Student Profiles Archive - URSP 2014-2015
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.
| Jimmy Zheng
Mentor:Dr. Michael Alfaro
Funding: Boyer Award
Jimmy Zheng is a third year undergraduate majoring in Biology and minoring in Evolutionary Medicine and Anthropology. He has been working in the Alfaro Laboratory under the mentorship of Dr. Michael Alfaro since Winter Quarter of 2014. Jimmy is currently running two computational phylogenetic studies to better understand vertebrate diversification dynamics across the tree of life.
The uneven distribution of organismal diversity is a fundamental and unsolved evolutionary phenomenon. The cichlid species that inhabit the African Great Lakes represent the most iconic model system of vertebrate functional diversity, yet no phylogenetic models can viably account for their unparalleled adaptive radiation. The answer to this macroevolutionary problem may lie in a mechanism called hybridization. Within a particular habitat, genetically diverged populations occasionally interbreed and generate hybrids that express phenotypic distributions outside of the parental range. This process, known as transgressive segregation, might manifest novel traits at the genetic level, leading to rapid diversification. Using next-generation sequencing and cutting-edge target-enrichment strategies, Jimmy aims to discover whether transgressive segregation and hybridization increase rates of functional diversification in these cichlid lineages.
Jimmy plans to graduate with a Bachelor's Degree in Spring of 2016 and pursue further studies in evolutionary medicine and anthropology subsequently. He would like to thank Dr. Michael Alfaro for his guidance, support, and mentorship in the past year. He would also like to express his gratitude to the Boyer Family and URC-Sciences for their generous contribution to his research and academic development.
| Johnathan Zhao
Mentor: Dr. Hanna Mikkola
Funding: Honorary Award
Project Title: The role of transcription factor MYCT1 in activating human fetal hematopoietic stem cell self-renewal
Johnathan Zhao is a UCLA senior majoring in Molecular, Cell, and Developmental Biology and minoring in Biomedical Research. Since spring 2012, he has worked under the direction of Dr. Hanna Mikkola, whose lab studies the generation of hematopoietic stem cells (HSC) during embryonic and fetal development.
HSC are capable of producing all mature blood cell types. Human HSC harvested from donor bone marrow are utilized in transplant therapies against blood disease, but such therapies are vastly limited by low cell counts and tissue-type mismatch between donor and recipient. Thus, learning how to generate sufficient supplies of transplantable HSC in culture would boast major implications for hematological medicine. Critically, HSC rely on their long-term self-renewal ability to expand in number without differentiating. However, the network conferring and maintaining self-renewal during development is unknown.
Johnathan's project focuses on the role of transcription factor c-Myc target protein 1 (MYCT1) in HSC self-renewal acquisition. MYCT1 was found to be highly upregulated in self-renewing HSC compared to non-self-renewing hematopoietic progenitors. In culture, knockdown of MYCT1 expression in HSC ablated self-renewal capacity, while its overexpression delayed HSC exhaustion. After confirming the absence of off-target effects, Johnathan aims to elucidate how MYCT1 imparts self-renewal by both assessing its effect on global transcriptional profiles and identifying its direct gene targets in HSC.
Johnathan would like to thank Dr. Mikkola, postdoctoral mentor Dr. Vincenzo Calvanese, the Mikkola lab, and the Amgen Foundation for their generous guidance and support for his research endeavors.
| Zijun Zhao
Mentor:Dr. Thomas Graeber
Funding: Hilton Award
Sophie is a 4th year undergraduate student, studying biochemistry and biomedical research. She has been conducting research in Dr. Graeber’s lab since Fall 2013. Our lab uses systems biology to study cancer metabolism.
Cancer cells perform aerobic glycolysis, which is the conversion of glucose to lactate despite the presence of oxygen. Normal cells perform cellular respiration in the presence of oxygen. The genetic basis of aerobic glycolysis in cancer cells has remained elusive. Based on the recurrent pattern of DNA copy number alterations (CNAs) in breast cancer patient samples, the Graeber Lab has implicated certain metabolic genes and regulators that assist in tumorigenesis. My current project seeks to understand the pattern of CNAs of cancer cells in relationship to their protein expression and metabolic properties. Mouse embryonic fibroblasts (MEFs), which are prone to become genomically unstable in culture, are exposed to different stressors including oxidative stress. Depending on the stress factor, the MEFs are predicted to respond with less or more copy number alterations. Western blot and NOVA are employed to measure the protein and metabolite levels.
After graduation, Sophie plans to obtain additional research experience and pursue a medical degree. She thanks the members of the Graeber lab for their generous guidance and support. She would also like to thank Ms. Wilson for her generous funding towards her research.
| Alia Welsh
Pictured (Left to Right): Kendra Nyberg, Alia Welsh, Dr. Amy Rowat
Mentor: Dr. Amy Rowat
Funding: Gottlieb Award
Project Title:The effects of physical stresses and changes in cell deformability on cancer progression.
Alia Welsh is a third year Microbiology, Immunology, and Molecular Genetics major. Under the guidance of Dr. Amy Rowat and graduate student researchers Kendra Nyberg and Angelyn Nguyen, she is investigating both the factors that characterize tumor cells and those that may affect cell metastatic potential.
Cancer cells are known to be softer and more deformable than their benign counterparts. To quantify cell deformability, cells and particles were driven through a microfluidic device with constricted 5µm channels. For each particle or cell type, videos were captured as they were driven through the device at a constant pressure. The individual transit times were measured as a function of cell viscosity, elastic moduli, and surface tension—all of which contribute to physical properties that may affect metastatic potential. Through image analysis, the transit time was determined as a quantitative measure of cell deformability.
Tumor cells are also subject to increased pressure in their microenvironment. Cancer cells could, as a result, have higher levels of Reactive Oxygen Species (ROS). Increased ROS levels could damage DNA, proteins, and may provide an alternate pathway through which cancer cells could acquire additional mutations that promote cancer progression. Numerous pancreatic cancer cell lines and one non-cancerous line were stained with ROS-specific dyes. They were then subjected to specific levels of hydrostatic pressure. ROS levels were detected with fluorescent imaging. The levels in cancerous cells were compared to those of non-cancerous cells. To examine other types of stress, individual cell lines were subjected to varying amounts of compressive stress. These cells were stained with fluorescent dyes to give measurements of cell area and nuclear size. These types of pressures partially recreate the microenvironment and allow for further examination of tumor cell characteristics.
Future experiments will examine the effects of mechanical stress on gene expression, specifically Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-kB) and Activated Protein 1 genes (AP-1). The expression levels of these genes will be compared to ROS levels to determine any correlation. This could reveal a broader cross-section of genes that may be implicated in both mechanical and oxidative stress.
Alia would like to thank Dr. Rowat, Kendra Nyberg, Angelyn Nguyen, and the Gottlieb family for their continued support in her research endeavors.
| Alice Shih-Yu Wang
Mentor: Dr. Kate M. Wassum
Funding: Hilton Award
Title: Inactivating the dorsolateral striatum as a means to elucidate the underlying psychological processes guiding decision-making under conditions of uncertainty produced by a novel motivational state.
Alice Wang is a 3rd year Neuroscience major who has been working in the Wassum lab since June 2013. The Wassum lab studies the neural mechanisms that control reward-related learning, motivation, and decision-making. In the past year, with the help of her mentor, Dr. Kate Wassum, and lab manager, Venuz Greenfield, she conducted an independent project in which she found that basolateral amygdala glutamatergic neurotransmission acts on AMPA, but not NMDA glutamate receptors to mediate the ability of reward-predictive stimuli to influence decision-making.
The project Alice is now conducting aims to elucidate the psychological processes guiding action selection under circumstances of uncertainty produced by novel motivational states. Using behavioral neuroscience techniques including instrumental conditioning, she is investigating the balance between habitual and goal-directed control systems referred to in computational modeling as model-free and model-based, respectively. In particular, Alice hopes to provide an empirical test of a recently proposed computational hypothesis that novel motivational states create uncertainty for the model-based system, thereby forcing behavioral control by the model-free system until such uncertainty is reduced through experience. Alice will train rats to lever press to earn sucrose when sated and then will test them hungry for the first time without allowing them to experience the sucrose hungry. On test, Alice will inactivate the dorsolateral striatum - a structure required for the development and use of model-free habits - to determine if the model-free system is turned off and if in a new motivational state subjects will use the model-based system to guide reward seeking. Control subjects should show no change in their responding when hungry relative to sated, if this is the result of model-free control of reward seeking then subjects with the dorsolateral striatum inactivated should show elevated responding for the sucrose when hungry, suggesting they are suing a model-based system that has access to the value of the sucrose in the new need state. The potential findings of this project could be important for understanding the behavioral strategies used to guide reward-seeking action under conditions of uncertainty and are also important for understanding disorders of behavioral control including addiction to drugs or alcohol.
Alice plans to graduate in June 2015 and to enter an M.D./Ph.D. program to train to become a psychiatrist-scientist. She would like to thank Kate and Venuz for their guidance and assistance since June 2013, as well as the Wasserman family and the Hilton family for their contribution and support.
| Brandon Tsai
Mentor: Dr. Xia Yang
Funding: Gottlieb Award
Brandon Tsai is a second-year pursuing a major in Molecular, Cell and Developmental Biology and minor in Biomedical Research. He joined Dr. Xia Yang’s lab during the winter of his first year. The Yang lab investigates the interaction between genetic and environmental risk factors, perturbation of gene networks and molecular networks, and their effect on common metabolic diseases such as, obesity, diabetes, and coronary artery disease. The lab employs an integrative genomics and systems biology approach to analyze large molecular datasets and identify specific causal candidates within networks as targets for therapy.
Brandon’s current research primarily focuses on endocrine disrupters termed “obesogens” and their causal role in metabolic diseases such as cardiovascular diseases, type 2 diabetes, and obesity. However, the molecular mechanisms underlying the disease-inducing effects of obesogens, remain poorly understood. One such obesogen that has captured recent attention is bisphenol A (BPA) due to its widespread prevalence in everyday products. Using the C57BL/6 mouse model treated with BPA, Brandon can observe both phenotypic and genotypic effects from BPA treatment. Phenotypes, including body fat composition, blood glucose, lipids, insulin, and glucose tolerance, will be measured before DNA methylome and transcriptome analyses through Reduced Representation Bisulfite Sequencing and RNA sequencing. Construction of tissue-specific gene networks can then point to key regulators that mediate the molecular toxicity of BPA as well as its effect on metabolic diseases.
Brandon would like to sincerely thank Dr. Yang for being a supportive, encouraging, and motivating mentor. He would also like to thank Qingying Meng and the rest of the Yang Lab for their mentorship and guidance. Finally, Brandon would like to thank the Gottlieb Foundation for their generous scholarship.
| Melissa Truong
Mentor: Dr. Dana Jones
Project Title:Characterizing the Role of headcase in Drosophila melanogaster Stem and Progenitor Cells
Melissa Truong is a senior at UCLA studying Molecular, Cell and Developmental Biology with a minor in Biomedical Research. 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 revolves 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 after RNAi-mediated knockdown.
After graduation, Melissa plans to pursue a Ph.D. in developmental and 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.
| Hamilton Trinh
Pictured: Elizabeth Guenther, Hamilton Trinh, Dr. David Eisenberg
Mentor: Dr. David Eisenberg
Project Title:Characterization of Fibril Forming Regions of TAR DNA Binding Protein 43, TDP-43
Hamilton Trinh is a third year student at UCLA majoring in biochemistry. Since the spring of 2013, he has been working with graduate student Elizabeth Guenther in the laboratory of Dr. David Eisenberg studying the structure of transactive response binding protein 43 (TDP-43).
TDP-43 is a transcriptional repressor and splicing regulator implicated in amyotrophic lateral sclerosis (ALS), a debilitating disease that is characterized by the death of motor neurons. Similar to other neurodegenerative diseases such as Alzheimer’s and Parkinson’s Diseases, research on ALS has revealed that accumulation of proteinaceous deposits is found in affected neuronal cells. In many cases, these deposits contain filamentous aggregates that contain C-terminal fragments of TDP-43. Although aggregation of TDP-43 is apparent, the atomic structure of these aggregates, as well as the mechanism behind the formation of these structures and how they affect the nervous system, is not clearly known. It is hypothesized that the C-terminal domain and truncated second RNA recognition motif of TDP-43 forms aggregates with structures similar to the fibrillar model, an atomic structure that amyloid deposits of Alzheimer's patients display. Hamilton's project involves the structural determination of short segments of TDP-43 aggregated into orderly assemblies of fibrils using computational predictions and x-ray crystallography and screening the toxicity of these structures in mammalian cell lines.
| Daniel Tran
Mentor: Dr. Volker Hartenstein
Funding: Van Trees Award
Project Title: Lineage-based Wiring Properties in the Drosophila Brain
Daniel Tran is a fourth-year UCLA undergraduate majoring in Molecular, Cell, and Developmental Biology. Because of his interest in the cell biology of the brain, Daniel joined Dr. Volker Hartenstein’s laboratory in the beginning of his third year. His work specifically involves characterizing the gene expression patterns of certain neuronal lineages, including DALv2 and DALv3, in the Drosophila melanogaster brain. The genes or markers Daniel studies are GMR48B12, engrailed, and more recently, Gooseberry. The ultimate goal of Daniel’s project is to determine how neurons form functional circuits in the brain by expressing many, different genes.
Daniel wishes to thank Dr. Hartenstein as well as Jennifer Lovick and Jaison Omoto for their kind mentorship and support throughout his time doing research. He would also like to thank the donors of the Van Trees scholarship for their generous investment into his research and future career. After graduating in the spring of 2015, Daniel plans to pursue an M.D. and possibly specialize in neurology.
| Justin Toh
Pictured (left to right): Dr. Peter J. Bradley, Justin Toh and Dr. Allan L. Chen
Mentor: Dr. Peter J. Bradley
Funding: Van Trees
Project Title: Characterization of novel Inner Membrane Complex (IMC) Identified from a BioID approach
Justin Toh is a 4th year Microbiology, Immunology, and Molecular Genetics major with a minor in Biomedical Research at UCLA. He works in Dr. Peter J. Bradley's lab studying Toxoplasma gondii, an important pathogen for AIDS patients and congenitally-infected neonates. Justin's current project focuses on the Inner Membrane Complex (IMC), a compartment within this parasite that is essential for the parasite's replication.
T.gondii belongs to the large phylum Apicomplexa, a group of obligate intracellular parasites that causes many veterinarian and medical diseases. The two most significant apicomplexan parasites affecting humans are T.gondii and its close relative Plasmodium falciparum, the causative agent of malaria. T.gondii infects about a third of the human population and is transmitted through the ingestion of raw meat or feline feces.
While the IMC is known for its role in replication, the mechanics of this process remains largely unknown due to the fact that many of these proteins have not yet been identified. Thus, Justin's project focuses on exploiting a protein interaction method known as BioID within T.gondii to identify novel IMC proteins and characterize these IMC proteins' function by CRISPR/CAS9-mediated knockout. Ultimately, Justin hopes to find IMC proteins that can be used as therapeutic drug targets for this important parasite.
After graduation, Justin plans to pursue a Ph.D. in Microbiology. Justin would also like to express his gratitude to every member of the Bradley lab, and the Van Trees Scholarship for their generous support of his undergraduate research and science education.
| Cho Ki Tam
Pictured (from left to right) Front row: Allen Yih Shin Huang, Cho Ki Tam, Cathy Yan Yin, Richard Sportsman. Back row: Christian Beren, Adam Biddlecome, Dr. William Gelbart.
Mentors: Dr. William M. Gelbart, Dr. Charles M. Knobler, Rich Sportsman
Funding: Oppenheimer Award
Project title: In Vitro Envelopment of Virus Like Particles with Applications for Gene Therapy
Cho Ki is a fourth year undergraduate majoring Physiological Sciences at UCLA. She has
been working under the guidance of Dr. William Gelbart and Dr. Charles Knobler in the
Department of Chemistry and Biochemistry since the beginning of her third year. The
Gelbart-Knobler Lab is investigating on how viruses “work” using physical chemical principles to explore generic aspects of the viral life cycle. The experiments conducted in the GelbartKnobler Lab are designed to elucidate the fundamental aspects of viral infection cycles of bacteriophage lambda (λ) and Cowpea Chlorotic Mottle Virus(CCMV) from entry and delivery of the genome, to replication of the virus, to the packaging of a new generation of virions and their subsequent escape from the host cell. The Gelbart-Knobler Lab has studied, both experimentally and theoretically, the pressurized bacterial viral capsids, coselfassembly of RNA and its capsid protein in plant viruses, and the budding behavior of enveloped animal viruses. Cho Ki’s project will focus on plant virus selfassembly and their envelopment.
Cho Ki is currently working with CCMV, a spherical RNA viruses that spontaneously
selfassemble from capsid protein constituent and RNA using the viral RNA or heterologous RNAs. As a result, CCMV has potential as a gene delivery system. The assembled protein shell carries a negative surface charge which, as recently shown in the GelbartKnobler lab, allows it to be wrapped by a cationic lipid bilayer that should enhance its ability to enter cells. Brome Mosaic Virus(BMV) is closely related to CCMV and it too is able to selfassemble; however, its surface charge is positive. In her project, she will first develop a way to wrap BMV with an anionic lipid bilayer, which shares the same chemical properties as a mammalian lipid bilayer. By doing so, she hopes that this will enhance viral transport into cell by promoting fusion with the cell membrane, further envelopment should enhance its ability to “hide” it from the mammalian immune system. If this is successful, Cho Ki will use capsid protein of CCMV to delivery genetically modified RNA into mammalian cell and examine how the charge on the lipid facilitates the entry. The results of her research can help guide thedevelopment of vaccine using CCMV as gene delivery system.
After graduation, Cho Ki plans to pursue either a MD/PhD or MD. She would like to thank Dr. Gelbart and Dr. Knobler and the members of the Gelbart/Knobler Lab for their mentorship and support. She would also like to express her gratitude to the Oppenheimer Foundation for its generous support in her research.
| Naomi So
Mentor: Dr. Edward Lee
Funding: Wasserman Award
Project Title: The Application of Image-Guided Transjugular Intrahepatic Portosystemic Shunts in the Treatment of Liver Disease
Naomi So is a 4th year Physiological Science major. She has been conducting research under the guidance of Dr. Edward Lee since the fall of 2012. Under Dr. Lee, she is involved in both clinical and translational research in the field of interventional radiology.
Naomi currently focuses on the application of iGuide Transjugular Intrahepatic Potosystemic Shunts (TIPS) in the treatment of liver disease. TIPS is an interventional procedure that connects two veins together within the liver under X-ray guidance. It is often performed for patients with liver disease to ultimately reduce portal hypertension along with any other resulting complications such as ascites as well as gastic and esophageal varices. While there are complications with TIPS, the safety and performance of TIPS can be improved to limit these complications and thus prove to be an important therapy for liver disease. These improvements can take the form of gaining a real-time knowledge of the location of the portal vein relative to the needle in the hepatic vein to thus prevent unnecessary punctures. iGuide TIPS is a new and innovative method, which improves the imaging of the vessels by fusing two 2D images into one 3D path to guide the TIPS procedure. Naomi aims to evaluate the feasibility and reproducibility of performing iGuide TIPS using enhanced real-time 3D image guidance in a swine model so that TIPS can become safer and more efficient and eventually be translated into the clinical setting.
In the future, Naomi plans to pursue a career in academic medicine. She would like to thank Dr. Edward Lee for his mentorship and guidance over the past three years as well as the Wasserman family for their generosity and support of her research endeavors.
| Sarah Simko
Mentor: Dr. David Shackelford
Funding: Wasserman Award
Project Title: Inhibition of Glycolysis and Glutamine Metabolism for the Treatment of KRAS and LKB1 Mutant Lung Tumors
Sarah Simko is a fourth year Physiological Science major with a great interest in translational research. She has worked with Dr. David Shackelford’s in the Pulmonary Department since the summer of 2011, and she has learned a great deal under his tutelage. The Shackelford lab studies mutations in the AMPK and mTOR signaling pathways that lead to altered metabolism and cell growth in human tumors, investigating targeted therapies to LKB1-mutant lung cancer lines.
Currently, there are few effective, targeted therapies for the treatment of non-small cell lung cancer (NSCLC) and no effective strategies for the chemoprevention of lung cancer. The scarcity of targeted approaches is largely due to our incomplete understanding of the molecular mechanisms driving lung cancer pathogenesis. Successful targeted therapies for NSCLC treat predominantly lung cancers with EGFR or ALK mutations, leaving patients with KRAS, P53 and LKB1 mutations fewer options. There is a great need to find targeted therapies for NSCLC in order to extend survival, improve quality of life and potentially cure these patients. The objective of Sarah’s research is to identify new therapeutic strategies targeting tumor metabolism in KRAS and LKB1 mutant NSCLC. Techniques include metabolic characterization of lung tumors and metabolic analysis of glycolysis, oxidative phosphorylation (OXPHOS) and glutamine metabolism in human and mouse NSCLC cell lines. We will perform a genetic analysis of the MYC pathway – a critical driver of both glucose and glutamine metabolism in our KRAS and LKB1 mutant tumor cell lines. This study will also actively investigate the effectiveness of combinatorial inhibition of glycolysis and glutamine metabolism using targeted therapies against mTOR and glutaminase 1 for the treatment of KRAS and LKB1 mutant lung tumors.
Sarah plans to graduate in Spring 2015, and hopes to pursue an MD and a masters in clinical science. She would like to thank her mentor, Dr. David Shackelford, for supporting her and for his willingness to answer any and all questions. She would also like to express her gratitude to the Wasserman family and the Undergraduate Research Scholars Program for their generosity and kindness.
| Sara Shu
Mentor: Dr. Ting-Ting Wu
Funding: Ehrisman Award
Project Title: Characterization of the Interaction of Murine gamma-herpesvirus 68 Open Reading Frame 34 and RNA Polymerase II
Sara Shu is a fourth 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 between Murine gamma-herpesvirus 68 Open Reading Frame 34 and RNA Polymerase II.
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. Like all other herpesviruses, progression of gene expression during lytic infection is highly regulated. A subset of genes known as viral late genes are important in 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. Sara is studying the novel interaction between ORF34 and RNA polymerase II, the primary player in transcription, using murine gamma-herpesvirus 68 (MHV-68) as a model. Using site-directed mutagenesis to map critical residues on ORF34 for this interaction, mutants will then be tested in order to demonstrate the functional significance of this specific interaction during the gamma-herpesvirus life cycle.
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 Ehrisman family and the Undergraduate Research Scholars Program for their generous support.
| Martina Shoukralla
Featured from the left to the right: Dr. Steven Welc, Martina Shoukralla, Dr. James Tidball
Mentor: Dr. James Tidball
Martina Shoukralla is a senior student majoring in physiological science. She has been conducting research since summer 2013 under the guidance of a postdoctoral fellow, Dr. Steven Welc, and her faculty mentor, Dr. James Tidball. Research in the Tidball lab is directed towards exploring interactions between the immune system and skeletal muscle during muscle injury and how they function during regeneration and growth processes.
Muscle injury is a significant clinical problem that is seen in muscular dystrophy, sarcopenia and muscular trauma. Muscle inflammation is an important step of muscle repair and regeneration. The lab’s research has shown that immune cells play an important role in modulating muscle injury and repair that occur in chronic, muscle wasting diseases and following acute injuries. This is essentially important for regulating disease progression and opens the horizon to exploring potential therapeutic molecules for treating the disease.
Martina’s research seeks to understand how Klotho protein can affect skeletal muscle inflammation following injury. Her study focuses on Klotho’s effect on macrophage phenotype changes during muscle repair. Previous studies showed that during inflammation, pro-inflammatory M1 macrophages switch to an anti-inflammatory M2 phenotype. This switch from M1 to M2 macrophage is critical to regeneration and growth following muscle atrophy, acute injury or disease.
After graduation, in spring 2015, Martina plans to become a medical researcher after obtaining a medical degree. She would like to thank Dr. Tidball for the invaluable research experience, Dr. Welc for his continued guidance and support and all other members of the Tidball lab for their encouragement. Finally she would like to thank the MacDowell Foundation and Vice Provost Turner for their generous funding and support for her resear
| Saumya Shah
Mentor: Dr. Denis Evseenko
Funding: Hilton Award
Project Title: FUNCTION OF OPIOID KAPPA RECEPTOR (OPRK)/DYNORPHIN SIGNALING PATHWAY IN HUMAN CHONDROCYTES
Saumya Shah is currently a fourth 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 Hilton family for their generous financial support.
| Tiasha Shafiq
Mentor: Dr.Amander Clark
Funding: Wasserman Award
Project Title: A molecular study of the human germline
Tiasha Ayumi Shafiq is a fourth year Molecular, Cell and Developmental Biology major, with minors in Biomedical Research and Neuroscience. She has been pursuing undergraduate research with Dr. Amander Clark in the department of Molecular, Cell and Developmental Biology since September 2013. Her current research focuses on understanding both in vivo and in vitro Human Primordial Germ Cells.
Primordial germ cells are responsible for creating the gametes that carry DNA to the next generation. Abnormalities in germ cell development can cause infertility problems, which affect about 10% of men and women in the US. To understand human germ cell development and potentially treat infertility, both in vivo primordial germ cells (PGCs) from human fetal gonads and in vitro derived primordial germ cells from pluripotent stem cells need to be analyzed transcriptionally and epigenetically. Recently, we carried out a transcriptional and epigenetic study using RNA-Sequencing and Whole Genome Bisulfite Sequencing respectively on PGCs from human fetal gonads at different developmental time points. Tiasha wishes to further analyze the dynamic reprogramming process of the in vivo PGCs by determining the expression of different histone marks. Moreover, for the in vitro part, she aims to increase the efficiency of generating germ cells from human embryonic stem cells, by creating a reporter line using TALENS/CRISPR, so as to sort germ cells effectively for further analysis.
Tiasha plans to pursue a PhD in Developmental and Stem Cell Biology after graduation. She would like to thank Dr. Amander Clark, Dr. Sofia Gkountela and the rest of the Clark lab for their on-going mentorship and support. She would also like to thank the Wasserman Family for their generous support to her
| David Shabsovich
Mentor: Dr. Carlos Tirado
Funding: Gottlieb Award
Title: Conventional and Molecular Cytogenetic Characterization of Pancreatic Carcinoma
David Shabsovich is a third-year Microbiology, Immunology, and Molecular Genetics major and Public Health minor at UCLA. He has been conducting research at the UCLA Clinical and Molecular Cytogenetics Laboratory under the guidance of Dr. Carlos Tirado since his freshman year, focusing on the elucidation of cytogenetic abnormalities in pancreatic carcinoma.
Pancreatic cancer is the fourth-leading cause of cancer death in the United States, with a 5-year survival rate of approximately 6 percent. Despite its known intratumor cytogenetic heterogeneity, there are currently no cytogenetic assays utilized in the diagnosis or clinical management of the malignancy. Furthermore, although recurrent cytogenetic abnormalities have been identified, most have not been correlated with phenotypic features of the disease, and as a result, their clinical significance is not known. Using conventional Giemsa banding, fluorescence in situ hybridization (FISH), and array comparative genomic hybridization (aCGH), David seeks to pinpoint recurrent cytogenetic abnormalities in pancreatic carcinoma and correlate them with phenotypic features of the disease. Ultimately, such information can provide insight into the chromosomal and molecular nature of the disease, and allow for the development of cytogenetic assays that can be used in clinical settings to more precisely determine diagnoses and prognoses for patients with pancreatic malignancies.
David would like to thank Dr. Carlos Tirado and the staff at the UCLA Clinical and Molecular Cytogenetics Laboratory for their continued guidance over the course of the past couple of years. Additionally, he would like to thank the Undergraduate Research Scholars Program and the Gottlieb family for their generous funding and support of this research. After graduation, David plans to pursue a career in medicine and public health.
| Shaina Sedighim
Mentor: Dr. Robert Prins
Funding: MacDowell Award
Glioblastoma multiforme (GBM) is amongst the most predominant types of high-grade brain tumors and despite the many efforts made in treating patients with this disease, in both conventional and novel fashions, the mean survival of such patients has stagnated at about fourteen-and-a-half months. Thus, many physicians are now turning to the tool of active-immunotherapy as an alternative means to treat GBM patients; one such therapy is dendritic-cell vaccination (DC-Vax).
Shaina utilizes FLOW cytometry in order to monitor changes in DC-vax and DC-vax-direct patient PBMC's. Results should reveal dynamic shifts immune-cell surface markers in treated patients; patterns in such shifts will be useful in order to predict which patients may respond to the treatment more effectively. Next-generation sequencing takes this idea forward by helping reveal parallel changes in the T-cell receptor (TCR) repertoires in both primary tumor and patient PBMC's due to DC-Vax.
Shaina is a fourth-year Neuroscience major and Biomedical Research minor who hopes to pursue an M.D./Ph.D degree in the future. She would like to wholeheartedly thank the Prins lab, who has opened its doors to teaching her about the very unique field of neuro-immunology; she cannot wait to further her progress there over the next year or so. She would also like to thank Dr. Rafael Romero and Dr. Ira Clark who head the Biomedical Research Minor and initially inspired her career in research. She finds great value in undergraduate research and would like to applaud the UCLA community as a whole for cultivating the minds of young scientists and thinkers.
| Benjamen Schoenberg
Mentor: Dr. James Byrne
Funding: Wasserman Award
Project Title: Investigating the Osteogenic Potential of Skin Cells and Their Response to a Bone Inducing Protein (BMP-2)
Ben is a fourth year student majoring in Biology with a minor in Biomedical Research. Since Fall 2013, he has been involved with the Byrne lab team researching ways to create and use patient-specific induced pluripotent stem cell technology to treat various diseases.
Ben and the Byrne lab have been involved with a spinal fusion project, which deals with finding a novel approach to inducing bone growth for patients who suffer from degenerative spinal conditions. The project involves obtaining skin cell derivatives and genetically modifying them to express BMP-2 (Bone Morphogenetic Protein-2). This is an important protein shown to induce bone growth both in vitro and in vivo. After we modified our cells we saw reduced levels of inflammation and a higher quantity of bone growth at the site of implantation (when compared to the standard protocols of spinal fusion) in a rat model.
He wishes to thank the Wasserman endowment foundation, his principal investigator Dr. James Byrne, mentor (Agustin Vega-Crespo), graduate advisors (Patrick Lee and Brian Truong), and the faculty of the Biomedical Research Department for their unending support. Ben aspires to pursue a career in Sports Medicine, continue to give back to the Los Angeles and Inland Empire communities, and start his own clinic.
| Marci Rosenberg
Pictured (left to right): Dr. Jeff Rasmussen, Ms. Marci Rosenberg, and Dr. Alvaro Sagasti
Mentor: Dr. Alvaro Sagasti
Project Title: Morphogenesis of basal skin cells during sensory axon ensheathment
Marci Rosenberg, a fourth year Neuroscience major and Biomedical Research minor, has been conducting research in the Sagasti lab since March 2013. With guidance from post-doctoral scholar Jeff Rasmussen, Marci studies the process by which sensory axons are ensheathed by skin cells in embryonic zebrafish.
Touch-sensing neurons innervate the skin with elaborate peripheral arbors. These arbors are devoid of associated glia, which normally ensheath axons to provide mechanical and metabolic support. In an ultrastructural analysis, the Sagasti lab found that basal skin cells ensheath these touch-sensing endings in zebrafish. Similar ensheathment channels have been described in the skin of a wide variety of other organisms, suggesting they perform essential functions; however, neither the mechanisms leading to channel formation nor the impact they have on sensory function is known. To understand the morphogenetic processes that lead to ensheathment, Marci has been using transgenic zebrafish and confocal microscopy to visualize the progression of ensheathment in live animals. She found that cellular components are recruited in a specific order to skin cell-axon contact points. Furthermore, blocking peripheral sensory axon development prevented the formation of ensheathment channels. With these data, Marci proposes a model in which an axon-derived signal polarizes the basal skin cell, leading to remodeling of the actin cytoskeleton, forming a channel for the extending axon. Adherens junctions then seal the opening over the axon to stabilize the sheath. This year, Marci will continue to test the robustness of her model by tracking the development and breakdown of sheaths using time-lapse imaging. Marci also plans to block ensheathment channel formation via a basal cell-specific deletion of alpha-catenin, an essential component of adherens junction; in doing so, she hopes to gain insight into how the skin modulates sensory axon function and/or survival.
After graduation, Marci intends to apply to MD/PhD programs in her pursuit of a career as a physician-scientist. She is very grateful to the Hilton endowment 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 the entire Sagasti lab for creating a driven, exciting, and fun lab environment where questions are always encouraged.
| Dylan Rees
Mentor: Dr. Stuart Brown
Funding: Norton Rodman Award
Project Title: NMR Studies of Strain-Induced Phases in Molecular Solids
Born and raised in Los Angeles, Dylan is a fourth-year physics major at UCLA. His father attended UCLA for undergraduate and graduate school and his grandfather was a professor of literature for 25 years at UCLA. With Dr. Stuart Brown, Dylan studies nematicity in crystal structures and is working on a project to relate strain with structural and electrical properties of materials through nuclear magnetic resonance (NMR) measurements. NMR is a phenomenon in which nuclei interact with radiofrequencies of light and emit radiation. Nuclear spin, crucial to this phenomenon, is an intrinsic magnetic dipole moment produced by a nucleus. The spin of nuclei in a material interact with applied magnetic fields and emit their own magnetic fields as a product of their motions. NMR measurements in iron-arsenide, a class of crystal structures, can tell us about its properties in exotic low-temperature states of matter. Iron arsenide is an unconventional superconductor—it becomes a superconductor at temperatures higher than the conventional superconductors, 38K as opposed to around 4K. While conventional superconductors are well-understood, an accepted theory behind high-temperature superconductors has not yet been formulated. Like many problems in the history of condensed matter physics, experimental understanding of this phenomenon could provide the basis for new theoretical insight into the phenomenon.
Dylan plans on pursuing a PhD in physics after graduating and will likely stay within the condensed matter branch of physics. He would like to thank Dr. Brown and the physics department for their support in his research and academics, and their help preparing him for graduate school.
| Navneet Ramesh
Mentor: Dr. Julian Martinez-Agosto
Title: Exploring Variants of Unknown Significance in Autism with Macrocephaly
Navneet is a fourth 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 specific gene variants may be implicated in overgrowth phenotypes in autism.
Autism spectrum disorders (ASDs) are a group of neurodevelopmental diseases characterized by impaired social interaction, reduced motor coordination, and repetitive and stereotyped patterns of behavior. The Centers for Disease Control (CDC) and Prevention estimates that 1 in 68 children are affected with ASDs, with the disorder being four to five times more common among boys than girls. Numerous studies have identified genetic, environmental and epigenetic factors that may contribute to the development of autism. However, a singular unifying molecular basis of ASDs remains illusive.
Navneet’s current project seeks to characterize the role of certain gene variants previously reported in macrocephaly and autism patients. Macrocephaly refers to a head circumference greater than three standard deviations above the mean and is the most reproducible finding in ASDs. Navneet aims to identify the mechanism by which the mutated proteins affect growth signaling, and subsequently develop strategies to rescue the abnormal growth. Furthermore, he would like to assess if there is cross-talk among several different pathways to generate the ultimate phenotype.
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 Ehrisman Foundation for their generous contribution towards his research.
| Nanetta Pon
Mentor: Dr. Richard Kaner
Funding: Wasserman Award
Title: Growth and Transfer of Graphene for Use as a Nanoporous Membrane
Nanetta is a third-year chemistry-materials science student. With the help of her mentor, Jaime Torres, she has been conducting research in the Kaner lab since February 2014. The Kaner lab focuses on the synthesis, characterization and application of both inorganic and organic materials, including graphene supercapacitors, conducting polymers, and superhard materials. Nanetta’s research has been towards the application of graphene as a reverse osmosis membrane.
Graphene’s extraordinary physical properties give it the potential to serve as a desalination membrane to facilitate inexpensive, energy-efficient desalination to relieve water-scarce areas. Current research to scale up the production of graphene has produced methods of transferring it roll-to-roll, making its size theoretically unlimited. However, these efforts have focused on maintaining graphene’s electronic properties, and a process to produce large-area graphene with the physical requirements to serve as a nanoporous membrane is still to be discovered. This project focuses on the production of large-area, high strength graphene that can withstand the high pressures of flow-cell tests. Parameters for investigation include metal growth substrates for chemical vapor deposition (CVD), etchant [iron (III) chloride and ammonium persulfate (APS)], and support membrane [polycarbonate and polytetrafluoroethylene (PTFE)]. The graphene produced is characterized using Raman spectroscopy, UV-Vis spectroscopy, and microscopy methods.
Nanetta would like to thank Dr. Richard Kaner, Jaime Torres, the Undergraduate Research Scholars Program, and the Wasserman family for their generous guidance and support.
| Brandon Pham
Pictured, left to right: Dr. Ram Raj Singh, Brandon Pham, Dr. Isela Valera
Mentor: Dr. Ram Raj Singh
Funding: Gottlieb Endowment
Title: Mechanism of Gender Bias in Autoimmune Disorders
Brandon Pham is a second year student majoring in Microbiology, Immunology, and Molecular Genetics and minoring in Biomedical Research. Since joining the Singh lab in Spring 2014, Brandon has been studying how gender bias occurs in autoimmune disorders.
Autoimmune disorders occur when the body’s immune system mistakenly attacks its own healthy tissue. Although there are over 80 types of autoimmune disorders, the most common diseases are rheumatoid arthritis, multiple sclerosis, and systemic lupus erythematosus. In general, autoimmune disorders occur more frequently in women but more severely in men. Although the cause of autoimmune diseases is still unknown, a class of proteins called toll-like receptors (TLRs) has been identified as an important factor that can affect the development of autoimmune disorders. TLRs are important in the innate immune response, which provides a relatively nonspecific mode of attack on pathogens. The function of these receptors is to identify a broad range of pathogens and microbes, as well as a wide variety of other molecules that may cause tissue damage. However, the innate immune response can result in damage to healthy tissue if prolonged. Because this “self-targeting-self” damage is characteristic of autoimmune disorders, TLRs have become a central focus of research regarding the development of such disorders. To investigate the role of TLRs in autoimmune disease, the Singh lab focuses on two TLRs: TLR7 and TLR8. Genes for these TLRs are located on the X chromosomes. Using flow cytometry, qRT-PCR, and immunohistochemistry, the Singh lab hopes to determine whether the double dosage of TLR7 and TLR8 genes, Tlr7 and Tlr8, respectively, alters the responsiveness to the respective TLR ligands in XXF vs. XYF and XXM vs. XYM splenocyte samples.
Following graduation, Brandon plans to pursue a career in the medical field and academic research. He would like to express his gratitude toward the Gottlieb Endowment for supporting his research in immunology. He would also like to sincerely thank Dr. Rafael Romero and Dr. Ira Clark of the Biomedical Research Minor for their dedication to promoting undergraduate research. Finally, Brandon would like to thank his mentors Dr. Ram Raj Singh and Dr. Isela Valera for their kindness, guidance, and support.
| Nina Petrosyan
Pictured, left to right: Dr. Kenneth Bradley, Nina Petrosyan, and Dr. Matthew Hatkoff
PI: Dr. Kenneth Alan Bradley
Mentor: Dr. Matthew Hatkoff
Funding: Boyer Award
Title: Characterization of Mechanism of Cholesterol Efflux
Nina Petrosyan is a 3rd year Microbiology, Immunology, and Molecular Genetics Major. She has been conducting research in the Dr. Bradley’s Laboratory under the guidance of postdoctoral fellow Dr. Matthew Hatkoff since September 2013.
In the Bradley laboratory Dr. Hatkoff and Nina focus on understanding novel mechanisms of cellular cholesterol homeostasis. Previously, the Bradley Lab discovered a new protein which when repressed in Chinese Hamster Ovary cells (CHO) leads to a 50% reduction in cellular cholesterol. To determine the mechanism by which this protein regulates cholesterol, Nina performed immunoprecipitation (IP) experiments followed by mass spectroscopy, which was done in collaboration with Dr. James Wohlschlegel. This allowed her to determine the protein-binding partners of the protein of interest (POI). Twenty-five proteins were consistently enriched in the POI IP compared to the control samples, including a number of key components of the retromer complex, which is important for protein trafficking within the cell. Currently she is working on identifying which of these proteins, if any, plays a role in conjunction with the POI in controlling cholesterol homeostasis. In order to do so, she is currently developing knock down cell lines using shRNA targeted against specific members of the retromer complex. Once stable knock down cell lines have been established in both wild-type cells and cells that have the POI knocked down, she will measure cholesterol levels in order to begin to understand if these proteins work in a complex to regulate cholesterol levels in the cell. Nina’s research will provide insight into the mechanism with which the POI alters cholesterol levels and reveal important therapeutic targets for cholesterol regulation in cardiovascular diseases.
Nina would like to thank Dr. Matthew Hatkoff, her post-doctoral mentor, for his limitless patience, guidance and encouragement. She would also like to thank Dr. Kenneth Bradley for the opportunity to conduct undergraduate research and for his valuable input and support. She would like to extend her gratitude to members of the Dr. Bradley Lab for creating a welcoming and educationally stimulating environment in which to conduct research. Additionally, she would like to thank the Boyer Family and the URC Undergraduate Research Scholars Program for their generous support of her research.
| Parth Patel
Mentor: Dr. Dino Di Carlo
Funding: Honorary Award
Project Title: Elucidating the role of Annexin A1 in the formation of B-ALL
Parth Patel is a fourth year undergraduate at UCLA studying Microbiology, Immunology, and Molecular Genetics. He has been working with Dr. Dinesh Rao since October 2012, both during the academic year and the summer.
Researchers in Dr. Rao’s lab are trying to understand mechanisms behind formation of B cell acute lymphoblastic leukemia (B-ALL), which occurs when mutations cause leukemic transformations in B-lymphoid precursor cell stages in the bone marrow. There are recurrent translocations in B-ALL, three of which are being studied extensively in the Rao Lab. The first two translocations are specific gene fusions. The third is a variable translocation in chromosome 11, and involves the MLL (mixed lineage leukemia) gene. It is of interest as it occurs in young infants and has a high mortality rate. Of the three ALL subtypes being studied, it has the worst prognosis. Several translocation partners have been identified, and the mechanism of transformation is thought to involve the upregulation of MLL target genes.
Parth will be studying the putative role of ANXA1 in B-cell oncogenesis. ANXA1 is a calcium dependent phospholipid-binding protein. It has a variety of roles, acting as an apoptosis mediator, as well as interacting with glucocorticoids to inhibit cell proliferation and regulate cell migration. Microarray data of 44 B-ALL patients shows that Annexin A1 (ANXA1) is differentially expressed amongst the three different translocation subtypes of B-ALL, with an up-regulation in the MLL subtype. This indicates that ANXA1 may play a role in the oncogenesis of this specific subtype. Many cancers have shown ANXA1 suppression, while others display an increased expression in ANXA1. ANXA1 interacts with the NF-κB pathway, which is often exploited by cancers to evade apoptosis, by binding to the p65 subunit.
After graduating, Parth plans on pursuing a degree in medicine. He would like to thank Dr. Rao for his continued mentorship and assistance, and Norma Iris Rodriguez-Malave for support and planning and direction of the project, as well as the rest of the Rao lab for their continued help and encouragement.
| Katie Pannell
Mentor: Dr. Jerome Zack
Funding: Wasserman Award
Project Title: The role of Wnt/Beta-catenin signaling in lymphocyte development from human embryonic stem cells
Katie Pannell is a fourth-year Microbiology, Immunology, and Molecular Genetics major with a minor in Biomedical Research. She works in 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 multiple projects aimed at optimizing lymphocyte differentiation from human embryonic stem cells (hESC), ultimately for use in cell-based therapies for HIV and other diseases of the blood.
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 hESC, 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 both hematopoietic precursor formation and T cell development.
Katie would like to thank Dr. Scripture-Adams and Dr. Zack for the incredible education and support, as well as both the Undergraduate Research Scholars Program and the Wasserman family for the opportunity to further her passion for research.
| Justin Ondry
Pictured, left to right: Shauna Robbennolt, Justin Ondry, Dr. Sarah Tolbert
Faculty Mentor: Sarah Tolbert
Funding: Lau Award
Project Title: Synthesis of Mesoporous Films of Semiconducting Nanocrystals by Cross Linking Inorganic Capped Nanocrystals with Transition Metal Ions
Justin is a fourth 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 projects focus on developing new methods to assemble semiconducting nanocrystals into nanostructures with porosity on the nanometer length scale. Semiconducting nanocrystals have a variety of interesting size dependent optical and electronic properties. However current methods for assembling nanocrystals into porous films require thermal treatments to remove the pore template. Unfortunately these heat treatments also cause the size of the semiconducting nanocrystals to change, which subsequently changes their optical properties and for many applications this is detrimental. Justin is working to use chemical treatments in lieu of thermal treatments to process semiconducting nanocrystals into porous films. In addition these materials have a lot of promise for applications in photovoltaics and other optoelectronic applications and is currently working on synthesizing devices with his materials.
Justin would like to thank the generosity of the numerous undergraduate research programs that have provided him with funding. In particular, this year he is grateful for the generous support of the Lau award.
| Ross Mudgway
Mentor: Dr. Erika Nurmi
Funding: Boyer Award
Project Title: Genetic Contributions to Obesity and Metabolic Risk in Mexican-American Children
Ross is currently in his third year at UCLA and is majoring in Psychobiology. He is pursuing undergraduate 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 and psychiatric disorders. Ross is investigating genetic polymorphisms previously shown to be associated with obesity in a new sample of Mexican-American children.
Hispanic populations tend to suffer higher rates of obesity in all age groups. Identifying genetic moderators of growth, weight, and metabolic factors can help explain vulnerability to obesity in children with Mexican-American background and may help target for intervention those at risk and suggest personalized treatment strategies. While many genes have been assayed in the lab, after a review of his literature, Ross’ research has highlighted paraoxonase 1 (PON1) as an additional compelling candidate. PON1 is a high density lipoprotein associated enzyme that detoxifies oxon derivatives of organophosphate pesticides, and is associated with diseases characterized by high oxidative stress. It has shown association with obesity phenotypes and a particular relevance to Mexican-American populations. Ross hopes to find that common genetic variation in energy balance, monoamine, and growth factor candidate pathways for obesity will be associated with early onset weight and metabolic profile in Mexican-American children.
Ross would like to thank Dr. Nurmi and the members of the Nurmi/McCracken Lab for their continued guidance and support, and for the incredible opportunity to conduct undergraduate research. He is honored to have Dr. Nurmi as his mentor and is very excited to continue his scientific investigations. He would also like to express his gratitude to the Boyer Scholarship and the Undergraduate Research Scholars Program for their support of his research endeavors.
| Eva Ma
PI: Dr. Rachelle H. Crosbie-Watson
Mentor: Dr. Elizabeth M. Gibbs
Funding: Lau Award
Project Title: Sarcospan as a Therapeutic Target in Treating Duchenne Muscular Dystrophy
Eva Ma is a fourth year Molecular, Cell, and Developmental Biology major and Global Studies minor. She is investigating a novel treatment strategy for Duchenne muscular dystrophy in Dr. Crosbie-Watson’s lab in the Department of Physiology and Integrative Biology. Her interest in scientific research first led her to join a cardiovascular research lab in 2008 where she studied the accuracy of multidetector CT angiography measured regional ejection fraction of the left ventricle in diagnosing coronary artery disease. Later, she was accepted into the 2011 LA BioMed Summer Research Fellowship Program where she investigated the H2AX gene and its role in corneal epithelial cell repair post-damage.
Currently, Eva is researching in the Center for Duchenne Muscular Dystrophy under the supervision of her mentor, Dr. Gibbs. Duchenne muscular dystrophy (DMD) is a progressive muscle wasting disorder that inevitably leads to death in teenagers and young adults affected by the disease. Children with DMD lack a protein called dystrophin, which results in the loss of the dystrophin-glycoprotein complex and renders the sarcolemma susceptible to contraction-induced damage. The main focus of her study is sarcospan (SSPN), a dystrophin-associated protein that enhances multiple compensatory mechanisms in the mdx mouse model of Duchnne. Human SSPN was previously shown to improve muscle integrity in mdx mice, but was lethal at high doses. Eva has contributed towards clarifying the role of species-specific sarcospan by showing that mice overexpressing murine SSPN do not display signs of toxicity and also ameliorates the dystrophic pathology. This information will be highly relevant and necessary to move forward with clinical trials using SSPN as a therapeutic target for curing DMD in humans.
Eva would like to take the time to thank Dr. Crosbie-Watson for her guidance and inspiration, Dr. Gibbs for her continued support and mentorship, and the rest of the Crosbie-Watson Lab for their companionship and encouragement through her undergraduate years. Finally, Eva would like to express her gratitude towards Mr. Lau for his generous contribution to her research.
| Laura Liu
Mentor: Dr. Ting-Ting Wu
Title: Characterizing the Significance of ORF34 in Gamma-Herpesviruses’ Late Gene Regulation
Laura is a junior majoring in Biochemistry with a minor in Biomedical Research. She started working in research early on in her freshman year in the Molecular and Medical Pharmacology department. Her work focuses on understanding late gene expression in the gammaherpes-virus by characterizing Open Reading Frame 34 in the virus.
Kaposi’s Sarcoma-associated Herpesvirus (KSHV) and Epstein-Barr Virus (EBV) are two human gamma-herpesviruses associated with cancers in immuno-compromised patients. Like all herpesviruses, progression of gene expression during lytic replication consists first of immediate early genes, followed by early genes, and finally late genes. The late genes encode structural components of virions and their expression is essential for the completion of the viral lytic cycle. In hopes of eventually developing a strategy to prevent persistent infection and identify potential targets to inhibit prior to virion production, late genes will be analyzed. Late gene expression can only occur after DNA replication has been completed so it is hypothesized that there exists a link between the two processes. There are currently six known viral Open Reading Frames (ORFs) that are part of the late gene complex and ORF 34 is one of those six. Laura will be identifying an interaction between ORF 34 and a component of the DNA replication complex in the hopes of determining a linkage. Mutations on ORF 34 will be made once an interaction is confirmed to determine which amino acids in the sequence are essential for this interaction.
Upon graduation, Laura intends to pursue a Ph.D. in graduate school. Laura would like to thank Dr. Ting-Ting Wu, Dr. Ren Sun, as well as the members of the Sun Lab for giving her the opportunity to work under their guidance. She would also like to thank URC Sciences and URSP for their generous support.
| Andrew Lin
Pictured (from left to right): Dr. Santhosh Nadipuram, Andrew Lin, Dr. Peter Bradley
Mentor: Dr. Peter J. Bradley
Funding: Honorary Award
Title: Functional Characterization of Novel Rhoptry Transporter Proteins in Toxoplasma gondii
Andrew Lin is a third-year majoring in Microbiology, Immunology, and Molecular Genetics. He began as an undergraduate researcher with Dr. Bradley in the winter quarter of his freshman year. The Bradley lab studies the host-pathogen interactions of the apicomplexan parasite, Toxoplasma gondii. Andrew’s research focuses on two novel proteins that localize to a compartment that has been shown to be essential for T. gondii’s survival, the rhoptry.
The Apicoplexa are a phylum of parasitic protozoa that includes Plasmodium falciparum, a parasite responsible for malaria, and Toxoplasma gondii, a widespread pathogen considered to be the leading cause of death attributed to foodborne illness. These parasites use a sophisticated strategy for infection, involving active invasion of their host cell, creation of a protective niche, and finally egress from the host cell. A hallmark of apicomplexans is the rhoptry, a specialized secretory organelle that plays an essential role in host cell invasion. Secreted rhoptry proteins are involved in both the hijacking of cellular machinery and the formation of a moving junction structure by which the parasite is able to pull itself into the host cell. While much is known about these released constituents of the rhoptry, very little is known about the transporter proteins in the delimiting membrane of the organelle. By studying these novel transporters, Andrew hopes to gain insight into the uncharacterized resident proteins of the rhoptry with the goal of ultimately contributing to the development of better therapies for these deadly parasites.
Andrew would like to thank Dr. Peter Bradley and all the members of the Bradley lab for their assistance and guidance through his research, as well as for creating a great environment to develop as a scientist. Additionally, he would like to thank the URC-Sciences office for their support in his research endeavors.
| Brianna Lam
Mentor: Dr. Scott Kitchen
Funding: Oppenheimer Award
Title: Knockdown of PD-1 in anti-HIV specific CD8+ T cells
Brianna Lam is a fourth year Microbiology, Immunology, and Molecular Genetics major pursuing a minor in Biomedical research. She has been working in the Kitchen lab since spring quarter of her sophomore year. The Kitchen lab focuses on engineering the immune system to better combat HIV infection, and Brianna focuses specifically on CD8 T cell exhaustion.
Human immunodeficiency virus is notorious for evading human immune response as the bodies’ CD8+ or “killer” T cells become exhausted from chasing down the constantly mutating virus, and eventually go through cell death, or apoptosis. The markers that are up regulated during chronic viral infection were discovered in previous studies, and include Tim-3, PD-1, LAG-3, and CTLA-4. The purpose of Brianna’s project is to knockdown PD-1 using an shRNA in HIV specific CD8 T cells in hopes of preventing their exhaustion. She incorporated the shRNA into the T cells through a lentiviral vector, and is now assessing T cell function against antigen presenting cells that have been exposed to an HIV peptide. This project will hopefully allow HIV specific T cells to live longer and kill more virally infected cells before AIDS ensues.
Brianna would like to thank Dr. Scott Kitchen, Dr. Anjie Zhen, and all others working in the Kitchen lab for their continual instruction, support, companionship, and for creating an incredible opportunity for undergraduate research. Brianna would also like to express gratitude towards the Oppenheimer scholarship for generously funding her research.
| Hei Tong Lam
Mentor: Dr. Catherine F. Clarke
Funding: Wasserman Award
Project Title: Screening for potential protein partners in coenzyme Q biosynthesis
Hei Tong Lam is a junior at UCLA studying Biochemistry. She has been working in the laboratory of Dr. Catherine F. Clarke since the summer of her freshman year in 2013 at UCLA.
The Clarke Lab works with Ubiquinone (Coenzyme Q or Q) to examine details on their biosynthetic pathways, including their site of synthesis, mechanisms of inter- and intra-cellular transport, and the regulation of the pathway involved. Previous work in lab has identified eight of the eleven polypeptides required for Q biosynthesis, as well as a potential model for a high molecular mass Coq polypeptide biosynthetic complex, named the CoQ synthome.
Hei Tong’s project focuses on examining the effects of twelve potential proteins in the Q biosynthesis of yeast Saccharomyces cerevisiae. Using chromosomally-integrated tandem affinity tags (CNAP tag) and further analyzes by HPLC-MS/MS, Allan C.M. found several proteins that co-precipitated with several Coq subunits. The twelve potential proteins associated with the CoQ synthome were then identified due to their localization in the mitochondria. Future studies this year will focus on examining the effects of null mutants on each of the twelve strain’s ability to grow in minimal medium and in medium containing nonfermentable carbon source, as well as their levels of Q biosynthesis. We aim to identify which proteins could be physically associated with the CoQ synthome, and characterize their functions in the Q biosynthetic pathway.
After graduation, Hei Tong hopes to pursue a career in the medical field. She would like to thank Dr. Clarke for her ongoing mentorship and the incredible opportunity to conduct undergraduate research, Dr. Theresa Nguyen and D. Chris Allan for their mentorship and guidance, and the rest of Clarke Lab for their incredible advice and support. She would also like to thank the Wasserman Family and the Undergraduate Research Scholars Program for their generous support in undergraduate research.
| Sahana Kribakaran
Mentor: Dr. Carlos Portera-Cailliau
Funding: Lau Award
Title: Functional Role of Cajal-Retzius Neurons in the Postnatal Mouse Neocortex
Sahana Kribakaran is a fourth year Neuroscience major and Biomedical Research minor
who has been working in Dr. Carlos Portera-Cailliau’s laboratory in the Department of
Neurology since September 2012 under the guidance of Postdoctoral Fellow, Dr. Amaya
Miquelajauregui. Her current project is focused on understanding the early postnatal role of Cajal-Retzius (CR) neurons in the mouse neocortex in vivo.
Cajal Retzius neurons, found in layer one of the neocortex, play a vital role in neuronal migration and cortical lamination during development, but the functional role of these cells in the postnatal neocortex is still poorly understood. Here, Sahana performs in vivo electrophysiology with optogenetics, where channelrhopsin 2 (ChR2) is expressed in Ebf2-Cre mice, to selectively stimulate CR neurons at postnatal ages (P) 6 to 10, and to simultaneously record local field potentials and single-cell patch-clamp recordings from layer 2/3 (L2/3) of the mouse neocortex.
Preliminary results show that optogenetic stimulation at P10 leads to distinct local field potential responses in L2/3 as well as in deeper cortical layers. To confirm the specificity of the response, Sahana is performing further experiments at younger ages (P6), a time point during which more CR neurons are present and the labeling is more specific. She expects that optogenetic activation of CR neurons will trigger post-synaptic currents in pyramidal neurons in L2/3, and possibly early network oscillations. If excitatory LFPs that are time-locked with the light stimulation are
recorded, this will give strong evidence that the CR neurons of L1 are synapsing onto the L2/3 pyramidal cells. Understanding this neocortical circuit could further elucidate underlying mechanisms for neurodevelopmental disorders such as autism spectrum disorders, epilepsy, schizophrenia, and bipolar disorder in future studies.
Sahana would like to thank the Undergraduate Research Scholars Program and Mr. Lau
for his generous funding. She would also like to thank Drs. Ira Clark and Rafael Romero of the Biomedical Research Minor for their immense support and dedication to undergraduate research. Finally, she would like to thank Dr. Portera-Cailliau, Dr. Amaya Miquelajauregui, and everyone in the Portera Lab for their continuous encouragement and guidance.
| Yeon Sun (Christy) Kim
Mentor: Dr. Brigitte Gomperts
Title: Chemoprevention drugs for the reversal of premalignancy to lung squamous cell carcinoma
Christy Kim is a senior majoring in Molecular, Cell, and Developmental Biology with a minor in Gender Studies. She began her undergraduate research in Dr. Gomperts’ lab in 2012 and has since been studying under the mentorship of postdoctoral fellows Dr. Manash K. Paul and Dr. Bharti Bisht. Currently, Christy’s project studies the premalignant stages to lung squamous cell carcinoma (LSCC) and aims to find drugs which will allow for a reversal of LSCC premalignancy through high-throughput-assay drug screening.
LSCC is a particular subtype of lung cancer which is thought to progress through distinct premalignant stages. Knowledge of the progression of LSCC is vital for its early diagnosis, treatment, and prevention; however, the genetic alterations specific to each stage of this premalignant progression have yet to be clarified. Previous literature has revealed pathways that are significantly implicated in LSCC. By chemically modulating some of these known pathways in airway basal stem cells, the presumed cells of origin for LSCC, my mentors and I have built an in vitro mouse model of LSCC which demonstrates hyperplasia, metaplasia, and dysplasia—the progressive stages of LSCC premalignancy. This model has substantial clinical significance: using this in vitro model, our next goal is to develop a high-throughput-assay to screen for compounds in order to build a targeted chemoprevention strategy. Successful chemoprevention drugs may ultimately stop the premalignant progression of LSCC.
Christy would like to thank Dr. Brigitte Gomperts, Dr. Manash K. Paul, Dr. Bharti Bisht, and the members of the Gomperts lab for their constant guidance and support.
| Grant Higerd
Mentor: Dr. Carlos Portera-Cailliau
Funding: Ehrisman Award
Title: Canonical Cortical Remapping after Targeted Stroke
Grant Higerd, a fourth year Neuroscience major and Biomedical Research Minor, has
been conducting research in the Portera-Cailliau lab since September of 2013. Under the
guidance of Dr. Máté Marosi, Grant is studying processes of neural plasticity after stroke
Remarkably, many stroke survivors exhibit significant recovery of deficits after the
stroke. This functional recovery, often incomplete, is presumably mediated by neural
plasticity in regions that were performing similar functions as the ischemic area but were
spared by the stroke. The mechanisms of this “remapping” are poorly understood and
increasing our knowledge of this plasticity will be crucial to the development of novel
pharmacologic and rehabilitative treatments. Grant is investigating this functional
remapping phenomenon in mice using optical intrinsic signal imaging and multi-photon
laser scanning microscopy to observe changes in the cortex during photo-thrombotic
stroke. The Portera-Cailliau lab has shown that when the whisker sensory representation
is targeted by stroke, it consistently remaps to a distant region in the supplementary
somatosensory cortex (S2c). This data suggests that functional remapping is not simply
determined by regional blood-flow, but rather by pre-determined (canonical) pathways.
The goal of Grant’s project is to investigate the changes in neural structure, connectivity,
and activity underlying this remapping, and determine its functionality.
Grant plans to graduate in the fall of 2015 and will pursue graduate training in an MDPhD
program. He is very grateful to Mr. Lewis and the Ehrisman Foundation for their
generous support. He would also like to deeply thank Dr. Portera-Cailliau, Dr. Máté
Marosi, and the rest of the Portera-Cailliau lab for their patient guidance and support.
| Joshua Hedtke
Mentor: Dr. Eddy M. De Robertis
Funding: Wasserman Award
Project Title: Endocytic Trafficking in Wnt/Beta-catenin signaling and Its Effect on Protein Stability
Josh is a fourth year Molecular, Cell, and Developmental Biology major. He has been conducting research in the De Robertis lab, under the direct supervision of Hyunjoon Kim, since Spring 2013.
The De Robertis lab focuses on, among other things, the developmental and cellular biology of the Wnt signaling pathway. The lab has uncovered a novel signaling method by which beta-catenin, the Wnt effector protein, becomes sequestered inside large multivesicular endosomes, thereby leading to its and other proteins’ stabilization(the other proteins also become sequestered and thus temporarily immune to proteasomal degradation). Many questions remain as to what molecular events are required in the sequestration process and what the effects of sequestration are on general protein stability within the cell. To study the stabilizing effects of sequestration, Josh created stable cell lines expressing a Glycogen Synthase Kinase 3 (GSK3) “biosensor” gene. This gene is a proxy for general proteins within the cell, and thus gives a readout of the Wnt effect on general protein stability. To study how the sequestration process occurs, Josh has been studying the proteins Axin, Adenomatous Polypopsis Coli (APC), Ubiquitin which are involved in various capacities in this process. Josh has done Axin and ubiquitin knockdown experiments and currently is working on creating APC knockout cell lines and Axin mutant constructs to study these two integral proteins’ roles in the Wnt signaling pathway.
Josh Will graduate in Spring 2015. He is very grateful to Eddy for the invaluable experience and support he has received in Eddy’s lab. He would like to thank Hyunjoon for his mentorship and the Wasserman Foundation for supporting young scientists such as himself.
| Sarah Heath
Mentor: Dr. Jack Feldman
Funding: Wasserman Award
Title: The Effects of Inhibition on Respiratory Rhythm and Pattern Generation
Sarah Heath is a 4th year neuroscience major and biomedical research minor, completing her undergraduate degree at UCLA. Sarah has been working under Dr. Jack Feldman since March, 2013, in collaboration with post doctorate scholar Kaiwen Kam. The Feldman Lab focuses on the neural circuitry of breathing and the generation of respiratory rhythm and pattern. What gives the neural circuitry of breathing it's rhythmic quality has not been clearly defined. The Feldman Lab is exploring this by using the model system of an isolated brainstem. This allows for observations of cellular, molecular, and synaptic properties, but also exploration of interactions at a network level by recording motor output to the hypoglossal nerve. By bridging the gap between cellular properties and behavior, The Feldman Lab hopes to elucidate some of the rhythmogenic mechanisms present in the brainstem.
Sarah is currently using electrophysiology in order to examine the role of synaptic inhibition on rhythm and pattern generation in the brainstem. She applies both inhibitory neurotransmitters and their antagonists to brain stem slices in order to observe neuronal and motor activity in the presence and absence of these molecules. So far, her results point towards the conclusion that synaptic inhibition is not necessary for rhythmogenesis in the brain stem.
| Jack Hale
Mentor: Dr. Bennett Novitch
Funding: Wasserman Award
Project Title: Optimizing motor-neuron differentiation of mouse embryonic stem cells
Jack Hale is currently a fourth year majoring in Neuroscience with a minor in Biomedical Research. He has been conducting research in the laboratory of Dr. Bennett Novitch for just over a year. The Novitch lab studies the intricate patterns of signals affecting motor neurons as they progress throughout embryonic development in the developing spinal cord, and their place within the larger sphere of neural circuitry.
We are also concerned with the dysfunction of this development and the diseases that manifest when lower motor neuron development goes awry—in particular Spinal Muscular Atrophy, a family of muscle wasting diseases that cause profound muscle weakness or death in 1 in 6000 infants. Under the direct supervision and guidance of Dr. Ken Yamauchi, Jack is currently investigating optimal procedures for efficiently differentiating mouse embryonic stem cells into motor neurons and culturing them with muscle cells, with the intention of making a “disease-in-a-dish” model of an SMA-type synapse between nerve and muscle utilizing light-based stimulation methods. We are looking to apply this optimized in-vitro assay to induced-pluripotent stem cells of SMA patients, with the intention of eventually using this patient-specific assay for screening possible drugs to combat SMA.
Jack would like to express his deep gratitude to Dr. Novitch and Dr. Yamauchi for their guidance and support in the laboratory, to the faculty in the Biomedical Research department and URC for their invaluable advice and assistance, and to URSP and the Wasserman family for their generous support of undergraduate research at UCLA.
| James Haggerty-Skeans
Mentor: Dr. Patricia Phelps
Funding: Van Trees Award
Title:The Effect of Olfactory Ensheathing Cells on Noradrenergic Axon Presence After Spinal Cord Injury.
James Haggerty-Skeans is a fourth-year student majoring in Neuroscience and minoring in Biomedical Research. James has studied with Dr. Phelps and Ph.D. candidate Rana Khankan since September, 2012. A major focus of the Phelps lab is to investigate the role that Olfactory Ensheathing Cells (OECs) play in axonal regeneration after spinal cord transection. OECs are unique glial cells found in both the olfactory epithelium and olfactory bulb, and are known to support axonal regeneration even after a complete spinal cord transection. The OEC treatment improves hindlimb stepping ability, and increases axon density in the normally inhibitory injury site. The extent of OEC survival after transplantation, and their migratory pattern in the spinal cord, however, still remain unclear.
James is currently using fluorescent immunohistochemistry to visualize OECs, and study their survival, migration, and interactions at the injury site. He also is quantifying the regenerative capacity of noradrenergic axons near the injury site in rodents with OEC or Fibroblast cell implantation following a complete transection. Further, he is analyzing the effect that immunosuppression has on OEC-graft survival and axon presence in the injury site after a complete spinal cord transection.
| Ayaka Hachisuka
Mentor: Dr. Pascal Ravassard
Funding: Gottlieb Award
Ayaka Hachisuka is a third year undergraduate student with a major in Neuroscience and a minor in Biomedical Research. She began working in the W. M. Keck Center for Neurophysics Laboratory in summer 2013 under the guidance of Dr. Pascal Ravassard. The W. M. Keck Center for Neurophysics focuses on understanding how the neural representation of the physical world is generated by measuring the activity of ensemble of neurons in the hippocampus and related cortical areas.
The hippocampus and entorhinal cortex are involved with spatial learning and navigation. In particular, specialized hippocampal cells called place cells have been shown to increase their firing rate within specific spatial locations of the environment - the place fields, leading to the hypothesis that these place fields could be the support for a neural representation of space and form a cognitive map used for spatial navigation. However, it is unknown exactly how and in what proportion environmental and internal cues affect place cell firing properties. When a rat runs back and forth on a linear track to collect rewards successively placed on either end, a property of place cell firing called directionality is observed. Directional place cells preferentially fire when the rat is running in one direction, while remaining silent in the opposite running direction. Interestingly, this property is not observed when the rat is allowed to forage in a two-dimensional arena, where place cells are found to fire within their respective place fields from any running directions. Ayaka is currently investigating what are the environmental factors susceptible to induce or suppress place cells directionality by measuring their activity in behaving animals running in a virtual linear track, in which features of the virtual environment (visual and auditory cues, reward amount) are precisely presented and modulated, while features of the physical world (such as odors) are not spatially relevant to the task. Ayaka hopes her research will provide a better understanding of the hippocampus system function that could lead to implications for Alzheimer's patients, whose episodic memory and sense of location is affected.
In the future, Ayaka plans to attend graduate school to work towards a Ph.D. in neuroscience, as well as pursue a career in education. Ayaka would like to thank all of the members of the lab for their continual guidance and encouragement. She would additionally like to thank the Biomedical Research Minor Department, the Gottleib Foundation, and the Undergraduate Research Scholars Pr
| Alexander Grunfeld
Mentor: Dr. Louis-Serge Bouchard
Funding: Boyer Award
Project Title: Nanoparticle catalysts for heterogeneous phase para-hydrogen induced polarization in water
Alex Grunfeld is a fourth year neuroscience major studying in the lab of Dr. Louis Bouchard. The Bouchard group aims to advance magnetic resonance technology through research in a variety of subfields, including catalysis and biomedicine. Under the supervision of Dr. Stefan Glöggler, Alex is working to optimize platinum nanoparticles to be used as heterogeneous catalysts in hyperpolarized magnetic resonance imaging.
Hyperpolarization is a technique that enhances the signal observed in nuclear magnetic resonance (NMR) by several orders of magnitude. Hyperpolarization can be achieved by various methods, one of which is para-hydrogen induced polarization (PHIP). In a typical PHIP experiment, an alkene or alkyne substrate is hydrogenated with para-hydrogen, followed by polarization transfer to a heteronucleus (typically carbon-13) in a low-strength magnetic field and signal acquisition in a high-strength magnetic field. Previous PHIP experiments have employed a homogeneous phase, rhodium based catalyst for the hydrogenation; however, the toxicity of this catalyst in the human body is not well understood. Alternatively, heterogeneous catalysts such as nanoparticles have also shown potential in producing hyperpolarized substrates. These nanoparticles are advantageous over homogeneous catalysts in that they can be filtered from the hyperpolarized product, thereby reducing issues of toxicity. Currently, Alex is assisting in the optimization of platinum nanoparticles to maximize the observed enhancement factor in PHIP experiments. Ultimately, this work in hyperpolarized imaging can be used to observe cell metabolism in real-time.
Alex would like to thank Dr. Louis Bouchard and Dr. Stefan Glöggler for their support and guidance throughout his time so far with the group. Additionally, he would like to thank the Boyer Scholarship Foundation for generously funding his research.
| Monish Patel
Mentor: Jay Jiang
PI: Dr. Kang Ting
Funding: MacDowell Award
Title: Temporospatial Expression of Nell-1 in Developing Murine Cartilaginous Tissue
Monish Patel is a senior 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.
| Tracy Lin
Mentor: Dr. Thomas Otis
Funding: Honorary Award
Project Title: Involvement of CamKII and calcineurin in cerebellar nuclear plasticity during associative motor learning
Tracy Lin is a fourth year UCLA undergraduate majoring in biochemistry and pursuing a minor in neuroscience. She has been conducting research since February 2014 in Dr. Thomas Otis’s laboratory under the guidance of Katrina Choe (Post-Doc). The Otis lab aims to dissect the cerebellar circuit by using the combination of optogenetic tools, stereotaxic surgery, and associative motor learning paradigms. The lab is interested in where plasticity occurs within the cerebellar circuit, how these changes are induced, and how these changes alter signaling and cerebellum-dependent behavior.
Cerebellar learning is thought to depend on plastic changes in the synaptic strengths of its neuronal circuits. Current hypotheses propose that learning results in part from plasticity in the glutamatergic synapses between mossy fibers (MFs) and cerebellar nuclei neurons (CNNs). As an effort to reveal the underlying mechanisms to how the cerebellum generates learned movement and alter the MF-CNN synaptic connection, Tracy has done previous research performing immunohistochemistry on brain sections from mice which were trained to establish associative memories by pairing optogenetic stimulation of Purkinje neurons with auditory tone. In these mice, she noted the increase in VGLUT2-positive puncta, signifying the presence of glutamatergic presynaptic terminals, to correlate with the increase in synaptic connections.
The mechanism for this structural plasticity is currently unknown. In previous literature, CamKII and calcineurin have been shown to be required for LTP induction in vitro in CNNs. CaMKII is involved in many signaling cascades and is thought to play a role in learning and memory. To further explore this idea, Tracy is focusing her current research work on the roles of CaMKII and calcineurin in establishing the synaptic plasticity between MFs and CNNs during associative motor learning induced by optogenetic stimulation. Tracy hopes to find a positive correlation by comparing the magnitude of learning obtained by behavioral analysis with the degree of change to the staining of CaMKII and calcineurin.
Tracy plans to graduate in Spring of 2015. Tracy would like to take this time to thank Dr. Otis and Dr. Choe for their continual support and mentorship and giving her the opportunity to work in the Otis lab. She would also like to thank the Undergraduate Research Scholars Program for giving her this honor and opportunity to further her passion for research.
| Amy Lie
Mentor: Dr. Albert Lai
Funding: Wasserman Award
Amy Lie is a third year Molecular, Cell, and Developmental Biology major and has been working in Dr. Albert Lai’s laboratory since the spring of 2014. The Lai Laboratory focuses on improving outcomes and ultimately finding a cure for patients with primary brain cancer through the development of personalized targeted therapies and associated biomarkers. Amy’s current research involves investigating the role of human telomerase reverse transcriptase (hTERT) promoter mutations both as a biomarker for gliomas and to understand the mechanism of how these promoter mutations increase expression.
Gliomas represent an incurable disease in which significant improvements in treatment outcome remain elusive. Telomerases, enzymes that add repeated sequences to the 3’ end of DNA strands, are responsible for extending telomere length in cells. In normal telomerase activity, telomeres shorten after each cell division eventually leading to cell senescence and death. However, in cancerous tissues, telomerase activity is believed to be high because of mutations in the hTERT promoter, which increase expression. This leads to maintenance of telomere length and unrestricted cell growth. Along with hTERT promoter mutations, co-deletions of chromosomal arms 1p and 19q can occur in varying frequencies within glioma patients. Current diagnosis using percentages of 1p19q co-deletions determined by fluorescent in situ hybridization and converted into a negative or positive diagnosis is subjective, because of an unclear percentage cutoff of 1p19q co-deletions. hTERT promoter mutations, unlike the 1p19q co-deletion reported in percentages, is binary, either the mutation is present or absent. Therefore, it is proposed that hTERT promoter mutations could be a better prognostic and diagnostic marker, replacing the 1p19 co-deletions to molecularly characterize gliomas. Two hot spot mutations and a polymorphism on the hTERT promoter have been reported in a high percentage of gliomas; however, prognostic value of these genetic alternations still remains controversial. Amy’s research under the main goal of investigating the role of hTERT promoter mutations as a biomarker for gliomas will be to study the correlation between the hTERT promoter mutations and 1p19q co-deletion within the subset of IDH1/2 mutant gliomas and to determine a phenotypic effect of hTERT promoter mutations on IDH1/2 wild type glioblastomas (GBMs). Additionally, the project aims to understand the effect of mutations on expression and the role of increased hTERT in promoting glioma growth. This study will potentially provide an alternative to characterize glioma patients using TERT promoter mutations instead of 1p19q co-deletions and elucidate the effect of these mutations on glioma patient prognosis.
Amy would like to thank Dr. Lai for his continued guidance and the incredible opportunity to conduct undergraduate research, and all the members of the Lai Laboratory for their ongoing support and mentorship throughout this project. She would also like to thank the Wasserman family and the Undergraduate Research Scholars Program for their support of her scientific endeavors.
| Derek Le
Mentor: Dr. Anthony Aldave
Funding: Wasserman Award
Title: Identification of Candidate Genes for a Novel Bowman Layer Corneal Dystrophy
I am a fourth year student in the Molecular, Cell, and Developmental Biology department. I joined Cornea Genetics Laboratory, directed by Dr. Anthony Aldave at the Jules Stein Eye Institute, in Summer 2013. The Cornea Genetics Laboratory focuses on characterizing the genetics of corneal dystrophies, a group of rare, inherited diseases that result in opacification of the cornea.
In particular, my research project focuses on identifying the genetic basis of a novel corneal dystrophy of the Bowman layer (CDB) of the cornea. Clinical symptoms of CDB include loss of vision and recurrent erosions of the corneal epithelium. Two CDBs have been clinically characterized: Reis-Bückler corneal dystrophy and Thiel-Behnke corneal dystrophy. Both of these dystrophies are dominantly inherited Mendelian disorders and are associated with conserved mutations in the transforming growth factor beta-induced (TGFBI) gene. However, a report exists of a family affected by an atypical CDB that is not associated with mutations in TGFBI. In addition, we have clinically assessed an Argentinian family with similar CDB-like opacifications. Screening of TGFBI in the Argentinian family was performed to also exclude mutations in this gene as the cause of the corneal opacities, supporting the possibility that these families are affected with a novel CDB. Currently, I am utilizing high-throughput genome sequencing to identify the putative variants in both families that are responsible for this atypical CDB. Once the causative mutation is identified, I plan to follow up with investigation of the functional impact that the mutation has on the function of the gene or gene product.
After graduation, I plan on pursuing a PhD. I would like to thank Dr. Anthony Aldave, Dr. Doug Chung, Ricardo Frausto, and the members of the Cornea Genetics Laboratory for their guidance and support. I would also like to thank the Wasserman family and the Undergraduate Research Scholars Program for supporting my research and research in the undergraduate community.
| Rina Kim
Mentor: Dr. Kent Hill
Funding: Boyer Award
Title: Dissecting Social Motility in African Trypanosomes using RNA-Seq Transcriptome Analysis and RNAi Functional Analysis
Rina Kim is a fourth year UCLA undergraduate majoring in Microbiology, Immunology, & Molecular Genetics. She has been conducting research in Dr. Hill’s laboratory since the Winter Quarter of her freshman year. Dr. Hill’s lab studies a protozoan parasite called African Trypanosome that is a causative agent of the African Sleeping Sickness.
Cell-cell communication and social behavior are widespread in microbes, such as fungi or bacteria. Social behavior was recently discovered in protozoan parasites. However, its contributions to disease pathogenesis and transmission are poorly understood. African trypanosomes (Trypanosoma brucei) are flagellated protozoan parasites that cause sleeping sickness in humans and related diseases in livestock in Sub-Saharan Africa. T. brucei parasites engage in social behavior or “social motility” when cultivated on semisolid agarose surfaces. This behavior is characterized by trypanosomes assembling into multicellular communities that engage in polarized migrations across the agarose surface and cooperate to divert their movements in response to external stimuli. In bacteria, transition from planktonic (suspension) conditions to a multicellular lifestyle on a surface is associated with a series of adaptations, which is reflected in changes in gene transcription. Similarly, developmental transformation from single cell to multicellular life-style in T. brucei is also expected to be regulated by changes in gene expression. To identify the mechanisms underlying social motility, in collaboration with the Merchant and Pellegrini labs, the Hill lab therefore performed a transcriptome comparison of trypanosome cultured in suspension versus surfaces from two somo + strains and one somo - strain using Whole Transcriptome Shotgun Sequencing. The results indicate that a set of genes is differentially regulated between the two culture conditions, suggesting that these genes might contribute to social motility. By applying a series of filters: (1) differential expression under surface versus plate (2) p-values and (3) RPKM values, we selected 7 genes to prioritize for functional (RNAi) studies. These genes are expected to contribute to the adaptation of trypanosomes to a multicellular life-style on surfaces. Current effort is focused on dissecting the contribution of identified genes to social motility on the molecular level using RNA interference (RNAi) knockdown approaches.
In order to assess whether a gene is required for social motility, Rina’s work focuses on knocking down 7 top priority candidates genes individually using a tetracycline-inducible RNA interference (RNAi) strategy and further characterizing them using quantitative real-time PCR (qRT-PCR), growth curve, motility assays, and social motility assays.
The study of social behavior in these microbes is expected to open new paradigms for considering host-parasite interaction and cell-cell communication, giving way to new strategies for therapeutic intervention.
As an aspiring physician-scientist, Rina plans to pursue an MD/PhD degree in immunology, researching diseases. She believes that understanding the anatomy and medical struggles of a patient is important in researching the mechanism of that patient’s disease, and coming up with a clinical cure for the disease. The dual degree will provide a synergy in recognizing new, instrumental ways for dissecting disease mechanisms, through the utilization of both experimental and clinical thinking as a physician-scientist.
Rina would like to thank Dr. Green and Dr. Whitcome for their generous contributions to her research. She would also like to express gratitude and appreciation for her mentor Dr. Kent Hill for his continued support and guidance.
| Chae Yoon Kim
Pictured, left to right: Dr. Stephanie White, Chae Kim, Dr. Nancy Day.
Mentor: Dr. Stephanie White
Funding: Wasserman Award
Title: Effects of Overexpression of FoxP2 in Area X on Male Zebra Finch Song
Chae Kim is a fourth 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 Wasserman endowment.
| Joonhee Kim
Mentor: Dr. Reza Ardehali
Funding: Wasserman Award
Title: Elucidation of the differences between male and female hearts at cellular and tissue level
Joonhee is a fourth-year student majoring in Molecular, Cell, and Developmental Biology. He began his undergraduate research with Dr. Reza Ardehali in the Medicine/ Cardiology department late April of 2014. Currently, his research focuses on elucidating the differences between male and female hearts at cellular and tissue level.
Cardiovascular disease (CVD) remains the leading killer of both women and men in the United States. Population studies have shown that there are fundamental differences between males and females when it comes to CVD. The absolute numbers of women living with and dying of CVD and stroke exceed those of men, as does the number of hospital discharges for heart failure and stroke. In addition, the risk of heart disease in women is often underestimated due to the misperception that females are “protected” against cardiovascular disease. The underrecognition of heart disease and differences in clinical presentation in women lead to less aggressive treatment strategies and a lower representation of women in clinical trials. Thus, it is crucial to conduct experiments that examine the gender difference in CVD.
Joonhee works in a discovery-driven project to determine the existence of differences between female and male mice hearts following myocardial infarction (MI) and transverse aortic constriction (TAC) surgeries. He is using frozen tissue sections for immunocytochemistry to determine the vascular density. Hearts will also be homogenized and gap junction proteins will be quantified by Western Blot and ELISA.
Joonhee would like to thank Dr. Reza Ardehali, Dr. Peng Zhao, and all the members of the Ardehali Lab for their ongoing mentorship and for creating an environment that is welcoming and highly educational. He also would like to thank Wasserman Family for the scholarship.
| Il Seok Jeong
Mentor: Dr. Kuk-Wha Lee
Funding: Lau Award
Title: A Potential Antioxidant Role of Humanin in Human Trophoblast Cells under Various Conditions of Oxidative Stress
Il Seok Jeong is a fourth-year undergraduate student majoring in Biochemistry. His involvement in the laboratory started in June 2013. Currently, he is working with Dr. Gina C. Capodanno, a 3rd year clinical fellow specializing in Pediatric Endocrinology, and conducting his research under the mentorship of his principal investigator, Dr. Kuk-Wha Lee. The Lee lab is investigating a novel peptide called Humanin (HN), focusing on its origin, characterization, and molecular mechanism of action; particularly its cytoprotective effect in many cell-types and disease models.
Intrauterine growth restriction (IUGR) is a pathological condition affecting pregnancy. Although the frequencies of the condition are about 3 percent of all pregnancies, the affected babies are at risk of significant medical problems during pregnancy and delivery, and after birth. These problems include low birth weight, hypoxia, hypoglycemia, attenuated immune system, and increased risk of chronic disease in adulthood. This clinical manifestation is a consequence of various stressors such as hypoxia-ischemia, maternal malnutrition, maternal diabetes, vascular disease, and substance use during pregnancy. The pathogenesis of IUGR is currently poorly understood, but a likely mechanism involves an oxidant-antioxidant imbalance. Humanin (HN) is a potent biopeptide initially cloned from a surviving portion of Alzeheimer’s patient’s brain. HN has already exhibited cytoprotective effects in various oxidant-induced disease models such as amyloid-β-induced Alzeheimer’s disease and atherosclerosis. We hypothesize that HN is a potent antioxidant that grants protection against various oxidants. We predict that HN will be endogenously induced in the first trimester human trophoblast cells (HTR8) under hypoxia and that exogenous delivery of HN will antagonize the hypoxic effects. HN-induced protection of HTR8 cells will demonstrate HN’s protective role in an previously unexplored disease model and will be instrumental to the development of therapeutic agents for IUGR.
Il Seok plans to pursue a medical degree. Il Seok would like to thank Drs. Lee and Capodanno for their priceless mentorship and support, as well as to everyone in the Lee lab for providing a friendly and comfortable environment to work in. Il Seok would like to show his appreciation to the Undergraduate Research Scholars Program for coordination of the program and Mr. Lau for the gracious funding of his research work.
| Shankar Iyer
Mentor: Dr. Thao Nguyen
Funding: Gottlieb and Wasserman Awards
Title: Ventricular Arrhythmia Triggers Induced By Fibroblasts in Co-cultures with Myocytes
Shankar Iyer is a third year undergraduate student majoring in Physiological Science with a minor in Biomedical Research. He began his research with Dr. Thao Nguyen in the Cardiovascular Research Laboratory during the spring quarter of his first year. His research focuses on understanding how fibrosis and stress synergistically promote the emergence of cardiac arrhythmias.
A leading cause of death around the world results from cardiovascular diseases. Sudden cardiac death are often caused by arrhythmias such as ventricular tachycardia and fibrillation (VT/VF). However, current antiarrhythmic drugs and cardiac defibrillation have limited efficacy in preventing the emergence of VT/Vf. During cardiac remodeling following injury, the heart attempts to repair itself: fibrosis develops as myofibroblasts (scar-forming heart cells) arise and deposit collagen bundles. It has been long accepted that fibrosis passively interrupts the normal electrical conduction system across the heart, leading to arrhythmias. However, recent evidence suggests a more active role of fibrosis in arrhythmogenesis. The goal of this study is to uncover the mechanisms underlying how fibroblasts may actively facilitate the emergence of VT/VF triggers in myocytes. Shankar hypothesizes that in the presence of stress (such as oxidative or ionic stress), fibroblasts influence neighboring myocytes to become more prone to develop arrhythmias by either physically coupling with the myocytes or by secreting paracrine fibroblast factors. Shankar will examine how different stressors promote arrhythmias in co-cultures of neonatal rat ventricular myocytes and myofibroblasts (NRVM, NRVF) using voltage and calcium optical mapping technique. Shankar hopes that the insights from his investigation may pave the way for future discovery of novel effective antiarrhythmics. His findings may even be relevant for the field stem cell therapy, in which exogenous stem cells may, just as myofibroblasts do, interact with endogenous myocytes and promote arrhythmias.
Shankar would like to extend his most heartfelt appreciation to Mrs. Gottlieb and the Wasserman Family for their generous support. He would also like to thank his mentor, Dr. Thao Nguyen, for her guidance as well as the Nguyen Lab for providing such a supportive, nurturing, and fun environment to conduct research.
| Amy Huang
Mentor: Dr. Peter John Bradley
Funding: Boyer Award
Project Title: Characterization of novel Inner Membrane Complex (IMC) proteins in Toxoplasma Gondii
Amy Huang is a third-year student in the Department of Microbiology, Immunology, and Molecular Genetics with a minor in North African and Middle Eastern Studies. She conducts research in Dr. Peter Bradley’s laboratory which studies the protozoan parasite Toxoplasma gondii. T. gondii is an obligate intracellular parasite that is especially dangerous to immunocompromised patients and congenitally-infected neonates. In immunocompromised (e.g. AIDS, transplant, lymphoma) patients, Toxoplasma is known to cause ocular and neurological disease and encephalitis. If acquired as a primary infection during pregnancy, vertical transmission of T. gondii can result in miscarriage, ocular lesions, or mental retardation. Toxoplasma also serves as a model system for Plasmodium falciparum, the causative agent of malaria.
Amy’s project focuses on a unique structure of Toxoplasma called the inner membrane complex (IMC), which underlies the parasite’s plasma membrane and functions in daughter cell formation and host invasion. Specifically, Amy is studying the apical cap region of the IMC, from which secretory organelles are released during host invasion. The apical cap also serves as a scaffold for replication by an internal budding process called endodyogeny. Using the CRISPR-Cas9 system for genome editing and a protein-protein interaction identification method called BioID, Amy hopes to gain a better understanding of apical cap proteins, their associated partners, and the role they play in Toxoplasma biology.
Amy would like to thank Dr. Bradley, Dr. Allan Chen, and the members of the Bradley Lab for their unwavering guidance and patience, as well as the Boyer Foundation for their generous support of undergraduate research and science education.
| Alexandria Hoffman
Mentor: Dr. Rhonda Renee Voskuhl
Funding: Honorary Award
Project Title: Identifying ERβ binding targets during oligodendrocyte maturation in primary cultured oligodendrocytes
Alexandria is a fourth year Molecular, Cell and Developmental Biology and Anthropology double major. She works in Dr. Rhonda Voskuhl’s lab in the multiple sclerosis program under the neurology department and studies the effect of estrogen receptor-beta on the progression of symptoms in experimental autoimmune encephalomyelitis (EAE), a mouse model for multiple sclerosis.
Multiple sclerosis is an autoimmune disease that is characterized by inflammation and demyelination in the central nervous system. Previous studies have shown that introducing an estrogen receptor-beta agonist ameliorates the severity of the disease scores and pathology of EAE mice. In an effort to better understand the role of ER-beta in neuroprotection Alex will be working with primary cultured oligodendrocyte precursor cells (OPC) which develop into myelin-producing oligodendrocytes. By mimicking the inflammatory environment of EAE in vitro and using DPN (an ER-beta specific ligand) Alexandria hopes to gain a better understanding of the mechanisms by which ER-beta affects this maturation process and the overall process of remyelination.
Alexandria will be graduating with her bachelor’s degree in spring 2015 and hopes to continue on to graduate education where she will pursue a PhD. She is extremely thankful for all of the help and guidance provided by Dr. Voskuhl and the members of the lab. Their constant support has been instrumental in her pursuit of a career in science.
| Victor Fung
Mentor: Dr. Mohamad Navab
Funding: Oppenheimer Award
Project Title: The oxidized phospholipid lysophosphatidic acid in induction of atherosclerosis in the atherosclerosis-susceptible animal model LDL R-/- mouse
Victor Fung is a 4th year Physiological Science major. He has been under the guidance of Dr. Mohamad Navab since the spring quarter of his second year. He is currently studying the effects of oxidized lipids and lipid metabolites on hyperlipidemia and atherosclerosis. His project focuses on determining the extent of lesioning as a result of these oxidized lipids and how effective oral HDL-mimetic peptides are at preventing lesion formation and removing these lipids.Hyperlipidemia is a disorder characterized by high lipid, cholesterol, and/or triglyceride levels. It is linked to atherosclerosis, the formation of hardened fatty plaques in blood vessels. These conditions occur as a result of dysfunctional mechanisms in lipid influx and efflux.
Phospholipids are natural lipids necessary for cell structure and function. Under certain inflammatory conditions, phospholipids like phosphatidic acid can be oxidized into lysophosphatidic acid (LPA), a toxic and potent growth promoter. When these oxidized lipids accumulate at levels beyond what is physiologically normal, they can promote systemic inflammation and contribute to plaque buildup. The working hypothesis is that LPA can induce atherosclerosis in LDL R-/- mice by contributing to systemic inflammation, a crucial step in the initiation and propagation of atherosclerosis. Our lab has produced an oral-mimetic peptide 6F that can act similarly to HDL by removing oxidized lipids from cells and reducing the risk for atherogenesis. The goal of this laboratory is to study and understand how oxidized lipids can lead to hyperlipidemia and atherosclerosis, and create novel treatments to them.
Victor would like to sincerely thank Dr. Mohamad Navab and Greg Hough for their dedication and mentorship in supporting his growth and curiosity as a researcher. He also wishes to thank Mr. O’Connell and URC-Sciences for the Oppenheimer Award and their tremendous support for future scientists and scholars. In the future, Victor plans to continue his research on lipids and cholesterol, and how they affect atherosclerosis and other cardiovascular diseases.
| Wakana Fujiwara
Mentor: Dr. April Pyle
Funding: Gottlieb Award
Project Title: Deriving Skeletal Muscle Progenitor Cells from Human Pluripotent Stem Cells by Manipulating Critical Pathways in Embryonic Myogenesis
Wakana Fujiwara is a third year student majoring in Biochemistry, with a minor in Biomedical Research. She has been conducting research in Dr. April Pyle’s laboratory under the guidance of Dr. Pyle and postdoctoral fellow Dr. Haibin Xi since August 2013. The Pyle lab is interested in understanding the potential of human pluripotent stem cells (hPSCs) in deriving skeletal muscle progenitor cells (SMPCs), which can be used to treat degenerative muscle diseases such as Duchenne Muscular Dystrophy (DMD).
DMD is an X-linked recessive disease due to mutations in dystrophin. Loss of dystrophin function causes muscle degeneration due to the progressive loss of endogenous muscle stem cells. One potential approach for treating DMD is to transplant genetically corrected SMPCs to replenish the exhausted muscle stem cell population in DMD patients. Wakana’s current project involves deriving SMPCs from hPSCs by following the developmental path of embryonic myogenesis. In the developing embryo, cells undergo multiple stages of differentiation under the influence of various embryonic patterning cues including paraxial mesoderm and somite/dermomyotome specification before becoming muscle satellite/progenitor cells. Derivation of paraxial mesoderm, an early step of embryonic myogenesis, can be induced by activation of the canonical wingless-type MMTV integration site family/ β-catenin (WNT/ β-catenin) signaling pathway. Wakana is working on improving the efficiency of SMPC derivation by inducing each stage of myogenesis through treatment of growth factors/small molecules that act as embryonic cues for skeletal myogenesis. Derivation of a robust SMPC population is critical for studying the engraftment potential in vitro and in vivo in animal models of DMD and provides the opportunity to generate novel regenerative approaches to treat patients with DMD.
Wakana would like to thank Drs. Pyle and Xi for their continued guidance and for the valuable opportunity to conduct research. She would also like to express her sincere gratitude to the Gottlieb family and the Undergraduate Research Scholars Program for their generous support.
| Sina Famenini
Mentor: Dr. Julian A. Martinez-Agosto
Funding: MacDowell Award
Title: The Role of Mutations in DICER-1 and Misregulation of Autophagy in Overgrowth and Cancer Phenotypes
Sina is a fourth year undergraduate pursuing a bachelor of science in Molecular, Cell, and Developmental Biology and minoring in Biomedical Research. Since January 2015, Sina has been working in Dr. Julian Martinez-Agosto’s laboratory. He is currently researching how mutations in specific genes may be implicated in overgrowth phenotypes in associated with DICER1 Syndrome.
MicroRNAs are short non-coding interfering RNA molecules that modulate the expression levels of specific proteins through binding to the complementary mRNA sequences. As a key player in miRNA production, Dicer1 is an RNase III enzyme responsible for cleaving double-stranded hairpin RNA molecules. Mutations in Dicer1 have been identified in patients with familial pleuropulmonary blastoma, cystic nephroma, medulloepithelioma, and Sertoli-Leydig cell tumor. Furthermore, whole exome sequencing has identified a recurrence of a missense mutation in the RNase IIIb domain of Dicer1 which corresponds to exon 25.
Dr. Martinez-Agosto and his colleagues at David Geffen School of Medicine have identified individual patients with mutations in Dicer1 and known autophagy genes. Autophagy is a tightly regulated intracellular catabolic process involving the lysosomal degradation of cytoplasmic organelles and proteins. Autophagy is essential for maintaining homeostasis through the elimination of damaged and old organelles and protein complexes. Inspired by these clinical findings, inspired Sina to investigate how microRNAs regulate autophagy and affect organismal growth. Furthermore, he would like to assess whether there is cross-talk among several different pathways to generate the ultimate phenotype.
Sina would like to thank Dr. Julian Martinez-Agosto and Dr. Steven Klein for their continued guidance and support in the laboratory. He would also like to sincerely thank the MacDowell Foundation for their generous contribution towards his research.
| Kathryn Dern
Mentor: Dr. Daniel T. Kamei
Funding: Ehrisman Award
Title: Surface Plasmon-Resonant Block Copolypeptide Vesicles for Photothermal Therapy and Triggered Drug Release
Kathryn Dern is a fourth year student in the Department of Bioengineering and has been conducting research in the lab of Dr. Daniel T. Kamei since March 2013. The focus of her research during this time has been the development of various drug delivery vehicles for the improved treatment of cancer. Currently, Kathryn is working on a project utilizing gold-coated block copolypeptide vesicles to improve the spatial and temporal control of cancer treatment through photothermal therapy and triggered drug release. After graduating from UCLA, she plans to pursue a medical degree.
Cancer is the second-leading cause of death in the United States. While current standard-of-care treatments such as chemotherapy effectively kill cancer cells, they cause many undesirable side effects due to nonspecific toxicity. There is therefore a need for a treatment that specifically targets cancer cells while leaving healthy tissues unharmed. The Kamei Lab has previously investigated the use of a novel vesicle system comprised of poly(L-lysine)60-block-poly(L-leucine)20 copolypeptides to target the delivery of an encapsulated chemotherapeutic agent to tumor tissues. We are now investigating the application of the vesicles for photothermal therapy, which utilizes energy from light to ablate cancer tissues. This often involves the use of gold nanostructures, which absorb light energy and convert it to heat due to the surface plasmon resonance of the gold electron cloud. Gold nanoshells, consisting of a spherical core coated in a thin gold shell, are of particular interest because they exhibit surface plasmon resonance in the near-infrared region of light, which has the ability to penetrate biological tissues to reach deep-seeded tumors. Our lab is interested in creating a gold nanoshell using the vesicles as the core to treat tumors through the combined effects of induced hyperthermia and triggered release of encapsulated chemotherapeutic drug. This year, Kathryn’s research focuses on optimizing the vesicle system and showing that it induces cell death in cancer cells in vitro under near-infrared irradiation.
Kathryn would like to thank Dr. Kamei and the members of the Kamei Lab for their continued guidance and support. She would also like to thank the Ehrisman Scholarship and the URC-Sciences for their generosity.
| Justin Rafael Ovalles De La Fuente
Mentor: Dr. David Brooks
Funding: MacDowell Award
Project Title: Identifying Interleukin-10 Producting Cells During Persistent Viral Infection
Justin Rafael De la Fuente is a fourth year Microbiology, Immunology, and Molecular Genetics student and has been a part of Dr. David Brooks’ lab since August 2013. The Brooks Lab studies the mechanisms that lead to immune dysfunction during persistent viral infection. Specifically, Justin’s work in the lab has focused on the upregulation of the immunoregulatory cytokine, Interleukin-10 (IL-10), during viral persistence.
Immunosuppression is a hallmark of several persistent viral infections such as HIV and Hepatitis C and is a major obstacle to the clearance of these pathogens. Previous studies by the Brooks lab have established IL-10 as a key mediator of this effect; high levels of the cytokine have been tied to exhaustion of the T cell functions necessary for effective anti-viral response. Justin’s current project involves mapping IL-10 production in key secondary lymphoid tissues through different phases of persistent infection. To accomplish this goal, the Lymphocytic Choriomeningitis Virus Clone 13 variant will be used to produce a persistent infection within IL-10 reporter mice, allowing production of the cytokine to be tracked by immunohistochemistry.
After graduating from UCLA in the upcoming spring, Justin plans to pursue a career in medicine. He would like to thank Dr. Brooks, Dr. Laura Snell, and Ivan Osokine of the Brooks Lab for their guidance and providing him with this unique learning experience. He would also like to thank the URSP and the MacDowell Scholarship for their generous support of his education.
| Kelly Darmawan
Pictured, left to right: Dr. Brigitte Gomperts, Kelly Darmawan, and Dr. Preethi Vijayaraj
Mentor: Dr. Brigitte Gomperts
Funding: Boyer Award
Project Title: Identifying Molecular Pathways of Idiopathic Pulmonary Fibrosis."
Kelly Darmawan is a third year Microbiology, Immunology, and Molecular Genetics major. She has been working in Dr. Brigitte Gomperts’ lab, in the department of Pediatrics, under Preethi Vijayaraj, PhD, since October 2012. Kelly is grateful for the opportunity to be involved in this lab as her project focuses on identifying the pathways that lead to the fatal lung disease, Idiopathic Pulmonary Fibrosis.
Idiopathic Pulmonary Fibrosis is a disease in which the lungs scar from unknown causes, such that the affected person is unable to exchange oxygen and carbon dioxide. Idiopathic Pulmonary Fibrosis is characterized by the formation of fibrotic foci, the build-up of extracellular matrix, and remodeling of the lung structure. Currently, there is no good model of the disease and therefore a poor understanding of its pathophysiology. Because of our lack of understanding of the mechanisms involved in the development and progression of IPF, there is no cure for the disease and currently the only available therapies may slow progression of the deterioration in lung function slightly, at best. Kelly is researching this disease process in patient samples in order to find a therapy for this terrible disease. She specifically aims to identify the mechanisms that result in the development of fibrotic foci and that are intrinsic to the mesenchymal compartment of the lung. She will be using a number of cell biology and molecular biology techniques in order to understand this process.
Kelly wants to thank the Gomperts Lab for all of their support, especially her mentor Preethi Vijayaraj and PI, Dr. Brigitte Gomperts. She also wants to thank the Boyer family for their generosity in funding her research.
| Joan Chou
Mentor: Dr. Ellen Carpenter
Funding: Honorary Award
Project Title: Loss of Reelin in the Tumor Environment Inhibits Metastasis of Primary Breast Cancer Cells
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.
| Allan Chong
Mentor: Dr. Ann Hirsch
Funding: Oppenheimer Award
Project Title: Optimizing motor-neuron differentiation of mouse embryonic stem cells
Allan Chong is a fourth-year Molecular, Cell, and Developmental Biology Major. He has been working under the guidance of faculty member Dr. Ann Hirsch since Summer 2013. Dr. Hirsch's lab focuses on the early stages of the symbiotic interaction between nitrogen-fixing Rhizobium bacteria and legumes such as alfalfa, pea, and soybean in order to determine why this interaction occurs exclusively with leguminous plants. The newest projects focus on beneficial plant-microbe interactions especially those related to “the plant’s guts”, i.e. the rhizosphere microbiome.
One such bacteria in question is Burkholderia tuberum STM 678, a beta-rhizobia that is predominantly found in the dry and acidic soils of South Africa.There is not much known about this specific species and how it interacts with its hosts and environment. By studying B. tuberum and several of its mutants, Allan hopes to establish a basic understanding of its symbiotic genes. The mutants used in his research have mutations in a subunit of pili, the formation of lipopolysaccharide, and the formation of exopolysaccharide. It should be noted that these are novel mutants for the B. tuberum species. Although the homologous mutations in other bacteria have been well studied, this is the first time that research has been done on these mutants.We would ultimately like to utilize its adaptability to living in tough conditions to help crop production in other parts of the world.
Allan is planning on graduating in the Spring of 2015 and hopes to either continue his academic studies by pursuing a graduate degree or establish himself in the science industry. He wants to deeply thank Dr. Hirsch for her mentorship, guidance, and support thus far. He also wants to thank the Oppenheimer fund for their generosity and support of undergraduate research.
| Joshua Chiou
Mentor: Dr. Hong Zhou
Funding: MacDowell Award
Project Title: Structural characterization of a Propionibacterium acnes phage
Joshua Chiou is a fourth year Microbiology, Immunology, and Molecular Genetics student who has been working under the guidance of Dr. Hong Zhou since the fall of 2013. Dr. Zhou’s laboratory focuses on structural biology and specializes in applications of high resolution cryo-electron microscopy. Joshua is currently researching the structure of a Propionibacterium acnes phage capsid protein at the atomic level.
P. acnes phages infect and lyse bacteria associated with the cosmetic skin disease acne. Phage therapy, the use of these phages to treat acne has recently emerged as an alternative treatment option to topical antibiotics. However, therapeutic use of these phages to counteract antibiotic-resistant strains of P. acnes bacteria still requires considerable research, particularly concerning structural stability and potential modification points.
Joshua’s current project seeks to elucidate the structure of a P. acnes phage for comparison to previously determined viral structures, and for identification of potential bioengineering applications. It is his hope that the results of his project will impact the development of phage-based therapeutics to treat acne.
Joshua would like to thank Dr. Hong Zhou for his continued guidance and support and acknowledge other members of the laboratory for their input on the project. He would also like to express his sincere gratitude for the MacDowell endowment.
| Sonal Chaudhari
Pictured, left to right: Dr. Ziwei Li, Sonal Chaudhari, Dr. Amander Clark
Mentor: Dr. Amander Clark
Funding: Wasserman Award
Project Title: Evaluating the Role of PRMT5 in Different States of Pluripotency
Sonal Chaudhari is a 3rd year Molecular, Cell, Developmental Biology major and Biomedical Research minor. She has been working in Dr. Amander Clark's laboratory since Summer 2013 alongside Dr. Ziwei Li. The Clark Lab explores the molecular regulation of stem cells and germline biology.
Ten percent of the U.S. population faces the health concern of infertility. The Clark Lab focuses on exploring the development of germ cells and the use of pluripotent stem cells (PSCs) as a source to derive functional germ cells in vitro. Understanding the basics of pluripotency guides future studies of regenerative medicine including differentiation of germ cells. Two pluripotent states of interest in my project are ground state and naïve pluripotency. Ground state PSCs are cultured with MAPK and GSK inhibitors and LIF. The naïve state PSCs are cultured in serum with LIF. Protein Arginine Methyltransferase 5 (PRMT5) is a key enzyme that is hypothesized to play a role in germ cell specification and maintenance. The two research studies – one from Tee et al. and other from our lab – show that the loss of PRMT5 have different phenotypes and thus PRMT5 shows different roles in pluripotency. Knockdown using shRNA of Prmt5 in serum ESCs shows down regulation of H2AR3sme2 (both nuclear and cytoplasmic), down regulation of pluripotent markers, and upregulation of somatic genes, resulting in change of morphology and loss of AP staining. However, preliminary data from our lab, using an inducible KO of Prmt5 through a lox-Cre-4OHT system, shows dramatic change of neither morphology nor reduced AP staining nor up-regulation of somatic genes. Instead, the phenotypes of reduced proliferation, increased cell death and a dramatic abnormal splicing of RNAs were discovered. The difference between these two studies could be either due to the different pluripotent states or the different tools used for the loss of Prmt5. Sonal's particular project aims to explore whether PRMT5 has different roles in pluripotency through connecting two studies and investigating their differences to ensure proper contribution to the scientific field of pluripotency about the role of PRMT5, a splicing regulator and transcriptional cofactor hypothesized to play a role in germ cell specification and maintenance. Both previous studies of Tee and Li have confirmed that PRMT5 is essential to regulate and maintain pluripotency; however, this project will be able to show whether or not the roles of PRMT5 are distinct in each unique pluripotent state.
Sonal would like to thank Dr. Clark and her direct mentor Dr. Ziwei Li for their ongoing support and invaluable mentorship, as well as for providing a friendly and welcoming educational environment to learn. Sonal also wants to extend her immense gratitude to the Wasserman Foundation for funding her research.
| Susan Chang
Mentor: Dr. Erika Nurmi
Funding: Wasserman Award
Project Title: Glutamatergic Biomarkers of Cognitive Behavior Therapy (CBT) Response in Pediatric Obsessive Compulsive Disorder (OCD)
Susan is a fourth-year biology major who hopes to pursue a career that combines both pharmacy and translational research. Toward this goal, Susan is conducting pharmacogenomics research under the guidance of Dr. Erika Nurmi in the Department of Psychiatry and Biobehavioral Sciences.
Susan’s current project focuses on improving treatment outcomes for obsessive-compulsive disorder (OCD). More than 40% of patients diagnosed with OCD respond inadequately to existing treatments, and response rate is even lower in those with comorbid disorders, family history, or adverse psychosocial factors. It has been shown, however, that brain glutamate levels measured by magnetic resonance spectroscopy predict outcomes with cognitive behavioral therapy. Susan is seeking to identify a genetic biomarker that can help explain these differential glutamate levels and can predict treatment response. 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.
| Andrea Chaikovsky
Mentor: Michael Teitell
Funding: Honorary Award
Project Title: Investigating the Role of Purine Biosynthesis in Human Pluripotent Stem Cell Maintenance and Differentiation
Andrea Chaikovsky is a senior majoring in Molecular, Cell, and Developmental Biology with a minor in Biomedical Research. Since January 2013, Andrea has been working in the laboratory of Dr. Michael Teitell in the Department of Pathology and Laboratory Medicine. Her current project seeks to understand how changes in stem cell metabolism interact with the process of differentiation.
Human pluripotent stem cells (hPSCs) rely heavily on glycolysis as their main energy source in order to support their rapid proliferation. This glycolytic metabolism allows for increased activity in the pathways that synthesize macromolecules needed to build new cells, including purine nucleotides. The altered metabolism of hPSCs is closely linked to differentiation, as the cell adopts a more oxidative metabolism as it differentiates. Andrea’s project thus aims to understand the role that purine biosynthesis plays in stem cell identity. She is investigating the molecular basis of upregulated purine biosynthesis in hPSCs, as well as the effects of purine biosynthesis manipulation on stem cell self-renewal and differentiation.
Andrea would like to thank Dr. Teitell and the members of the Teitell lab for their continuous support and guidance. After graduation, Andrea plans to pursue a Ph.D. in molecular and cell biology.
| Michael Basin
Mentor: Dr. Andrea Kasko
Funding: Honorary Award
My name is Michael Basin and I am a fourth year biochemistry major at UCLA. Since January 2013, I have been working as an undergraduate researcher in the laboratory of Dr. Andrea Kasko. My project has been focused on spatially and temporally controlling the degradation of hydrogels and drug release within them.
The objective of tissue engineering is to create functional tissues from biological and/or synthetic materials. In most cases bone healing can occur on its own after a simple trauma/fracture but in some instances such as bone cancer or severe trauma, natural bone restoration process is impaired. Tissue engineering addresses this issue by creating a way to repair and replace damaged tissue. The 14-amino acid peptide, osteogenic growth peptide (OGP), was isolated and linked to bone regeneration as well as having cell proliferation effects. The activity of OGP can be mimicked with just the last five amino acids in its sequence, OGP 10-14. Our interest is in the proliferation effects of the peptide. By conjugating OGP 10-14 to a light-sensitive linker that is incorporated into a degradable scaffold, we are able to control the release of the peptide using light. By regulating the release of this five amino acid peptide, we can effectively spatially and temporally control the exposure of OGP 10-14 to cells, and ultimately recreate damaged or lost tissues and bones.
I would like to thank Dr. Kasko and all the members for the Kasko lab for their never-ending support, guidance, and mentorship, as well as including me into the laboratory family.
| Maral Bakir
Mentor: Dr. Martin Cadeiras
Funding: Lau Award
Title: Development Of A Nomogram Of The Immune Response After Heart Transplantation
I am a fourth year student studying nursing at UCLA. I have been conducting research under Dr. Martin Cadeiras since February 2013, and I am grateful to be involved in this lab. I am graduating UCLA in Spring 2015, and I am interested in continuing my research after graduation.
The focus of my lab is on interactions between the cardiovascular system and the immune system using gene expression profiling. My research focuses on post-heart transplant patients and their clinical trajectory after heart transplantation. Rejection and infection are common complications after heart transplantation, and one of the biggest challenges that clinicians face is the management of patients’ immunosuppressant levels. My research is focused on the assessment of the immune monitoring strategies using novel molecular assays. My goal is to create a multivariable nomogram that best defines the individual immune response among groups of different rejection and infection risks over time. Ultimately, using this nomogram, immunossupression will be managed in a more informed way. In creation of the nomogram the following clinical variables have been used; Brain Natriuretic Peptide (BNP), Echocardiogram, and Angiogram which have been used to assess for changes in the allograft function, Allomap which has been created by Dr. Mario Deng, the PI of our lab to assess cellular rejection, Cylex which has been used to assess infection, and human leukocyte antigens which have been used for evaluation of antibody mediated rejection. The nomogram will serve as a framework of reference for health care providers and will allow clinicians to compare individual patient’s immune status to better manage their immunosuppressant levels to prevent any complications. Nomogram will also allow for future predictions to be made, and it will give clinicians the opportunity to make changes to the immunosuppression therapy before patients develop any complications. Ultimately, on the longer term, we will evaluate if making medical decisions using this strategy is linked to improved patient outcomes.
I want to thank Dr. Martin Cadeiras for his continuing support and mentorship as well as Mr. Lau and URSP for their generous support.
| Daniel Baghdasarian
Pictured, from left to right: Nicole Darling, Daniel Baghdasarian, Dr. Tatiana Segura.
Mentor: Dr. Tatiana Segura
Funding: Blad and MacDowell Awards
Title: Acrylated Hyaluronic Acid (HA-Ac) Biomimetic Scaffolds for Culturing Limbal Stem Cells: An Alternative for Clinical Transplantation
Daniel Baghdasarian is a fourth year majoring in Molecular, Cell, and Developmental Biology and double minoring in Biomedical Research and Asian Humanities. He has been conducting research under the guidance of Dr. Tatiana Segura Lab since December of 2013 and under the direct mentorship of Ph.D. candidates Giovanny Acosta and Nicole Darling. One of the main focuses of the Segura lab is to design and engineer hydrogel based biomaterials containing biological signals that can enhance the wound-healing rate of hard to treat wounds. Current projects focus on the introduction of gene, protein and peptide based bioactive signals into hydrogel scaffolds and the culture of adult stem cells inside these hydrogel materials.
Daniel is interested in engineering biomimetic platforms that can serve to preserve limbal stem cell pluripotency and promote proliferative expansions for extended culture periods. As stem cell fate can be influenced by bioactive signals in the extracellular matrix (ECM), engineering cell instructive biomaterials that mimic ECMs is of great value to the fields of tissue engineering and regenerative medicine. Hydrogels are networks of hydrophilic polymer chains that can be used as tissue culture systems that mimic the natural stem cell niche. Because hydrogels have mechanical properties similar to natural tissues and can be functionalized with bioactive signals, hydrogels are promising platforms to direct stem cell differentiation. Daniel aims to develop a hydrogel system, which can be spatially functionalized with bioactive signals via enzyme-assisted bioconjugation or conjugate addition reactions. It is hoped that such a hydrogel system will allow for the synthesis of complex biochemical patterns and gradients to emulate the in vivo microenvironment of the corneal epithelium for limbal stem cell expansions. Such a hydrogel system would have importance in the fields of tissue engineering and regenerative medicine, as it would present the opportunity to have a patient’s own cells grown and used for transplantation as opposed to the traditional clinical transplantation procedures involving donor/cadaver tissues.
Daniel hopes to pursue a medical degree after graduating from UCLA in Spring of 2015. He would like to thank the Blad family and the MacDowell award for their generous donation, Dr. Tatiana Segura for the opportunity to be a member of her lab, and his mentors Nikki and Gio for their continued guidance and support.