The URSP Scholarship is awarded to Juniors and Seniors who have a strong commitment to research, and who are completing an honors thesis or a comprehensive 199 project during their senior year.
| Marlene Arceo
Marlene Arceo is a fourth year student majoring in Psychobiology. She has been conducting research under the guidance of Dr. Bo Yu since Fall 2016. Her lab has focused on molecular interactions between inflammation and bone metabolism, with the long-term goal of developing novel agents to treat inflammation-driven bone diseases such as periodontitis.
Periodontitis is an extremely prevalent chronic inflammatory disease, and results from microbial infection around the teeth. This infection triggers inflammatory responses that degrade the bone and connective tissues surrounding the teeth. Current treatment approaches for periodontitis mostly focus
on the removal of bacteria without sufficiently addressing the often-unresolved inflammation. Marlene’s lab recently turned attention to PGC-1a, a master metabolic regulator that has shown to attenuate inflammation-related skeletal muscle aging by enhancing mitochondrial biogenesis. In previous studies, it was found that depletion of PGC-1a led to enhanced bone loss by exacerbating the pro-inflammatory NF-kB signaling pathway in a mouse model for osteoporosis. Translating this finding in the long bone to the oral cavity, Marlene’s lab is investigating if PGC-1a could play a similar role in a mouse model for periodontitis. Findings will further the understanding of the effects of PGC-1a in inflammation-driven bone loss, and may allow PGC-1a to be identified as a potential therapeutic agent to treat bone loss resulted from periodontitis.
After graduating from UCLA, Marlene hopes to continue conducting research for a year before attending dental school. She would like to thank her mentor Dr. Bo Yu for his guidance and support.
| Patricia Bunda
Patricia Bunda is a senior majoring in Molecular, Cell, and Developmental Biology, with a minor in Biomedical Research. She joined Dr. Stephanie Correa’s lab as an undergraduate researcher in Winter 2017.
The Correa lab focuses on how reproductive hormones affect metabolic health and disease. A region of the hypothalamus known as the ventromedial hypothalamus (VMH) has been found to have neurons that express estrogen receptor α (ERα). Coincidentally, the VMH has been linked to a number of physiological processes including locomotion, feeding, thermoregulation, mating, and anxiety. Recent work by Dr. Correa identified a subpopulation of neurons within the VMH that specifically mediates locomotion in female mice. Thus, one of the main focuses of the lab is determining whether other distinct subpopulations of neurons exist in the VMH and whether they facilitate specific physiological processes. Patricia’s project focuses on characterizing sex differences in the VMH using in situ hybridization and axonal tracing. This will help visualize sex differences in neuronal populations of the VMH, which can then aid in understanding the underlying physiological responses associated with these differences.
Outside of lab, Patricia serves as the medical outreach director for Pilipinos for Community Health, a service-oriented club on campus. She is also a part of a Christian fellowship called Locality. After graduation, she is doing a post-baccalaureate program at the Merlino Lab at NIH while applying to MD-PhD programs. Patricia would like to thank Dr. Stephanie Correa for her guidance towards her research and future career plans. She would also like to thank URSP and Mr. Tanner for their generous financial support.
| Emma Carley
Emma Carley is a fourth year biochemistry major and biomedical research minor. She works in Dr. Margot Quinlan’s lab in the Department of Chemistry and Biochemistry where she studies proteins that interact with actin. Actin is a small, globular protein that can be assembled to form filaments. During oogenesis, or egg development, in many species, an actin mesh is created, a process necessary for proper establishment of cell polarity in the developing oocyte. Emma is studying the role that the actin nucleator Spire and the motor protein Myosin V play in controlling the structure of the actin mesh using microscopy, genetic, and biochemical techniques. Emma plans to attend graduate school and hopes to continue studying the cytoskeleton. She aims to become a professor so that she can teach others about the joys of working as a scientist. She would like to thank the Undergraduate Research Scholars Program for supporting her pursuit of these goals.
| Elaine Cheung
Elaine Cheung is a fourth year at UCLA and majoring in Neuroscience. She has been working in Dr. Fong’s UCLA Gambling Studies lab since January 2017. The Fong lab uses a wide range of research methods to continually investigate the biological, psychological, and social factors associated with the onset, severity, and treatment of pathological gambling.
A lack of restorative, quality sleep can be detrimental to an individual’s overall health, which includes increased risk for cardiovascular disease, metabolic & immune dysfunction, and decreased alertness. Previous studies on community samples of pathological gamblers have shown that gamblers were more likely to have issues with sleeping compared to respondents without gambling pathology. Additionally, previous sleep studies demonstrate that disturbances in sleep-wake cycles negatively impact the circadian rhythm of individuals with neurological or behavioral disorders.
This study seeks to understand the relationship between gambling disorder treatment and sleep disturbances. Specifically, we examine whether problem gambling treatment can improve sleep-wake cycles, a topic of behavioral neuroscience. The UCLA Gambling Studies Program (UGSP) collected data from residential patients with gambling disorder in collaboration with Beit T'Shuvah (BTS), a local residential treatment center with a program for clients with gambling disorder. The overall goal is to characterize the sleep/wake cycles of problem gamblers with the type of pathological gambling behavior expressed. Understanding the circadian dysfunction that occurs in gambling disorder is a novel topic of interest.
After graduating, Elaine plans to pursue medicine and obtain an MD. She would like to thank Dr. Timothy Fong, Dr. Chris Colwell, and other members of UGSP lab for being very invaluable and helpful in her research endeavors. She would also like to thank the Boyer family and URSP for their generous support.
| Taylor Ely
Taylor Ely is a senior majoring in Marine Biology with a minor in Environmental Systems and Society. Since her sophomore year she has been working in Dr. Barber’s lab. Originally she helped Kelcie Chiquillo, a graduate student, with her research on an invasive species of seagrass, Halophila stipulacea. Now she works with Zack Gold, another graduate student, with his research on marine environmental DNA, eDNA, and how it can help assess the effectiveness of marine protected areas, MPAs. Taylor helps with DNA extractions, amplification, quantification, and purification to be sent off for sequencing. Environmental DNA can be used to quickly and effectively assess the composition of marine organisms in an area. This method is much more accurate, especially with identifying rare or cryptic species, than fish counts or any other method of sampling. However there remains much to be learned about the potential biases of this technique, limiting its implementation as a biomonitoring tool. This is why Taylor started her project to investigate the degradation rate of eDNA in the marine environment. Previous studies have only conducted experiments in laboratory conditions but her experiment seeks to find in situ decay rates. The results from this study will provide crucial insights into the temporal variation of eDNA in marine environments, helping address one of the key uncertainties of using eDNA to monitor marine biodiversity.
| Elisa Fazzari
Elisa Fazzari is a senior Neuroscience major with a minor in Biomedical Research. She has been working in the Lai Lab under the mentorship of Dr. Albert Lai since Fall 2015. The Lai Lab is focused on determining the underlying mechanisms behind primary brain cancer the goals of developing treatments and improving patient outcomes. With a concentration on diffuse glioma, the most common type of primary brain cancer, the members of the Lai Lab are dedicated to using methylation profiling techniques on patient tissue resources and glioma cell models to identify novel epigenetically silenced tumor suppressor genes in glioma, to validate their use as biomarkers of outcome, and to determine their mechanistic and therapeutic significance. Elisa’s project is aimed at uncovering methods of modulating intratumoral oncometabolite formation in IDH1WT and IDH1MUT glioma cell lines. The goal of this study is to further elucidate the mechanism for establishment of the hypermethylated phenotype in IDH1MUT tumors that ultimately leads to silencing of tumor suppressor genes. Eventually, knowledge garnered from this undertaking can hopefully lead to an effective treatment for a devastating disease.
| Sierra Foshe
Sierra Foshe is a senior Neuroscience major with a Bioinformatics minor. She has worked in Dr. Marcus Roper's Myco-fluidics lab since her freshman year.
Her project investigates cooperation between spores of the filamentous fungus Neurospora crassa. When spores germinate, they sprout tubes called hyphae that elongate and fuse to form the fungal transport network. Quorum sensing--the ability for cells to detect their neighbors--has been observed in bacteria and other fungal species. The goal of this project is to determine whether spores cooperate (grow faster with more neighboring spores), and whether this cooperation is dependent on membrane fusion or diffusible signaling molecules.
After graduation, Sierra plans to earn a Ph.D. and pursue a career in cellular/molecular biology research.
| Wendy Fung
Wendy Fung is a 4th year Neuroscience major and has been working in Dr. Elissa Hallem’s lab since Winter 2015. In the Hallem lab, Wendy investigates how neural circuits are modulated in response to changes in the environment of an organism to generate appropriate behaviors.
The free-living nematode C. elegans is an ideal model organism for our study, because a near-complete wiring diagram of its neural network has already been established. This makes it possible to examine the mechanisms by which neurons work together to produce responses to specific stimuli. One of the cues that C. elegans sense in their environment is CO2. CO2 is an ambiguous cue that may signal the presence of food, mates, and predators. The possibilities are so diverse that C. elegans must sense other stimuli to help them determine how to appropriately respond to CO2. Previous members of the lab have shown that the C. elegans response to CO2 is modulated by the internal feeding state. Wild-type worms avoid CO2 in the fed state but shift their response and are attracted to CO2 when starved. Wendy has helped identify which neurons drive this behavioral shift in CO2 response as feeding state changes. Currently, she is exploring the potential mechanisms that can modulate the activity of these neurons in the fed and starved states.
Wendy plans to attend graduate school after graduating from UCLA. She would like to sincerely thank Dr. Elissa Hallem, all members of the Hallem lab, and URSP for their continued support and guidance and for inspiring her to pursue a PhD in Neuroscience.
| Kevin Hakimi
Kevin Hakimi is a fourth year Microbiology, Immunology, and Molecular Genetics major. Since joining Dr. Antoni Ribas’ cancer immunotherapy lab in the Fall of 2016 under the mentorship of Dr. Anusha Kalbasi (junior faculty), his research has focused on studying the effect of interferons on tumor progression.
Immune checkpoint blockade as treatment for metastatic melanoma has had a profound impact on the prognosis of this disease, but remains ineffective for many patients. Recent literature has described interferon dependent signaling as a mechanism for primary and acquired resistance to immune checkpoint blockade, including anti-PD1 and anti-CTLA4 therapy. Interferons (IFN) have been shown to be an important regulator of anti-tumor responses, with IFN gamma (IFNG) directly contributing to these anti-tumor responses. However, in a subset of patients who responded to anti-PD1 immune checkpoint blockade initially, but then later developed tumor progression, genetic defects in the IFNG signaling pathway were found in relapsed tumors (eg. JAK1 and JAK2 mutations). These mutations eliminated the anti-tumor effects induced by IFNG, thereby allowing for ICB resistance.
While the mutations explained the resistance of tumors to interferon mediated anti-tumor activity, they did not explain the ineffectiveness of tumor-specific T cells. To model the efficacy of tumor specific T cells in vivo against tumors with mutations in JAK1 and JAK2, we utilized the B16-pmel adoptive cell transfer model. In this model, activated T cells bearing a gp100-specific TCR are adoptively transferred into wildtype mice bearing gp100-expressing murine melanoma (B16). Using CRISPR technology, we generated B16 cell lines in which JAK1, JAK2, IFNAR1 or B2M was genetically deleted.
We hypothesize that direct T-cell killing mechanisms will continue to allow tumor cell death in the pmel-B16 model, despite the lack of interferon signaling. Our studies will also allow us to determine the relative importance of type I versus type II interferon signaling within tumor cells to direct T cell mediated anti-tumor activity.
| Yi-Yun Ho
Peggy is a 4th year Microbiology, Immunology, and Molecular Genetics major with a minor in Entrepreneurship. She is currently working in Plath Lab in the Biological Chemistry department studying the X-chromosome inactivation (XCI) in mouse embryonic stem cells (mESCs). In particular, she is investigating the changes in the organization of the X-chromatin configuration during initiation of XCI.
XCI is demarcated by the expression and the cis-spreading of the long noncoding RNA (lncRNA) Xist from its transcription locus along the entire future inactive X-chromosome (Xi), which mediates silencing and chromatin compaction. Female ESCs provide an excellent model for XCI studies as both X chromosomes are active and XCI is induced upon differentiation.
To understand the higher-order X-chromatin changes that occur during XCI at the single-cell level, Peggy performs a series of multicolor RNA-DNA FISH experiments to label different parts of the X-chromosome in differentiating mESCs and apply high-resolution fluorescence microscopy to uncover the chromosome configuration. She is currently establishing an approach where she partitions the X-chromosome by fluorescently-labeled probes that will detect individual 35- to 45Mb-long segments or ‘patches’ that span sequentially across the chromosome linear map. By examining the distribution of the chromosomal patches with high-resolution confocal microscopy, she will be able to delineate the spatial organization of the X-chromosome at the multi-Mb level and examine how it changes during XCI.
| Vivien Ho
Vivien Ho is a senior majoring in Molecular, Cell, and Developmental Biology with a Specialization in Computing and a Minor in Biomedical Research. She has been working in the laboratory of Dr. Utpal Banerjee since March 2016. Her current project involves studying and characterizing Combined Hematopoietic Intermediate Zone (CHIZ) cells as a unique cell population in Drosophila blood cell development to better understand their identity and function. These CHIZ cells are located between the mature and progenitor cell zones in the lymph gland, an organ in which blood cells develop in Drosophila larvae. These cells express both the mature and progenitor cell markers at lower levels than true mature and progenitor cells. These CHIZ cells might be under unique regulatory mechanisms or have special functions that are not characteristic of solely the mature or progenitor cells.
Recently, she found that CHIZ cells are present among the circulating blood cells in Drosophila larvae. She also found that most CHIZ cells in circulation colocalize with a mature plasmatocyte marker. She will investigate the origin and identity of CHIZ cells in circulation and perform various experiments to find a potential explanation for their colocalization with plasmatocytes. She will also determine the fate of lymph gland CHIZ cells and their contribution to the mature cell population and zones of the lymph gland. As CHIZ cells are a key transitional cell population where progenitor cells decide which differentiated cell to become, and as pathways that influence differentiation are most likely acting specifically in these cells, the results obtained in this study may provide insights into blood development-related research.
Vivien plans to graduate in the Spring of 2018. She is motivated towards pursuing a research career in either academia or industry in the future. With this goal in mind, she will be applying to Ph.D. programs in the biological sciences in the Fall of 2017 for admission in Fall 2018. She would like to express her utmost gratitude to her post-doctoral mentors Dr. Carrie Spratford and Dr. Juliet Girard, Dr. Banerjee, and members of the Banerjee Lab for their encouragement, guidance and support.
| Kaitlyn Honeychurch
Kaitlyn Honeychurch is a fourth year majoring in Molecular, Cell, and Developmental Biology and minoring in Biomedical Research. Upon graduating from UCLA, she intends to pursue an MD/PhD degree. Kaitlyn works in Dr. Samantha Butler’s lab in the Department of Neurobiology. She is investigating the role of netrin in axon guidance in the chicken embryonic spinal cord. Axon guidance is critical since the diverse functions of the nervous system, from movement to cognition, require that the neural circuits are precisely connected to their synaptic targets during development. While the role of netrin as a guidance cue acting at a long range is well established, netrin’s function in creating an adhesive boundary, that axons grow along but do not cross, has only recently been discovered in mice. Since many experimental procedures in the developing spinal cord are more effectively done in chicken, Kaitlyn aims to determine if this new model of netrin guidance is conserved in chicken before future experiments can be done to further understand netrin in the embryonic spinal cord.
| Wendy Hung
Wendy Hung is a fourth-year student majoring in Molecular, Cellular, Developmental Biology. She has been working in the laboratory of Dr. Dong Sung An since Spring 2015. The An lab is interested in the study of genetic modification for Human Immunodeficiency Virus (HIV) resistance. HIV targets the immune cells of its host, such as Lymphocyte T CD4+ (T4) cells and macrophages. If left unattended, the levels of CD4 cells will decrease dramatically, leaving the patient extremely vulnerable to even a mild infection. HIV continuously attacks the host’s immune system until the body is unable to fight off antigens and the patient has thus entered the last stage of HIV: Acquired Immunodeficiency Syndrome (AIDS). CCR5 chemokine receptors on macrophage cells are the main entryway for HIV infection. Binding of HIV envelope glycoproteins to both CD4 and its co-receptor CCR5 on macrophage causes fusion of HIV into immune cells, which often leads to the spread of HIV infection. Currently, with the use of highly active antiretroviral therapy (HAART), the viral load can be suppressed with a cocktail of drugs that is to be administered daily, which allows the HIV patients to live extended lives. In recent years, more attention has been placed upon the possibility of altering the patient’s genes to combat HIV/AIDS due partly to the development of the CRISPR/CAS9 system. By knocking down CCR5 expression by small hairpin RNA sh1005, HIV glycoproteins are unable to bind to immune cells and therefore prevent infection. Wendy’s project focuses on the utilization of a next generation Cas9 system derived from Staphylococcus aureus, which has a lower rate of off-site targeting as well as the ability to cleave genomic sequences that might not be available to the original Streptococcus pyogenes system. She plans to utilize this Cas9 system to perform double stranded cleavages at two genes simultaneously: one for selection, and the other for HIV resistance, such as CCR5. Wendy plans to graduate in Spring 2018, hoping to pursue a career in biomedical research by applying to Ph.D. programs in the biological sciences. She would like to thank her Ph.D. mentor Dr. Olivier Pernet, Dr. An, and all of the members of the An lab for their support, encouragement, and guidance.
| Ian Hurst
Ian Hurst is currently a third year undergraduate Microbiology, Immunology, and Molecular Genetics major and studies the effect of amino acid substitutions, metal ions, and small-molecule inhibitors on the aggregation of amyloid beta, the protein believed to cause the neuropathology associated with Alzheimer’s disease. He has been conducting research in the lab of Dr. Gal Bitan since his freshman year.
Alzheimer’s disease (AD) is a progressive, degenerative disease that typically results in cognitive impairment and dementia. Amyloid-β (Aβ) oligomers are believed to be the proximal toxic agents causing the neuropathology of AD. Therefore, targeting the oligomerization of Aβ is a promising strategy for designing AD therapeutics. The Bitan lab has previously characterized a series of Aβ42 C-terminal fragments (CTFs), which have been shown to incorporate themselves into Aβ oligomers, disrupt their structure, and inhibit Aβ induced neurotoxicity. Ian plans to continue his labs research and examine whether three CTFs maintain their ability to prevent fibril formation in the presence of Zn2+ and assess whether CLR01, a small-molecule inhibitor, is another possible candidate for therapy development. He plans to study how Zn2+ affects the ability of three CTFs to inhibit fibril formation by following changes in secondary structure with circular dichroism (CD) spectroscopy. He will substantiate these results by using transmission electron microscopy (TEM) to study the resulting morphology. His research will help elucidate the effectiveness of CLR01 and CTFs as aggregation and cell death inhibitors. Ian’s work will also provide insight into possible AD therapeutics and improve our understanding of how Zn2+, CLR01, and CTFs effect Aβ42 aggregation, structure and toxicity.
Ian would like to thank his principle investigator, Dr. Gal Bitan, and the entire Bitan Lab group for their continued support, mentorship, and kindness. He would also like to thank the UCLA Undergraduate Research Center for encouraging undergraduate research in the sciences.
| Juka (Soohyang) Kim
I am a third year undergraduate majoring in Psychobiology at University of California, Los Angeles. I was born in Japan, and moved to North California to attend a high school in Los Altos six years ago. The goal of my research is to develop a method for medium-throughput screening of compounds against the toxic protein oligomers that is currently suggested to be the most likely culprit for amyloidoses. Inhibitory potency of compounds in modulating self-assembly of amyloidogenic proteins will be analyzed by quantifying the change in the oligomer size distribution of these proteins generated by photo-induced cross-linking of unmodified proteins (PICUP) when incubated with varied concentration of the modulators. The new PICUP-based method will analyze inhibitors for formation of oligomers rather than for post-oligomerization proteins, which has already been previously established.
| Kristina Kunes
Kristina has worked in the Quinlan Lab, a biochemistry lab, at UCLA since January of 2016. She investigates delphilin, a formin that accelerates actin filament formation within dendritic spines in the brain. Previously, she examined the importance of the C-terminal tail of delphilin in actin polymerization. Currently, she is working on determining the structure of delphilin using crystallization techniques. She studies biology and hopes to one day become a physician and researcher. She would like to thank URSP for supporting her as an undergraduate researcher at UCLA.
Delphilin is a mammalian formin that accelerates actin filament formation localized specifically to dendritic spines in Purkinje cells. There is a link between decreased dendritic spine number and neurodegenerative diseases. The actin cytoskeleton provides support for dendritic spines, so understanding proteins that assemble actin may yield a mechanism of dendritic spine loss or maintenance. We have previously determined that delphilin preferentially accelerates the polymerization of certain actin isoforms. These properties differ from those of other formins, suggesting differences between the structure and function of delphilin and other formins. I therefore aim to determine the crystal structure of delphilin using a metal-mediated synthetic symmetrization technique. By uncovering the structure of delphilin, I will gain valuable information regarding delphilin’s role in actin dynamics within the brain.
| Michael Le
Michael Le is a third-year undergraduate student completing his degree in Neuroscience with a minor in Biomedical Research. Since December of 2016, he has been an active contributor to the Portera-Cailliau Lab, a project that aims to elucidate the synaptic and network mechanisms of neuronal plasticity underlying functional recovery after stroke. Stroke is a devastating neurological condition caused by an acute interruption of blood flow to an area of the brain. It is the 5th leading cause of the death in the U.S., and the leading cause of adult onset disability. While advancements have been made in preventative and acute care of stroke patients, there are currently few treatments aimed at improving functional recovery after stroke. Fortunately, many patients demonstrate limited spontaneous recovery, suggesting an endogenous repair mechanism exists in the brain. Michael is interested in investigating this repair process with the goal of eventually finding methods to accelerate recovery. To do so, the lab utilizes an experimental mouse model of stroke targeted to the somatosensory cortex that processes inputs from whiskers on the snout. Michael trains mice on a whisker-based tactile discrimination “go/no-go” task to assess the loss and subsequent recovery of sensory function over time after stroke. Preliminary data shows that mice can learn this task within 2-3 weeks. After learning the task, the mice are randomized into two groups. For the control group, a stroke is targeted to an area of the forepaw representation in the mouse primary somatosensory cortex (S1) whereas for the experimental group, the stroke is targeted to the barrel field, the region specific to receiving whisker inputs. Behavior testing then continues for one month after the stroke. Through these sets of experiments, the Portera-Cailliau Lab hopes to better understand whether functional deficits revealed by this are specific to the barrel cortex and to directly study the neuronal and circuit level changes that might mediate functional recovery after stroke. After graduation, Michael aspires to pursue a career in the medical field and in academic research. He would express his deepest gratitude to the entire Portera-Cailliau lab for their never-ending guidance and support. Furthermore, he would like to thank both Dr. Romero and Dr. Clark from the Biomedical Research Minor for providing him the opportunity to step into the world of research.
| Yoon Lee
Yoon Lee is a third-year Molecular, Cell, and Developmental Biology major, with a minor in Gerontology and Biomedical Research. Since Fall 2015, she has been working under the guidance of faculty mentor Dr. Zhefeng Guo to study the elongation rate of amyloid-β.
The amyloid β (Aβ) protein, more specifically the growth of the Aβ protein, is paramount to the pathogenesis of Alzheimer’s disease (AD). Aβ aggregation is marked by several micro-processes, including nucleation, elongation, and plateau. A complete mechanistic understanding of Aβ aggregation requires the delineation of all the aggregation steps, including the rate constants of these steps. Yoon aims to use seeding experiments to directly measure the fibril elongation rates and to better define the rate constants of the aggregation of Aβ.
Besides research, Yoon is involved with The iKNITiative (UCLA’s needlecraft club), the UCLA Companion Care program and Locality Christian Fellowship. She is planning to pursue medicine.
Yoon would like to thank Dr. Zhefeng Guo for his guidance and mentorship, as well as the Wasserman family for their generosity and support of undergraduate research.
| Eumene Lee
Eumene Lee is a fourth year bioengineering student and has been conducting research in Dr. Daniel T. Kamei’s lab since the summer after freshman year. His research has focused on developing a point-of-care screening device for cervical cancer.
Though easily curable if detected in its early stages, cervical cancer continues to be one of the leading causes of death for women in resource-poor regions. Current standard screening procedures require the direct sampling of the cervix by a medical professional and the use of laboratory equipment, which consequently make these tests unsuitable and inaccessible for women in third-world countries. Thus, the objective of Eumene’s current project is to develop a self-administered, paper-based diagnostic device that can rapidly determine a woman’s risk for cervical cancer by detecting for the human papillomavirus type 16, which is the greatest risk factor. Specifically, the device will detect for the virus’s major capsid protein, L1. As a self-administered swab will present difficulty in sampling cells, an aqueous two-phase system (ATPS) will be utilized to concentrate L1 prior to detection. Furthermore, the ATPS will simultaneously serve to lyse the sample cervical cells and allow the release of the L1 from the cells.
After graduating, Eumene plans to pursue a PhD in bioengineering. Eumene would like to thank Dr. Kamei and the members of the Kamei Lab for their continued support and guidance, as well as the Undergraduate Research Scholars Program for this opportunity.
| Liang Liu
Liang Yen (Larry) Liu is a 4th year Biology Major at UCLA currently conducting research in the Lai Laboratory, which focuses on conducting research on diffuse gliomas, particularly glioblastoma, which is the most common form of primary brain cancer. Since the end of his freshman year, he has been a part of the Lai Laboratory, and as a URSP Scholarship recipient for the 2016-2017 year he is continuing his research on the hTERT gene and telomerase in glioblastoma cells, expanding on the findings from his URSP project from the previous year.
In his previous project, Larry studied the effects mutations on the promoter of the hTERT gene, which codes for the reverse transcriptase catalytic subunit TERT on the human telomerase ribonucleoprotein complex that functions to extend telomeres and prevent cell apoptosis. While telomerase is not expressed in normal somatic cells, cancer cells generally have higher telomerase expression, and those with mutations on the hTERT gene promoter show an even more upregulated gene expression. Larry discovered in his previous URSP project that this hTERT overexpression driven by hTERT promoter mutations increased sensitivity in MGMT methylated U87 glioblastoma cells to temozolomide, a chemotherapeutic agent. Despite these findings, there is currently a gap in the mechanistic understanding of how hTERT promoter mutations interact with MGMT promoter methylation to increase temozolomide sensitivity. Larry’s URSP 2017-2018 project therefore aims to explain the mechanism of interaction between hTERT promoter mutation and MGMT promoter methylation to increase temozolomide sensitivity.
In the future, Larry plans on applying to medical school after graduating in Spring 2018, and he hopes to continue conducting scientific research throughout his career. He would like to thank Dr. Albert Lai, Tie Li, Christopher Cox, and all the members of the Lai Laboratory for their mentorship and guidance. He would also like to thank the Van Trees and Boyer Endowment as well as the URSP Program for their gracious support for his research endeavors.
| Tiffany Lu
I am a third year Biophysics major and I joined the Sagasti lab in October 2016. My project focuses on the role of cell-cell junctions in the formation of microridges, fingerprint-like actin-based protrusions on the surface of mucosal epithelial cells. Other members of the Sagasti Lab found that microridge formation may be affected by tension of the apical membrane, which could be mediated by tight junctions. I have found that tight junctions are likely required for microridge formation. Microridges were severely disrupted by the knockdown of ZO-3, a tight junction protein, with a morpholino. I am further testing whether tight junctions are required for microridge formation by using other methods to inhibit tight junction function, such as an inhibitory peptide that affects claudin B, another tight junction protein. Other work in the lab has also found that myosin-based contractions of the apical membrane are required for microridge formation. I observed that embryos injected with the ZO-3 morpholino had an increased number of myosin-based contractions. To determine the role of these contractions in microridge formation, I will treat fish that have been injected with the ZO-3 morpholino with blebbistatin, a myosin inhibitor. Determining the role of tight junctions in microridge formation will provide more insight into how cells change their shape to fit a specific function. A better understanding of microridge formation would also provide insight into how microridges affect epithelial cell function in human tissues, and how defects in epithelial cell structure can lead to disease.
I would like to thank Dr. Alvaro Sagasti, my graduate student mentor Aaron van Loon, and the rest of the Sagasti lab for their teaching, mentorship, and support.
| Justin Mak
Justin Mak is currently a fourth year undergraduate majoring in Molecular, Cell, and Developmental Biology. Since Winter 2017, he has been working in Dr. Luisa Iruela-Arispe’s laboratory where he researches how dysfunctional NOTCH3 signaling is involved in the development of CADASIL, a form of vascular dementia. Particularly, Justin’s project aims to shed light on the role of NOTCH3, a protein primarily expressed in the vascular smooth muscle cells of adults, in the maintenance of vascular homeostasis.
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is most common form of familial vascular dementia, with incidence rates as high as 1 in 1000. Mutations in the gene NOTCH3 have been known to cause CADASIL for over 20 years, yet the role of NOTCH3 in cellular homeostasis is not well understood. Loss of NOTCH3 signaling has been implicated in impaired microvasculature function and the resultant widespread multifocal white matter lesions in the brain typical of CADASIL. RNA-Seq data, generated by the Arispe Lab, from the vascular smooth muscle cells (vSMCs) of Notch3 knockout mice has shown decreased expression of several genes contributing to the dystrophin glycoprotein complex (DGC), a multimeric protein complex linking the myocyte contractile apparatus to the sarcolemma and extracellular matrix. Failure to form the DGC impairs contractile stability and results in muscle damage in response to normal contraction. While most work characterizing the DGC and pathologies associated with its loss have largely focused on skeletal and cardiac muscle, many of components of the DGC are highly expressed in vSMCs at the transcriptional level. Thus, Justin’s project, using immunohistochemistry to characterize the vasculatures of Notch3 knockout mice, will provide further insight into the NOTCH3 signaling pathway and lead to a better understanding of CADASIL pathology.
| Manan Mehta
Manan Mehta is a fourth-year student majoring in Biology. He has worked with Dr. Patricia Phelps since August 2014, and currently works in close collaboration with graduate student Katie Ingraham. A major focus of the Phelps lab is to investigate the role that Olfactory Ensheathing Cells (OECs) play in axonal regeneration after a complete spinal cord transection. OECs are unique glial cells found in the periphery associated with the olfactory epithelium and in the outer layers of the olfactory bulb. After a complete spinal cord transection of the rat thoracic spinal cord, OECs were grafted near the lesion site and appear to support axonal regeneration. Rats that received the OECs have improved in their stepping ability, and have increased axon density in the normally inhibitory injury site. Descending serotonin (5-HT) positive axons are a specific axonal population that can be evaluated for functional connections across the injury site because there are few intrinsic serotonergic neurons in the spinal cord. These serotonergic axons descend from the brain stem motor regions (Raphe) and are vital to the production of coordinated movement. Specifically, Manan is working with OEC- or fibroblast-transplanted spinal rats that also were treated with epidural stimulation and climb training for 6 months.
Manan is currently using fluorescent immunohistochemical techniques to visualize 5-HT-labeled axons that cross the injury site in these rats. A recent advancement in spinal cord injury analysis is 3D visualization of the injury site environment and this is important to understanding the entire architecture of the injury site. Using Neurolucida software, Manan reconstructs the injury site of the rodents and uses the 3D reconstruction to quantify the regenerative capacity of 5-HT serotonergic axons post injury with quantitative volume analysis to gain further insight on the behavior at the injury site with axon bundle tracing. This research ultimately seeks to help those who are paralyzed, ultimately seeking to help regain motor function and improve overall quality of life for the over 5.6 million people who suffer from some degree of paralysis in the United States.
| Patrick Minassians
His current project focuses on both assaying the thermal stability of NELL-1, a protein shown in animal trials to promote bone regeneration, and fine-tuning the process required to perform such assessment. Using a process known as a thermal shift assay, the melting temperature of NELL-1 will be determined under several formulation conditions, including after the addition of various excipients. The results of this project will help to establish the optimal storage and processing conditions for NELL-1 to increase its potential as an effective therapeutic for osteoporosis.
Patrick would like to thank Dr. Benjamin Wu, his postdoctoral mentor Dr. Yulong Zhang, and all the members of the Wu Lab for their guidance and support. He would also like to thank Mr. Diener and the Undergraduate Research Scholars Program for supporting his project.
| Aditi Newadkar
Aditi Newadkar is a fourth-year undergraduate student completing her degree in Neuroscience with a minor in Biomedical Research. She has been a part of the Portera-Cailliau Lab since March 2016, where she is interested in understanding the behavioral deficits seen in mice with Fragile X Syndrome (FXS).
FXS is the most commonly inherited form of mental impairment, affecting 1 in 4000 males, but there is currently no effective treatment for the condition. It is caused by the lack of a protein that is crucial for shaping neural connections, resulting in autistic traits such as delayed learning, challenges in social interaction, and abnormal sensory processing, which is the focus of this project. Abnormal sensory processing results in sensory hypersensitivity, where patients with FXS experience an overload of sensation that often leads to anxiety. Her research has focused on reversing these deficits in visual processing in FXS using a mouse model. She trains mice on a behavioral paradigm, uses histological techniques to analyze brain tissue, and images these slices to look for expression of certain proteins. Her project aims to identify a reversible brain circuit deficit in an experimental model of FXS that holds promise for the treatment of autism.
In the future, Aditi aspires to practice medicine, and she hopes to integrate research into her medical career. Aditi would like to express her gratitude towards Dr. Carlos Portera-Cailliau for his sincere and excellent guidance in both her research and future career. She would also like to thank Dr. Anubhuti Goel for her superior mentorship and support.
| Kiana Nguyen
Kiana Nguyen is a fourth year student majoring in Biology and has been conducting research under the mentorship of Dr. Joanne Weidhaas since Winter 2016. The Weidhaas lab studies the KRAS-variant, a let-7 miRNA binding site mutation located in the 3’ UTR of the KRAS oncogene. The KRAS-variant has been clinically utilized as a marker for increased risk of non-small cell lung cancer, premenopausal triple negative breast cancer, and ovarian cancer, in addition to differential response to cancer treatments.
Kiana’s specific aim is to characterize the underlying signaling pathways used by cells with the KRAS-variant to drive differences in cellular signaling and enhanced oncogenesis. Using perfectly-matched, isogenic normal breast epithelial cells with (MCF10AKRAS+/-, MT) and without (MCF10AKRAS-/-, WT) the KRAS-variant, Kiana currently investigates the role of estrogen receptor and growth factor receptor signaling on malignant tumorigenesis and its dependency on the KRAS-variant.
KRAS-variant cells also exhibit a dramatic acquisition of mesenchymal phenotypes, suggesting a baseline epithelial-to-mesenchymal transition (EMT). Because cancer metastasis heavily depends upon EMT, understanding how KRAS-variant signaling promotes EMT may provide insight on cancer cell invasiveness and motility. Since 1 in 5 breast cancer patients have the KRAS-variant, understanding the impact of different molecular inhibitors of these pathways is crucial, and our investigation will contribute to the development of novel breast cancer therapeutics and targeted therapies. Ultimately, Kiana aims to improve the prognosis of women with KRAS-variant breast cancer and empower them with information to take charge of their own health.
Upon graduating, Kiana plans to pursue a career in medicine and academic research. Kiana would like to express her deepest gratitude towards Dr. Porteus and the Boyer family for their generous support of her research. Kiana would also like to thank Dr. Weidhaas, Dr. Jung, and Emily Rietdorf for their continued mentorship and unwavering support.
| Christopher O'Connor
Since its launch in 2009, the Kepler satellite has provided astronomers with extensive demographic data on planetary systems, many of which bear little resemblance to our Solar System. For instance, many of these systems contain one or more planets intermediate in size and composition between Earth and Neptune -- so-called “super-Earths,” of which the Solar System has none. These planets can be broadly explained if they formed from a nebula more massive than that which birthed the Earth and its siblings, but certain statistical properties of the Kepler planet sample remain unexplained by this model. Meanwhile, other observations show that up to one-fifth of stars similar to the Sun host planets analogous to Jupiter or Saturn, gas giants which are hundreds of times more massive than the Earth and several times more distant from their stars. It is likely, therefore, that some of the Kepler systems contain such planets, which, due to their large orbits, have eluded detection. How does their gravitational influence affect the formation of interior planets? Can their presence account for any of the unexplained properties of the Kepler systems? What might this imply about the history of the Solar System? These are some of the questions which Chris is investigating, primarily by way of computer simulations of planet formation.
When he is not poring over a computer screen or a physics textbook, Chris can be found playing saxophone and clarinet in the UCLA marching and symphonic bands. Following graduation, he intends to pursue his Ph.D. in astronomy and astrophysics and an academic career thereafter. He gratefully acknowledges the mentorship of Prof. Hansen and the generous support of the Litton Endowment for his research.
| Kelsey Ouyang
Kelsey Ouyang is a third year student majoring in Microbiology, Immunology, and Molecular Genetics and minoring in Art History. Since joining Dr. Jenny Kim’s laboratory in Spring of 2016, she has explored the mechanisms of immune response in common skin conditions.
Affecting 17 million people in the United States alone, acne vulgaris is the most common skin disease, affecting people regardless of race or gender. The pathogenesis of acne is considered multifactorial with several significant pathogenic factors including increase in the production of sebum due to androgen stimulation, hyperkeratinization and clogging of sebaceous follicles, inflammation, and perhaps most importantly, the growth and proliferation of Cutibacterium acnes, or C. acnes, previously named Propionibacterium acnes. Most humans harbor C. acnes, but not all of them are affected. At the strain level, C. acnes distributions are different among healthy and acne patients, suggesting that different C. acnes strains may play differing roles in acne vulgaris. Understanding these differences between the strains is crucial to understanding how C. acnes is involved in the pathogenesis of acne. Though there are increasing amount of studies aimed at understanding the mechanisms by which acne associated C. acnes and healthy associated C. acnes strains differ in their modulation of adaptive responses, there is still a gap in understanding of the relative fitness of the different C. acnes strains. Thereby, Kelsey plans to perform competition assays to identify which acne strains outcompete other strains in an effort to determine whether certain healthy associated strains can triumph certain acne strains and vice versa.
Kelsey would like to thank Dr. Jenny Kim, her postdoctoral mentors, Dr. George Agak and Dr. Min Qin, as well as the other members of the Kim lab for all their continuous support.
| Roshni Patil
I am a fourth-year student majoring in Physics with an interest in solid state physics and nanotechnology. I have been working in Professor B. C. Regan’s laboratory since February 2017 on microscale thermoelectric coolers.
The thermoelectric effect is a phenomenon where an electromotive force applied across the junction between two different electrical conductors either accumulates or extracts heat at the junction. Thermoelectric coolers and generators are practical applications of this effect, which could be used to improve refrigeration and store waste heat. However, these devices are uneconomical because of their low efficiency, which is quantified by the dimensionless figure of merit, ZT. ZT is directly proportional to the electrical conductivity and inversely proportional to the thermal conductivity. Phonons and electrons contribute to the thermal conductivity of these materials. Suppressing phonon modes reduces the thermal conductivity without affecting the electrical conductivity. This is achieved in 2D materials, so 2D microscale thermoelectric devices should achieve better ZT values than their 3D counterparts as suggested theoretically by Mildred Dresselhaus. We fabricate these thermoelectric devices using the wet and dry transfer processes.
We use a technique called Plasmon Energy Expansion Thermometry (PEET), which is based on Electron Energy Loss Spectroscopy (EELS), to map the temperature changes at the junction of the thermoelectric devices when they are reverse biased. From the data obtained from PEET, we will measure the temperature gradients in the thermoelectric coolers. We expect to observe cooling at the junction and a significant improvement in the ZT values of the world’s tiniest thermoelectric devices as compared to their 3D counterparts.
I plan on attending graduate school next year in either experimental condensed matter physics or materials science.
| Divya Prajapati
Divya is a third year Molecular, Cell, and Developmental Biology major and Global Health minor. She has worked in Dr. Luisa Iruela-Arispe’s lab since the spring of her first year and currently studies endothelial barrier function and its relevance to tumor cell extravasation.
Endothelial cells line the interior surface of blood vessels to form a physical barrier which selectively regulates substance exchange between blood vessels and tissues. Previously, the Arispe Lab identified VAV3 as a barrier-regulating molecule and characterized barrier heterogeneity in diverse vascular beds. In particular, Divya has helped characterize VAV3’s heterogeneous distribution in mural tissue and its effects on junctional and cytoskeletal protein localization and expression. In addition, she has investigated how various compounds protect the endothelial barrier against tumor cell extravasation. Divya is now testing barrier resistance and protein expression in endothelial cells with mutated or knocked down VAV3, Rap1, and Rac1 in hopes of elucidating the VAV3 mechanistic pathway.
Divya would like to sincerely thank Dr. Luisa Iruela-Arispe, her postdoctoral fellow mentor Dr. Georg Hilfenhaus, and the members of the Arispe Lab for their mentorship, support, and kindness. She would also like to thank the UCLA Undergraduate Research Center for encouraging undergraduate research.
| Kendal Reeder
Kendal Reeder is a fourth-year student majoring in Psychobiology with a specialization in Computing. Since September 2016, Kendal has served as a research assistant in the Child FIRST Laboratory under the supervision of Dr. Bruce Chorpita. The Child FIRST Lab aims to improve child mental health services by exploring innovative treatment designs, clinical decision-making processes, and mental health system structures.
Currently, Kendal is exploring the effects of common elements of evidence-based treatments. The elements of in-session role-play, homework assignment, and caregiver involvement have been identified as strategies that may make evidence-based treatments more effective; while these approaches are promising, it is still unclear whether they improve treatment outcomes in community mental health settings. Kendal’s study aims to answer this question by investigating whether treatments that include these strategies are associated with reduced rates of reenrollment in mental health services at 1- and 2-year follow-ups, which is a marker of successful treatment.
| Daniel Sanford
Daniel is a fourth year Biology major and Geography minor at UCLA. He is an Undergraduate Researcher at the West Los Angeles, VA Medical Hospital in the department of Gastroenterology and Hepatology and has been actively researching since 2015. He works on multiple projects, but his main project investigates the neuropeptide Calcitonin Gene-Related Peptide (CGRP) and its impact on obesity and metabolism. Peripheral proteins serve as key regulators of metabolic characteristics, appetite and weight gain/loss. This makes these proteins relevant and important research targets that can help address the obesity epidemic with non-surgical remedies. Using state of the art metabolic cages, he is able to analyze energy expenditure, activity, food and water consumption, as well as the metabolic profile of mice that have been injected with the peptide of interest. The data from these experiments provides novel information on the relevance and potential benefit of these neuropeptides. He additionally helps with long term diet studies that analyze the impact of diet on fatty liver disease and on body composition.
Following graduation, Daniel plans to pursue a career in the medical field as a surgeon. Daniel would like to thank Mrs. Gottlieb for her generosity in supporting his research endeavors. He would also like to thank his faculty mentors Dr. Patrizia Germano and Dr. Joseph Pisegna for their guidance and support.
| Yao Chang Tan
Yao Chang Tan is a fourth year student majoring in Molecular, Cell, and Developmental
Biology, and minoring in Biomedical Research. He joined Dr. Amander Clark’s lab in
Spring 2016, and has been researching the role of critical regulators in germ cell
For multicellular organisms, germ cells represent the origin of new individuals, and are
essential for passing genetic material to future generations, providing genetic diversity,
and driving evolution. The germ cell lineage originates early during development, and
goes through a series of intricate developmental processes to generate fully mature
gametes. One of these processes is epigenetic reprogramming, where most of the
genome’s epigenetic marks, such as DNA methylation, are erased. Certain parts of the
genome are protected from this reprogramming, but the exact genes and mechanisms
responsible for this protection are unclear. A gene that is thought to play a key role in
this protection is Trim28. Trim28 functions as a co-repressor that mediates gene
silencing, by recruiting downstream effectors like SETDB1, HP1, and the HDAC
complex. My project aims to uncover the role of Trim28 in the maintenance of DNA
methylation in primordial germ cells (PGCs), and how the selective deletion of Trim28
affects mouse PGC development and fertility.
After his graduation, Yao Chang plans to pursue a career in medicine. He would like to
wholeheartedly thank his incredible mentors, Dr. Amander Clark and Dr. Yu Tao, as well
as the rest of the Clark lab for their continued guidance, kindness, and support. He
would also like to express his gratitude to the Gottlieb Endowment for their generous
| Vincent Tran
Random mutations in the retroviruses, especially human immunodeficiency virus type 1
(HIV-1), are constantly occurring. These mutations may result in drug resistance that
complicates a patient’s treatment. If drug resistant mutants could be identified beforehand, the
process of finding the most effective treatment for the patient could be shortened, saving valuable
time and resources. In this study, a drug screening of a mutant HIV-1 library, with mutations
made in the integrase (IN) gene, was conducted in order to determine drug resistant HIV-1
mutants. The mutant library was created using the transposon directed base-exchange
mutagenesis (TDEM) method. Using an in vitro infection assay with a human T cell reporter
line, a drug screening of the mutant library was carried out using the well studied IN inhibitor
(INI), raltegravir, and a novel INI, BI-D. Specific drug resistant mutants were selected, and each
mutant’s drug resistance was confirmed and characterized via another in vitro infection assay
using the same human T cell reporter line. In addition to identifying drug resistant HIV-1
mutants, the data can be used to infer the molecular mechanisms that confer the drug resistance.
| Juna Yi
A hallmark characteristic of cancer cells is uncontrolled proliferation. This is the consequence of impaired cell cycle checkpoints and results in an increased demand for nucleotides, the building blocks for DNA replication. At any given time, cancer cells possess an insufficient supply of nucleotides for genome replication, thus, the ability to produce or nucleotides is essential for cancer cell growth and proliferation. The two metabolic pathways that produce nucleotides are the de novo pathway (DNP) and the nucleoside salvage pathway (NSP). These pathways are convergent and interchangeable, in that inhibition of a single-pathway can be compensated by the other. In response to nucleotide pool insufficiency, the replication stress response (RSR) pathway is activated to decrease nucleotide consumption and increase nucleotide production. Our group has shown that pharmacological inhibition of the RSR pathway along with DNP and NSP using potent and selective small-molecule inhibitors leads to extensive DNA damage and programmed cell death in leukemia cells and is well-tolerated in vivo. A better understanding of the environmental and signaling mechanisms that regulate the metabolic pathways necessary to synthesize the building blocks for DNA replication may reveal potential therapeutic targets against tumor cells.
| James Zhen
James Zhen is a third-year undergraduate student at UCLA pursuing a major in Biochemistry with a minor in Biomedical Research. He has been working in Dr. Zhefeng Guo’s lab since Winter 2017. The Guo lab investigates the structural biology of amyloid-related neurodegenerative diseases, such as Alzheimer’s disease, focusing on studies in protein structure and aggregation.
James’s current research is on the determination of Abeta oligomer structures using electron paramagnetic resonance (EPR) spectroscopy. EPR is an underutilized method that detects unpaired electrons in spin labels in a sample, which can provide valuable information about the microenvironment of a protein, including distances between residues and the presence of secondary structures. Compared with other structural techniques such as NMR and X-ray crystallography, EPR has some unique advantages which make it a power technique for the studies of Abeta oligomers. Drugs are reliant on protein structure for targeting specific pathogenic pathways, and further structural characterization of Abeta oligomers will be crucial for progress towards the treatment of Alzheimer’s disease.
James would like to thank Dr. Zhefeng Guo and the other members of the Guo Lab for their guidance and support.
| Philip Zhou
My name is Philip, and my hometown is Dallas, TX. I am a third year MCDB major working in Nakano Lab. I have been engaged in research for a little over a year now, and my current project researches how glucose affects heart development. My participation in research has greatly influenced my ability to critically assess and interpret new information, both in outside of academic settings. One of my most enjoyable research experiences was this past summer when I participated in the Amgen Scholars Program in Japan. I travelled to Japan to perform breast cancer research at Kyoto University for 8 weeks. Outside of lab, I enjoy swimming and taking urban dance workshops.
Congenital heart disease (CHD) is the most common birth defect in the United States. Its risk greatly increases in diabetic pregnancies, which indicates that there is a correlation between hyperglycemia and the development of CHD. Our lab has research on the mechanistic basis behind how high glucose concentrations negatively affect cardiac development, and I am now working on how chemical inhibitors can counteract the effects of hyperglycemia. Through manipulating human embryonic stem cell derived cardiomyocytes, I can analyze how these inhibitors can act as drugs which offer rescue from inhibited cardiac development. These findings could translate over to clinical applications for congenital heart disease. The prospects for this research are exciting since my work can contribute to a possible treatment for a birth defect that affects tens of thousands of infants per year.