Student Profiles Archive - URSP 2012-2013
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.
| Ms. Jane Wang
In Photo from Left to Right: Ren Sun, Jane Wang, Jiaying Feng
Ms. Jane Wang
Mentor: REN SUN
Title: Murine Gammaherpesvirus 68 Open Reading Frames 40 and M1 Aid in Modulation of the Unfolded Protein Response
Jane Wang is a third-year student in the department of Molecular, Cell, and Developmental Biology. Under the guidance of graduate candidate Jiaying Feng and faculty mentor Dr. Ren Sun, Jane has been characterizing the Murine Gammaherpesvirus 68 Open Reading Frames 40 and M1 expression kinetics and their relation to viral modulation of the Unfolded Protein Response.
The Gammaherpesvirinae subfamily of Herpesviridae is known for its inclusion of the cancer-implicated Epstein-Barr virus (EBV) and Kaposi’s sarcoma-associated herpesvirus (KSHV). EBV and KSHV are characterized by their abilities to establish lifelong latent infection and evade host immune responses. A preliminary screen of the MHV-68 genome, a model for EBV and KSHV, identified the M1 and ORF40 genes to be strong regulators of the unfolded protein response (UPR) within the viral host. UPR, brought on by the onset of endoplasmic reticulum (ER) stress, activates in response to the accumulation of unfolded or misfolded proteins in the lumen of the host ER and aims to restore normal cell function by halting protein translation and increasing the production of protein chaperones. Because viruses exploit host cellular machinery, viral synthesis often leads to ER stress and consequentially triggers the UPR. Surprisingly, in vitro studies have concluded that ORF40 represses activation of UPR while M1 gene induces activation of the response. Jane seeks to determine the order of ORF40 and M1 expression kinetics in hopes of elucidating the mechanism by which these two genes elude host detection and promote viral replication.
Jane would like to thank Dr. Ren Sun, Jiaying Feng, and the members of the Sun lab for their continued guidance and the incredible opportunity to conduct undergraduate research. She would also like to thank the Gottlieb family and the Undergraduate Research Scholars Program for their support of her scientific endeavors. Upon graduation, she hopes to pursue a career in the medical and public health fields.
| Mr. David Vu
In Photo from Left to Right: Mirjam Schenk, David Vu, Robert Modlin
Mr. David Vu
Mentor: Robert Modlin
Title: Effect of IL-1beta on Macrophage Development and Function in Mycobacterial Infections
David Vu is a third year Neuroscience major at UCLA. David is in his second year working in Dr. Robert Modlin’s immunology lab, which uses leprosy as a model to study the mechanisms of host defense in humans. He has been working on the role of IL-1beta in the human immune response against the intracellular pathogen Mycobacterium leprae.
At a site of infection, monocytes are recruited from the blood and differentiate in situ into diverse macrophages and dendritic cell (DC) populations. The Modlin Lab has shown that innate immune signaling, such as Toll-like receptor 2/1 (TLR2/1) activation, induces the differentiation of monocytes into phenotypically and functionally diverse macrophages (CD209+) and DC (CD1b+) subsets. Their research also demonstrates that IL-1beta also induces rapid differentiation of monocytes into CD209+ macrophages and to a lower extent CD1b+ DC at a later time point. David is currently analyzing whether these macrophages have different functional capacities. As the IL-1beta induced macrophages express higher levels of Fc-receptors, markers of phagocytosis, and HLA-DR, David hopes to determine whether these cells will exert higher phagocytic activity and potentially better antigen-presenting functions than TLR2/1 induced macrophages.
David is thankful for his lab training and for the opportunity to learn from both Dr. Modlin, MD and visiting research assistant Mirjam Schenk, PhD. Currently, David's career research interests center around the improvement of effective therapeutic strategies against infectious disease.
| Ms. Mericien Venzon
Ms. Mericien Venzon
Mentor: Michael Alfaro
Title: Phylogenomic Study of Coral Reef Fish Faunas using ultra-conserved DNA elements (UCEs)
Mericien Venzon is a 3rd year Pre-Computational Systems and Biology major. After taking an introductory biology course with Dr. Michael Alfaro last fall, she discovered her interest and enthusiasm for evolutionary biology. She has been working in the lab of Dr. Alfaro in the department of Ecology and Evolutionary Biology since the spring quarter of her second year. Her current research project employs a new phylogenomic method that uses target enrichment and massively parallel sequencing of >1300 ultra-conserved DNA elements (UCEs) to investigate hypotheses regarding the evolutionary relationships and histories of coral reef fish faunas.
Coral reefs are home to over half of all the ocean’s fish species, yet the evolutionary history of these species remains as one of the most longstanding problems in vertebrate systematics. UCE’s represent a new set of genetic markers that more efficiently identify and isolate ideal regions of genomes for comparative analysis, better matching the capacity of next generation sequencing technologies. As the first application of UCEs to this group, Mericien aims to generate a more resolved phylogeny that will enable further investigations regarding the biogeographic history and tempo of diversifications of both reef and non-reef lineages. After sampling the 10 core reef associated fish families, Mericien’s long term goals include increasing the density of sampling within these groups as well as extending this method to 22 additional poorly studied reef clades.
Aside from phylogenomics, Mericien’s broader research interests include molecular evolution, disease ecology and evolution, and bioinformatics. After graduation, she plans to pursue an MD-PhD degree and ultimately hopes to use evolutionary medicine to develop new approaches to disease pathology and treatment. Mericien would like to thank Dr. Michael Alfaro for recognizing her potential, for his daily mentorship, the opportunity to learn in his lab, and above all, for introducing her to the endless possibilities in the world of evolution and computational biology. She would also like to extend her gratitude to Bernard Kim, her previous graduate student research mentor, her fellow members of the Alfaro lab, and her family for all their continued support. Finally, she would like to extend her gratitude to the URC Sciences and the Howard Hughes Medical Institute for providing opportunities in undergraduate research.
| Ms. Kimberly Tsui
Ms. Kimberly Tsui
Mentor: Stephen Zipursky
Title: Elucidating Role of CDC-42 in Layer Specificity
Kimberly Tsui is a third year Molecular, Cell, and Developmental Biology major and is pursuing a minor in biomedical research. She joined the Zipursky lab of the Department of Biological Chemistry Spring Quarter of her second year. Her research currently focuses on investigating how cytoskeleton regulation gives rise to layer specificity in the brain.
Brain function relies on precise networks of synaptic connections. The segregation of these connections into layers allows for the parallel processing of information, and is fundamental to the function of the Central Nervous System in vertebrates and invertebrates. However, the molecular mechanisms that underlie layer assembly are poorly understood. Preliminary work from the Zipursky lab indicates that the Rho-GTPase CDC-42, a regulator of the actin cytoskeleton, acts in a cell type specific manner to control layer specificity within the Drosophila visual system. Kimberly plans to investigate how CDC-42 regulates layer specificity. Understanding how layer specificity is achieved through the precise regulation of cytoskeleton will provide insight on the molecular mechanism of layer assembly in the brain.
Upon graduation, Kimberly plans to pursue a PhD program and continue research in the biomedical sciences. She would like to thank Dr. Larry Zipursky, her postdoctoral mentor, Matthew Pecott, graduate mentor, Yi Chen, and the entire Zipursky lab for their unfailing guidance and support. She would also like to thank the Wasserman Foundation for their generous funding support for her research.
| Ms. Janie Trinkkeller
Pictured: Janie Trinkeller with mentor Dr. David Glanzman
Ms. Jane Trinkkeller
Mentor: David Glanzman
Title: Murine Gammaherpesvirus 68 Open Reading Frames 40 and M1 Aid in Modulation of the Unfolded Protein Response
| Ms. Tam Tran
Ms. Tam Tran
Mentor: Thomas Vondriska
Title: Global Changes in Chromatin Structure and Localization during Cardiac Hypertrophy
Tam Tran (pictured, right) is a third-year undergraduate student majoring in neuroscience at UCLA. She has been conducting research in the laboratory of Dr. Thomas Vondriska (pictured, left) since September 2011. Her project, “Global Changes in Chromatin Structure and Localization during Cardiac Hypertrophy,” explores the relationship between cardiac hypertrophy and fetal gene re-expression, both of which are major components of heart disease.
It has been established that heart disease leads both to cardiac hypertrophy or cell enlargement, and to fetal gene re-expression, but what role hypertrophy itself has in inducing changes in gene expression is unknown. To investigate this, neonatal rat ventricular myocytes will be treated with hypertrophic agonists, after which overall changes in chromatin structure will be examined. This examination will be accomplished both through looking for certain histone post-translational modifications, each of which can be associated either with gene expression or repression, and through DNA digestions, which can show nucleosomal positioning and thus genes' accessibility to transcriptional machinery. By seeing if hypertrophic agonists alone can induce global changes in chromatin structure, the manner in which heart disease-induced hypertrophy is related to fetal gene re-expression can be better understood, which itself will be essential to comprehending how the heart adapts to or fights against disease.
| Ms. Diana Tran
In Photo from Left to Right: Douglas L. Black , Diana Tran
Ms. Diana Tran
Mentor: DOUGLAS L. BLACK
Title: Characterizing the Protein-protein Interactions of RBFox with hnRNP H and hnRNP M in Alternative Splicing
Diana Tran is a 4th year UCLA student majoring in Microbiology, Immunology and Molecular Genetics and minoring in Biomedical Research. She has been conducting research in Dr. Douglas Black¹s lab since the Spring quarter of her third year. The Black Lab studies the mechanisms of alternative splicing and its role in neuronal differentiation. Under the mentorship of Andrey Damianov (Ph.D.) she has been studying the effects protein-protein interactions of heterogeneous nuclear ribonucleoproteins (hnRNP) with proteins of the RNA-binding feminizing on X (RBFox) family, known to play a role in the regulating alternative splicing events, and have been implicated in a variety of neurological disorders including spinal cerebellar ataxia type II and autism spectrum disorders.
The RBFox family of proteins are involved in regulating splicing by binding to the sequence (U)GCAUG on pre-mRNA. The hexanucleotide sequence has been found in different species and is not limited to neurons. RBFox proteins act as splicing activators when bound downstream of a regulated exon or splicing repressors when bound
upstream or within an intron. The RBFox proteins were recently found in a large complex with other proteins, among which are the alternative splicing factors hnRNP M and hnRNP H. Diana has been working on determining the functional consequences of these protein-protein interactions upon exon inclusion or skipping. Understanding mechanisms behind Fox-mediated regulation may hopefully lead to a greater insight into the
splicing code that determines splicing products of a given gene in particular cell-types and microenvironments, as well as how their misfunction might lead to disease.
Diana plans on graduating in Spring 2013 and hopes to pursue a PhD. She would like to thank Douglas Black and Andrey Damianov for their incredible amount of patience and excellent guidance in the lab. She would also like to thank the MacDowell foundation for their considerate support.
| Ms. Lisa Ta
Ms. Lisa Ta
Mentor: Caius Radu
Title: Exploring the Role of Replication Stress Response in Cancer
Lisa Ta is a fourth-year undergraduate student majoring in Molecular, Cell and Developmental Biology at UCLA with a minor in Biomedical Research. She has been part of the Radu Lab since her first year. Under the guidance of her post-doctorate mentor, Dr. David Nathanson and her principle investigator, Dr. Caius Radu, she is currently working on exploring the role of replication stress response in cancer.
Many aggressive cancers upregulate nucleotide biosynthesis and possess proficient intra-S phase checkpoints. These features could be essential for enabling the high proliferative potential of malignancies with high degrees of genomic instability and mutability. Therefore addressing these characteristics may represent novel therapeutic targets. Previous studies have shown that various cancer cell types undergo replications stress and early S phase arrest when treated with thymidine (dT), which expands dTTP pools to levels that are inhibitory for de novo biosynthesis of dCTP. The Radu lab has shown that thymidine therapy combined with inhibition of deoxycytidine kinase (dCK), the rate-limiting enzyme in the salvage pathway, induce dCTP insufficiency followed by cell cycle arrest. Cell cycle arrest is attributed to the activation of the Replication Stress Response (RSR) pathway. She hypothesizes that RSR activation safeguards dCTP depleted cancer cells from accumulating additional DNA damage that is incompatible with cell survival. To test this hypothesis, we have explored the effects of inhibiting the RSR pathway, in particular the effector kinases Chk1 and Chk2, in dCTP depleted cancer cells. Data in multiple cancer cell types show increased apoptotic response and decreased viability, following RSR effector kinase inhibition in dCTP-depleted cells. She proposes that combining dCTP starvation with abrogation of intra-S checkpoint kinase activity may represent a new potential therapeutic option for rapidly growing cancers that are resistant to both conventional and targeted therapies.
Lisa plans to graduate in Spring 2012 and pursue her research and medical interests in graduate school. She would like to thank her enthusiastic mentor, Dr. David Nathanson for his guidance and mentorship, and for the entire Radu Lab for their support and patience for these past three years. Lastly, Lisa would like to thank the Wasserman family for their generous support.
| Ms. Lily Sung
In Photo from Left to Right: Lily Sung, Dr. Stephanie White, Zachary Burkett
Ms. Lily Lai-Ling Sung
Mentor: Stephanie White
Title: The Genes Involved in Zebra Finch Syntax Learning
Lily Sung is a fourth year biophysics major. She has been conducting research in Dr. Stephanie White’s lab since Fall 2010. Currently, she is working with graduate student Zachary Burkett to find the genes involved in syntax learning, using the zebra finch as a model for human vocal learning.
Like human speech, birdsong has syntax; while humans can create different sentences by rearranging words, songbirds can sing different motifs by rearranging syllables. By studying the genetic basis of how zebra finches learn song syntax, Lily hopes to gain insights into vocal learning and generalize this information to further understand human speech and language disorders.
Lily would like to thank Dr. White, Zachary Burkett, and the rest of the lab for their help, guidance, and continued support. She would also like to express her gratitude for the Ehrisman endowment.
| Mr. Amit Sumal
Mr. Amit Sumal
Mentor: Benhur Lee
Title: Examining the Differences in CD4 and CCR5 Usage Efficiency of Paired Maternal and Infant Human Immunodeficiency Virus Isolates
Amit Sumal is a 4th year Microbiology, Immunology, and Molecular Genetics major. With the help of his mentor, Kelechi Chikere (Ph.D.), he has performed research in Dr. Benhur Lee’s laboratory since his sophomore year. The Lee Lab investigates the viral envelopes of HIV and Nipah Virus with a focus on viral entry and cell surface receptor interactions.
Specifically, Amit’s research studies the perinatal transmission of HIV. HIV infects cells through the engagement of its envelope glycoprotein with CD4 and the coreceptor CCR5. Thus, a virus’s relative usage of the CD4 and CCR5 receptors during infection can elucidate its means of viral pathogenesis. Making use of a GGR Affinofile cell line that can simultaneously and independently induce CD4 and CCR5 at up to 48 different combinations, Amit will be able to able to quantitatively determine the relative efficiencies that maternal and infant HIV envelopes use CD4 and CCR5 during infection. Using this system, Amit hopes to provide insight on the perinatal transmission of HIV with respects to the means of viral pathogenesis of maternal and infant HIV envelopes, the selective pressures behind perinatal HIV transmission, the differences between transmitter/founder and chronic envelopes, and lastly, therapies and vaccines that prevent HIV entry.
In the future, Amit plans to graduate in the Spring of 2014 and subsequently, become a doctor specializing in infectious diseases. He would like to thank Kelechi for his guidance and assistance over the past year, as well as Dr. Benhur Lee for the unique opportunity to work in his laboratory. He would also like to thank the Wasserman family for their contribution and support.
| Ms. Jennifer Shieh
Ms. Jennifer Shieh
Mentor: Giovanni Coppola
Title: Mechanisms of Toxicity in the C9ORF72 Hexanucleotide Repeat Expansion in Frontotemporal Dementia
Jennifer Shieh is a fourth year Physiological Science and Neuroscience major and has been working in the Coppola lab since September 2011. Under the guidance of Giovanni Coppola and Mochtar Pribadi, she is studying the effects of the C9ORF72 hexanucleotide repeat expansion, currently the most commonly identified cause of familial ALS and Frontotemporal Dementia (FTD).
The long-term goal of the Coppola Lab is to advance our understanding of the genetic architecture and construction of neuropsychiatric diseases such as Friedrich’s ataxia, dementia, Alzheimer’s and Schizophrenia. The lab uses a combination of genetic, genomic, and bioinformatics approaches to sequences genes from patients with neurodegenerative conditions at the single-gene and whole-genome level and record this information in large-scale datasets.
FTD is a degenerative brain disease resulting in gradual changes in behavior, personality and other executive functions. For those under 60, FTD is the most common cause of dementia. Recent studies have reported a hexanucleotide repeat expansion in gene C9ORF72 of up to 10,000 base pairs and this novel gene repeat is suggested to be the most common cause of familial FTD. Jennifer’s work focuses on determining the pathogenic mechanisms of this gene repeat in order to develop treatment for patients with dementia by using lymphoblast cell lines from patients and expression studies to see whether the responses to stressors (e.g. inflammatory agents) is different in patients’ cells compared to normal cells. By using Western blot analysis, Jennifer has been able to study the C9ORF72 protein in lymphoblast cell lines. Using Southern Blot analysis, she has also been quantifying the length of the repeat in FTD patients versus healthy individuals in order to determine the minimal repeat size needed to cause FTD. This would be helpful for correlating the repeat length with disease presentation and useful in the clinical setting to screen for patients with FTD.
Jennifer plans to graduate in Spring 2013 and pursue a career in medicine. Jennifer would like to thank Dr. Coppola and her fellow researchers for their mentorship and guidance as well as the Boyer family for their endowment and the Undergraduate Research Center for their support.
| Ms. Vivian Shi
In Photo from Left to Right: Vivian Shi, Dr. Ren Sun
Ms. Vivian Shi
Mentor: Ren Sun
Title: Antiviral Activity of IFITM1 and 3
Vivian’s project aims to uncover the specific anti-HIV function of a family of interferon stimulated genes (ISGs) called interferon induced transmembrane proteins (IFITMs). ISGs are a collection of hundreds of proteins whose transcription is activated as part of the cell's innate immune response upon viral challenge. ISGs are key proteins in fighting off viral infections. HIV is a known pathogen that evades the innate immune response. Therefore the goals of Vivian’s project are to first uncover the specific mechanisms of IFITM antiviral HIV activity, and secondly, how HIV deactivates and/or evades this function during natural infection. The research program in Vivian’s lab has long aimed to uncover the interplay between viral pathogens and the innate immune response.
| Ms. Sara Sanadiki
Ms. Sara Sanadiki
Mentor: Donald Kohn
Funding: Van Trees
Title: Enhancing Zinc-Finger Nuclease Mediated Gene Correction by Small Molecule Inhibitors of DNA-PKcs
Sara Sanadiki is a fourth year transfer student majoring in Microbiology, Immunology and Molecular Genetics. Sara has been with Dr. Kohn’s lab since January 2012 and has been working with Ph.D Candidate Alok Joglekar. The Kohn lab focuses on using gene therapy to correct particular diseases involving blood cells, with an interest in stem cells.
Sara is currently working with a fairly new mode of gene therapy using Zinc Finger Nucleases (ZFNs). These nucleases create a site specific double stranded break in the genome recognized by the zinc finger motifs and catalyzed by the Fok1 domain. Once the double stranded break is introduced into the cell, it can be repaired in one of two ways: homologous recombination (HR) or non-homologous end joining (NHEJ). The occurrence of HR in the cell allows for the introduction of a corrected donor template that can be used to repair the double stranded break. This allows for potential site specific gene modification of a particular disease causing gene. Nu7441 is a DNA-PKcs inhibitor, a key enzyme required for the NHEJ pathway. Treating the cells with an NHEJ inhibitor is hypothesized to cause an increase in HR, leading to an increase in gene modification.
Sara plans to graduate in June 2013 and persue a PhD. to become a professor. She would like to thank Dr. Kohn for giving her such a wonderful opportunity to be a part of the Kohn lab and also express her great appreciation for her graduate student mentor Alok for his guidance. Last but not least, Sara would like to thank the Van Trees family for their generous contribution and Ms. Knapp for her support.
| Mr. Robert Rovner
In Photo from Left to Right: Dr. Jerome Zack, Robert Rovner, Dr. Dimitrios Vatakis
Mr. Robert Rovner
Mentor: Jerome Zack
Title: Quantitation of 2-LTR Circular HIV DNA Species
Robert Rovner is a fourth year Molecular, Cellular, and Developmental Biology major. Robert started his research in the Zack laboratory during April of 2012 and is currently researching the development of a spectratyping assay that quantifies HIV 2-LTR circle diversity.
Dr. Zack’s laboratory studies the molecular mechanisms underlying HIV infection and pathogenesis. An in depth knowledge of HIV infection is believed to ultimately inform rational approaches to the development of therapeutics for the treatment of AIDS. Recent studies have utilized levels of episomal viral cDNA such as 2-LTR circles as a measure of viral replication both in the presence and absence of anti-retroviral drugs. However, where the 2-LTR circle population has been recently reported to be quite diverse, current protocols are not adequate to quantitate and characterize episomal HIV cDNA. To this end, Robert’s research project in the Zack laboratory has involved the use of spectratyping to more effectively quantitate 2-LTR circle diversity. Ultimately, it is hoped that this assay will become more widely used to measure the true sequence state of the HIV provirus for therapeutic and diagnostic applications in a clinical setting.
Robert plans to graduate in the Spring of 2013, and will be pursuing a PhD/MBA. Robert would like to thank Dr. Zack and Dr. Vatakis for their tireless support and effort in making him the researcher he is today. Additionally, Robert would also like to thank Mr. O’Connell for his generous support and funding.
| Mr. Steve Roberts
Mr. Stephen Roberts
Mentor: Alvaro Sagasti
Title: The Role of Collagen XVIIIa1 in Somatosensory Axon Guidance
Steve Roberts is currently a fourth year Molecular, Cell and Developmental Biology major conducting research in the Sagasti laboratory since April 2012. His current research focuses on elucidating the molecular attractants essential for peripheral axon guidance to the skin.
Early in zebrafish development, the peripheral axons of somatosensory neurons innervate the skin between two epithelial layers. The correct guidance of these axons to the skin relies on interactions between several receptor protein tyrosine phosphatases (PTPs) and the presence of heparan sulfate proteoglycan (HSPG) ligands. Collagen XVIII is modified with heparan sulfate disaccharide chains and is the focus of Steve’s current research. He will use strong morpholinos that block collagen XVIII expression to determine whether somatosensory innervation is defective. In addition, he will co-inject weak collagen XVIII morpholinos with other morpholinos against components of the axon guidance pathway to elicit a synergistic defect. Utilizing fish selectively expressing GFP in somatosensory neurons and RFP in the skin, he will use confocal microscopy to assess axon innervation defects. Finally, Steve will be involved in the production and screening of TALEN collagen XVIII mutants to determine how sensory neuron innervation is affected in collagen XVIII ablation. Steve believes this research may have important implications for Knobloch syndrome, an autosomal recessive disorder caused by mutations in the collagen XVIII gene (COL18A1).
After graduation, Steve will take a year off from academics, marry his beautiful fiancé, and engage in the growing biotechnology industry before pursuing a medical degree. He would like to extend his sincere appreciation to all of the inspirational members of the Sagasti laboratory and for the gracious support on behalf of the Oppenheimer Foundation.
| Mr. Ramin Rajaii
In Photo from Left to Right: Ramin Rajaii, Dr. Tom Carmichael
Mr. Ramin Rajaii
Mentor: STANLEY CARMICHAEL
Title: BDA Quantification of Neuronal Proliferation following Hydrogel and BDNF Treatment Post-Ischemia
Ramin Rajaii is a 4th year Neuroscience major and Spanish minor. He has conducted research since his first year, and has been investigating neuronal proliferation following ischemia with Dr. Tom Carmichael since February of 2011. The Carmichael lab focuses upon the implantation of a bioengineered hydrogel with other compounds as a novel treatment for a photothrombotic (PT) mouse model of ischemia.
Ramin is investigating the efficacy of the bio-polymer hydrogel infused with Brain-Derived Neurotrophic Factor (BDNF), a peptide released by cells that encourages nearby neuronal growth following injury to the central nervous system (CNS). He uses the hydrogel as a vehicle for BDNF injection into the peri-infarct, a region adjacent to the stroke site and otherwise unsuitable for cellular growth. He currently leads an independent project that involves biotinylated dextran amine (BDA) as an axonal tracer to quantify recovery following hydrogel/BDNF injection. By labeling axonal sprouting near the injury and peripheral areas, BDA will allow a direct, quantitative comparison of the density of new neuronal networks in treatment groups to that of control and Sham. If effective, this approach will possess immense potential for clinical translation and stroke recovery in humans.
Upon graduating from UCLA, Ramin plans to pursue a 1-Year Master’s program in either biotechnology, health sciences or health care management. He will be applying to MD programs in June of 2013, with the ultimate career goal of obtaining a dual MD/MBA to effect change in healthcare management and reform. Ramin would like to express his gratitude to Dr. Carmichael and Hyun Chun for their unwavering support, as well as all other members of the laboratory. In addition, he thanks the Carter Family and the staff members of the URC - Sciences for generously aiding undergraduate researchers.
| Ms. Stacey Pun
Ms. Stacey Pun
Mentor: Felix Schweizer
Title: Plasticity in the Vestibular System Studied Under Microgravity Conditions
Stacey Pun is a 4th year Biochemistry major. She has been conducting research since her freshman year in Dr. Felix Schweizer’s laboratory with the help of Patricia M. Quinones. The Schweizer lab studies the molecular mechanisms of neurotransmitter release, its diversity between different secretory systems, and its regulation by activity and by intra- and intercellular signaling events, especially with regards to short-term plasticity.
About one third of the US population of 40 years or older is affected by a dysfunction of the vestibular system, which contributes to debilitating falls, especially in the elderly. The utricle of the vestibular system is sensitive to linear acceleration and uses hair cells to sense and transmit this information to the brain. Previous work in our lab showed that exposure to microgravity as experienced during space-travel elicits significant alterations in the number of synapses per hair cell in the rodent utricle. These findings indicate that there is synaptic plasticity in the vestibular system, which has important implications for sensory physiology and for translational research. In order to further investigate this plasticity in an earth based system, Stacey cultures rat utricles in a clinostat, which simulates microgravity. Stacey analyzes the effect of microgravity on these tissues using immunohistochemical characterization and hopes to eventually elucidate the molecular mechanisms of this synaptic plasticity.
Stacey plans to graduate in the Spring of 2013 and attempt to get an MD/PhD. She would like to thank Yuki for her many years of guidance and Dr. Schweizer for the opportunity to learn in his lab. Finally, Stacey would like to thank the Wasserman family for their generous support.
| Ms. Chalisa Prarasri
Ms. Chalisa Prarasri
Mentor: Bennett Novitch
Title: Investigating the Role of Sprouty Proteins in Motor Neuron Axon Branching and Pathfinding
Chalisa Prarasri is a third year Neuroscience major who is also pursuing a Biomedical Research Minor and a Mathematics minor. She began working in the Bennett Novitch Laboratory at the start of her second year under the guidance of post-doctoral fellow Caroline Pearson. Her research is currently centered on understanding the role of the Sprouty family of proteins in motor neuron development and axon branching.
Growth factor signaling pathways are commonly transduced through receptor tyrosine kinases (RTKs) and are responsible for controlling a broad spectrum of developmental processes, including proliferation, differentiation, migration, and survival. In vertebrates, Sprouty 1,2,3, and 4 constitute a family of intracellular inhibitors of RTK signaling. Knockout of each of the Sprouty proteins has been shown to result in phenotypes associated with excess growth factor signaling -- most notably, increased axonal branching in a variety of tissues. Few studies, however, have investigated the role of Sprouty proteins in motor neurons. So far, Chalisa has characterized the expression of Sprouty 1,2, and 4 in mouse and chick spinal cords during the period of motor neuron development. She has created a misexpression construct designed to conditionally overexpress Sprouty genes in motor neurons, and is currently working on analyzing the data gathered from electroporating the construct in vivo into chick spinal cords. She hopes this research will further our understanding of the intracellular interpretation of environmental signals in developing motor neurons.
After graduation, Chalisa intends to attend graduate school to pursue a Ph. D. in neuroscience. She would like to thank all of the members of the Novitch lab for their guidance, along with the Gottlieb foundation for their generosity.
| Mr. Aanand Patel
In Photo from Left to Right: Dr. Herman Lelie, Aanand Patel, and Dr. Joan Valentine
Mr. Aanand Patel
Mentor: Joan Valentine
Title: Conformational Antibodies against Cu/Zn Superoxide Dismutase Mutants Linked to Amyotrophic Lateral Sclerosis
Aanand Patel is a 4th year Molecular, Cell, and Developmental Biology major and Biomedical Research minor. He has been working in Dr. Joan Valentine’s lab in the Department of Chemistry and Biochemistry since September 2010, under the guidance of Dr. Herman Lelie and Dr. Madhuri Chattopadhyay.
Amyotrophic Lateral Sclerosis (ALS), also known as Lou-Gehrig’s disease, is a fatal neurodegenerative disease characterized by a degradation of motor neurons. Mutations to the antioxidant enzyme copper/zinc superoxide dismutase (SOD1) account for approximately 20% of familial ALS cases. These mutants acquire toxicity through a gain-of-function, in which misfolding and aggregation are thought to play major roles.
Conformation-restricted antibodies have been developed as an important tool to probe for SOD1 misfolding. These antibodies only recognize a subset of SOD1 that adopts a specific conformation. Importantly, positive staining with the conformational antibody C4F6 in sporadic ALS provides some of the first indications that wild-type SOD1 can also misfold and potentially contribute to disease. However, the lack of information regarding what exactly these antibodies recognize limits the conclusions that can be drawn using conformational antibodies. In particular, SOD1’s complex maturation pathway, which includes metal acquisition, disulfide bond formation, and dimerization, significantly impacts its conformation, and therefore may influence recognition by conformational antibodies. Aanand’s project addresses these limitations by characterizing the affinity of these conformational antibodies for wild-type and mutant SOD1 in a variety of states. Through this work, these antibodies can become a more powerful tool and provide more specific information about the state of SOD1 in vivo.
Aanand plans to graduate in the spring of 2013 and pursue an MD/PhD degree in preparation for a career as a physician-scientist. He would like to thank the members of the Valentine lab, the Biomedical Research Minor, and URC – Sciences for their continued mentorship, support, and encouragement.
| Mr. Victor Oshita
Mr. Victor Oshita
Mentor: Tatiana Segura
Title: Recombinant Production of Cross-Linkable Platelet-Derived Growth Factor
Victor Oshita is a fourth-year Biomolecular Engineering Option Chemical Engineering major. In the summer of 2011 he began working in Dr. Tatiana Segura’s laboratory with then-Ph.D. candidate Dr. Anandika Dhaliwal and he is now working with Dr. Allyson Soon.
The Segura Laboratory researches tissue engineering, specifically angiogenesis and blood vessel formation in the target tissue, which is currently a major setback in successful tissue engineering. Growth factors signal the proliferation of the cells that form blood vessels, but freely floating growth factors are quickly lost to diffusion and can no longer signal cells to form the vessels. Victor is currently working with Dr. Allyson Soon using E. coli to produce a specific growth factor platelet-derived growth factor (PDGF) with an additional peptide sequence containing glutamine that can be linked to another peptide sequence containing lysine. Crosslinking occurs via Factor XIIIa, which is involved in the formation of blood clots. The goal of this research is to link these growth factors to peptide sequences in hydrogels containing cells so that the growth factors can remain present throughout the duration of treatment.
Victor is planning to graduate in the spring of 2013 and attend graduate school next year to obtain a Ph.D. He would like to thank Tatiana for her mentorship and the opportunity to begin research and Allyson and Anandika for their guidance. Victor would also like to thank Sparks and Mr. Jones for their generous funding and support of his research.
| Ms. Jessica Ong
In Photo from Left to Right: Jessica Ong, Dr. Karen Lyons
Ms. Jessica Ong
Mentor: Karen Lyons
Title: The Overlapping yet Discrete Functions of the Secreted Proteins CCN1 and CCN2 during Long Bone Development
Jessica Ong is a fourth year Molecular, Cell, and Developmental Biology Major and Biomedical Research Minor currently working in Dr. Karen Lyons’ laboratory. Her research focuses on a family of proteins, the CCN proteins, within the context of skeletal development.
Her current project focuses on the first two family members of the CCN proteins (CCN1-6) called CCN1 and CCN2 during bone development. In bone development, bone is made from a cartilaginous mold called the growth plate. Proper signaling is essential to growth plate development. Both CCN1 and CCN2 play vital roles in angiogenesis and cartilage differentiation in vitro. However, although CCN2 has been shown to be essential for proper cartilage formation in vivo, less is known about the role of CCN1. In order to examine whether CCN1 and CCN2 have overlapping functions during bone development, they are using cartilage-specific depletions of CCN1 and/or CCN2 from mouse growth plates use Cre/LoxP technology. They hypothesize that if CCN1 and CCN2 do have overlapping functions during bone development, the double mutant will have a more severe mutant phenotype. Such studies are pertinent to understand proper growth factor signaling pathways in the cartilaginous growth plate. In the future she hopes to examine how the other CCNs (CCN3-6) are affected.
Jessica is pursuing a career as a translational researcher, and aspires to become a medical scientist. She appreciates the generous support from URSP, Dr. Karen Lyons, and the Lyons Lab members.
| Ms. Jessica Oh
Ms. Jennifer Oh
Mentor: Rachelle Crosbie-Watson
Title: Sarcospan Overexpression in Mice Lacking Dystrophin and Utrophin
Jennifer Oh is a fourth year undergraduate student majoring in Biology. She began research during her first year in Dr. Crosbie-Watson’s laboratory under the guidance of Jamie Marshall (Ph.D.). The Crosbie-Watson laboratory studies the effects of the protein sarcospan in Duchenne muscular dystrophy.
Duchenne muscular dystrophy is an X-linked disease associated with progressive muscle wasting, resulting from mutations in the dystrophin gene. Sarcospan is an integral membrane protein of the dystrophin glycoprotein complex and utrophin glycoprotein complex. Along with the alpha7beta1 integrin complex, these three complexes function to stabilize the sarcolemma from contraction-induced injury. The Crosbie-Watson laboratory hypothesizes that the utrophin glycoprotein complex and integrins are necessary for the improvement of pathology with sarcospan overexpression. Jennifer will be analyzing mice overexpressing sarcospan that are deficient in dystrophin and utrophin, a homolog of dystrophin. She will perform various histological staining, immunofluorescence assays, and quantifications to determine the level of dystrophy occurring in these mice. She will explore whether the overexpression of sarcospan will rescue this mouse model, ameliorating pathology.
Jennifer would like to thank Dr. Crosbie-Watson for graciously accepting her as an undergraduate researcher, as well as Jamie Marshall for all the guidance and support over the years. She would like to thank UCLA’s Undergraduate Research Center-Sciences for giving her this opportunity. Lastly, she would like to thank Ms. Boyer Ballas and Mr. Boyer for their generous support through the Albert C. Boyer Scholarship.
| Mr. Brandon Nguyen
Mr. Brandon Nguyen
Mentor: Ali Salim
Title: Prevention of Toxic Neuronal Calcium Influx After Traumatic Injury Through Adrenergic Receptor Inhibition
Brandon Nguyen is a third-year Physiological Science major and Classics minor conducting research in the lab of Ali Salim in the Department of Surgery. He currently focuses on how neurons and astrocytes respond to after traumatic injury and hopes to show that inhibition of adrenergic receptors will prevent the toxic neuronal calcium influx that initiates apoptosis in stretch injured cells. After graduation Brandon hopes to pursue an M.D./Ph.D and ultimately a career as a pediatric trauma surgeon
Traumatic brain injury initiates a prolonged cascade of neurotoxic biochemical changes in the brain, yet there are no treatments available to address this post injury dysregulation. Injured brain cells exhibit a characteristic increase of cytoxolic calcium derived from extracellular and intracellular stores. By using a stretch-plate model, Brandon hopes to show that inhibition of beta adrenergic receptors results in reduced calcium enzyme activity, as shown by a reduction i reduction in cleaved spectrin fragments. Cells treated with beta adrenergic receptor inhibitors should also demonstrate a reduced fraction of apoptotic cells, with an increased fraction of surviving cells. Understanding the in vitro effects of adrenergic inhibitors on injured cells will inform the design of future studies and suggest a means of measuring the efficacy of drug delivery and activity in vivo.
Brandon would like to thank Dr. Ali Salim, Dr. Eric Ley, the Undergraduate Research Scholars Porgram, and Mrs. Gottlieb for their generous support and continual guidance.
| Mr. Matthew Murkidjanian
Mr. Matthew Murkidjanian
Mentor: Harley Kornblum
Title: Proteasome Activity and Drug Resistance of Glioblastoma Stem Cells
Matthew Murkidjanian is a third year Neuroscience major. He has been working in the laboratory of Dr. Kornblum since Fall 2011 under the guidance of Dr. Jack Mottahedeh. The Kornblum lab is interested in understanding the fundamental biology of cells within brain tumors that have many characteristics of neural stem cells, so called “brain tumor stem cells”.
Glioblastoma (GBM) is amongst the most lethal of all cancers. GBM consist of a heterogeneous population of tumor cells amongst which a tumor initiating and treatment resistant subpopulation, here termed GBM stem cells (GSC), have been identified as primary therapeutic targets. Matthew’s research focuses on the effect of drug treatments on this population of cells, and a potential mechanism by which these cells might resist treatment. The results might indicate a potential mechanism by which tumorgenic cells resist treatment. Therefore, future research might lead to better treatments of glioblastomas which focuses on alterations of this mechanism of resistance. The hope is that future treatments will be effective and lead to a increased survival rate in patients.
Matthew would like to thank the Undergraduate Research Scholars Program, Dr. Kornblum and all the members of the Kornblum Lab, and the Wasserman family for their generous funding.
| Ms. Katherin Misogas
Ms. Katherine Misogas
Mentor: Barbara Knowlton
Title: Effects of Neutral vs. Negative Emotional Stimuli on Inhibition Response
Katherine Misogas is a third year undergraduate student majoring in Psychobiology at UCLA. Under the guidance of Dr. Barbara Knowlton and Tara Patterson, Katherine has been conducting behavioral neuroscience research for the past year. Her research focuses on investigating how negative emotion and early-life adversity affect human cognition and neurological pathways using behavioral and neuroimaging techniques.
Early life stressors (ELS) experienced before the age of eighteen have been shown to negatively affect physical and emotional health in adulthood. Experiences such as parental separation, family members with mental disorders, criminal activity, and physical, emotional, and verbal abuse cause emotional distress and have long-term effects on a person’s life; these stressors have all been linked with adverse behaviors and physiological illnesses. These harmful life consequences could potentially arise from enduring behaviors instilled through habitual learning processes. Habitual responses are effects of depending on the dorsolateral striatum to learn behaviors instead of using goal-directed responses as mediated by the medial prefrontal cortex, medial orbital cortex, and dorsomedial striatum. Since people using their habitual learning system are more focused on performing the action than thinking about the outcome, a telltale sign of habit learning is continuing to perform a devalued action. By analyzing differences in ELS participant responses with non-ELS participant responses during the extinction phase of an instrumental reward learning task, Katherine investigates the contributions of declarative memory systems and habit learning memory systems to a human response to repeated but devalued stimuli.
As an expansion of investigating the effects of negative experiences on long-term behavior, Katherine is involved in research regarding the effect of negative emotions on immediate response inhibition. Previous work has shown that exposure to negative emotional stimuli prior to performing a stop-signal task increases the delay between hearing a stop signal and successfully inhibiting one’s reaction. Collected fMRI data reveals reduced neural activity in the right inferior frontal gyrus, middle frontal gyrus, and medial superior frontal gyrus—three brain regions were previously found to participate in successful stop actions. The reduced activity suggests that negative emotional cues interfere with neurological pathways involved in typical inhibition response to the signal. Katherine is investigating other neural networks and pathways involved in the stopping response and if and how negative emotion stimuli effect their role in successful inhibition. Furthermore, interesting results concerning the role of the brain’s emotional center, the amygdala, suggest additional brain regions become involved with the inhibition pathway when added layers of processing are involved, such as the added component of negative emotion.
Katherine would like to thank Dr. Barbara Knowlton for her guidance and the opportunity to be a part of her behavioral neuroscience research team and to all the post-doctoral and graduate students of the Knowlton laboratory who continuously offer support and encouragement. Katherine would like to extend a very special thank you to the ongoing and dedicated mentorship of Tara Patterson, with whom Katherine works closely with on her research. Finally, Katherine is sincerely grateful and appreciative to the Gottlieb family for their generous contribution to undergraduate research and for their personal recognition and support of her research.
| Mr. Arek Melkonian
Mr. Arek Melkonian
Mentor: Louis Bouchard
Title: Heterogeneous Catalysis Utilizing Metal-Organic Frameworks
Arek Melkonian studies physical and inorganic chemistry, in addition to physics, mathematics, materials science, and computation. He has been working with Professor Louis Bouchard since September of 2011 in the field of chemical catalysis. The catalysis group of the Bouchard lab employs various techniques from physical chemistry to study the catalytic properties and applications of metal-organic frameworks (“MOFs”) in collaboration with the Yaghi group at UC Berkeley.
The synthesis of MOFs has proliferated in the field of inorganic chemistry in the last 15 years. Invented by Professor Yaghi, MOFs are crystalline compounds that are composed of metal clusters and organic molecules that connect the clusters together. Thanks to their chemical robustness, MOFs show potential for use in heterogeneous catalysis, in which the catalyst and reaction mixture are in different physical phases. The porosity of the frameworks enables them to act as hosts to catalytically-active coordination complexes such as nickel cross-coupling catalysts. These complexes are usually homogeneous catalysts—they are dissolved in the reaction mixture, and their separation after a reaction requires a work up. By eliminating this need, in addition to being relatively inexpensive to make, MOFs could be viable and inexpensive catalysts in the chemical industry.
| Mr. Harding Luan
Mr. Harding Luan
Mentor: Ting-Ting Wu
Title: Characterizing the Interaction of Murine gamma-herpesvirus 68 Open Reading Frame 34 and RNA Polymerase II
Harding Luan is a third-year student majoring in Molecular, Cell, and Developmental Biology with a minor in Biomedical Research. He began his undergraduate research with Dr. Ting-Ting Wu in the Molecular and Medical Pharmacology department in the middle of his first year. His research focuses on characterizing the interaction of Murine gamma-herpesvirus 68 Open Reading Frame 34 and RNA Polymerase II.
The gamma subfamily of herpesviruses, including Kaposi’s sarcoma-associated herpesvirus and Epstein-Barr virus, is known for its ability to establish life-long infections that cause a variety of diseases, including a number of cancers, in immunocompromised patients. In immune compromised patients, gamma-herpesviruses will undergo occasional lytic replication. Through studying a mouse gamma-herpesvirus, Murine gamma-herpesvirus 68 (MHV-68), the lytic replication of gamma-herpesviruses has been well characterized. Gene expression occurs in a regulated cascade divided into immediate early, early, and late genes. The regulation of late genes, mostly coding for structural proteins of the virus, is poorly understood. Through co-immunoprecipitation and mass spectrometry screen of five viral proteins identified to be essential for late gene expression, it was identified that MHV-68 Open Reading Frame 34 strongly interacted with RNA Polymerase II, the critical enzyme in transcribing DNA to RNA. Harding seeks to confirm this observation, characterize the interaction of the two proteins, and identify how this interaction affects viral replication.
Harding would like to thank Dr. Ting-Ting Wu, Dr. Ren Sun, and all the members of the Sun Lab for their ongoing mentorship and for creating an environment that is both fun and highly educational. Harding would also like to extend his gratitude to the Gottlieb Foundation for their generous support of his research and to URC – sciences for promoting scientific discovery in the undergraduate community.
| Mr. Jerry Lou
In Photo from Left to Right: Jerry Lou and Dr. Albert Lai
Mr. Jerry Lou
Mentor: Albert Lai
Title: Evaluation of 2-HG in Proliferation Inhibition and Role in IDH1 Mutant GBM Phenotype
Jerry Lou is a third year Neuroscience major pursuing minors in Biomedical Research and Public Health. He has been working in Dr. Lai’s lab since Fall of his second year where he has contributed to studies concerned with improving therapies for malignant gliomas, a type of brain cancer.
Gliomas are a form of brain tumor that affects over 20,000 new patients in the United States each year and the survival rate for gliomas, especially glioblastomas (GBM), are severely low. Patients with GBM have 50% probability to live about 12 months after their diagnosis. Recently arginine to histidine substitutions at codon 132 of the isocitrate dehydrogenase 1 gene (IDH1MUT) were discovered in up to 65% of GBM. The IDH1MUT is a gain and loss-of-function alteration that leads to increased intracellular 2-hydroxyglutarate (2-HG), decreased NADPH, and decreased α-ketoglutarate (α-KG). Recent evidence indicates that patients with IDH1MUT GBMs have better prognosis and longer median survival than those with IDH1WT tumors. IDH1MUT also sensitizes GBM cells to undergo apoptosis after radiation. Jerry aims to investigate the effects of increased intracellular 2-HG on cancer cell proliferation, migration, and radiation sensitivity in vitro and animal median survival in vivo. Possibly, 2-HG has potential as a future cancer treatment for GBM brain cancer.
Jerry extremely thankful for the support of Dr. Albert Lai, Sichen his post-doctoral mentor, and all the members of the lab. Their guidance and daily encouragement have been instrumental to her motivation within this field. Jerry would also like to sincerely thank the Gottlieb Foundation for their generous funding, recognition, and support of his research.
| Ms. Connie Liu
Ms. Connie Liu
Mentor: Lily Wu
Title: CSF1R Mediated Inhibition of Alternatively Activated Macrophages to Augment Androgen Receptor Blockade Therapy
Connie is a 4th year Molecular, Cell Developmental Biology major. She has been conducting research since her sophomore year in Dr. Lily Wu’s laboratory with help from Jemima Escamilla (Ph.D. Candidate). The Wu lab studies the mechanisms of prostate cancer progression and uses a pharmacological means to target the cancer.
The traditional means of treating prostate cancer (PCa) is through androgen receptor (AR) blockade therapy. However, treatment with anti-androgen drugs such as MDV3100 (a second generation prostate cancer drug), acquires resistance 186 days after treatment. (Tran et. al., Science 2010) Various reports show that androgen deprivation results in increased inflammatory response in PCa and suggest a potential role of inflammatory cells, such as macrophages, in the acquisition of castration-resistant prostate cancer (CRPC).
Connie is working on that inhibiting of recruitment of tumor associated macrophages (TAMs) with a CSF-1R inhibitor, GW2580; in combination with AR blockade therapy to hopefully attain synergistic results in prostate cancer treatment.
Connie is graduating in the spring of 2013 and is attempting to pursue a PhD in biomedical sciences. She would like to thank Jemima for all of her guidance and teaching and Lily for the opportunities to learn in the lab. She would also like to thank the Hilton Foundation for their generous support.
| Ms. Michelle Lissner
In Photo from Left to Right: Dr. Stephen Smale, Michelle Lissner
Ms. Michelle Lissner
Mentor: Stephen Smale
Title: Age-Dependent Deficiencies in Immune Signaling Pathways
Michelle Lissner is a fourth-year Microbiology, Immunology, and Molecular Genetics major and Biomedical Research minor. She has been conducting research in the laboratory of Dr. Stephen Smale since January 2011. Under the guidance of Dr. Smale and Ann-Jay Tong, she has been examining age-dependent differences in immune signaling that lead to neonatal and geriatric susceptibility to intracellular infection.
Deficiencies in the immune systems of newborns, pregnant women, and the elderly lead to susceptibility to a variety of intracellular pathogens. Part of this increased vulnerability in newborns is caused by an impaired ability to mount T helper (Th) 1 immune responses. Efficient responses from adult Th1 cells lead to cell-mediated immunity though the activation of phagocytes and the release of cytokines. Data suggest that the defect in newborn Th1 response is due to the reduced activation of genes dependent on interferon regulatory factor 3 (IRF3).
Michelle is using RNA-seq to characterize the transcriptional program of newborn, adult, and elderly peripheral blood monocytes in response to infection by either LPS, a component of Gram-negative bacterial cell walls, or Listeria monocytogenes, an age-dependent intracellular pathogen. This project will both identify subsets of genes that are differentially regulated throughout the life cycle as well as provide new insights into the causes of age-dependent susceptibility to infection.
| Mr. Justin Lin
Mr. Justin Lin
Mentor: Genhong Cheng
Deciphering Mechanisms of Type I Interferon Regulation of Antibacterial Response Genes
Justin is a fourth year Microbiology, Immunology, and Molecular Genetics major pursuing a career in pharmacy. He has been working in Dr. Cheng’s lab since spring quarter 2011, and under the guidance of Dr. Cheng as well as graduate student Shankar Iyer, Justin has been researching the role of Type 1 Interferon in the inhibition of antibacterial response.
Viral infections such as influenza cause the human body to generate type I Interferon (IFN). These IFNs function as signaling molecules that alert the immune system of a viral infection and activates genes that are involved in antiviral defense. IFN signaling, however, has recently been shown to inhibit a set of genes that are activated in mounting antibacterial defense, and thus, confer susceptibility to secondary bacterial infections. Activation of type I IFN signaling activates two transcription factors, STAT1/STAT2, which are involved in anti-viral gene expression. The pathway by which they activate these genes has been well studied, and these proteins have been mapped out. However, STAT1/STAT2 also play a role in inhibiting antibacterial response genes. The mechanism by which they inhibit antibacterial responses has not been well studied, and the goal of his research will be to elucidate the mechanism by which they inhibit antibacterial genes.
Justin is grateful to Dr. Cheng, as well as the Cheng lab, for the valuable help and mentorship they have provided. He would also like to thank the Wasserman family for their support, as well as the Undergraduate Research Center in making this partnership possible.
| Mr. Jeffrey Lin
In Photo from Left to Right: Jeffrey Lin, Dr. Linda Liau, Sylvia Odesa, Horacio Soto
Mr. Jeffrey Lin
Mentor: Linda Liau
Title: Hybrid Immuno-Gene Therapy for Malignant Gliomas
Jeffrey Lin is currently a 4th year undergraduate at UCLA majoring in Molecular, Cell, and Developmental Biology. He has been working in Dr. Linda Liau’s lab in the Department of Neurosurgery since the summer of his senior year in high school.
Of all primary brain tumors that affect humans, glioblastoma multiforme (GBM) is the most common and the most aggressive. Prognosis for patients with GBM is poor and GBM malignancy may come from a lack of immunogenic surface antigens. This trait allows GBM to evade the host immune surveillance mechanisms and could render it resistant to certain potential immunotherapies. However, dendritic cell (DC) vaccine therapy has shown promise in treating GBM, but the therapy needs to be refined so the effects can be broadened and can benefit more patients. Replication-competent retrovirus (RCR) vectors can help enhance the immune response. When the RCR vector is engineered to contain a pro-drug activator and delivered into tumor tissue, administration of the pro-drug systemically results in selective destruction of the transduced tumor cells. Also, tumor cells that have been successfully transduced with an RCR vector also likely express an array of viral antigens. Jeffrey’s research will focus on characterizing the anti-viral and anti-tumor immune responses induced by peripheral dendritic cell vaccination in a syngeneic mouse model of RCR-mediated suicide gene therapy. In the future, the combination of RCR-DC therapy has the possibility of translating into a new clinical therapy.
Jeffrey would like to thank Dr. Liau for her patience and guidance. He would also like to thank all the members of the Liau lab for their help and support throughout his time at the lab.
| Mr. Billy Lin
In Photo from Left to Right: Dr. Johann Schredelseker, Billy Lin, Dr. Jau-Nian Chen
Mr. Billy Lin
Mentor: JAU-NIAN CHEN
Title: Hybrid Immuno-Gene Therapy for Malignant Gliomas
Billy is a 4th year undergraduate double-majoring in Physiological Sciences and Philosophy. He has been a part of Dr. Jau-Nian Chen’s lab since fall of 2010.
Billy’s current research deals with uncovering the physiological roles of the outer mitochondrial Voltage-Dependent Anion Channel 2 (VDAC2) in zebrafish, specifically focusing on the heart. His previous work investigated whether the mitochondria plays a role in regulating calcium levels and cardiac contraction via VDAC2. Now, Billy is generating VDAC2-null models using morpholino antisense oligonucleotides for knockdown and zinc-finger nucleases for knock-out generation to study VDAC2 and its physiological function in the heart.
Billy is currently genotyping candidate VDAC2 ZFN mutants. When he has found a null-mutation, he will outcross the mutant to lines with GFP-labeled hearts, GFP-labeled cell membranes, or GFP-labeled calcium sensors to better study the VDAC2-null phenotype.
| Mr. Joon Ha Lee
Mr. Joon Ha Lee
Mentor: Elissa Hallem
Title: Olfactory Plasticity in Entomopathogenic Nematodes
Joon Ha Lee is a third year Neuroscience major and has been working in Dr. Elissa Hallem's lab in the Microbiology, Immunology, and Molecular Genetics department since June 2011. The lab is interested in the neurobiology of olfaction in nematodes, and Joon's project focuses on the effect of environmental conditions on the olfactory preference of entomopathogenic nematodes.
Olfaction is a critical component of host-seeking behavior in parasitic nematodes to locate potential hosts, but little is known about how these parasites respond to olfactory cues and the neurons mediating olfactory response. Entomopathogenic nematodes (EPNs), used as model systems for studying host-seeking behavior, are closely related to human-parasitic nematodes such as Strongyloides stercoralis, and have much potential in agriculture as biocontrol agents for insect pests and disease vectors. Joon's work in the Hallem lab so far has shown that although the infective juveniles of EPNs are developmentally arrested prior to infection of a host, their response to odorants appears to be plastic and influenced by environmental cues such as temperature and time. Joon aims to characterize the environmental condition-dependent changes in EPN olfactory behavior. Furthermore, he plans to identify neurons responsible for olfactory response, and ultimately identify chemosensory genes that are differentially expressed at different cultivation temperatures. This work will provide insight into how environmental conditions can influence behavior and improve EPNs' efficacy as biocontrol agents.
After graduation, Joon plans to pursue a Ph.D. program. He would like to thank Dr. Hallem and everyone in the Hallem lab for their guidance and support. He would also like to thank the Howard Hughes Medical Institute and the Holmes O. and Margaret R. Miller Scholarship for their generous funding and support of his research.
| Ms. Debora Lee
In Photo from Left to Right: Julie Miller, Debora Lee, Stephanie White
Ms. Debora Lee
Mentor: Stephanie White
The Relationship Between Dopamine Levels and Vocal Motor Deficits in Zebra Finch after Injection of 6-hydroxydopamine (6-OHDA) into area X
Debora Lee is a third year biology major and has been conducting research in Dr. Stephanie White’s Lab since the beginning of her first year. Under the guidance of Dr. Julie Miller, Debora is working on using the zebra finch Parkinson’s model to better understand the relationship between dopamine levels and speech deficits seen in Parkinson’s patients.
Parkinson’s disease (PD) is a movement disorder caused by the loss of dopaminergic neurons in the midbrain. Though PD is typically associated with abnormal limb movement, most patients show speech deficits which may precede non-vocal motor deficits (Harel et al. Brain Cogn, 2004). This raises the prospect of using vocal deficits in zebra finches as early biomarkers for PD. Our laboratory has shown that the neurotoxin 6-hydroxydopamine (6-OHDA) depletes dopamine input to area X, the song-specific region of the basal ganglia in zebra finches, resulting in changes in song that resemble human PD vocal deficits. Debora will further examine how these vocal deficits are linked to the amount of dopamine loss in area X and the midbrain. Results from this project will provide insight into the link between dopamine depletion and vocal behavior in the zebra finch Parkinson’s model as well as a better understanding of the relationship between dopamine levels and speech deficits in PD patients.
Debora would like to thank Dr. White for the opportunity to conduct research as well as Dr. Miller and George Hafzalla for their mentorship and continued support. She would also like to express her gratitude to the Hilton Foundation for their generosity in funding her research.
| Mr. Brian Lee
Mr. Brian Lee
Mentor: Daniel T Kamei
Title: Targeted Delivery of Chemotherapeutics Using Novel Block Copolypeptide Vesicles
Brian Lee is a 4th year bioengineering student. He has performed research in Daniel T. Kamei‘s lab under the guidance of Dr. Kamei and graduate student Mike Choe since his sophomore year. The Kamei Lab focuses on designing drug delivery vehicles for the treatment of cancer as well as developing diagnostic tools.
Cancer is the 2nd leading cause of death in the United States. One type of cancer treatment is chemotherapy, the use of drugs to kill cancer cells. However, many drugs used for the treatment of cancer cannot distinguish healthy cells from cancer cells, which give rise to undesirable side effects such as vomiting and hair loss. The Kamei Lab, in collaboration with the Deming Lab, has studied novel poly(L-glutamate)60-poly(L-leucine)20 block copolypeptide vesicles as drug delivery vehicles that may overcome the nonspecific side effects. Brian will focus on investigating different approaches for loading doxorbucin (DOX), a common chemotherapeutic, into the vesicles while preventing the vesicles from being disrupted or aggregated, since both of these outcomes will limit the ability of the vesicles to deliver the drug. Once DOX is efficiently encapsulated in the vesicles, to get selective targeting to cancer cells, these nanoparticles will be decorated with transferrin, a protein that binds to its receptor that is overexpressed on cancer cells relative to normal cells. The goal of this project is to develop this nanoparticle that will be efficient at killing cancer cells while not harming normal cells.
Brian is planning to attend medical school after graduating in Spring 2013. Aside from research, he is an active member of the Biomedical Engineering Society since entering UCLA. He would like to thank the entire Kamei Lab for its continued guidance and support. Finally, he would like to thank the Lau family for their generous funding.
| Mr. David Le
In Photo from Left to Right: Dr. Amy Rowat, David Le
Mr. David Le
Mentor: Amy Rowat
Title: Mechanical Properties of the Arabidopsis thaliana Nucleus
David Le is a 4th year Microbiology, Immunology, and Molecular Genetics major. He has been working in the Rowat Lab since November 2011. Currently, he is working to characterize the mechanical properties of the nucleus in Arabidopsis thaliana.
In the mammalian cell nucleus, lamin proteins form a mesh structure underneath the inner nuclear membrane and are essential for the mechanical stability of the nucleus. Plant cells lack the genes encoding lamins; therefore, how they maintain nuclear mechanical stability remains a question. One possibility is that other proteins fulfill a similar structural role. Previous research revealed a family of nuclear-localizing proteins in Arabidopsis called LINC. Mutations in LINC proteins have been shown to affect nuclear morphology, but little else is known about their role in the mechanical stability of the nucleus.
David aims to investigate the contribution of LINC proteins to nuclear structure by characterizing the mechanical properties of the nucleus in wild type and LINC mutant Arabidopsis plants. To do this, he will subject plant cells to sorbitol solutions of varying osmolarities and measure the forces exerted on the nucleus by the vacuole. In addition, he will mechanically deform nuclei with microfluidic devices and image the resulting deformations using fluorescent labels. By seeking to understand the role of LINC proteins, this research will help illuminate key differences between plant and animal cell physiology.
David would like to thank Dr. Rowat for her invaluable guidance and assistance, and the rest of the Rowat Lab for providing a welcoming and supportive research environment. He would also like to thank the Boyer Foundation for its generous support.
| Mr. Robert Lamm
Mr. Robert Lamm
Mentor: Daniel Kamei
Title: Targeting Chemotherapeutics for Prostate Cancer Using the A11 Minibody
Bob Lamm is a fourth year bioengineering major at UCLA. He currently works in the laboratory of Dr. Daniel T. Kamei in the department of bioengineering, where he has been working since April of 2011. After graduating from UCLA, Bob plans on pursuing a PhD in bioengineering and subsequently receiving postdoctoral training in preparation to lead a lab in academia.
Current chemotherapeutic treatments for prostate cancer can be improved; despite clinical success, these treatments exhibit toxic side effects due to lack of specificity, where the drugs kill both normal and cancerous cells. There are two main strategies to decrease these off-target side effects, encapsulation and targeting. One goal of the Kamei Lab, and that of Bob’s research, is to improve cancer therapy by engineering drug delivery systems that utilize these two strategies to minimize toxic side effects.
With encapsulation, normal cells in the body are protected from the cytotoxic properties of the drug. Another benefit of encapsulation is that it provides nonspecific targeting through the enhanced permeability and retention effect.
Specifically, Bob’s project involves encapsulating a commonly used chemotherapeutic, doxorubicin, in PLGA nanoparticles and targeting them with the novel targeting ligand, A11 minibody. Prostate cancer cells overexpress the prostate stem cell antigen (PSCA) throughout all stages of cancer. The lab of Dr. Anna Wu at UCLA developed the A11 minibody, a shortened form of an antibody. A11 shows a very high binding affinity to the PSCA and has been successfully investigated as an imaging agent for prostate cancer, but has never been used as a drug-targeting agent.
Bob’s research involves the first characterization of A11-targeted drug delivery vehicles.
| Ms. Cindy La
Ms. Cindy La
Mentor: Christina Charles-Schoeman
Title: Animal Model of Atherosclerosis and Rheumatoid Arthritis
Cindy La is a fourth-year student majoring in Human Biology and Society and minoring in Biomedical Research at UCLA. Since June 2010, she has been interested in the interdisciplinary fields of Rheumatoid Arthritis and atherosclerosis and has performed research in the Molecular and Medical Pharmacology Department.
The overall focus of the laboratory is to study the role of pro-inflammatory HDL and associated proteins in the development of atherosclerosis. Studies have shown that atherosclerosis significantly increases risk of cardiovascular disease in patients with rheumatoid arthritis (RA). Cindy’s research project aims to develop an animal model of RA and atherosclerosis to characterize the disease mechanisms leading to increased atherosclerosis. The triggering event for the development of fatty streaks and atherosclerosis is the accumulation and retention of oxidized LDL within the sub-endothelial layer of the arterial wall. This causes the endothelium to express adhesion molecules, which in turn recruit more monocytes and macrophages leading to vessel wall injury. Previous studies have shown that genetic differences in atherosclerotic susceptibility in mice are due to variations in inflammatory responses of endothelial cells to oxidized lipids. To study these correlations, Cindy proposes to develop an animal model of atherosclerotic background (apoE-null) that will be subjected to a serum injection gathered from a K/BxN mice breed with RA background. This work will allow the study of mechanisms leading to increased atherosclerosis in patients with RA.
Cindy is grateful for the support and mentorship of Dr. Christina Charles and Dr. Srinivasa Reddy and other members in the lab. Their guidance has fostered her curiosity and they have been integral in enriching her undergraduate experience and interest. Furthermore, she would also like to thank the Boyer and the Undergraduate Research Center foundation for their generosity and assistance.
| Ms. Meghana Kumar
Ms. Meghana Kumar
Mentor: Tatiana Segura
Title: The Effects of Clustered Versus Soluble Vascular Endothelial Growth Factors (VEGFs) on Proliferation and Migration of Human Umbilical Vein Endothelial (HUVEC) Cells
Meghana is a third year undergraduate majoring in Chemical and Biomolecular Engineering with a Biomolecular emphasis. She has been working in Segura Laboratories since winter 2012 with graduate student and mentor, Shiva Gojgini, and is currently researching the promotion of angiogenesis using clustered vascular endothelial growth factors.
Angiogenesis is the growth and development of blood vessels from pre-existing vasculature. Angiogenesis is essential for development and survival, and is especially important in tissue re-growth and wound healing. The ability to inhibit or induce migration, proliferation and differentiation of endothelial cells would be a significant step in wound healing following diseases such as diabetes or stroke. VEGF regulates angiogenesis and initiates a phenotypic switch in endothelial cells to tip cells, which is necessary for the formation of branching vasculature and consequent wound healing. Meghana will be covalently binding VEGF to heparin to allow for the phosphorylation of VEGF receptors. It is expected that VEGF clusters will more effectively increase levels of VEGF receptor-2 and phenotypic switch from endothelial cells to tip cells than soluble VEGF. Consequent downstream signaling will result in controlled angiogenesis; specifically, controlled migration, proliferation, and differentiation of endothelial cells. Meghana will test this increase in VEGF activity by quantifying cell migration and proliferation.
Meghana would like to thank the Wasserman Family for their generous contribution towards her research. She is looking forward to sharing her findings with the Wasserman Family. She would also like to express gratitude for her mentor, Shiva Gojgini, for her help and training in the laboratory, and Dr. Tatiana Segura, for her continued support and guidance. Meghana has currently been accepted as a summer intern at a chemical engineering company, and hopes to continue pursuing a career in industry after graduation while working towards a Masters in chemical engineering.
| Ms. Justine Ko
Ms. Justine Ko
Mentor: Samuel French
Title: Chemokine SDF-1 and Chemokine Receptor CXCR4 Axis for Improving liver Regeneration:
A Tissue Culture Based Model
Justine Ko is a 3rd year Physiological Sciences major who is also pursuing a minor in Spanish. She has been conducting research in the lab of Dr. Samuel W. French’s collaborator, Dr. Vaithi Arumugaswami (Cedars-Sinai Medical Center) since her freshman year. Dr. French and Dr. Arumugaswami have been focused on understanding the factors involved in liver cell engraftment and liver regeneration. Justine’s project focuses on a chemokine SDF-1 and its role in chemoattracting stem cells to damaged liver tissue. After college, Justine hopes to pursue an M.D./Ph.D and ultimately a career as a physician.
Viral hepatitis can lead to chronic liver injury as characterized by scarring (cirrhosis) and loss of liver function. While liver is the second most commonly transplanted organ, there is a shortage of liver donors. Recent advances in the generation of patient specific induced pluripotent stem cells provide cellular therapeutic options for liver regeneration. The major challenge is to identify the donor cell and host factors critical for the successful engraftment of the human liver progenitor cells to regenerate the damaged liver. A mouse model lacking a liver enzyme fumaryloacetoacetate dehydrogenase (Fah) has been reported for engraftment of human liver cells. Deficiency of Fah enzyme leads to buildup of hepatotoxic tyrosine metabolites, which allows the positive selection of implanted Fah+ human liver cells.
A chemokine SDF-1 (also called CXCL12) has been shown to be up-regulated in partially hepatectomy liver tissue, which plays an important role in liver regeneration by chemoattracting stem cells to damaged liver tissue. Justine will study the role of SDF-1 as a specific ligand for a chemokine receptor CXCR4 to induce the migration of target cells. Justine hypothesizes that exogenously produced SDF-1 can be used for attracting the CXCR4 expressing progenitor cells to the damaged tissue. Justine will focus on the construction and characterization of an adenovirus vector expressing the SDF-1 gene as well as the functional verification of SDF-1 using CXCR4 expressing target cell migration.
Justine would like to thank both Dr. French and Dr. Arumugaswami for their patience, academic mentorship, as well as inspiration. She would also like to thank the Arumugaswami lab for their support.
| Mr. Jason Kerr
Mr. Jason Kerr
Mentor: Andrea Kasko
Title: Developing Photodegradable Drug Delivery Molecules that Diffuse Therapeutic Agents through a Hydrogel
Jason Kerr is a third year biochemistry major at UCLA working in the bioengineering department under Professor Andrea M. Kasko. His interests in research started during the summer of sophomore year to delve into the world of tissue engineering and biomaterials. Currently, Jason is developing photodegradable drug delivery molecules that diffuse therapeutic agents through a hydrogel.
Hydrogels are water-swollen, polymer networks that provide physical and chemical support during tissue growth. To encourage this growth, hydrogels tether different therapeutic agents into their own scaffold to be released, but current methods of release have some limitations. Therapeutics can be physically encased within a hydrogel and released based on their diffusion coefficients. However, this approach does not allow sustained release of small to moderately sized therapeutics resulting in a bolus release. Furthermore, current methods of release in therapeutics are controlled by the surrounding environment, either by hydrolysis or enzymolysis, and the rate of release cannot be changed post-fabrication.
To overcome these limitations, therapeutics can also be covalently tethered to the scaffolding network through degradable linkers; specifically photodegradable linkers. The Kasko lab has designed these photodegradable macromers that release therapeutic agents by shining light. The group has developed a computational model that allows them to predict concentrations that can be released from a hydrogel.
To further understand the interaction of Kasko group’s photodegradable macromers with proteins, Jason will calculate the amount of exchange that a photodegradable macromer undergoes. Different proteins and hydrogel lengths can sterically hinder the exchange site. Understanding this interaction will allow the Kasko lab to have a better model of the exchange and how proteins can be utilized as a therapeutic agent.
Jason plans to pursue graduate school in biomedical engineering for a doctorate degree. Afterwards, he intends to continue the advancement of tissue engineering in either an academic or industrial setting. Jason would like to express his deepest gratitude to the Gottlieb endowment for their generous donation.
| Mr. Kevin Junus
Mr. Kevin Junus
Mentor: Yi Sun
Title: The Expression and Mechanisms of microRNAs in Epigenetic Regulation in Neural Progenitor Cells
Kevin Junus is a fourth-year undergraduate Pyschobiology major at UCLA. He has been a part of Dr. Yi Sun’s lab since the Fall of 2011. The Sun lab investigates the how gene regulation controls the cell lineage determination and differentiation in central nervous system (CNS). Her lab has published several important findings in regards of how epigenetic regulation such as DNA methylation, histone modifications, and small non-coding RNA, affects development and lineage switch in the CNS.
Kevin is now working on the project in understanding how microRNA expression affects the histone modification and/or DNA methylation in neural progenitor cells (NPCs). microRNAs are short sequences of RNA processed by specialized enzymes and can regulate the expression of target genes by three different pathways. MicroRNAs can bind to target mRNA and signal degradation, bind to the target mRNA and prevent protein synthesis, or can change the chromatin modifications by blocking or recruiting the chromatin modifiers. In plants, microRNAs have been shown to recruit DNA methylase and induce DNA methylation to silence gene expression. Previously, Dr. Sun’s group showed DNA methylation can also induce gene activation depending on the methylation site relative to the promoter regions. Although, it hasn’t been shown in mammals, DNA methylation can be controlled through microRNAs, and the mechanism of other small non-coding RNAs (piwi-interacting RNAs) suggest the existence of such regulation pathways. Through previous analysis, students in the Sun lab found the choices of cell lineage for postnatal NPCs can be altered in absence of de novo DNA methylase, DNMT3a. In addition, the removal of Dicer (the key protein to generate mature microRNAs) in conditional Dicer KO cells in adult neural progenitor zone also shows the changes of NPC behavior. Kevin hopes to gain a better understanding of this type of gene regulation through the study of NPCs by comparing genome-wide DNA methylation and RNA sequencing in wild-type vs. Dicer KO NPCs. His participation is focused on bioinformatics analyses.
Upon graduating from UCLA, Kevin plans to attend medical school and pursue further research in the field of neurology. He would like to thank Dr. Sun for giving him the wonderful opportunity to partake in research as an undergraduate and also everyone in the Sun lab for their continual support. Kevin would also like to express his gratitude to the Carter family and the URSP program.
| Mr. James Jung
Mr. James Jung
Mentor: Jerome Zack
Title: The Effect of Cocaine on HIV Infection in Quiescent CD4+ T Cells
James Jung is a fourth year undergraduate under the major of Microbiology, Immunology and Molecular Genetics. He has been conducting research in Dr. Jerome Zack’s lab since the January of 2012, being closely supervised by Dr. Dimitrios Vatakis. Research in the Zack lab focuses on the pathogenic processes of the Human Immunodeficiency Virus-1 infection and the development of therapies to confront infection.
While cocaine is commonly known for its effects on the central nervous system, recently a growing interest has been directed towards its implications on immune system dysfunction. Moreover, further investigations have also begun to link HIV susceptibility to cocaine, demonstrating a significantly increased viral load and decreased CD4+ T cell count when compared to non-cocaine exposure. To better understand its effect on HIV progression, our lab is investigating how it is affecting quiescent CD4+ T cells, the greatest potential target of HIV, but nonetheless strongly resistant to infection while in the quiescent (resting) state. Ultimately, the overall purpose of this research is to better elucidate how drugs of abuse affect HIV infection and how such knowledge can lead to more effective antiretroviral therapies for substance abusers.
Upon graduating from UCLA, James hopes to pursue graduate school to receive a PhD and further study viral pathogenesis in relation to the human immune system. He would like to thank Dr. Zack and Dr. Vatakis for their guidance and support. He would also like to thank the Lau family for their generous financial support.
| Ms. Somya Jalan
Ms. Somya Jalan
Mentor: Kenneth Bradley
Title: Determining the Role of COMMD5 in the Regulation of Cholesterol Homeostasis in Mammalian Cells Altering Sensitivity to CDCs
Somya Jalan is a fourth year undergraduate student, majoring in Physiological Sciences at UCLA. Her work began in Dr. Bradley’s M.I.M.G. lab, with research on the gram positive cholesterol dependent cytolysin (CDC), Anthrolysin O. The Bradley lab identified a gene, COMMD5, which modulates the sensitivity of the mammalian cell to CDCs. They created a Chinese Hamster Ovary (CHO-P3) cell line that represses the expression of COMMD5 in the absence of doxycycline, resulting in decreased levels of cholesterol in the plasma membrane and resistance to ALO. Somya studies the mechanism by which the COMMD5 gene alters cholesterol levels and thus affects mammalian cell sensitivity to intoxication by cholesterol dependent cytolysins. Her research plan involves determining which cholesterol pathway, efflux, biosynthesis, or uptake is regulated by COMMD5.
CDCs play a vital role in causing successful host infection and disease. They are a highly conserved group of virulence factors, expressed by 20 different human pathogens. Thus knowledge about factors affecting intoxication can contribute greatly to pathogenesis and clinical signs caused by various strains including ALO, which kills cells of the immune system, degrades the barrier in epithelial cells, and also causes lysosomal degradation. Determining the role of cholesterol in CDC intoxication also provides integral information about physiological and cellular functions such as inflammation, steroid biosynthesis, and membrane structure. Insight into the mechanism by which CHO-P3 cells maintain cholesterol levels could provide immeasurable tools for studying biophysical membrane properties such as membrane repair and biogenesis.
Somya truly appreciates the support of Dr. Bradley and the hardworking members of her lab. She is grateful for their encouragement and help, which has allowed her to be successful in the progression of her project. She hopes her research will help her attain her ultimate goal of becoming a medical professional. Finally, she would like to thank the Wasserman family for their support and generosity.
| Mr. Sinan Jabori
On the right, Dr. Brian DeRubertis
On the left side, Dr. Juan Jimenez
Back right, Dr. Peter Lawrence
Back left, Dr. David Rigberg
Mr. Sinan Jabori
Mentor: Brian G. DeRubertis
Funding: Van Trees
Title: MRA Assessment of the Aortic Arch: Relationship between Arch Anatomy and Age
Sinan is a senior undergraduate student majoring in psychobiology biological sciences at UCLA. His deep interests in medicine, particularly in vascular surgery has led him to join the department of vascular surgery at UCLA, where he has been working as a clinical research assistant for the last 3 years under the supervision of Dr. Brian DeRubertis, an assistant professor of surgery and vascular surgery at UCLA. Sinan has presented multiple abstracts at national and local meetings and published papers in prestigious journals. Sinan received recognition scholarships and awards from the Society of Vascular Surgery and recently, he was honored the first place Presidential Resident/Student Award for the best scientific abstract presentation at the Sothern California Vascular Surgical Society (SCVS).
Under Dr. DeRubertis’s supervision, Sinan’s project focuses on the utilization of endovascular therapy for aortic diseases and pathology and the use of high resolution non-invasive imaging technology (i.e. MRI and CT-Scan) to accurately assess and evaluate vascular malformations such as complex aortic arch artery anatomy for appropriate patient selection for surgery. Previous studies have shown that older patients are at a higher stroke rates with Carotid Artery Stenting (CAS) than younger cohorts. Some have suggested that increased age is a surrogate for disadvantaged arch anatomy, though age-related morphologic arch changes have not been well-characterized. These changes in aortic diameters, arch morphology, and degree of atherosclerotic disease that occur in elderly patients can lead to increased procedural complexity and heightened risk during interventional procedures involving the aortic arch and its branches. While the cause for this is likely multi-factorial, growing evidence suggests that age-related changes in aortic arch morphology may be a significant contributing factor. We sought to analyze these arch changes using high-resolution Magnetic Resonance Angiography (MRA). The primary aim of the study includes the use of MRA to provide characterization of the morphological and geometrical changes that occur in the aortic arch as patients age and offer description of the prevalence of various anatomic anomalies of the aortic arch that occur in this patient population. Additionally, to quantify the amount of aortic arch atherosclerotic disease present in this patient population by examining corresponding CT angiograms in the subjects when available.
Upon graduation, Sinan hopes to in incorporate the knowledge and expertise he has gained from his research experience to his practice as he aspires to pursue a career as an academic and clinical vascular surgeon. He would like to sincerely thank his encouraging mentor, Dr. Brian DeRubertis, for his continued intellectual guidance and valuable support, and express his gratitude to the Van Tree foundation for their generous financial assistance, and URSP program for this opportunity.
| Ms. Elizabeth Huang
In Photo from Left to Right: Dr. Otto Yang, Elizabeth Huang, and Dr. Ayub Ali
Ms. Elizabeth Huang
Mentor: Otto Yang
Title: Investigating HIV-1 Envelope (Env) Function Using Isolated and Cloned Full-length Env from Acutely Infected Individuals
Elizabeth Huang is a fourth year undergraduate majoring in Microbiology, Immunology, and Molecular Genetics and minoring in Asian Humanities. She has been working in Dr. Otto Yang’s laboratory since her freshman year in 2009. She is currently working on investigating HIV-1 Envelope (Env) function using isolated and cloned full length Env from acutely infected individuals.
The research project focuses on the study of the human immunodeficiency virus-1 (HIV-1), which is the causative agent of AIDS, a disease that has killed nearly 25 million people since the start of the AIDS epidemic in 1981. For vaccine development, it is important to characterize HIV-1 escape mutations to prevent the possibility of viral escape from the vaccine induced immunity. The research project will focus on studying the properties and functions of HIV-1 Env mutations generated under immune pressure. This project will investigate the dynamic interaction between the host immune response and viral mutations under immune pressure, and will shed light on the regions of HIV-1 Env that are functionally constrained and can serve as vaccine agents that trigger the human immune response.
Elizabeth intends to participate in a two-year public health internship. Afterward, she plans to pursue a Ph.D. in public health. Elizabeth would like to thank Dr. Otto Yang, Dr. Ayub Ali, Dr. Jun Zuo, and the Yang lab members for their guidance and support. Elizabeth would also like to thank the Wasserman family for their generous support. Lastly, Elizabeth would like to thank her parents and her sisters, Diana Chen and Christiana Chen, for their unconditional love and encouragement.
| Ms. Tiffany Hsyu
In Photo from Left to Right: Dr. Christian Johnson, Tiffany Hsyu, Dr. R. Michael Rich
Ms. Tiffany Hsyu
Mentor: R. Michael Rich
Funding: Norton Rodman
Title: Chemical Abundances of Red Giant Branch (RGB) Stars in the Globular Cluster NGC288
Tiffany Hsyu is a fourth year undergraduate student majoring in Astrophysics. Since her junior year, she has been conducting research under the mentorship of Dr. R. Michael Rich and postdoc Dr. Christian Johnson. Her current research focuses on the formation and evolution of globular clusters, specifically the RGB stars in the globular cluster NGC288.
Recent improvements in technology have shown that some globular clusters, once thought to contain stars of a single age and chemical composition, have extreme light element (i.e. C, N, O, Na, Mg, Al) abundance variations from star to star. The variations were furthermore found to correlate: stars high in Na and Al were low in O and Mg. Astronomers have also observed that in some globular clusters, there are multiple giant/ main sequence branches instead of the previous conception of a single evolutionary branch.
Tiffany is working on a project that seeks to answer: why don’t all globular clusters demonstrate multiple evolutionary sequences and in ones that do, how do the different populations differ in their chemical compositions? So far, she has confirmed cluster membership with radial velocity measurements for NGC288 and is working on deriving an average metallicity. She will look to examine whether or not there is a connection between central concentration and light element abundance, and to study the detailed chemistry of stars on the two giant branches to see if and how they are different.
Tiffany will graduate in the Spring of 2013 and eventually pursue a PhD after graduation. She would like to thank Dr. Rich and Dr. Johnson for the opportunity to conduct research in a field she is so passionate about, as well as for the guidance and help along the way. She would also like to thank the Orszag family for their generous support and contribution to undergraduate research.
| Ms. Lyolya Hovhannisyan
In Photo from Left to Right: Dr. Alex Platt, Wilson Lee, Dr. John Novembre
Ms. Lyolya Hovhannisyan
Mentor: ANDREW C CHARLES
Title: Mechanisms of Low Frequency Oscillations in Brain Activity
Lyolya Hovhannisyan is a third year student majoring in neuroscience. She has been a member of Dr. Andrew Charles’ laboratory since spring 2012. The lab studies mechanisms underlying migraine and tests potential therapeutic agents.
Lyolya is studying how low frequency brain oscillations may be disrupted by cortical spreading depression (CSD). CSD is a wave of increased and then quiescent brain activity that slowly sweeps across the cortical surface, and it is believed to be the underlying cause of migraine aura. She studies brain oscillations by making optical and electrophysiological recordings of the exposed cortex and vasculature in anaesthetized female mice. Female mice are used as a model system because in humans, migraine is much more prevalent in females and are known to be affected by hormonal changes related to the menstrual cycle. During normal and even aberrant states, the brain tissue and vasculature exhibit a number of different oscillatory patterns of activity and it is unclear how these are related to or impacted by CSD. Studying the relationship between oscillatory patterns between brain tissue and vasculature and how they are impacted by CSDs can help us to better understand mechanisms related to migraine and to general brain function.
Lyolya plans to pursue a dual MD/Ph.D. in neuroscience after graduation. Lyolya would like to thank her mentors Dr. Andrew Charles and Dr. Serapio M. Baca for their continual support and guidance as she pursues her individual research project. She would also to thank Mrs. Gottlieb for her scholarship funding and general support of undergraduate research.
| Mr. Vincent Heng
Mr. Vincent Heng
Mentor: Gerassimos Orkoulas
Title: Simulated Phase Diagrams for Protein Systems
Vincent is a senior chemical engineer working with Professor Gerassimos Orkoulas in the Molecular Simulation Laboratory in the Department of Chemical Engineering. He looks to go to graduate school in chemical engineering to achieve his PhD. Currently, Vincent has been working on novel techniques to simulate fluid-solid coexistence in protein systems, with the end goal of creating complete protein phase diagrams. Motivation for this research comes from the difficulty in crystallization of proteins, which would assist in x-ray crystallography and batch crystallization. To analyze equilibrium between the two phases, fluid and solid are simulated separately in an isothermal-isobaric ensemble, where the fluid and solid phases are simulated separately. To simulate the solid phase, the simulation volume is divided into equal volume Wigner-Seitz cells where each particle is confined to Monte-Carlo particle displacements that keep the particle within the cell. The fluid phase is simulated without any such boundaries. An external field is introduced into the system such that at high external field values, the system behaves as a constrained cell solid and low external field values allow it to behave as an unrestrained fluid. By modifying this external field, semifluid/semisolid characteristics are seen and the two phases can be linked. This model is shown to be applicable to multiple potential functions and is desirable due to its computational simplicity.
Future work looks at the same system in a binary setting with two particles. This is equivalent to protein crystallization in a solvent, which is more realistic experimentally. This problem is much more computationally taxing, but is necessary and will be tested against experimental data. Vincent would like to thank the Wasserman Foundation for funding his research along with Professor Orkoulas for mentoring him.
| Mr. Sean Full
Mr. Sean Full
Mentor: Sepideh Hagvall
Title: The Effect of Vitronectin on the Differentiation of Embryonic Stem Cells in a 3D Culture System
Sean Full is a Molecular, Cell, and Developmental Biology major with a minor in English. He has been conducting research in Dr. Sepideh Hagvall and Dr. Richard Shemin’s laboratory since fall of 2009. Sean’s primary focus is on three-dimensional culture systems that promote cell differentiation and proliferation. Following his undergraduate career he will be attending a D.M.D/Ph.D program. He plans to practice as well as conduct research in an academic setting for the remainder of his career.
While stem cell niches in vivo are complex three-dimensional (3D) microenvironments, the relationship between the dimensionality of the niche to its function is unknown. In this experiment a 3D microenvironment is created through electrospinning in order to study the impact of geometry and different extracellular proteins on the development of cardiac progenitor cells from resident stem cells and their differentiation into functional cardiovascular cells. We have investigated the effect of collagen IV, fibronectin, laminin and vitronectin on the adhesion and proliferation of murine ES cells as well as the effects of these proteins on the number of cardiac cells cultured in 2D conditions compared to 3D system in a feeder free condition. Thus far we have found that the number of cardiac cells was significantly higher in 3D scaffolds coated with laminin or vitronectin compared to colIV-coated scaffolds. Our results show the importance of defined culture systems in vitro for studying the guided differentiation of pluripotent embryonic stem cells in the field of cardiovascular tissue engineering and regenerative medicine. This research conducted adds another stepping-stone towards regenerative medicine in hopes of devising a method for limited rejections of tissue implants into diseased, damaged, or destroyed host tissue. This could range anywhere from replacing damaged cardiovascular tissue due to a heart attack or even replacing a torn anterior cruciate ligament. The potentials are limitless.
| Ms. Jessica Fan
In Photo from Left to Right: Jessica Fan, Dr. Timothy Deming
Ms. Jessica Hwei-Jay Fan
Mentor: Timothy Deming
Title: Applications of Diblock Copolypeptide Hydrogels in Neuroengineering
Jessica Fan is a fourth year bioengineer who works as an undergraduate researcher in Dr. Timothy Deming’s lab. Her current research involves polymer hydrogels that may be injected into the brain and spinal cord to treat disease or injury.
Polymer hydrogels can be used to deliver therapeutics in the brain in a localized, controlled fashion. Currently, brain cancer treatments often involve systemic administration of therapeutics that are toxic to cancer cells. However, these therapeutic agents may also damage non-cancer cells throughout the body, leading to undesirable side effects. Injectable polymer hydrogels hold the potential to deliver these therapeutics in a controlled fashion directly to the tumor site, which would lead to more effective treatment with fewer side effects.
Polymer hydrogels may additionally be used as a scaffold to support stem cell growth. Since neurons in the central nervous system do not regenerate after injury, brain and spinal cord injury are often permanent. Injection of hydrogels with stem cells may encourage neuronal regrowth into the injury site, leading to restoration of nerve function.
Polymer hydrogels hold the potential to create a large impact on the medical field, and Jessica hopes to continue this impact by becoming a physician after graduation. She would like to thank the Deming and Sofroniew Labs and the Hilton Foundation for supporting her research efforts.
| Ms. Shannon Esswein
In Photo from Left to Right: Boris Brumshtein, Shannon Esswein, David Eisenberg
Ms. Shannon Esswein
Mentor: David Eisenberg
Title: Investigation of the Involvement of an Immunoglobulin Variable Domain Segment in Light-chain Amyloidosis (AL) Disease
Shannon Esswein is a 3rd year Physiological Science major. She has been conducting research since Summer 2011 in Prof. David Eisenberg’s laboratory, which focuses on amyloidogenic proteins. Under the guidance of Boris Brumshtein, she is researching the involvement of a segment in the variable domains of the immunoglobulin light-chains in causing light-chain amyloidosis.
Amyloid deposits are responsible for a group of diseases in which proteins misfold and form toxic, insoluble fiber-like aggregates. In systemic light-chain amyloidosis (AL) disease, which in most cases correlates to multiple myeloma, white blood cells overproduce light chains and secrete them into the blood. High concentrations of light-chains cause the protein to form non-physiological dimers, also known as Bence-Jones proteins, which partly misfold and polymerize into amyloid fibers. Fiber deposits in vital tissues result in organ failures and eventual death. Many mutations and various types of the protein have been studied: some variants are more stable and less susceptible to form fibers, and others quickly polymerize into fibers. However, all of them can assemble into amyloids and no common mechanism or structural determinants that drive this polymerization have been identified.
Using computational methods developed by Prof. Eisenberg, several segments within variable domains of the immunoglobulin light-chains have been calculated to be able to form amyloid fiber backbone. The objective of this study is to investigate the involvement of one of these segments in light-chain amyloidosis by introducing point mutations that hinder formation of amyloid backbones into the segment of interest.
Shannon plans to graduate in Spring 2013 to pursue an MD/PhD. She would like to thank Boris Brumshtein for his guidance and Prof. David Eisenberg for the opportunity to conduct research in his lab. Furthermore, Shannon would like to express her appreciation for the generosity and support of Ms. Boyer Ballas and Mr. Boyer.
| Ms. Bibi Eghtedari
Ms. Bibinaz Eghtedari
Mentor: Neil Harris
Funding: Van Trees
Title: The Effects of Chondroitinase ABC on Neural Activation and Plasticity After Traumatic Brain Injury
Bibi Eghtedari is currently a fourth year Psychobiology major and Biomedical Research minor. She has been conducting research in Dr. Neil Harris’s lab, in the Neurosurgery department, since her second year. The Harris lab focuses on the potential for brain plasticity and functional recovery after traumatic brain injury (TBI). Bibi is currently studying the effects of the bacterial enzyme chondroitinase ABC on the neurotrophic support system that is upregulated post- TBI.
Traumatic brain injury results in devastating behavioral and structural deficits. After TBI, endogenous levels of growth inhibitory molecules are upregulated as part of the neurotrophic support system in response to injury. With this upregulation comes a non-growth permissive environment that hinders axonal sprouting, which is the underlying mechanism promoting brain plasticity. Previous studies have shown that the reduction of one of such growth inhibitory molecules, chondroitin sulfate proteoglycans (CSPGs), with the bacterial enzyme chondroitinase ABC, led to an increase in axonal sprouting. Furthermore, with the addition of rehabilitation, a reduction in behavioral deficits was observed as well. Bibi is currently looking at brain activation, as measured by c-FOS (a cellular proto-oncogene) expression, as an indicator of increased functionality, and as the potential linkage between axonal sprouting and behavioral improvement that has been demonstrated in post-TBI models after treatment with the chondroitinase ABC enzyme. In addition, she is currently working on quantifying novel synapse formation, as a measure of improved brain circuitry.
Bibi would like to thank Dr. Neil Harris and the Harris lab for their continued mentorship and guidance over the past few years. She would also like to thank the Van Trees family for their utmost generosity and support of her research, as well as the URC- Sciences program for this opportunity. Bibi plans to attend medical school after graduation.
| Mr. Dhaval Dixit
In Photo from Left to Right: Dr. Jerome Zack, Dhaval Dixit, and Dr. Dimitrios Vatakis.
Mr. Dhaval Dixit
Mentor: Jerome Zack
Title: Characterization of HIV Infection in Hematopoietic Stem Cells Using Humanized Mouse Model
Dhaval Dixit is a 4th year Microbiology, Immunology, and Molecular Genetics major with a Biomedical Research Minor. He has a strong fascination and interest in studies involving infectious diseases and immunology. This inspired him to join Dr. Jerome Zack’s laboratory, where he has been conducting research since his sophomore year. The focus of his mentor’s research, Dr. Dimitrios Vatakis, is to study why distinct cell types are differentially susceptible to HIV infection and how this impacts HIV replication and disease progression.
HIV infected patients demonstrate hematopoietic abnormalities mainly related to HIV replication in the bone marrow. Yet, HIV infection of bone marrow stem cells is an area of intense debate. The requirement for continuous use of Highly Active Antiretroviral Therapy due to persistent low-level virus production has intensified the focus on alternative ways to eradicate HIV. Dhaval’s interest is to study the impact of hematopoietic stem cell infection on the latent resevoir.
Under the mentorship of Dr. Dimitrios Vatakis, Dhaval is looking to characterize hematopoietic stem cell HIV infection in a humanized mouse model. Towards this aim, he will conduct studies to determine whether they preserve persistent low-level virus through cell expansion, contain viral DNA without expressing viral protein, and lastly determine whether infected hematopoietic stem cells can give rise to a clonal, differentiated population of infected cells. Studying whether HIV can infect hematopoietic stem cells is crucial for the characterization of HIV latency and the development innovative stem cell and gene therapy.
Dhaval will be graduating this year and plans to pursue a MD/PhD degree. He would like to Dr. Dimitrios Vatakis and Dr. Jerome Zack for their continuous support, and to the rest of the Zack lab for creating a stimulating working environment. He would also like to thank the Wasserman family for their generosity.
| Mr. Sai Devana
In Photo from Left to Right: Sai Devana, Dr. Dwayne Simmons, Aubrey Hornak
Mr. Sai Devana
Mentor: Dwayne Simmons
Title: The Role of Oncomodulin in the Functionality of Outer Hair Cells within the Cochlea
Sai Devana is currently a 3rd year undergraduate majoring in Molecular Cell and Biology. He has a strong passion for studies involving auditory function which led him to join the lab of Dr. Dwayne Simmons.
Age-related hearing loss or presbyacusis, affects about 1/3rd of adults over the age of 65. Calcium-sensitive pathways involving the calcium binding protein oncomodulin (Ocm) may play a role in progressive hearing loss. Sai’s project involves studying the function of Ocm in the outer hair cell of the inner ear and testing its effects on cell motility and functionality. He will be testing the hypothesize that Ocm modulates intracellular calcium [Ca2+]i levels in outer hair cells of the inner ear by acting as a buffer. By regulating intracellular calcium, Ocm not only effects cell hyperpolarization but also cell motility via actin polymerization and depolymerization which is largely dependent on [Ca2+]i. The long term goal of the lab’s studies is to understand progressive hearing loss and develop a platform upon which investigation of therapeutics could be possible.
| Mr. Stephen Chang
Mr. Stephen Chang
Mentor: Albert Lai
Title: Determining if Isotretinoin Can Have a Synergistic Effect on Inhibiting Growth of Glioblastoma Cells Treated With Temozolomide.
Stephen Chang is a fourth year Neuroscience major. He has been working in Dr. Lai’s lab since Spring 2011 where he has contributed to numerous studies concerned with improving therapies for patients diagnosed with gliomas. Currently, Stephen’s work is on determining if isotretinoin, a form of retinoic acid, can add a synergistic effect to the alkylating agent, temozolomide, in inhibiting growth of glioblastoma cells.
Gliomas are a form of brain tumor that affects over 20,000 new patients in the United States each year and the survival rate for gliomas, especially glioblastomas (GBM), are severely low. One of the most effective treatments against gliomas today is temozolomide. Previous research has identified patients with the mutation of the gene isocitrate dehydrogenase 1 (IDH1) to respond better to treatments such as temozolomide. Additionally, there is evidence that retinoic acid can induce differentiation and stop proliferation in neuroblastoma cells, which may cause an increase in the time of survival for glioma patients. As a result, Stephen is currently studying several glioblastoma cell lines containing either the wild-type or mutant IDH1 gene and determining if isotretinoin in combination with temozolomide has a synergistic effect in stopping growth of tumor cells in vitro. Through this in vitro study, Stephen hopes to provide evidence of a synergistic effect in the combination of isotretinoin and temozolomide to allow patients a greater chance of prolonging their survival.
Stephen would like to thank Dr. Albert Lai for the opportunity to conduct research in his laboratory and all members of the laboratory for their ongoing support. Stephen would also like to sincerely thank the Oppenheimer family for their generous funding, recognition, and support of his research.
| Ms. Le Chang
In Photo from Left to Right: Dr. Kang Ting, Le Chang
Ms. Le Chang
Mentor: Kang Ting
Title: Optimum dosage of Nell-1 and Perivascular Stem Cells on Osteoinductive Growth
Le Chang is a third year Biology major and has been an undergraduate student researcher under Dr. Kang Ting since 2011. Her research is under the Dental and Craniofacial Research Institute at UCLA.
Le has studied the effects of Nell-1, a novel growth factor, and the role of multipotent stem cells in osteogenic differentiation. Currently bone grafts are the standard for treating non-healing skeletal defects; however, significant disadvantages associated with bone graft harvests have propelled studies to identify other potential methods of bone regeneration. Our laboratories have identified Human Perivascular Stem Cells (hPSCs) as an alternative stem cell source. This purified mesenchymal stem cell line is derived from the pericytes surrounding microvessels and capillaries as well as adventitial cells that surround larger blood vessel. This cell type has the added benefit of differentiating into bone both in vitro and in vivo without the need for culture which ensures precise product characterization. hPSCs are also known to maintain endothelial cell function as well as secrete angiogenic factors such as vascular endothelial growth factor (VEGF). When used in conjunction with Nell-1 there is a noted increase in endochondral and intramembranous ossification as well as promotion of VEGF expression. This present study aims to create a bone graft substitute using an implant combined with PSCs and Nell-1 in varying dosages in order to optimize their combined osteogenic and vasculogenic effects.
After graduation Le is planning on attending medical school to obtain either an MD or MD/PhD. She would like to thank all the member of Ting lab for their continued support and the Milton Gottlieb Scholarship for supporting her endeavors in both academics and research.
| Mr. Jason Chang
Mr. Jason Lin Chang
Mentor: Shimon Weiss
Title: Determination and Optimization of Imaging Buffer and Conditions for Super-resolution Optical Fluctuation Imaging Usage
Jason Chang is a 3rd year Biochemistry major. He has been conducting research in Dr. Shimon Weiss’s Laboratory under the guidance of postdoctoral fellow Jianmin Xu since the summer of his freshman year. The Weiss lab studies and develops technique for super-resolution imaging of living systems on the nanoscopic level through fluorescence imaging.
Fluorescence imaging is a powerful technique for probing cellular structure and activity in a minimally invasive way. The ability to study live cells utilizing fluorescent probes, such as organic dyes or fluorescent proteins, enable investigating the dynamic aspects of the cellular machinery and observing in real-time its response to various stimuli. Despite the many advantages of fluorescent imaging, the main limitation of fluorescence microscopy is the low resolution due to the diffraction limit of light. Through the use of advanced mathematics in super-resolution imaging strategies, such as SOFI (Super-resolution Optical Fluctuation Imaging), this limit can be overcome as higher resolution images than the diffraction limit can be obtained. SOFI uses blinking labels in order to mathematically extrapolate a super-resolution structure. Unattained by other superresolution counterparts, SOFI’s capability of capturing dynamic states that occur on the nanoscopic level in real time is crucial in visualizing cellular processes and furthering man’s understanding of life. Because SOFI has only been applied to fixed cells due to biologically incompatible imaging buffer conditions, SOFI’s full potential in capturing rapidly changing cellular states has yet to be realized.
With his background in biochemistry, Jason is excited in pushing the frontiers of science and hopes to improve SOFI to the point that it becomes a successful and widely-utilized technique that can allow the visualization of a whole new dynamic nanoscopic world for the scientific community before he graduates in the Spring of 2014. He would like to thank Jianmin Xu for his patience, guidance, and inspiration, and Shimon for the opportunity to learn in his lab. Jason also thanks all the postdoctoral fellows and graduate students in the Weiss Lab for their advice and companionship. Finally, Jason is grateful for the generous support the Gottlieb family has provided.
| Ms. Liane Dallalzadeh
Ms. Liane Dallalzadeh
Mentor: Kelsey C. Martin
Title: MicroRNA-Mediated Translational Regulation of GluA2 in Mouse Hippocampal Neurons and its Role in Basal Synaptic Transmission
Liane Dallalzadeh is a fourth-year Neuroscience major who has been working in the laboratory of Dr. Kelsey Martin since March 2011. The Martin lab is interested in how neurons restrict gene expression to a subset of synapses, and focuses on the role of localized messenger RNA (mRNA) transcripts and their regulated translation. Recent studies from the lab and others have revealed that a subset of mRNAs is present in distal subcellular regions. Liane’s project focuses on GluA2, a subunit of the AMPA-type glutamate receptor (AMPARs), and its interaction with microRNA-124 (miR-124). After graduation, she plans to attend medical school.
Neurons are able to modify the strength of their synaptic connections in response to the environment through a process called synaptic plasticity. Changes in synaptic strength contribute to an array of cognitive processes, including memory storage. Long-lasting forms of synaptic plasticity require new protein synthesis and can occur in a synapse-specific manner. AMPARs play a central role in synaptic plasticity, since the levels of AMPARs at a particular synapse determines its strength. In order to selectively strengthen synapses, certain mRNAs are localized to distal subcellular regions. Furthermore, translation of these mRNAs can be regulated by miRNAs, which bind to the 3’ untranslated regions of mRNAs to suppress gene expression. Fluorescence in situ hybridization has been used to visualize the distribution of GluA2 mRNA and miR-124 in dissociated mouse hippocampal neurons. Current gain and loss of function studies aim determine if miR-124 regulates translation of GluA2 endogenously. A functional assay will be performed afterwards to determine changes in synaptic strength as a result of changes in GluA2 levels.
Liane would like to thank the Undergraduate Research Scholars Program and the Wasserman family for their generous support. She would also like to thank all members of the Martin Lab for their continual guidance.
| Mr. Nathan Cho
Mr. Nathan Cho
Mentor: Yi Tang
Title: Intracellular Protein Delivery Using Polymeric Nanocapsules
Nathan Cho is a third year undergraduate student majoring in chemical and biomolecular engineering. He is interested in the pharmaceutical applications of many organic compounds, which led him to conduct research in Dr. Yi Tang’s laboratory since his sophomore year. The Tang lab studies biosynthetic pathways of natural products and aims to characterize enzymes encoded in these pathways for possible biocatalysis applications. The Tang lab also works in the bionanotechnology field and aims to engineer biomaterials capable of delivering macromolecules intracellularly. In particular, research is focused on efficient delivery of various proteins to cells for applications in cancer-therapy, imaging, and reprogramming.
Nathan currently synthesizes polymeric nanocapsules that are effective in delivering proteins to the cytosol through the cell membrane. Nanocapsules are engineered to encapsulate various transcription factors that are important for the transdifferentiation of mammalian liver cells into pancreatic beta cells, which may help stabilize blood glucose levels for patients with Type I diabetes. He plans to iterate various synthesis parameters to prepare nanocapsules to determine the optimal ratio of monomers and crosslinkers required for effective nanocapsule formations. His goal is to detect successful intracellular delivery by synthesizing nanocapsules with rhodamine-tagged transcription factors, which can be visually observed through fluorescence microscopy. Nathan will also perform various biological assays to assess the ability of engineered nanocapsules.
Nathan plans to graduate in spring of 2014 and plans to get a Ph.D. in biomolecular engineering. He would like to thank Anu Biswas, the superb graduate student in the Tang Lab, for the year-long guidance and Dr. Yi Tang for providing the opportunity to learn more about the research behind applications of nanobiotechnology. Also, Nathan would like to express his gratitude to Mrs. Gottlieb for generously supporting his research and his endeavors to learn more about the potential impact of biotechnology to society.
| Ms. Katharine Chen
Ms. Katherine Chen
Mentor: Istvan Mody
Funding: Van Trees
Title: Changes in Newborn Dentate Granule Cells Within a Surrounding Epileptic Network
Katherine Chen is a 4th year Neuroscience major. She has been working in Dr. Istvan Mody’s laboratory under the mentorship of Ryan Jones (Ph.D. Candidate) since her freshman year. One research focus in the Mody lab includes elucidating basic mechanisms of temporal lobe epilepsy and investigating the consequences of abnormal neuronal excitability in the epileptic brain.
Epilepsy is a brain disorder that affects approximately fifty million people worldwide. Those affected suffer from spontaneous and unpredictable seizures, which have a profound impact on quality of life. Temporal lobe epilepsy (TLE) is the most common form of acquired epilepsies and is often resistant to drug treatment. The hippocampal formation is one of the most sensitive regions of the brain to seizure generation. Interestingly, the hippocampus is also one of the few brain regions in which new neurons are generated throughout life. These neurons are generated from stem cells and integrate into the local neural network. Currently, it is unclear how this developmental process may be affected during epilepsy and if abnormal development may exacerbate seizure frequency and severity.
Katherine’s project is focused on how developing neurons in the hippocampus can be adversely affected by epilepsy. To investigate how the development of single neurons are affected by an epileptic phenotype, Katherine is combining viral vectors and fluorescence imaging techniques to assess how neurons, at specific developmental stages, integrate into the local neural network in the normal and epileptic brain. Investigating changes in the neuronal network throughout affected areas in an epileptic phenotype may reveal basic mechanisms of how developing neurons are affected by local network activity as well as identify potential therapeutic targets to slow the progression of TLE in human patients.
Katherine plans to graduate in the Spring of 2012 and attempt to pursue an MD in the future. She would like to thank Ryan and Istvan for their many years of guidance. Finally, Katherine would like to thank the Van Trees family for their generous donation that allows her to pursue cutting edge biomedical research at UCLA.
| Ms. Iris Chen
Ms. Iris Chen
Mentor: Yibin Wang
Title: Long Non-Coding RNA in Hypertrophy and Heart Failure
Iris Chen is a fourth-year undergraduate student majoring in Psychobiology. Since spring quarter of 2011, she has been part of Dr. Yibin Wang's lab, which investigates the molecular basis of stress induced cardiomyopathy. Having studied the variability of heart failure pathogenesis via echocardiography previously, she is now taking a more microbiological approach with Dr. Zhihua Wang, focusing on long non-coding RNAs and understanding their functions with respect to hypertrophy and heart failure.
Chronic heart failure (CHF) affects 20 percent of the global population, causing high socioeconomic costs in its treatment. Its onset is induced by a compensatory response from the sympathetic nervous system and neurohormonal pathways, which increases the rate and intensity of heart contraction to sustain cardiac output. Chronic excessive activation of the sympathetic system, however, results in heart failure. The pathogenesis of heart failure is further complicated by the influence of various environmental and genetic factors, rendering the limited therapeutics available ineffective for a significant portion of CHF patients. Iris' research project implements a clinical purpose – by understanding the different genetic contributions to the variability of heart responses, the goal is to personalize medicine according to the patient’s genetic background.
Long non-coding RNAs have been shown to partake in biological activities, but the functions of the majority remain unknown, especially in the context of heart failure. Based on the previous studies, Iris specifies several long non-coding RNA candidates (C11-108m, C1-137m, and C2-118m) to investigate their impact on cell size and cell death. After validating the expression of these RNA in hypertrophy and heart failure models using Real-time PCR, she will clone the long non-coding RNA into the Adeno-virus and transfect neonatal rattus ventricular myocytes. Furthermore, she will inhibit these long non-coding RNAs using siRNA or antisense RNA to comprehend the signaling pathways underlying long non-coding RNA regulated heart function.
After graduating, Iris hopes to continue her education and research in an MD/PhD program. She would like to thank Dr. Yibin Wang and Dr. Zhihua Wang for their continued guidance and encouragement. Iris is also extremely grateful to Wasserman family for their generous contribution to her research.
| Mr. Ivneet Bhullar
Mr. Ivneet Bhullar
Mentor: Warren Grundfest
Title: Reflective Terahertz Imaging of Skin Burns on Rat Model
Ivneet Bhullar is a 4th year, Undergraduate at UCLA studying Bioengineering. To supplement his studies with practical experience, Ivneet is conducting research in the Minimally Invasive Surgical Systems Laboratory of Dr. Warren Grundfest. Working on the Terahertz (THz) Imaging project, Ivneet and his research team hope to produce a reliable system to image skin surface abnormalities.
Terahertz radiation occurs in the frequency range of 0.1THz to 10THz in the electromagnetic spectrum. Three main qualities make terahertz ideal for imaging skin irregularities and pathologies such as burns, scars, wounds and skin cancer: non-ionizing terahertz photon energy (0.4 – 40meV), extreme sensitivity to changes in water concentration, and the ability to penetrate clothing and gauze. Thus, the THz system can image and distinguish between regions of hydration and dehydration related to a burn site. This year, Ivneet will work with a team of graduate students to run trials on the rat model. The focus of these trials will be to test the efficacy of the device in differentiating between partial-thickness and full-thickness burn wounds, as determined by histology. A pilot study will be conducted on two rats to determine difficulties in the procedure. After the success of the pilot study, Ivneet and his team will conduct burn experiments on a statistically determined ten rats. Inventions such as the MRI and X-Ray machines have revolutionized healthcare and Ivneet hopes the Terahertz system can similarly provide imaging in a broader range of medical cases.
With his experience in research and his foundational bioengineering background, Ivneet plans to further focus his skills by attending graduate school. Upon receiving his graduate degree, Ivneet hopes to become a leader in the biomedical device field. His enthusiasm and aptitude for research can be attributed to the intriguing work being done in Dr. Warren Grundfest’s lab. Ivneet sincerely thanks Dr. Grundfest for the opportunity to contribute to this project and for his guidance throughout Ivneet’s Undergraduate studies.
| Mr. Andrew Berg
In Photo from Left to Right: Dr. Tom Carmichael, Dr. Pouria Moshayedi, Andrew Berg
Mr. Andrew Berg
Mentor: Stanley Carmichael
Title: Enhancing Host Cell Migration into Implanted Hyaluronan Hydrogels after Focal Ischemic Stroke
Andrew Berg is a 3rd year Bioengineering student who has been conducting research since his sophomore year. He joined the Carmichael lab in the Department of Neurology and works closely with postdoctoral fellow Dr. Pouria Moshayedi. The Carmichael lab seeks to identify mechanisms of recovery after stroke and develop novel therapies for neural regeneration.
Stroke is the leading cause of long-term adult disability in America. After stroke, the brain has a limited capacity for repair due to hostile infarcted tissue that is not amenable to significant cell growth. Many research strategies aim to create a favorable microenvironment in the stroke cavity so that endogenous repair processes are promoted. Engineered hyaluronan hydrogels may serve as a viable treatment option – they are biocompatible, injected through minimally invasive procedures, and maintain similar viscoelastic properties to the brain. However, host cellular migration into the implanted gel has not yet been seen in a robust manner. Andrew is working to enhance cell movement into the gel by attaching RGD, YIGSR, and IKVAV cell-adhesion motifs to the hyaluronan backbone. By injecting gels with different permutations of these motifs into mice after stroke injury, Andrew hopes to find which combination yields the most favorable gel environment for host cell migration. Promoting significant cell migration into the hyaluronan is a critical step in generating a sustainable tissue construct that could support neural reconnection in the stroke cavity.
Andrew plans to graduate in the Spring of 2014 and pursue a Ph.D. He would like to thank Dr. Carmichael, Dr. Moshayedi, and the rest of the Carmichael Lab. He would also like to extend his gratitude to the Gottlieb family and URC-Sciences for their generous support.
| Mr. Roland Azurin
Mr. Roland Azurin
Mentor: Patricia Gowaty
Title: Polyandry in Drosophila
Roland Azurin is a 4th Year Biology major also pursuing college honors. His fascination for animal behavior has driven him toward a research-oriented undergraduate education. He has been working under the mentorship of Dr. Patricia Gowaty and Dr. Sergio Castrezana in the Department of Ecology and Evolutionary Biology since the beginning of winter 2012. His research project in the Gowaty Lab is focused on polyandry in different species of Drosophila. He has performed a number of experiments and is currently learning how to consolidate and analyze data.
Polyandry is a natural observed behavior common in most animals including Drosophila. Polyandrous females mate with multiple males so that different fathers sire some or all of her offspring, but the potential fitness benefits are questionable. To understand better the ecological forces favoring polyandry, with funding from NSF the Gowaty lab is performing experiments on multiple species of Drosophila, notably species with sequenced genomes and/or with interesting ecologies or curious social behavior. Roland has performed experiments on three different species of Drosophila, including: D. subobscura, D. acanthoptera, and D. melanogaster. His experiments involve treatments of females with various male exposures. The data he has collected will provide insight on fitness benefits of single versus multiple mating for females.
After graduation, Roland plans to pursue a medical degree and aspires to become a physician in the United States Medical Corps. He would like to express his deepest gratitude to Professor Gowaty and Dr. Castrezana for their support, guidance, and encouragement; they have provided him an enriching, educational experience. Roland would also like to thank URC-Sciences and Mr. Lewis/Ehrisman fund for their generous support and for giving him this invaluable opportunity.
| Mr. David Ashby
Mr. David Ashby
Mentor: Suneel Kodambaka
Title: Electrodeposition on Carbon Nanotube Yarns to Improve Mechanical Properties
David Ashby is currently a third year undergraduate materials engineer. He has been undertaking research under Professor Kodambaka since winter quarter of second year in which he has been working with carbon nanotubes.
Carbon nanotubes have a wide range of applications in the real world because of their high tensile strength and because of their high thermal and electrical conductivity. The possibility in solar cells, heat sinks, and for light weight high strength materials can drastically change our energy production and what everyday machines are made with. The only problem is that commercially grown tubes usually do not get larger then several millimeters and are on a scale of a nanometer wide. Carbon nanotube yarns have just recently been able to be spun, but in the spinning process much of the desirable properties are lost.
David is currently working on improving the tensile strength and electrical conductivity of the carbon nanotube yarns through electrodeposition of metal onto the yarns. The hope is that the metal will be able to functionalize the carbon in the nanotubes leading to the bonding together of the carbon nanotube strands. The metal bonding is stronger than the Van Der Waal forces that hold the yarn together so the tensile strength should increase and because of the conductivity of the metal the electrical conductivity should increase.
David is expecting to graduate in June of 2014 after which he plans to continue on to graduate school in materials engineering where he plans to pursue a masters and eventually a PhD degree. He eventually after graduate school plans to pursue a career in nanotechnology focusing on the energy field. David would like to thank the Gottlieb Foundation for their generous donation.
| Ms. Nicole Arulantham
In Photo from left to right: Laura Vican, Nicole Arulanantham, Ben Zuckerman
Ms. Nicole Arulanantham
Mentor: Benjamin Zuckerman
Title: Searching for Young Stars in the Solar Neighborhood
Nicole Arulanantham is a 4th year Astrophysics major. She began working for Dr. Zuckerman and his colleagues, Dr. Joel Kastner at RIT and Dr. David Rodriguez at Univ. of Chile, in June 2012. The group is identifying young stars close to the Sun and classifying them as members of co-moving groups.
Co-moving groups consist of young stars that appear to move together through the plane of the sky. Their uniform motion indicates that the objects formed from the same molecular cloud but because of their youth have not yet dispersed across the sky. There are several young moving groups that have been identified within a small radius of the Sun. Dr. Zuckerman’s group has narrowed down a large initial selection of young star candidates to a list of 455 objects that are likely members of these moving groups. Nicole is now going through the list to ascertain whether any of the objects are worth further examination. The most promising young star candidates that she finds will be considered for spectroscopic follow-up, which means their chemical properties will be observed from a telescope to confirm their status as young stars. This is the first step towards studying the earliest stages of planetary evolution; young stars could be harboring newly-formed planets. The closer the host stars are to the Sun, the easier they will be to study.
Nicole will be graduating in June of 2013 and intends to pursue a PhD in Astrophysics. She would like to thank Dr. Zuckerman for the opportunity to participate in this research and grad students Laura Vican and Sarah Logsdon for introducing her to the project and providing guidance whenever needed. She also thanks Ms. Evers-Manly for her generous support.
| Mr. Tatsuya Araki
Mr. Tatsuya Araki
Mentor: Edward De Robertis
Title: A New Role for TAZ in Germ Layer Specification during Xenopus Embryonic Development
Tatsuya Araki is a third year Molecular, Cell, and Developmental Biology major who is also pursuing a minor in Biomedical Research. He has been conducting research since the summer before his sophomore year in Dr. Edward M. De Robertis's laboratory with the help of Hadrien Demagny (Ph.D. Candidate). The De Robertis lab studies cell-cell communication during embryonic induction with a focus on the effect of Wnt in early development.
Understanding how cells integrate different signaling pathways to induce specific germ layers is important in embryonic development. It is known that Bone Morphogenetic Protein (BMP) and Transforming Growth Factor Beta (TGF-beta) pathways signal are important during the early development. Both pathways signal through Smad proteins. It has been shown that Yes-associated protein (YAP) interacts with Smad1 (BMP-specific Smad protein), and this binding is required for the full Smad1 activity. It has also been shown that the YAP paralogue TAZ is required for the full activity of TGF-beta signaling. Tatsuya is currently studying whether TAZ also interacts with Smad4 to affect TGF-beta signals by studying the requirement of TAZ in mesoderm induction by TGF-beta in Xenopus embryo. Tatsuya hopes to uncover the condition required for TAZ to activate TGF-beta signaling. By elucidating that TAZ activates and is required for TGF-beta signaling and mesoderm induction, it may uncover a new role for TAZ in TGF-beta signaling during germ layer specification.
Tatsuya plans to graduate in the Spring of 2014 and hopes to pursue a MD/PhD degree. He would like to thank Hadrien for the years of instruction and guidance, Eddy (as Tatsuya would call him) for the opportunity to learn in his lab, and the Gottlieb family for their generous support.
| Ms. Teni Anbarchian
In the Photo from Left to Right: Diana Rigueur, Teni Anbarchian, Dr. Karen M. Lyons
Ms. Teni Anbarchian
Mentor: Karen Lyons
Title: Signaling Pathways of Chondrogenesis in the Absence of Smad4, in Smad4 Conditional Knockout Mouse Mutants.
Teni Anbarchian is a 4th year Molecular, Cell, and Developmental Biology major, minoring in Biomedical Research. She has been conducting research in Dr. Lyons' laboratory since February 2012, with the help of Diana Rigueur (Ph.D candidate). The Lyons lab studies signal transduction pathways of chondrogenesis.
Osteoarthritis (OA) is a common joint disorder in the United States, which results in disability. The wear-out of cartilage at the end of our bones leads to OA and can be due to several reasons such as genetics or aging. To find therapeutic treatments for OA, it must be studied at the genetic and molecular levels. Two of the pathways involved in the process of cartilage production and its replacement with bone are the Transforming Growth Factor beta (TGFb) and Bone Morphogenetic Protein (BMP) signaling pathways. Previous research found Smad4 to be essential for signal transduction in these pathways. However, recent data showed that Smad4 is largely dispensable for early chondrogenesis.
The research project consists of studying chondrogenesis in the absence of Smad4 in order to re-evaluate its function. Teni is currently examining downstream targets of the BMP pathway in transcriptional and translational levels, as well as the interaction of the members of the BMP and TGFb pathways with each other in Smad4-deficient mice models. She predicts the lab can find a bone and cartilage pathway that functions without the presence of Smad4.
Teni plans to graduate in Spring 2012 and continue conducting research in a Ph.D program. She would like to thank Dr. Lyons for her guidance and opportunity to participate in her research project, and Diana Rigueur, her graduate mentor for her extensive training and support. She would also like to thank the lab members for helping her have a great research experience. Teni also expresses her gratitude to Mr. Lau for his generosity, support and acknowledgment of her research.
| Mr. Abhi Amarnani
In Photo from left to right: Dr. Ivan A. Lopez, Abhi Amarnani, and Dr. Ram Raj Singh
Mr. Abhimanyu Amarnani
Mentor: Ivan Lopez
Title: A Study of Lupus Nephritis Disease Progression through
Abhimanyu Amarnani (Abhi) is a 4th year Psychobiology major who is interested in studying the disease mechanisms underlying systemic lupus erythematosus (SLE).
SLE is a chronic, potentially fatal illness. It is characterized by autoantibody production leading to the deposition of autoantibody-autoantigen immune complexes that subsequently cause tissue injury. Clinically, it is difficult to effectively monitor its complications because the pathogenesis of SLE is not completely understood. While there has been some progress in treatment, these treatments mainly include general anti-inflammatory drugs and cyclophosphamides. There have not been many effective treatment options developed to target the particular SLE disease progression. In particular, there is a high prevalence of renal involvement in SLE, lupus nephritis. As the highest cause of morbidity and mortality in SLE, there is a need to understand the specific etiopathogenesis that progresses from early stage lupus nephritis towards end stage renal disease.
Working with Drs. Ram Raj Singh and Ivan Axel Lopez, Abhi’s research goals include studying the mechanistic progression of lupus nephritis. Through a focus on its pathophysiological steps, their research team hopes to elucidate differentially expressed proteins that are linked to glomerular alterations in SLE.
To approach this research goal, they have built a collaboration with the UCLA Pasarow Mass Spectrometry Laboratory. For this, Abhi also works closely with with Drs. Julian Whitelegge and Chris Ryan so that he can gain a fundamental understanding of mass spectrometry based proteomics techniques. Through application of HPLC MS/MS techniques, we will be able to design important proteomics experiments that can elucidate the underlying mechanisms of lupus nephritis disease progression.
Abhi is currently applying to MD/PhD programs across the United States and hopes to train, medically, as a rheumatologist and continue studying Systemic Lupus Erythematosus as part of his combined career. He would like to thank his mentors and collaborators for their invaluable guidance and support, which allowed him to discover his major research interests and career goals. Finally, Abhi would like to express his utmost gratitude to the Wasserman Family for their generous contribution to undergraduate research.
| Ms. Eva Ng
Ms. Eva Ng
Mentor: Kent L Hill
Title: The Role of the Trypanosoma brucei BBSome in Flagellar Homeostasis and Pathogenesis
Eva Ng is a Microbiology, Immunology, and Molecular Genetics major and has been conducting research under the guidance of Dr. Kent Hill and Gerasimos Langousis since the beginning of her third year at UCLA.
The Hill lab uses trypanosomes as a model organism to explore flagellar mechanisms. Trypanosomes are single celled eukaryotic organisms that cause African sleeping sickness. They have a complex life cycle that involves development in the gut of a tsetse fly to virulence in humans or mammals. For this reason, the flagellum as a sensory organelle is crucial to trypanosomes for survival. Recently, a protein complex called the BBSome, composed of seven Bardet-Biedl syndrome (BBS) proteins (BBS1, 2, 4, 5, 7- 9) was found to mediate protein trafficking to and from the eukaryotic flagellum. In humans, C. reinhardtii and other organisms, depletion of BBS proteins disrupts homeostasis in the flagellum leading to pleiotropic defects such as defective responses to extracellular signals. However, the molecular basis of trypanosome infectivity remains enigmatic. The Hill lab seeks to explore the necessity of the BBSome in T. brucei for infectivity in the mouse model. Various knockouts of BBS proteins will be developed in lab and examined for the disruption of the BBSome, growth defects, and damped infectivity in the mouse model. Furthermore, the lab seeks to construct a tentative model of the BBSome in T. brucei by examining protein-protein interactions in the knockouts. If the BBSome has a direct affect on infectivity, the proteins it traffics will be examined to perhaps determine a good drug target for T. brucei to hopefully find a cure for the epidemic that plagues sub-Saaharan Africa.
Eva would like to thank Dr. Kent Hill and the Hill lab for their continued input and support, and Mrs. Gottlieb for her generous sponsorship.
| Mr. Peter Nauka
Mr. Peter Nauka
Mentor: Heather Maynard
Title: Exploring Linker Length as a Way to Increase Polymer-Protein Conjugation Yield
Peter Nauka is a 3rd year Chemical Engineering student. He has been working in Dr. Heather Maynard’s laboratory for over a year alongside Juneyoung Lee (Ph.D. Candidate). The Maynard lab specifically works on protein-polymer conjugates and how they can be used to stabilize various interesting therapeutic proteins.
Many therapeutic proteins suffer from limitations, including, short half-life in vivo, poor solubility, high immunogenicity and short shelf-life. Polymer conjugates can be used to correct some of these deficiencies. In particular, poly-ethylene glycol polymers and various derivatives have become increasing popular, and there are currently numerous polymer-drugs on the market. However, it has been observed that some polymers are relatively low or none yielding upon conjugation with a therapeutic. Peter is working on a way to improve the yield of polymer-protein conjugation by varying the linker length between the protein reactive end group and the polymer backbone. Specifically, he is synthesizing various linker sizes between the end group and backbone and then using reversible addition-fragmentation chain transfer (RAFT) to create poly(poly(ethylene glycol methyl ether) acrylate) (pPEGA). pPEGA-protein conjugation has been targeted in the past, but the modification is relatively low yielding. It is believed that a long linker length will reduce steric hindrance between the protein and bulky branched pPEGA polymer. Peter hopes that this research will help increase understanding in why certain polymer can only be conjugated onto proteins with difficulty, and what steps can be undertaken to rectify this problem.
Peter plans to graduate in the Fall of 2014. He would like to thank Dr. Maynard for her support and invaluable guidance over the past year and Juneyoung for his mentorship in the subject matter. He would also like to express his immense gratitude to the Gottlieb Foundation for funding his research.
| Ms. Haneul Yoo
Ms. Hanuel Yoo
Mentor: Margot Quinlan
Title: Purification and Characterization of Franken-Cappuccino Proteins
Haneul Yoo is a fourth year undergraduate student majoring in Biochemistry. She joined Professor Quinlan’s laboratory as an undergraduate researcher in Winter 2011. Since then she has been working under the guidance of a graduate student Elizabeth Roth on the purification and characterization of Franken-Cappuccino proteins.
Actin polymers, along with microtubules, play a crucial role in various cell functions. Cells polymerize actin by deploying several actin-assembling proteins that catalyze polymer nucleation and elongation. The Quinlan lab studies two kinds of such specialized proteins, Spire and Cappuccino, that are known to play an important role in fly oogenesis.
Cappuccino is classified as the formin class of actin-assembling proteins. All formin class proteins share highly conserved formin homology 1 (FH1) and 2 (FH2) domains, but the so-called tail regions next to the FH2 domain are much less conserved between the formin proteins. Recent work suggests that these tail regions contribute differently to the actin polymerization activities and/or the microtubule binding affinities of different formin proteins. For example, the tail regions of some formins bind microtubules well while others do not. Haneul is currently working on the purification and characterization of the so-called Franken-Cappuccino proteins, which has FH1/FH2 domains of Cappuccino but the tail regions of different formin proteins. She hopes this project will help us better understand of the role of the tail region in formin’s actin-assembling and microtubule-binding abilities.
After graduation, Haneul intends to pursue a doctoral degree in Biochemistry. Haneul would like to express her gratitude to Dr. Quinlan and Elizabeth Roth for providing mentorship and to the rest of the Quinlan lab for creating a comfortable research environment. She would also like to thank Mr. Lau for his generous support.
| Mr. Timothy Wu
In Photo from Left to Right: Dr. Volker Hartenstein, Timothy Wu
Mr. Timothy Wu
Mentor: Volker Hartenstein
Title: Tracing Lineage and Neural Stem Cell Development in the Drosophila Brain
Timothy Wu is a 4th year Molecular, Cell, and Developmental Biology major who is conducting research in Dr. Volker Hartenstein’s laboratory with the help of Jaison Omoto (Ph.D Candidate). The Hartenstein lab studies the developmental pattern of the Drosophila brain. The lab is centered on elucidating the mechanisms of neurogenesis and constructing an atlas of Drosophila brain development.
Neurons in the fly brain develop in a highly characterized matter. Cells proliferate in lineages, meaning that over the developmental continuum, a single parental cell in the embryo eventually give rise to a line of multiple cells types in the larva and adult. Timothy is attempting to generate a novel method in tracing these lineage formations by investigating different molecular markers. The conserved neural developmental pattern between vertebrate and invertebrates allow us to gain enormous insight to human neuronal development and disease using the Drosophila model.
Timothy plans to graduate in the Spring of 2013 and pursue a PhD in cancer biology. He would like to thank Dr. Hartenstein and Jaison for guidance and the opportunity to work in the lab. He would also like to thank Kathy Ngo for training him in the techniques used. Finally, he would like to thank Ms. Carter and the J.W. and Nellie MacDowell foundation for their generous support.
| Ms. Shannon Wongvibulsin
In Photo from Left to Right: Stephanie Reed, Shannon Wongvibulsin, and Dr. Benjamin Wu
Ms. Shannon Wongvibulsin
Mentor: Benjamin Wu
Title: Investigation of the Involvement of an Immunoglobulin Variable Domain Segment in Light-chain Amyloidosis (AL) Disease
Shannon Wongvibulsin is a third year undergraduate minoring in biomedical research, majoring in bioengineering, and performing research in Dr. Benjamin Wu's lab. Because of Shannon's interest in biomedical research, she has been a member of Dr. Wu's lab since the summer before her freshman year at UCLA. While projects of the Wu Lab range from the study of cell interactions with appetite bone matrix to dermal wound healing, they all center upon the study of biomimetic environments for the ultimate goal of tissue repair.
After working with 3D printing and developing a technique which allows 3D printed sugar preforms to serve as positive molds for infusion of aqueous-based scaffold solutions, such as chitosan-alginate, Shannon is currently working on implementing this system to create chitosan-alginate scaffolds with two zones, one that facilitates bone growth and one that facilitates cartilage growth. The long-term aim of this project is the creation of chitosan-alginate scaffolds with zonal micro- and macro-architecture for cartilage and bone regeneration. Additionally, these two zones of the scaffold will be created to have different pore sizes, larger pores for the bone region and smaller pores for the cartilage region; channels to facilitate the influx of endogenous progenitor cells will also be incorporated into the design of the preform.
Shannon would like to thank all her research mentors for enriching her undergraduate education with the opportunity for hands on experience in solving current biomedical challenges. After graduation, she hopes to pursue an MD-PhD dual degree and contribute to the medical field both as a physician and a member of the research community.
| Mr. Daniel Wong
In Photo from Left to Right: Daniel Wong and Dr. Julian A. Martinez-Agosto
Mr. Daniel Wong
Mentor: Julian Martinez-Agosto
Title: The Role of Pico, The Drosophila MRL Protein, in Growth Regulation
Daniel Wong is a junior at UCLA, majoring in Molecular, Cell, and Developmental Biology with a minor in Biomedical Research. Since March 2011, he has been working in the Martinez-Agosto laboratory in the department of Human Genetics. His current project investigates the molecular mechanism through which pico, the Drosophila MIG-10/RIAM/lamellipodin (MRL) protein, regulates systemic larval growth.
Control of tissue and organismal size is coordinated by a number of intracellular growth signal transduction pathways that respond to various extracellular cues. While these growth regulatory mechanisms are crucial to the normal growth and development of animals, dysregulation of these pathways can lead to overgrowth diseases such as cancer. Therefore, elucidating the points in growth signaling pathways at which dysregulation occurs is essential for the development of therapeutic strategies to treat and prevent disease processes such as tumorigenesis.
Daniel’s project seeks to characterize the role that MRL proteins play in the communication of these growth regulatory pathways. MRL proteins comprise a specific class of molecular adaptors that connects upstream events, for example, the binding of a ligand to a surface receptor, to downstream targets whose activation brings about a cell response, such as the initiation of proliferation. Using Drosophila melanogaster as a model to study and characterize MRL proteins, Daniel aims to illuminate the role of pico in the regulation of systemic larval growth through examining the link that Pico has to two specific growth signaling pathways: the PI3K/Akt/TOR pathway and insulin signaling.
Daniel would like to thank Dr. Julian Martinez-Agosto for his continued guidance in the laboratory, and Daniel greatly appreciates the generosity and support from the Gottlieb Foundation and the Howard Hughes Undergraduate Research Program. Finally, Daniel is grateful to Dr. Ira Clark, Dr. John Olson, the HHURP faculty, and the URC for their encouragement in his research endeavors.
| Mr. Wilson Mai
Mr. Wilson Mai
Mentor: Andre Nel
Title: Overcoming Multi-drug Resistant (MDR) Cancer Cells through the Dual Delivery of siRNA and Doxorubicin using Mesoporous Silica Nanoparticle (MSNP)
Wilson Mai is a fourth year biochemistry major, working under Dr. Huan Meng and Dr. Andre Nel for over two years. Wilson is involved in one of many projects in the group involving using nanoparticles for therapeutic purposes. Nanotechnology has been rapidly growing during the past years, and newly synthesized nanomaterials have become a hot topic for drug delivery.
Using nanomaterials for disease treatment has been primarily focused on cancer treatment, where patients undergoing modern chemotherapy often encounter several challenges. Modern chemotherapy often results in systemic toxicity due to unspecific drug delivery to normal tissues. In addition, chemotherapy has become less effective due to the development of multidrug resistant (MDR) cancer cells which have mechanisms preventing drug-mediated cell death. One critical component for MDR is P-glycoprotein (Pgp), an efflux pump overexpressed in cancer cells that reduces intracellular buildup of chemotherapeutic drugs within the tumor. Wilson plans on using an optimized mesoporous silica nanoparticle (MSNP) to deliver small interfering RNA (siRNA) to silence Pgp expression as well as doxorubicin to induce cytotoxicity within the cells. Wilson hopes by using MSNPs to co-deliver siRNA and doxorubicin, a synergistic treatment will result. The effective silencing of Pgp will result in more bioaccumulation of drugs within the cancer cells, and therefore increase efficacy of the treatment.
Wilson is currently in his last year at UCLA. He is currently applying to several Ph.D. programs, pursuing his dream of becoming a leading researcher in molecular and cellular biology. Wilson would like to thank the Nel lab for all their help, especially his mentor, Dr. Huan Meng, who has been extremely patient and helpful. Lastly, Wilson would like to thank the Lau family for all their generosity.
| Mr. Nova Wang
Mr. Nova Wang
Mentor: Yi Tang
Funding: Silva Trust
Title: Anticancer Protein Delivery Using Self-Degrading Nanocapsules
Nova Wang is currently a fourth year Bioengineering (B.S.) major. He has specific interests in oncology-related biotechnology, which led him to the drug delivery research sector of Dr. Yi Tang’s laboratory. The Tang research group is centered on natural product biosynthesis and biocatalysis, however interest in research at the interface of nanotechnology, biomaterials and drug delivery has significantly increased in the recent past. Specifically, the research focuses on the delivery of various biological molecules for several important clinical applications.
The goal of Nova’s research is to utilize an innovative method of therapeutic protein delivery to reactivate apoptosis in triple negative breast cancer, an extremely aggressive breast cancer subset that metastasizes fast and results in poor patient survival. The main focus is to deliver the most commonly mutated tumor suppressor protein, p53, via degradable protein nanocapsules (DPNCs). These DPNCs are engineered to penetrate cell membranes and subsequently dissociate in the reducing cytosolic environment to release the protein cargo in functional form. The project is extremely innovative because reversible encapsulation is a unique approach to protein delivery that circumvents permanent genome modification. The results from this research may enable the development of new treatments to breast cancer and other types of carcinomas alike.
Nova is scheduled to graduate in the Spring of 2013 and has a desire to gain several years of industry experience following graduation. He plans to later pursue a Ph.D in Biomedical Engineering with a focus on cancer therapeutics, staying close to the field of oncology. Nova would like to thank his mentor, Professor Tang, for his unwavering support, and also his supervisor Muxun Zhao for her invaluable guidance and counsel. Finally, he would like to express enormous gratitude for Mr. Henry and Silva Trust for their generous endorsement.