting of maturing hemocytes, and a posterior signaling center that serves as a hematopoietic niche. However, the lymph gland is known to dissociate during the developmental transition from the larval to the adult stage during the first 12 hours after puparium formation. No molecular markers exclusive for lymph gland cells are known at the time, making direct lineage tracing experiments for tracking the terminal fate of the lymph gland during the adult stage unfeasible. In order to circumvent this issue, Sunjong has developed a technique for in vivo cultures of Drosophila lymph glands via whole-organ transplantation. The technique consists of dissecting lymph glands from donor larvae and then transplanting them into the body cavities of the desired host larvae. The body cavities of host larvae serve as culture vessels and their hemolymph serve as incubation media. This novel technique allows the tracking of lymph gland cells into the adult stage by simply transplanting marked lymph glands into donor larvae. After further optimizing the technique, Sunjong’s long term goals include not only investigating the location of the lymph gland cells in adult Drosophila but also their identity and function in adult Drosophila.
After graduation, Sunjong plans to pursue an MD-PhD degree and ultimately aspires to become a medical scientist. He would like to thank Dr. Utpal Banerjee for his mentorship and for the opportunity to be a part of his laboratory. He would also like to extend his gratitude to Ting Liu, Dr. Cory Evans and Dr. Tina Mukherjee for their mentorship and Dr. Jiwon Shim, Dr. Bama Charan Mondal, Dr. Ira Clark, Dr. John Olson and the rest of the Banerjee laboratory for their continued support. Finally, he would like to thank the Undergraduate Research Scholars Program, the Minor in Biomedical Research, and the Wasserman Family for their generous support and for providing him with opportunities in undergraduate research.
| Christina Jayson
Ms. Christina Jayson
Mentor: Dr. Carla Koehler
Christina Jayson is a third-year pursuing a Biochemistry major and Spanish minor. She joined the Koehler lab of the Biochemistry department in the fall of her second year. Under the guidance of her post-doctoral mentor, Meghan Johnson, and principle investigator, Dr. Carla Koehler, she is characterizing mutants in mitochondrial assembly in the vertebrate model zebrafish.
Mutations in the Tim8 protein can lead to Mohr-Tranebjaerg Syndrome or Deafness Dystonia Syndrome. This disease is caused by defective mitochondrial import and is characterized by progressive sensorineural hearing loss, dystonia, mental deficiency and visual disability. Previous research by Dr. Koehler et al. indicates the disease results from a mutation in Deafness Dystonia Protein1 (DDP1) that affects mitochondrial protein import. Christina is generating a zebrafish line with germline mutations in Tim8A and Tim8B to phenotypically characterize the effects of this disease on a vertebrate model. Using zebrafish to recapitulate the resulting disease phenotypes from targeted protein mutation will allow her to generate a model organism that has more clinical and chemical relevance for studying mitochondrial protein translocation and the degenerative consequences that arise when the import system is compromised.
Christina would like to thank Dr. Carla Koehler, her post-doctoral mentor, Meghan Johnson, and the members of the Koehler lab for their guidance, and for the opportunity to conduct undergraduate research. She would additionally like to thank the Wasserman Foundation and the Undergraduate Research Scholarship Program for their generous support.
| Elisabeth Hodara
Pictured (left to right): Elisabeth Hodara, Robin Roychaudhuri
Ms. Elisabeth Hodara
Mentor: Dr. David Teplow
Elisabeth Hodara is a fourth year undergraduate student at UCLA, completing a degree in Molecular, Cell and Developmental Biology. Since the summer of 2012, Elisabeth, mentored by Dr. Roychaudhuri, has been working in Dr. Teplow’s laboratory where she first investigated the role of methionine 35 in the assembly of amyloid β-proteins. She then began working on the Icelandic variant of Aβ, conducting structural studies to elucidate the effect of two mutations at position 2 in Aβ42.
Aβ is responsible for the plaques that cause the most common progressive neurodegenerative disorder associated with aging, Alzheimer’s Disease (AD). Aβ42, a translational product of the amyloid precursor protein (APP) gene, is thought to be a major pathogenic contributor to AD. Elisabeth researches two naturally-occurring mutations at position 2 in Aβ42. The first, an alanine to threonine substitution, was previously shown to be associated with a protective effect against cognitive degeneration and AD, while the second, an alanine to valine substitution, was reported to be recessive for early onset AD. The fact that these two mutations occur at the same site but confer drastically different phenotypic effects indicates that position 2 plays a pivotal role in determining the nature and impact of Aβ42, making their investigation critical. To study these peptides, Elisabeth will use Photo-Induced Cross-Linking of Unmodified Proteins and subsequent SDS gel, ThT binding and fluorescence assays, CD spectroscopy, electron microscopopy, and toxicity assays. Through this research, Elisabeth aims to obtain a structural basis for the protective effect conferred by the newly discovered threonine mutation.
Elisabeth aspires to obtain a PhD degree after she graduates, and pursue a career in scientific research and education. She would like to thank Dr. Teplow and Dr. Roychaudhuri for opening the doors to the world of scientific research. She would also like to thank Mr. Lau for generously sponsoring her URSP scholarship.
| James Haggerty-Skeans
Mr. James Haggerty-Skeans
Mentor: Dr. Patricia E. Phelps
Funding: Van Trees
James Haggerty-Skeans is a third-year student majoring in Neuroscience and minoring in Biomedical Research. James has been studying under Dr. Phelps since September, 2012, in close collaboration with Ph.D. candidate Rana Khankan. One of the main focuses of the Phelps lab is an investigation of the role that Olfactory Ensheathing Cells (OECs) play in axonal regeneration after spinal cord transection. Olfactory Ensheathing Cells, unique glial cells found in the olfactory epithelium, have been shown to support axonal regeneration after a complete spinal cord transection in rodents when they are grafted near the lesion site. Animals that have received the OEC treatment have shown improved stepping ability, as well as increased axon density in the normally inhibitory injury site. It has not yet been shown that OECs survive after transplantation, nor what their migratory pattern may be.
James is currently using fluorescent staining in order to visualize OECs, and gain insight on their survival, migration, and behavior at the injury site. He is working to quantify the regenerative capacity of 5-HT serotonergic axons, post injury, in animals that received an OEC treatment after a complete spinal cord transection.
| Dewal Gupta
Mr. Dewal Gupta
Faculty Mentor: Dr. Dino Di Carlo
Title: High Throughput Cell Viability Assay using Deformability Cytometry
Dewal is currently a third year at UCLA majoring in computational and systems biology. He currently works in Dr. Di Carlo's lab in the Bioengineering department with microfluidic devices. His current project focuses on deformability cytometry and how epigenetic modifications to the DNA structure can be detected using deformability.
Microfluidics is a large field and generally deals with the behavior and manipulation of cells and fluids at a micro-scale level. One of the most important tools recently developed is the deformability cytometry. Deformability cytometry works by stretching cells at a junction while a high-speed camera records the elasticity of each cell as it passes through. It is high-throughput and has the capability of analyzing approximately 1,000 to 3,000 cells per second. It has been shown there are significant differences in the deformability of live and dead cells, differentiated stem cells, cancer cells, and many other cell populations. Therefore, deformability cytometry can be used as an efficient and high-throughput cell viability assay. Currently, Dewal is experimenting with different designs and methods to sort cells based on viability without the need of staining or labeling. His project looks to detect the epigenetic modifications of certain drugs on cancer cells, and how these changes can be quantified using deformability cytometry. By using the deformability cytometer, it will become much easier and cheaper to quantify viable cells and measure the effectiveness of DNA modifying drugs on specific cell populations.
Dewal would like to thank Dr. Di Carlo, the Di Carlo lab, and the Undergraduate Research Scholars Program and the MacDowell Scholarship for supporting his research endeavors. He is very grateful for their guidance and support that he has received over the past few years.
| Ishanee Dighe
Ms. Ishanee Dighe
Mentor: Dr. Suraj P. Bhat
Ishanee Dighe is a third year Biology major at UCLA. Ishanee has been working in the Vision Molecular Biology Laboratory headed by Dr. Suraj P Bhat in the Jules Stein Eye Institute, under the guidance of Dr. Rajendra K Gangalum (Assistant Research specialist) for an year and half now. Dr. Bhat’s laboratory studies the regulation and function of the small heat shock protein, alpha-B crystallin (αB-crystallin) in the eye as well as in various other tissues. It was Dr. Bhat’s laboratory that first reported on the expression of αB-crystallin outside of the ocular lens (Bhat and Nagineni, 1989). Soon it was recognized that this protein has important physiological functions in a number of tissues. B-crystallin is now known to be associated with many neurodegenerative diseases including Alzheimer’s disease (Renkawek et al., 1994), Parkinson’s disease and multiple sclerosis (van Noort et al., 1995) and many cancers. Mutations in this small heat shock protein also lead to cardiomyopathies and Cataracts.
αB-crystallin is one of the predominant proteins expressed in ocular lens. It is also expressed in the heart, muscle, kidney, retina, small intestine and the brain (Bhat and Nagineni, 1989). The Bhat lab has pursued regulation of the expression of the αB-crystallin gene and the physiological function of this gene product; αB-crystallin gene contains a heat shock promoter that interacts with heat shock transcription factor, HSF4 in a developmentally dictated fashion (Somasundaram and Bhat, 2004).αB-crystallin associates with the Golgi complex in a cell cycle dependent manner in human Glioblastoma cells (Gangalum et al., 2004). Work in the Bhat laboratory has shown that B-crsytallin is part of the detergent resistant membrane microdomains (DRMs)/lipids rafts and is secreted via exosomes (Gangalum et al., 2011). The mechanistic details of its association with membrane microdomains and its involvement in inter-cellular communication via exosomes still remain to be understood. Ishanee’s research project is focused on understanding the role of αB-crystallin in DRMs by characterization of the interacting proteins in these specialized membranes. She studies these membrane domains and their macromolecular composition(s) in membrane isolates from different cells and tissues.
Ishanee sincerely appreciates the support of Dr. Bhat and Dr. Gangalum. She is grateful for their encouragement and help, which has contributed to her understanding of the complex research problems and their resolution via focused experimentation. This learning experience will help her seek a productive career in medicine and health care. She would also like to thank Mr. O’Conell for his help and consideration and finally, she would like to thank the Oppenheimer family for the scholarship.
| Jaime De Anda
Mr. Jaime De Anda
Mentor: Dr. Gerard Wong
Jaime is a 4th year transfer student and the first member of his family to attend college. Before he transferred to UCLA, his passion for research spanned a variety of interesting and broad subjects from Astronomy to Tissue Engineering. Prior to his current position in Dr. Gerard Wong’s research group, he interned at the Monterey Institute for Research in Astronomy, under the supervision of Dr. Bruce Weber, where he worked on the design of the layout for a High-Resolution Echelle Spectrograph, in addition to writing computer algorithms in Fortran programing language to calibrate a CCD camera to be mounted at the 36-inch telescope at the Chews Ridge Observatory. The following year, prior to transferring to UCLA, Jaime interned at UC Davis, Physics Department, under the supervision of Dr. Daniel Cebra where he worked on a stochastic Glauber model for simulation of nuclear collisions of heavy ions at relativistic speeds, in addition to working with particle production spectra from the Relativistic Heavy Ion Collider at Brookhaven National Laboratory in New York.
Currently, Jaime is directing research under the supervision of Dr. Gerard Wong in the Department of Bioengineering at UCLA. Jaime also had a year as an undergraduate intern collaborator and has been trained on their procedures for data analysis and computer algorithm development. In Dr. Wong’s Laboratory, Jaime observes bacteria motility and behavior on surfaces with the help of powerful microscopes and high speed cameras. Jaime’s current project focuses on developing computer algorithms with the MATLAB software. This computer program processes the images taken by the cameras mounted on the microscope. This processing includes image filtering and region morphology identification for bacteria tracking. This allows us to view where every bacterium is located during a transient or long term cluster, on the field of view. Through these algorithms and green fluorescent tags, we set to study the second messenger cyclic di-GMP, which is used by bacteria as signal control for motility and biofilm formation. This protein plays a major role in bacteria interactions and growth into bacterial colonies. Such structures are required for chronic infection of the host; hence, the study of motility at early biofilm formation can give great insight towards the development of novel anti pathogenic treatments. The lab expect the bacteria to have specific affinity towards specific cyclic di-GMP producer trajectories.
Jaime would also take this time to thank Dr. Wong. His support and mentorship in his academic research has tremendously helped Jaime’s development in the Bioengineering field. In addition, Jaime would like to express my deepest gratitude to the Wasserman Family for their generosity.
| Joseph Conovaloff
Pictured left to right: Dr. David B. Teplow, Joseph Conovaloff, Dr. Eric Y. Hayden
Mr. Joseph Conovaloff
Mentor: David B. Teplow
Title: Isolation and Characterization of Amyloid Beta-Protein Oligomers
Joseph Conovaloff is a third year neuroscience major, minoring in biomedical research. He has been doing research in the Teplow laboratory since June 2012, under the direct mentorship of Dr. Eric Y. Hayden. The Teplow lab focuses on studying and understanding the amyloid beta-protein (Ab), a protein heavily implicated in causing Alzheimer’s disease (AD).
AD is a neurodegenerative disorder that can lead to difficulty in performing basic tasks, forgetfulness, and eventually death. Currently in the United States, over 5 million people have AD. This is estimated to increase to at least 15 million by 2050, amounting to over $1 trillion in healthcare costs. In AD, small clumps (“oligomers”) of Ab are responsible for the death of brain cells. To develop effective therapeutic agents for AD, it is necessary to understand how these oligomers form and to determine their three-dimensional structures. Medicinal chemists can then design specific agents that bind to the atoms that control this clumping phenomenon. Oligomers contain small numbers of Ab proteins, but no single type exists. Oligomers may contain two, three, or more individual Ab proteins (monomers). In addition, these oligomers can convert from one to another by losing or gaining monomers, making oligomer structure determination very difficult. Joseph is working on isolating these individual oligomers that contain different numbers of monomer units in one complex. The resulting isolated oligomers will enable many different characterization studies, providing a knowledge base for therapeutic agents against the most toxic species of Ab. As there are numerous disease that involve amyloid proteins, this process of isolating oligomers could provide insight into isolating oligomers associated with other diseases, such as Parkinson’s disease.
Joseph is a part of the Howard Hughes Undergraduate Research Program (HHURP) at UCLA, and is extremely grateful for the HHURP faculty’s support and guidance. He would also like to thank Drs. Ira Clark and Rafael Romero and the Biomedical Research Minor for their encouragement and dedication to promoting undergraduate research.
Joseph would like to express his sincere gratitude to Mr. O'Connell for sponsoring his URSP scholarship endowed by the Oppenheimer Award. He is also a part of the Howard Hughes Undergraduate Research Program (HHURP) at UCLA, and is extremely grateful for the HHURP faculty’s support and guidance. He would also like to thank Drs. Ira Clark and Rafael Romero and the Biomedical Research Minor for their encouragement and dedication to promoting undergraduate research.
| Laurel Clare
Ms. Laurel Clare
Mentor: Martha Lewis
Title: Studying the Patterns of Hepatitis C Co-transmission with HIV in a Los Angeles MSM Cohort Using Molecular Epidemiology
Laurel Clare is a fourth year UCLA undergraduate majoring in Microbiology, Immunology, & Molecular genetics and pursuing a minor in Environmental Systems & Society. She has been working in the Lewis Lab within the Division of Infectious Diseases since the start of her third year. The Lewis Lab focuses on the study of HIV in association to adaptive pressures of the immune system and also in relation to co-infection with other viruses such as Hepatitis B (HBV) and Hepatitis C (HCV), with a strong emphasis on phylogenetic analysis.
Her current project focuses on the study of HCV transmission within an HIV-positive cohort of men who have sex with men (MSM) in Los Angeles, called Metromates. HCV is the fastest rising co-infection in U.S. urban populations and a main contributor of mortality among HIV-infected persons. One goal of this study is to determine the prevalence of HCV and HIV co-infection in the cohort, as well as identify risk factors such as non-injected drug use or high risk sexual practices. The prevalence can be determined by detecting HCV specific cDNA synthesized from viral RNA extracted from patient serum samples. Another goal is to use phylogenetic analysis to clarify relatedness of HCV and HIV transmission networks among the cohort individuals. This will be useful for determining whether the transmission of HCV may have originated from one or multiple sources, thus applying epidemiologic principles to the study. One last goal for the study is to examine the association between transmitted HIV and HCV drug resistance and identify risk factors for resistance. These characteristics can be analyzed by sequencing key regions of HCV and HIV genomes and looking for drug resistance mutations. Overall, the improved understanding of HCV and HCV co-infection prevalence within the Metromates cohort will provide data to help improve HCV prevention efforts.
Laurel would like to thank Dr. Martha Lewis and all those working in the Lewis Lab for their continual guidance and support throughout the project. She would also like to express her gratitude to the Hilton Scholarship for generously funding her URSP scholarship.
| Joan Chou
Ms. Joan Chou
Mentor: Dr. Ellen M. Carpenter
Joan is a UCLA third year undergraduate student majoring in physiological science. She began working with graduate student Elvira Khialeeva in Dr. Ellen Carpenter’s lab in UCLA’s Department of Psychiatry and Biobehavioral Sciences in September of 2012. Her project focuses on the role of reelin in breast cancer metastasis.
Reelin is an extracellular matrix glycoprotein originally observed to play a significant role in cell migration during brain development. However, recent studies from the Carpenter lab and others have demonstrated that reelin signaling is also present in other tissues such as the mammary glands. There, reelin has been shown to inhibit the migration of mammary epithelial cells lining the lumen of mammary ducts. Recent findings in the Carpenter lab have shown that loss of reelin signaling affects breast cancer metastasis. In these studies, 4T1 mouse mammary tumor cells implanted into the mammary fat pads migrated to the lungs, lymph nodes and liver in wild-type mice, forming metastatic nodules. In mice carrying mutations in the genes encoding reelin or Dab1, an intracellular adaptor protein downstream in the reelin signaling pathway, no metastatic nodules were seen. Her goal is to determine what differentiates tumors raised in wildtype mice from those raised in reeler or Dab1 mutant mice.
| Le Chang
Ms. Le (Leslie) Chang
Mentor: Dr. Kang Ting
Title: Bone formation in osteoporotic mice is induced by systemic administration of NELL-1
Leslie Chang is a fourth year Biology major and has been an undergraduate student researcher under Dr. Kang Ting since 2011. Her research is under the Dental and Craniofacial Research Institute at UCLA.
Leslie has studied the effects of NELL-1, a novel osteoinductive protein, and the role of multipotent stem cells in osteogenic differentiation. Osteoporosis is a major health concern that plagues elderly and post-menopausal patients. Complications during treatment include a decline in the number, function and survival of osteoblasts and new therapies for the prevention and treatment of osteoporotic fractures are necessary. The NELL-1 protein has been found to promote endochondral and intramembranous ossification and is a potential future therapy for osteoporosis. NELL-1 is highly specific and promotes osteoblastogenesis while reducing osteoclast formation, which reduces bone formation. Localized delivery of NELL-1 has been found to produce bone regeneration, but a systemic delivery of NELL-1 would prevent osteoporotic fracture. This present study aims to use a murine tail injection model to study the capacity for recombinant NELL-1 to prevent ovariectomy (OVX)-induced osteoporosis. These findings will hold compelling implications for the use of NELL-1 as an anti- osteoporotic therapy for the aging population.
After graduation Leslie is planning on attending medical school to obtain either an MD or MD/PhD. She would like to thank all the member of Ting lab for their continued support and the generous Ehrisman Scholarship for supporting her endeavors in both academics and research.
| Jason Chang
Pictured left to right: Dr. Shimon Weiss, Dr. Jianmin Xu, Jason Kerr
Mr. Jason Lin Chang
PI: Dr. Shimon Weiss
Mentor: Dr. Jianmin Xu
Title: Determination and Optimization of Imaging Buffer and Conditions for Super-resolution Optical Fluctuation Imaging Usage
Jason Chang is a 4th year Biochemistry major. He has been conducting research in Dr. Shimon Weiss' Laboratory under the guidance of postdoctoral fellow Jianmin Xu since the summer of his freshman year. The Weiss lab studies and develops technique for super-resolution imaging of living systems on the nanoscopic level through fluorescence imaging.
Fluorescence imaging is a powerful technique for probing cellular structure and activity in a minimally invasive way. The ability to study live cells utilizing fluorescent probes, such as organic dyes or fluorescent proteins, enable investigating the dynamic aspects of the cellular machinery and observing in real-time its response to various stimuli. Despite the many advantages of fluorescent imaging, the main limitation of fluorescence microscopy is the low resolution due to the diffraction limit of light. Through the use of advanced mathematics in super-resolution imaging strategies, such as SOFI (Super-resolution Optical Fluctuation Imaging), this limit can be overcome as higher resolution images than the diffraction limit can be obtained. SOFI uses blinking labels in order to mathematically extrapolate a super-resolution structure. Unattained by other superresolution counterparts, SOFI's capability of capturing dynamic states that occur on the nanoscopic level in real time is crucial in visualizing cellular processes and furthering man's understanding of life. Because SOFI has only been applied to fixed cells due to biologically incompatible imaging buffer conditions, SOFI's full potential in capturing rapidly changing cellular states has yet to be realized.
With his background in biochemistry, Jason is excited in pushing the frontiers of science and hopes to improve SOFI to the point that it becomes a successful and widely-utilized technique that can allow the visualization of a whole new dynamic nanoscopic world for the scientific community before he graduates in the Spring of 2014. He would like to thank Jianmin Xu for his patience, guidance, and inspiration, and Shimon for the opportunity to learn in his lab. Jason also thanks all the postdoctoral fellows and graduate students in the Weiss Lab for their advice and companionship. Finally, Jason is grateful for the generous support the Gottlieb family has provided.
| Susan Chang
Ms. Susan Chang
Mentor: Dr. Erika Nurmi
Project Title: Genetic Moderators of Treatment Response to Dexmethylphenidate in Children and Adolescents with ADHD
Susan is a third-year biology major who hopes to pursue a career in pharmacy and pharmaceutical research. Toward these goals, Susan is conducting translational pharmacogenomics research under the guidance of Dr. Erika Nurmi in the Department of Psychiatry and Biobehavioral Sciences. The Nurmi/McCracken Lab studies genetic factors underlying brain functioning, psychiatric disorders, and effects of psychotropic medications. Susan’s current project focuses on elucidating the effects of genetic variation on treatment response to dexmethylphenidate (d-MPH) for pediatric attention-deficit hyperactivity disorder (ADHD). While d-MPH is an effective ADHD treatment, many individuals fail therapy due to lack of response or limiting side effects.
Susan is investigating whether genetic variation in drug targets (SLC6A3/DAT1, VMAT2) and metabolic enzymes and transporters impacting drug disposition (CES1A1, ABCB1) could help explain differential outcomes in treatment response to d-MPH. Common genetic variation represented by single nucleotide polymorphisms (SNPs) and variable number tandem repeats (VNTRs) is currently under examination for its impact on treatment outcomes. The results of her research can help guide the design of novel therapeutics and personalize treatment matching in the future.
Susan would like to thank Dr. Erika Nurmi and the members of the Nurmi/McCracken Lab for their mentorship and support. She would also like to express her gratitude to the UCLA URC and the Wasserman Family for their generosity and encouragement of undergraduate research.
| Alanna Chan
Pictured (left to right): Dr. Heather Christofk, Alanna Chan, Wen Gu.
Ms. Alanna Chan
Faculty Mentor: Heather Christofk
Title: MCT1 inhibition can promote the survival of dissociated human embryonic stem cells
Alanna Chan is a fourth year majoring in Molecular, Cell, and Developmental Biology with a minor in Biomedical Research. She began as an undergraduate researcher with Dr. Heather Christofk in the Molecular and Medical Pharmacology department during the spring quarter of her first year. Her research seeks to characterize how the metabolism of human embryonic stem cells (hESCs) can be altered to promote their survival upon dissociation.
There is a growing body of literature which suggests that during differentiation the metabolism of hESCs switches from a reliance on glycolysis in the undifferentiated state to a reliance on oxidative metabolism. Our lab has identified a possible regulator of this metabolic switch in hESCs. This regulator is a protein, monocarboxylate transporter 1 (MCT1). MCT1 functions in the proton linked transport of monocarboxylates, like lactate and pyruvate, across the plasma membrane. Furthermore it is know that hESCs tend to grow in colonies in vitro, but when hESC colonies are dissociated into single cells, they undergo apoptosis. It is important to be able to study the culture of single hESCs for regenerative medicine purposes since genetic manipulations can be carried out at the singular cell level and then clonally expanded. When examining the effects of MCT1 inhibition on dissociated hESCs, we observed that MCT1 inhibition can promote the survival of dissociated hESCs. Alanna's research aims to characterize the molecular pathway that promotes the survival of dissociated hESCs upon MCT1 inhibition.
Alanna would like to thank Dr. Heather Christofk, Wen Gu, and all the members of the Christofk lab for their assistance and guidance throughout her research, for creating a supportive and nurturing environment, and the incredible opportunity to conduct research at the undergraduate level. Alanna would also like to thank the Wasserman family and the Undergraduate Research Scholars Program for their generous support.
| Benjamin Boodaie
Pictured, left to right: Benjamin Boodaie, Dr.Garima Dutta
Mr. Benjamin Boodaie
PI: Dr. Marie-Francois Chesselet
Direct mentor: Dr. Garima Dutta
Benjamin Boodaie is a fourth-year neuroscience major who has worked at in the laboratory of Dr. Marie-Francois Chesselet since January 2012. At the Chesselet laboratory, we use various fascinating mouse models of Parkinson’s and Huntington’s disease to enhance our understanding of these disease while also examining the efficacy of potential therapeutics. Benjamin’s specific project focuses on a promising new drug that aims to stunt the progression of Parkinson’s disease (PD) by targeting Lewy Bodies, the toxic inclusions that manifest themselves in the brains of PD patients.
Parkinson’s disease is the second most common neurodegenerative disorder. Although great strides have been taken in the development of symptomatic treatments for PD, there are currently no treatments available to reverse, stop, or even slow down the progression of this devastating disease. Studies of PD patients show that the aggregation of a-syn is a key player in the formation of Lewy bodies. Benjamin is currently aiding in a study that focuses on a novel bicyclic peptidomimetic compound designed to target a region of a-syn that is responsible for its aggregation. He and other lab members are using a mouse model of PD to test the drug’s effectiveness in reducing behavioral and histological markers of the disease. The compound he is testing was recently recognized as one of the top three most promising PD therapeutics by the Michael J. Fox Foundation, so Benjamin is excited and honored to be able to contribute to the study of this potentially groundbreaking therapy.
Benjamin would also like to express his gratitude to the Wasserman family for generously support his research and his endeavors to help find a cure for PD.
Outside of the laboratory, Benjamin is very passionate about community service; he is privileged to be involved with several service-based student organizations at UCLA that help making a positive impact on his community. In his free time, Benjamin enjoys playing basketball and tennis, swimming, practicing yoga, working out, playing the piano, and going out with friends and family.
| Neda Bionghi
Pictured left to right: Dr. Marcus Horwitz, Neda Bionghi, and Dr. Michael Tullius
Ms. Neda Bionghi
Mentor: Marcus Horwitz
Title: Characterization of a novel heme iron acquisition system in Mycobacterium tuberculosis
Neda Bionghi is a fourth-year student in the department of Microbiology, Immunology, and Molecular Genetics. Under the guidance of associate researcher Dr. Michael Tullius and faculty mentor Dr. Marcus Horwitz, Neda has been conducting an independent research project focusing on characterizing a system for iron acquisition from heme in Mycobacterium tuberculosis (Mtb).
Like most bacteria, Mtb requires iron to survive, and its multiplication and consequent infection in a host is dependent upon an iron acquisition system. Previously, it was believed that Mtb utilized only its siderophore system to acquire free iron. Recently, the Horwitz lab demonstrated an alternative to the siderophore-mediated iron acquisition system in Mtb, namely, a heme iron acquisition system. Some of the genes involved in heme acquisition have been identified; however this alternative mechanism has not yet been fully characterized. The widely used tuberculosis vaccine strain, BCG, which is almost identical at the genome level to Mtb (yet severely attenuated in comparison to Mtb largely due to specific deletions), is severely compromised in heme utilization. Neda hopes to characterize this defect in BCG so as to identify other genes involved in Mtb heme acquisition. Understanding the biology of Mtb is essential in combating this disease-causing agent. Elucidating the dynamics of the siderophore-mediated iron acquisition system versus the heme acquisition system can provide vital information for potentially targeting Mtb with antibacterials or vaccines, and can further our understanding of the currently distributed BCG vaccine.
Neda would like to thank Dr. Horwitz and Dr. Tullius for the invaluable guidance and support they have provided, as well as the entire Horwitz lab for creating a comfortable environment to work and learn in. She would also like to thank the Undergraduate Research Scholars Program and the Ehrisman Scholarship for their generous funding.
| Andrew Berg
Pictured (Left to Right): Dr. Tom Carmichael, Dr. Pouria Moshayedi, Andrew Berg
Mr. Andrew Berg
Mentor: Dr. S. Thomas Carmichael
Funding: Silva Trust
Title: Directed Neural Stem Cell Differentiation with a Transplanted Hyaluronan Biopolymer Hydrogel in Stroke
Andrew Berg is a 4th year Bioengineering student who has been conducting research since his sophomore year. He joined the Carmichael lab in the Department of Neurology and works closely with postdoctoral fellow Dr. Pouria Moshayedi. The Carmichael lab seeks to identify mechanisms of recovery after stroke and develop novel therapies for neural regeneration.
Stroke is the leading cause of long-term adult disability in America. After stroke, the brain has a limited capacity for repair. Engineered hyaluronan hydrogels may serve as a viable treatment option – they are biocompatible, injected through minimally invasive procedures, maintain similar viscoelastic properties to the brain, and sustain neural stem cells. The hyaluronan can be modified to direct the differentiation of encapsulated cells with growth factors and oligopeptide motifs from the active domains of the extracellular matrix. Andrew is working to characterize the response of encapsulated neural stem cells to a hyaluronan gel containing bone morphogenetic protein-4, brain-derived neurotropic factor, and the RGD, YIGSR, and IKVAV cell adhesion motifs. Successfully directing the differentiation of encapsulated neural stem cells in the hydrogel could be a critical step in initiating neural reconnection and improving functional recovery after stroke.
Andrew plans to graduate in the Spring of 2014. He would like to thank Dr. Carmichael, Dr. Moshayedi, and the rest of the Carmichael Lab. He would also like to extend his gratitude to the Silva Trust and URC-Sciences for their generous support.
| Rajani Bansal
Ms. Rajani Bansal
Mentor: Dr. Shaily Mahendra
Funding: MacDowell Fund
Rajani Bansal is currently a third year Chemical Engineering major. She works with Dr. Shaily Mahendra in the Civil and Environmental Engineering department. The Mahendra lab studies bacterial and fungal degradation of organic water pollutants, such as 1,4-dioxane, a probable human carcinogen. Rajani's project is to measure the degradation of 1,4-dioxane in conjunction with chlorinated solvents that are typically found together in contaminated water sources.
1,4-Dioxane and trichloroethylene (TCE) are co-occurring contaminants of concern in groundwater at many polluted sites across the United States. Since both of these compounds are probable carcinogens, their removal from water supplies is essential to ensure protection of human and ecological health. In past decade, it has been reported that various monooxygenase-expressing bacteria, such as propane-oxidizer Mycobacterium vaccae (austroafricanum) JOB5, can biodegrade 1,4-dioxane or TCE separately under aerobic conditions. However, bacteria that use 1,4-dioxane as carbon and energy source, such as Pseudonocardia dioxanivorans CB1190, have not yet been tested for growth-supporting or cometabolic biodegradation of TCE. In Rajani's study, TCE biodegradation by propane-oxidizing and 1,4-dioxane-oxidizing bacteria will be investigated. In independent experiments, both strains will be grown in minimal salts media with their primary growth substrates; 1,4-dioxane for CB1190 and propane for JOB5. Rajani will add TCE to both strains and monitor TCE degradation over time. She will also evaluate metabolic biodegradation of TCE by analyzing any increase in bacterial cell density.
Rajani would like to thank the MacDowell Fund for their generous contribution to her research. She would also like to express gratitude for her mentor Peerapong Pornwongthong for his help and training in the laboratory, and Dr. Shaily Mahendra, for her continued support and guidance. Rajani plans to graduate in June 2015 and hopes to pursue a career in industry in the future.
| Khadij Assani
Pictured, left to right: Ciara Martin, Khadij Assani, Dr. David Krantz
Ms. Khadij Assani
Mentor: Ciara Martin
PI: Dr. David Krantz
Khadij Assani is a 4th year Physiological Science and Study of Religion double major. Under the guidance and mentorship of Ciara Martin and Dr. David Krantz, Khadij has been conducting research in the Krantz lab since October 2013. Khadij studies gene-environment interactions and their effects on Parkinson’s disease (PD) using the Drosophila fly model. Previous projects included the examination of the relationship between proteasome inhibition, pesticide exposure and PD.
This year, Khadij will examine how genetic variations in the ubiquitin proteasome system (UPS) may affect dopaminergic cells. PD is a neurodegenerative disorder characterized primarily by the loss of dopaminergic neurons. Epidemiological studies have shown that exposure to the pesticides ziram, maneb, and paraquat increases the risk of PD three-fold; however, the neurotoxic mechanisms of action are unknown. Dr. David Krantz’s lab uses Drosophila to study gene-environment interactions involved in PD. The PD-linked fungicide ziram inhibits E1 ligase, the essential first step in the UPS. Additionally, ziram has been shown to preferentially kill dopaminergic neurons in primary culture and inhibit the degradation of the protein alpha-synuclein, which is known to accumulate and aggregate in the brains of PD patients. Khadij hypothesizes that it is ziram’s ability to inhibit E1 ligase, and not other molecular mechanisms, that are responsible for its link to PD. To test this hypothesis in the fly, Khadij will specifically mimic the effects of ziram on E1 ligase through genetic constructs. The genetic construct, UAS-E1-RNAi, inhibits the E1 protein in the protein degradation pathway. Expression of the RNAi construct in dopaminergic cells is pupal lethal, due to the critical role of dopamine in cuticle development. Thus, in order to obtain viable adults, the GAL4-GAL80 temperature sensitive system will be used. GAL80 inhibits expression of RNAi by inhibiting GAL4 at 18ºC. Once the flies have hatched, they will be transferred to 30 ºC where RNAi can be expressed due to lack of inhibition by GAL80. Previous experiments in the lab demonstrated no dopaminergic cell loss in four week old adults, reared as just described, with one copy of RNAi.R Khadij will determine if more robust knockdown of RNAi is sufficient to cause dopaminergic cell loss.
Aside from research, Khadij plans to graduate with double bachelors in Spring 2014. Her current goals are to continue onto medical school in Fall 2015 and become a surgeon. In the future, she wishes work for a hospital in an impoverished country, continue research on PD, and travel the world.
Khadij wishes to express immense gratitude to Ciara Martin and Dr. David Krantz for their continued guidance, encouragement, and support. She would also like to thank Ms. Knapp and the Undergraduate Research Scholars Program for the generous scholarship and support of her research.
| David Ashby
Mr. David Ashby
Mentor: Dr. Suneel Kodambaka
Funding: Gottlieb Endowment
Title: The Study of the Growth Characteristics of Zinc Dendrites from Electrodeposition
David Ashby is currently a third year undergraduate materials engineer. He has been undertaking research under Professor Kodambaka since winter quarter of second year in which he has been working with carbon nanotubes.
The study of the growth characteristics of zinc can have serious implications on battery design. If the electrochemistry and physics that occurs during battery use is better understood then the batteries design can be changed to produce more optimal power and life span. The problem with zinc batteries currently is that during use the batteries tend to create dendrites which inhibit the batteries intended use. Energy storage will become an ever more important field as the need to store and distribute energy in the modern world will increase; this is best seen in the large number of electric cars being created recently.
David is currently working on understanding the different parameters and their effect of the growth characteristics of zinc from electrodeposition. The hope is to better understand the changes that cause certain morphologies in zinc batteries so that the batteries can be adjusted to lessen their detrimental effect. The understanding of the growth will allow zinc air batteries to be better designed and thus increasing their life span and energy density during its life. This study is focused on the growth of these dendrites to better understand how they are formed and thus what can be done to stop their growth.
David is expecting to graduate in June of 2014 after which he plans to continue on to graduate school in materials engineering where he plans to pursue a masters and eventually a PhD degree. He eventually after graduate school plans to pursue a career in nanotechnology focusing on the energy field. David would like to thank the Gottlieb Foundation for their generous donation.
| Tatsuya Araki
Pictured (From left to right): Dr. Edward M. De Robertis, Tatsuya Araki, Hadrien Demagny.
Mr. Tatsuya Araki
Mentor: Dr. Edward M. De Robertis
Title: Regulated Smad4 Phosphorylations Integrate TGF-beta, FGF and Wnt Signaling Pathways
Tatsuya Araki is a fourth year Molecular, Cell, and Developmental Biology major who is also pursuing a minor in Biomedical Research. He has been conducting research since July 2011 in Dr. Edward M. De Robertis's laboratory with the help of Hadrien Demagny (Ph.D. Candidate). The De Robertis lab studies cell-cell communication during embryonic induction, with a focus on the effect of Wnt in early development.
An embryo develops into an organism as a result of many complex cell-cell interactions. It is known that Bone Morphogenetic Protein (BMP) and Transforming Growth Factor Beta (TGF-beta) pathways are important during the early development, and they signal through Smad proteins. It has been shown that Wnt and mitogens like Fibroblast Growth Factor (FGF) can increase the BMP signal duration by affecting phosphorylations at the Smad1 linker region. Tatsuya is studying whether FGF and Wnt can also control TGF-beta signaling activity by regulating phosphorylations at the Smad4 linker region, which contains a similar linker motif found in the Smad1 linker. Tatsuya aims to elucidate the functional role of the phosphorylation sites at Smad4 linker region by generating Smad4 phosphorylation-resistant linker mutant cell lines or injecting the Smad4 mutant mRNA in Xenopus embryos to assess the effect of phosphorylation-resistant linker mutations. Although Smad4 is currently thought to be constitutively active, Tatsuya hopes to uncover Smad4 as a highly regulated center for integrating multiple developmental signals like FGF and Wnt.
Tatsuya plans to graduate in the Spring of 2014 and hopes to pursue a MD/PhD degree. He would like to thank Hadrien for the years of instruction and guidance, Eddy (as Tatsuya would call him) for the opportunity to learn in his lab, and the Gottlieb family for their generous support once again.
| Matthew Abrams
Mr. Matthew Abrams
Mentor: Dr. Paul Micevych
Matthew Abrams is a fourth year neuroscience major who has been working under Dr. Paul Micevych for over a year. Matt is grateful to be involved in this lab as his project focuses on the effects of rapid membrane estrogen signaling. This field is exciting and challenging as much is being discovered about the effects of this rapid signaling in the past decade.
Our lab has been focused on the regulation of the membrane initiated estrogen receptor-alpha signaling in neurons. Matthew’s project is to discover how estrogen regulates the cell signaling involved in the hormonal activation of the luteinizing hormone surge, the central event in reproduction. This process is mediated by the kisspeptin neurons in the anteroventral periventricular nucleus (AVPV). To explore how these neurons are regulated, Matthew will begin to explore the effects of estradiol on a AVPV mHypo51 cell line to see if there is progesterone receptor induction when treated with estradiol over a specified time course. After the time course has been optimized then Matthew will begin to explore how the receptor is trafficked by performing several different assays. At the end of the year, Matthew hopes that is research can give more information on the regulation of reproduct, specifically during the luteinizing hormone surge.
Matthew is currently in his fourth year at UCLA with plans to graduate in the Spring. He is exploring several options such as obtaining a graduate degree or going straight into the science industry. Matthew wants to thank the Micevych Lab for all of their support, including the support of his mentors Dr. Paul Micevych and Dr. Angela Wong. Matthew wants to thank the Wasserman Foundation for their generosity for helping him with his senior project.