urc-care home srp course info research funding and scholarships urc-care programs Summer Programs conferences profiles of students urc-care staff
URC-CARE logo urc-care home urc-care home UCLA Home Page
 

The Undergraduate Research
Scholars Program

2008-2009


        

Mr. Karan Mehta
Mr. Aaron Meyer
Ms. Vanessa Minassian
Mr. Furqan Muqri
Mr. Charles Ng
Ms. Marina Oster
Mr. Roland Palvolgyi
Ms. Michelle Peng
Mr. Parag Sampat
Mr. Ting-Chang Sheu
Ms. Stacey Shiigi
Ms. Sanaa Suharwardy
Mr. Hung Trinh
Ms. Wendy Tseng
Mr. Jonathan Vinea
Ms. Sue Wang
Mr. Samuel Wilson
Mr. William Wong
Ms. Katherine Wu
Mr. Fangfang Xing
Ms. JoJo Yang
Ms. Sophia Yang

Mr. Karan Mehta
Mentor: Dr. Benjamin Williams
Funding: Bonner Scholar
Title: Tunable phase elements for terahertz semiconductor lasers

Karan Mehta and Dr. Benjamin Williams

Karan Mehta is a third year Electrical Engineering and Physics major, and is currently working in Prof. Benjamin Williams’ lab in the Department of Electrical Engineering.

A lack of convenient lasers operating at frequencies in the terahertz range, as well as the range of promising applications of sources in this frequency range, has spurred much research into the development of terahertz quantum cascade lasers during recent years. The development of a frequency tunable source is a further challenge, with applications in terahertz spectroscopy. Designing a quantum cascade laser’s cavity as a transmission line incorporating voltage-tunable lumped-element capacitances based on metal-semiconductor junctions is one potential path to a tunable terahertz laser; by adjusting these capacitances, the “allowed” resonant frequencies in the cavity, and hence the operating frequencies of the laser, could potentially be adjusted. Karan will investigate the feasibility of such an approach to obtain widely-tunable terahertz semiconductor lasers, and phase-tunable elements for terahertz integrated circuits.

 

Back to top

Mr. Aaron Meyer
Mentor: Dr. Daniel Kamei
Funding: Sparks Scholar
Title: Concentration of Nucleic Acid Biomarkers Using Aqueous Two-Phase Systems

Aaron Meyer and Dr. Daniel Kamei

Aaron Meyer is a fourth-year bioengineering major. He has worked in the laboratory of Dr. Daniel T. Kamei in the Department of Bioengineering since September 2006, examining the use of novel two-phase surfactant systems in order to concentrate diagnostically significant biomarkers.

Researchers have noted the presence of unique markers in the saliva and urine of patients with certain disorders such as oral squamous cell carcinoma and bladder cancer. Identifying these markers would allow for the detection of the corresponding disorders, and early detection typically results in a much higher survival rate, even beyond the promises of currently experimental treatments. However, the tested fluids contain a wide array of molecules, very few of which are significant. Ideally, nascent disorders would be detected through regular screening; however, current detection methods require expensive equipment and special training, precluding their use in a clinical setting. Using the methods Aaron is investigating, the ability to selectively concentrate these markers might be increased, thus significantly increasing the sensitivity of current tests. The nature of surfactant systems additionally allows for their use in a clinical environment for screening purposes in cheaper, easier to use, and more environmentally friendly forms.

Aaron is extremely grateful for the guidance he has received from Dr.Kamei. He also appreciates the opportunities offered through URC/CARE and the assistance offered by its staff. Aaron is currently applying to graduate schools and plans to pursue a Ph.D. in bioengineering.

 

Back to top

Ms. Vanessa Minassian
Mentor: Dr. Linda Baum
Funding: Bonner Scholar
Title: Effects of alpha-2-6 sialic acid on T cell migration

Vanessa Minassian and Dr. Linda Baum

Vanessa Minassian is a fourth year undergraduate at UCLA majoring in Microbiology, Immunology, and Molecular Genetics. She has been a volunteer student researcher in the Department of Pathology and Laboratory Medicine since March of 2007, under Dr. Linda Baum.

Vanessa's research over the years has encompassed T cell migration and the various factors that regulate this process. T cell adhesion and migration is crucial for the efficient mounting of an immune response. Vanessa is currently studying the potential role of alpha-2-6 sialylation of N-glycans on T cell migration regulation. N-glycans are complex carbohydrate chains found on T cell surfaces, while sialic acids are 9-carbon monosaccharides that bind to these molecules to modify cell function. It has been previously shown that sialylation of cancer cells up-regulates their adhesion and migration. Since a specific correlation between T cell migration and sialylation has not yet been concluded, Vanessa aims to identify the specific role and mechanism of alpha-2-6 sialic acid in this process.

Vanessa would like to thank Dr. Linda Baum, Shuguang Bi, and all the members of her lab for their guidance and support, as well as Mr. Gaulke for the generous Margaret Bonner Estate scholarship.

 

 

Back to top

Mr. Furqan Muqri
Mentor: Dr. Asim Dasgupta
Funding: Van Trees Scholar
Title: Host Cell Interaction in Hepatitis C Infected Cells

Furqan Muqri and Dr. Asim Dasgupta

Furqan Muqri is a fourth-year undergraduate student majoring in Microbiology, Immunology, & Molecular Genetics (MIMG) and pursing a minor in Art History. After previously working in a lab researching the Epstein-Barr Virus, he joined Dr. Asim Dasgupta’s lab in the MIMG department in January 2008. Under the guidance of Dr. Dasgupta, he has learned more about the role of the Hepatitis C Virus (HCV) and its role in the tumorigenicity of liver cells into hepatocellular carcinoma.

Cell cycle deregulation and blocking of apoptosis are the two main causes of tumorigenicity in cancerous cells. In Hepatitis C Virus infected cells, many factors have been identified by microarray analysis to contribute to one of these two events. An increase in the Ese-1b gene, one of the Ets transcription factors has been shown to be upregulated in cells infected by the core protein, a transformative protein that is produced by the HCV. Furqan’s project is to test whether the upregulation of the transcription factor, which has been shown to be upregulated in other cancers, is on the mRNA and protein level as well, along with testing the effects that Ese-1b has on the cell. These results may help elucidate what role Ese-1b plays in the formation of hepatocellular carcinomas.

After graduating in the spring, Furqan plans to attend medical school with hopes of becoming an academic physician. He would like to thank Dr. Dasgupta for his guidance and support for his project as well as the lab members who help him daily. He would also like to thank the benefactors of the Van Trees Scholarship as well for the financial support as well as the Undergraduate Research Center for this amazing opportunity.

 

Back to top

Mr. Charles Ng
Mentor: Dr. Kenneth Bradley
Funding: Boyer Scholar
Title: Anthrax Toxin Receptor 1: Affinity Modulation of Protective Antigen Binding

Dr. Kenneth Bradley and Charles Ng

Charles Ng is a fourth year Biophysics Major with a minor in Biomedical Research. He conducts research under the guidance of Dr. Ken Bradley and graduate student Jordan Ramey. The Bradley lab investigates the biological actions of toxins produced by Bacillus anthracis, the causative agent of the disease Anthrax. Bacillus anthracis is a gram positive, rod shaped bacterium which forms endospores. Its toxin consists of three proteins, protective antigen (PA), lethal factor (LF), and edema factor (EF). Two cell surface receptors have been shown to bind PA, tumor endothelial marker 8 (TEM8) and capillary morphogenesis gene 2 (CMG2). A group of transmembrane αβ-heterodimeric proteins known as integrins have similarities to TEM8 and CMG2. Half of all integrin α chains contain an extracellular inserted (I) domain, a major ligand binding site. Both receptors contain an I-domain. Within the I-domain there is a conserved metal ion dependent adhesion site (MIDAS). In integrins with MIDAS containing I-domains, substitution of a threonine to an alanine is shown to disrupt ligand binding and metal coordination. The focus of Charles’s research will be to determine whether a mutation of this conserved threonine to alanine (T118A) in the MIDAS motif of TEM8 causes a similar change in affinity regulation as has been seen in integrins. Previous in vitro research has shown that the T118A mutation causes a marked decline in affinity towards PA. However it remains unclear whether this is due to a closed low affinity conformation. This is in contrast to CMG2 where the mutation has little effect. Therefore Charles seeks to elucidate the structure and affinity of TEM8 in this low affinity putatively closed state.

Charles would like to thank Dr. Ken Bradley and Jordan Ramey for their continued guidance as well as the generous support of the Boyers.

 

Back to top

Ms. Marina Oster
Mentor: Dr. Robert Wayne
Funding: Wasserman Scholar
Title: Genomic-scale SNP genotyping of the Arctic wolf: ecology and adaptation over space and time

 

Marina Oster and Dr. Robert Wayne

Marina is a fourth-year Biology major who started working in Dr. Wayne’s lab in 2007 under the mentorship of Dr. John Pollinger.

Her current research is on an NSF funded project on the SNP genotyping of the Arctic wolf. Using a canid genotyping chip, gray wolf variation from six ecotypes is in the process of being characterized to discover genome-wide variation patterns and define diagnostic SNPs that permit the assignment of wolves to these very ecotypes. Marina’s work in transcriptome cDNA preparation and post mass sequencer run comparisons will allow her to see if wolves exhibiting different behavior (e.g. migratory vs. nonmigratory) and living in different ecosystems have different RNA expression patterns.

Marina would sincerely like to thank Dr. Wayne for giving her an opportunity those two years ago and Dr. Pollinger for his patience and kindness. She is also grateful to all of the people working in the Wayne lab for the very healthy and friendly environment that they foster - a true reflection of their open personality and encouraging character.

 

Back to top

Mr. Roland Palvolgyi
Mentor: Dr. Judith Berliner
Funding: Wasserman Scholar
Title: Elucidating the mechanism of Ox-PAPC induced extracellular cleavage of VEGFR2 in human aortic endothelial cells

Dr. Judith Berliner, Roland Palvolgyi and Dr. Sangderk Lee

Roland Palvolgyi is a fourth-year pre-medical student majoring in Physiological Science. Having conducted research for 3 years and working in Dr. Judith Berliner’s pathology lab since the spring of 2007, he is now embarking upon his departmental honors thesis. His project concerns the physiological mechanisms by which oxidized phospholipids cause oxidative stress and ultimately lead to atherosclerosis. In human aortic endothelial cells, phosphorylation of the VEGFR2 integral membrane receptor is found to be important in the signaling pathway that stimulates the expression of pro-inflammatory cytokines such as Interleukin 8. Previous experiments have shown that Ox-PAPC, an oxidized phospholipid, induces the extracellular cleavage of VEGFR2, creating a novel 150 kDa band observed on western blots. Taking these data one step further, Roland will test whether this cleavage is caused by the Ox-PAPC induced activation of a matrix metallo-protease by silencing candidate enzymes with siRNA transfection.

This hypothesis is highly significant because it could expand our knowledge of the signaling pathway that leads to the formation of atherosclerotic plaques in human aortic endothelial cells. If plaque rupture occurs, it causes blood clots to form and occlude vessels, which results in heart attack and stroke. Through elucidating the mechanism for atherosclerosis, the development of new pharmaceuticals has the potential to reduce this leading risk factor for heart disease.

Roland will be graduating in 2009 and is currently applying to medical school with the hopes of becoming a surgeon. He would like to thank the Wasserman family and the URSP program for their generous support.

Back to top

Ms. Michelle Peng
Mentor: Dr. Debora Farber
Funding: Wasserman Scholar
Title:Interaction of a novel protein, ZBED4, with scaffold attachment factor B1

Dr. Debora Farber and Michelle Peng

Michelle Peng is a fourth year student majoring in Molecular, Cell, and Developmental Biology. She is currently conducting research under the guidance of Dr. Debora Farber in the Jules Stein Eye Institute retinal biochemistry laboratory.

The rod and cone photoreceptors of the vertebrate retina are the cells involved in vision. Mutations of the genes coding for the visual pigments leads to a variety of congenital color vision deficiencies, color blindness, and cone dystrophy. Dr. Farber’s laboratory is specifically working in the isolation and characterization of genes involved in hereditary retinal diseases. Once the protein/enzyme products of these genes have been identified, gene therapy will be implemented to deliver the normal form of these genes to the proper cells. Currently, they are also investigating non-viral and non-invasive delivery systems.

Michelle will be studying a novel ZBED4/KIAA0637 protein which was discovered through subtractive and differential screening in the retina of cone dystrophic dogs, particularly in regards to its interaction with scaffold attachment factor B1 (SAFB1). SAFB1 overexpression has been shown to play a key role in inhibiting proliferation of breast cancer cells by acting as an estrogen receptor co-repressor. The interaction of ZBED4 with SAFB1 suggests that ZBED4 may also serve as a regulator of proper cell response to estradiol, thus preventing estrogen- responsive breast cancer.

Michelle would like to thank Dr. Debora Farber, the Farber laboratory, and the Wasserman family for their support in her research interests.

 

Back to top

Mr. Parag Sampat
Mentor: Dr. Ben Wu
Funding: Oppenheimer Scholar
Title: Cytocombatibility of photoinitiation with cells

Parag Sampat and Dr. Ben Wu

Parag Sampat is a fourth year undergraduate majoring in bioengineering. He joined Dr. Ben Wu’s laboratory in his junior year, and currently works on a research project under the guidance of Haison Duong.

There is a need to find an effective delivery method to noninvasively implant a combination of cells and growth factors to optimize bone regrowth and regeneration. Parag’s project includes engineering a procedure in order to create an effective method to deliver a gel into a bone defect. This requires a combination of multiple elements, one of which is a specific growth factor that allows bone cells to grow. Through previous studies conducted in Dr. Wu’s laboratory, an effective and specific growth factor, Nell-1, is able to promote calvarial cell mineralization. In addition, chitosan and alginate are two biocompatible and biodegradable materials that have shown positive results in previous experiments. However, the bulk of this project includes creating a polymer with interspersed cells that are able to survive photoinitiation. Two effective photoinitiators are camphorquinone with a combination of triethanol amine, used specifically for visible light, and riboflavin, used specifically for UV light. Parag will be analyzing different concentrations of both these photoinitiators as well as varying cell amounts to find an optimal procedure to maximize bone growth in vivo.

Parag would like to thank the Oppenheimer Estate for their generous support. He would also like to thank Dr. Wu and Haison for their unwavering support and guidance in the research lab.

 

Back to top

Mr. Ting-Chang Sheu
Mentor: Dr. Genhong Cheng
Funding: Bonner Scholar
Title: STAT1-dependent downregulation of murine chemokine KC reporter

(from left to right): Dr. Jane Deng, Ting-Chang Sheu, Dr. Genhong Cheng

Ting-Chang (Shane) Sheu is a fourth-year Microbiology, Immunology, and Molecular Genetics student at UCLA. He has been conducting research in Dr. Genhong Cheng’s laboratory since fall quarter of his second year. Under the guidance of Dr. Ash Shahangian and Dr. Jane Deng, Shane is studying the phenomenon of influenza challenge sensitizing hosts to secondary bacterial infections in vitro.

In response to viral infections, infected cells secrete interferons that act on neighboring cells and prepare them in antiviral states through the JAK-STAT pathway. Interferons are suspected as the culprit in the downregulation of antibacterial genes during secondary bacterial challenge. The murine chemokine KC fights pneumococcal infection by recruiting neutrophils to the lung, but the study of Dr. Ash Shahangian has shown that influenza challenge preceding secondary bacterial infection significantly reduces KC production. It is possible that STAT1, an important signaling molecule in the interferon JAK-STAT pathway, plays an inhibitory role in p65-mediated expression of KC. Previous data have shown a putative STAT1 binding site inside the two NF-κB binding sites of KC promoter, but the actual mechanism of inhibition is unclear. Shane’s project aims to elucidate the means of inhibition by studying the effect of STAT1 on transient expression of KC-luciferase reporter in HEK293T cells. This project will hopefully shed light on the interaction between innate immune responses to influenza virus and pneumococcus, and provide an explanation for the ability of type I interferons to sensitize hosts to secondary bacterial challenges.

After graduation, Shane hopes to attend medical school and pursue a career in academic medicine. He would like to thank Bonner Scholar and Mr. Gaulke for their generosity, as well as Dr. Genhong Cheng, Dr. Ash Shahangian, Dr. Jane Deng, and all other members of Cheng Lab for their support and guidance.

Back to top

Ms. Stacey Shiigi
Mentor: Dr. Daniel Kamei
Funding: Bonner Scholar
Title: Enhancing the detection of UTI's with two-phase aqueous micellar systems

Stacey Shiigi and Dr. Daniel Kamei

Stacey is a fourth year Bioengineering major and has been conducting research under the guidance of Dr. Daniel T. Kamei. Her current project focuses on utilizing two-phase aqueous micellar systems to concentrate detectable biomarkers to enhance urinary tract infection diagnostics.

Urinary tract infections (UTI’s) are a leading cause of health expenditures, partly due to the expensive and lengthy diagnostic method that involves culturing the bacteria. New techniques have therefore been developed, including one that involves using a chip with labeled probes for ribosomal RNA (rRNA) that are unique for bacteria commonly found in UTI’s. Although this system has had much success, concentrating the bacteria or their rRNA in the urine sample prior to using the chip may allow for increased sensitivity. The Kamei Lab has been generating two-phase micellar systems with the nonionic surfactant, Triton X-114, to examine the partitioning behavior of biomarkers. These systems exploit the chemical properties of nonionic surfactants and their ability to self-aggregate into micelles in aqueous solutions. The solution will separate into a micelle-rich and micelle-poor phase, a process which drives biomolecules, such as RNA, preferentially to the smaller volume of the micelle-poor phase. Stacey works on extending the applicability of these two-phase systems to partitioning bacterial RNA. This methodology could be instrumental in increasing the sensitivity of diagnostic tools: allowing for earlier detection of a UTI and as such, more timely treatment decisions.

 

Back to top

Ms. Sanaa Suharwardy
Mentor: Dr. Joanna Jen
Funding: Bonner Scholar
Title: Relocalization of mutant TREX1 in human brain tissue

Sanaa Suharwardy and Dr. Joanna Jen

Sanaa Suharwardy is a fourth year undergraduate student majoring in Economics. Since Fall 2007, she has conducted research under the guidance and supervision of Dr. Joanna Jen and the Jen Neurology Lab. Sanaa will conduct her honors thesis on the structure and function of the TREX1 gene and its mutant forms. In humans, TREX1 is a 3’→ 5’ DNA repair exonuclease expressed in all cells. TREX1 recessive mutations, which occur in the enzymatic portion of the protein and cause a loss-of-function, are seen in autoimmune diseases such as Aicardi-Goutiéres Syndrome and familial chilblain lupus. Dominant mutations in TREX1 cause RVCL, a disease causing stroke-like symptoms but no autoimmune response. Since the dominant mutations affect mainly the C-terminus and not the enzymatic portion of TREX1, suggesting perhaps a gain-of-function. Sanaa will investigate the effect of the RVCL-causing mutation on the gene product, specifically its role in relocating TREX1 to the nucleus of the cell and the implications of this relocation. Since the mutations causing RVCL affect mainly the C-terminus and not the enzymatic sites of TREX1, she will look at the function of the C-terminus extension in relation to the position of the TREX1 protein. The varied phenotypic and clinical effects of mutations in TREX1 gene indicate that further investigation of the TREX1 enzyme is necessary to understand the basis and eventual treatment of these diseases.

Sanaa will graduate in June 2009 and hopes to begin medical school in the fall. She would like to thank Dr. Joanna Jen and her lab for their support and guidance and Bonner for their generous donation.

Back to top

Mr. Hung Trinh
Mentor: Dr. William Lowry
Funding: Oppenheimer Scholar
Title: The Generation of Tissue from Pluripotent Stem Cells

Hung Trinh and Dr. William Lowry

Hung Trinh is a fourth year Molecular, Cell, & Developmental Biology major and Biomedical Research minor. He plans to pursue a career in medicine and translational research after graduation. He has been working under the mentorship of Dr. William Lowry since the summer of 2007.

Human embryonic stem cells (hESCs) and human induced pluripotent stem cells (hiPSCs) hold much promise in regenerative medicine as a source of a nearly unlimited supply of cells and tissue due to their plasticity and capacity for self-renewal. Despite the potential for innumerable uses in the field of regenerative medicine, successful utilization of these cells to treat disease and create new tissue has been limited. In particular, there has been limited success in the generation of tissue derived from pluripotent cells and little data on the usage of hiPSCs to generate tissue. By directing hESC and hiPSC differentiation, it is hoped that these pluripotent derived cells will be comparable to multipotent progenitors in vitro and in vivo, and possess functional relevance.

Hung would like to thank Dr. William Lowry and his labmates for their support and mentorship, and Helga K. and Walter Oppenheimer for their contribution to undergraduate research.

Back to top

Ms. Wendy Tseng
Mentor: Dr. Yin Tintut
Funding: Wasserman Scholar
Title: Regulation of Interleukin-6 by Oxidized Phospholipids

Wendy Tseng and Dr. Yin Tintut

Wendy Tseng is a fourth-year student majoring in Physiological Science. She has been conducting research under the guidance of Dr. Yin Tintut in the Division of Cardiology, David Geffen School of Medicine since 2006.

Her ongoing research focuses on the oxidized phospholipids regulation of interleukin-6 (IL-6) expression by osteoblasts, bone-forming cells. IL-6 is one of the cytokines involved in stimulating differentiation of osteoclasts, bone-resorbing cells. Previously Dr. Tintut and colleagues have shown that oxidized phospholipids, which trigger pathogenesis of atherosclerosis, also regulate bone cell differentiation and maturation.  Investigating mechanisms of IL-6 expression will provide a better understanding of the regulatory role of atherogenic phospholipids in bone cells.  In addition, the findings may shed light on the prevalence of osteoporosis in patients with cardiovascular disease.
 
Wendy has found that oxidized phospholipids increase IL-6 mRNA expression and transcriptional activity in preosteoblast calvarial cells, MC3T3-E1. She has also found that this induction involves protein kinase A and extracellular signal-regulated kinase.  Wendy is currently extending her findings to elucidate the relationship of these two signaling pathways, as well as investigating the transcriptional regulation of IL-6 by oxidized phospholipids.

Wendy is grateful for the opportunities and guidance provided by Dr. Tintut and the support from her fellow colleagues. She especially thanks the Wasserman family for its generous financial support and the Undergraduate Research Center for an excellent research opportunity as she plans to pursue a joint MD/PhD program in the near future.

Back to top

 

 

Mr. Jonathan Vinea
Mentor: Dr. Chentao Lin
Funding: Wasserman Scholar
Title: Designing Artificial siRNA circuits in Arabidopsis thaliana

Dr. Hongtao Liu and Jonathan Vinea (not pictured: Dr. Chentao Lin)

Jonathan is working on using recently understood discovered siRNA pathways to engineer gene circuitry that uses mobile siRNA molecules to affect gene expression in plants. The purpose of this research is multi-fold: firstly it will add to the current body of knowledge of the plant response to siRNA cleavage metabolites, secondly if some of the ideas have efficacy, it will provide a new mechanism for systemic control of gene expression in Arabidopsis. Thirdly, it will provide a new method of controlling these genes- while typically gene expression needs to be controlled by a specific promoter and transcription factor, these artificial genes will be controlled only by siRNAs, which provide an infinitely customizable amount of different methods to control gene expression. The method of control will be by siRNA injection into a leaf, which theoretically will engage a chain-reaction throughout the plant, changing gene expression systemically. Up until now, systemic gene control was achieved by heat-shock or addition of a chemical to an entire plant, and injection of siRNA was determined to be practically ineffective for research. This research thus potentially provides an alternative to using inducible promoters, which all have their disadvantages, and it will allow for genetic engineering projects to require fewer genes transformed into the plant, which increases likelihood of success.

 

Back to top

Ms. Sue Wang
Mentor: Dr. Benhur Lee
Funding: Oppenheimer Scholar
Title: Galectin-1 regulation of dendritic cell activation and migration through the Syk signaling pathway

Margaret Chang, Sue Wang and Dr. Benhur Lee

Sue (Shuo) Wang is a fourth-year microbiology, immunology, and molecular genetics student with a minor in biomedical research. She started her research in immunology in Dr. Benhur Lee’s lab in March of 2007.  Dr. Lee’s lab has noted the function of the endogenous protein stimulus, galectin-1, in inducing functional maturation of dendritic cells in the immune response.  Sue is investigating the differences in the mechanistic pathway of galectin-1-induced maturation in comparison to LPS-induced maturation to examine the differences between endogenous activation and exogenous activation. She is studying the roles played by the spleen tyrosine kinase (Syk) and protein kinase C (PKC) in functional DC maturation as measured by cytokine levels, matrix metalloproteinase gene expression, and migration capabilities.

Sue will be graduating in spring of this year with the goal of continuing research in medical school. She would like to thank Dr. Benhur Lee for the opportunity to conduct research in this amazing lab, her mentors Dr. Jennifer Fulcher and Margaret Chang for their patience and guidance, and all the members of the Lee Lab that have made working the lab so much fun. Finally, Sue would like to express her sincere gratitude to the Oppenheimer Education Trust for their generosity and support.

Back to top

 


Mr. Samuel Wilson
Mentor: Dr. Burkard Baschek
Funding: Bonner Scholar
Title: Oceanic Gas Bubble Measurements Using an Acoustic Bubble Spectrometer

Samuel Wilson and Dr. Burkard Baschek

Samuel Johnson Wilson grew up in a small town on the Central Coast, attending a high school of only 250 students. Sam arrived at UCLA knowing that he enjoyed both math and surfing, and decided to combine the two with a degree in Math/Atmospheric and Oceanic Sciences. Working in the Ocean Physics Lab here on campus, he has been able to gain real world experience doing research that is directly related to Climate Change. Much of the lab's focus, with Burkard Baschek as the principle investigator, has been on air sea gas exchange.

Gas bubble injection by breaking waves contributes significantly to the exchange of gases between atmosphere and ocean at high wind speeds. In this respect, CO2 is primarily important for the global ocean and climate, while O2 is especially relevant for ecosystems in the coastal ocean. For measuring oceanic gas bubble size distributions, a commercially available Dynaflow Acoustic Bubble Spectrometer (ABS) has been modified. Two hydrophones transmit and receive selected frequencies, measuring attenuation and absorption. Algorithms are then used to derive bubble size distributions. Sam has been in charge of calibrating and testing this instrument, preparing it for use in the ocean.

While it may sound like it, Sam is not a complete nerd. He enjoys an active social life on campus, attending NCAA sporting events, taking part in community outreach programs for tutoring children, and playing rugby for the Bruins all four years he has been at UCLA. He is currently the Vice President of UCLA's Men's Rugby Club, and sees the team as an amazing way to get involved on campus. Sam Wilson has also taken advantage of EAP's Study Abroad programs, spending Fall of 2007 in Barbados.

Sam Wilson plans to graduate in Spring of 2009. After taking a year off to make money and hike the John Muir Trail with his father, he plans to return to school and earn a PhD in Physical Oceanography.

Back to top


Mr. William Wong

Mentor: Dr. Steve Jacobsen
Funding: Wasserman Scholar
Title: The role of UBA domains and DRM3 in DRM2-directed DNA methylation

From left to right: Ian Henderson, William Wong, Steve Jacobsen

William Wong is a 4 th year undergraduate majoring in Molecular, Cell, and Developmental Biology (MCDB). He has been working in Dr. Steven E. Jacobsen’s lab for over year, initially under postdoctoral fellow Dr. Ian R. Henderson. He will now continue on the project that he started with Dr. Henderson under the guidance of Dr. Angelique Deleris.

Dr. Jacobsen’s research focuses on characterizing the various factors that control targeting of DNA methylation, using Arabidopsis thaliana as a model. Cytosine methylation is a heritable marker associated with transcriptional repression, commonly used by eukaryotes to regulate gene expression and to silence selfish genomic elements such as transposons. All DNA methylation in A. thaliana is established by the de novo methyltransferase DRM2, a homologue of the mammalian de novo methyltransferase family Dnmt3. In mammals, Dnmt3-like (Dnmt3L), a catalytically inactive paralogue of the Dnmt3 family, is required for de novo methylation in vivo. Recent studies have shown that Dnmt3L forms a tetrameric complex with Dnmt3a, stimulates Dnmt3a activity, and guides Dnmta to sites of de novo methylation by binding histones via its N-terminal domain.

DRM3, a catalytically inactive paralogue of DRM2, is only partially required for de novo methylation. Furthermore, the DRM and Dnmt3 families seem to have evolved independently. DRM2 and DRM3 both have unique UBA domains in their respective N-terminal domains. DRM2 is also responsible for maintenance of DNA methylation in certain methylated cytosine contexts. Disruption of UBA function in DRM2 shows improper localization of DRM2 by immunohistochemistry. However, impairment of UBA function in DRM2 only shows a decrease in DNA methylation—to the extent observed in a drm3 knockout—at certain loci, as opposed a complete loss in a drm2 knockout. William has shown that the C-terminus of DRM3 binds to DRM2 in vitro. He will further investigate the interaction between the two proteins by generating a plant line with epitope-tagged DRM2 and DRM3. He will then perform coimmunoprecipitation to determine the extent of interaction between DRM2 and DRM3 in vivo. William will also generate a DRM2-UBA deficient and drm3-null double mutant to see if loss of UBA domains of DRM2 and DRM3 is sufficient to eliminate DNA methylation at certain loci.

William would like to thank all members of the Jacobsen lab for their support and guidance. William would also like to thank the Wasserman family and the UCLA Undergraduate Research for the generous scholarship and their continual support of undergraduate research.

Back to top


Ms. Katherine Wu
Mentor: Dr. Benjamin Bonavida
Funding: Bonner Scholar
Title: NO-mediated modulation of gene products involved in cancer metastasis and reversal of resistance to TRAIL -induced apoptosis

Dr. Benjamin Bonavida, Katherine Wu, Dr. Stavroula Baritaki

Katherine Wu is a fourth year Microbiology, Immunology, and Molecular Genetics major and Anthropology minor at UCLA. Since the summer after her second year, she has been conducting research in Dr. Bonavida’s laboratory. Under the guidance of Dr. Stavroula Baritaki, Katherine is studying the effect of nitric oxide on the NF-kB/Snail/RKIP loop in tumor metastasis and tumor resistance to drug-induced apoptosis.

Tumor metastasis is the leading cause of death in cancer patients. Raf kinase inhibitor protein (RKIP) is a novel metastasis-suppressor protein that inhibits the anti-apoptotic activity of NF-kB. Snail transcription factor is upregulated by NF-kB and promotes resistance and tumor metastasis. To complete the loop, Snail downregulates RKIP. Dr. Bonavida's lab is investigating a means to intervene in this loop and to reverse resistance and inhibit metastasis in prostate cancer using nitric oxide (NO) donors. It is hypothesized that NO inhibits NF-kB and Snail through the induction of RKIP. The focus of Katherine’s project is to test the above hypothesis using human metastatic prostate cancer cells. The results of these studies may help prove the potential for the therapeutic application of nitric oxide in cancer.

After graduating, Katherine hopes to attend medical school. Katherine would like to thank the Bonner Scholarship committee for their support for her research, UCLA’s URC/CARE program for their encouragement of undergraduate research, and Dr. Bonavida and the lab for their guidance and inspiration.

 

Back to top


Mr. Fangfang Xing
Mentor: Dr. Ren Sun
Funding: Wasserman Scholar
Title: Characterizing the role of Hepatitis C virus NS5A and cellular lipid metabolism enzyme HMGCR during virus replication

Dr. Ren Sun and Fangfang Xing

Fangfang Xing is a fourth-year student of Microbiology, Immunology, and Molecular Genetics. Under the guidance of Post-doctoral Fellow Vaithi Arumugaswami, Fangfang is characterizing the viral to cellular protein interactions essential for HCV replication in the context of host cholesterol biosynthesis.

The Hepatitis C virus (HCV) infects an estimated 130 million people worldwide. As a major health concern, HCV infection causes liver diseases including chronic hepatitis, cirrhosis, and hepatocellular carcinoma. In order to complete the viral lifecycle, the virus hijacks and/or counteracts cellular functions, including signaling pathways, cell cycle regulations, and innate and adaptive immune responses. Host organelles rich in sphingomyelin and cholesterol are essential for HCV replication and particle assembly. Dr. Sun’s lab, using genome scale yeast-two hybrid experiments identified several HCV- cellular protein interactions. Fangfang’s project is to characterize these hits using immunofluorescent and confocal microscopy. Then he will examine the importance of these protein interactions in the context of viral replication using siRNA knockdown approaches. In addition to elucidating fundamental mechanisms of the HCV lifecycle, findings from this project may also offer more sensitive targets against HCV.

Fangfang would like to thank Professor Ren Sun, Dr. Vaithi Arumugaswami, Shaoying Lee and all members of the laboratory for their mentorship and the opportunity to conduct research as an undergraduate. Research has been a transformative educational experience and will be an important aspect for the rest of his career. He would also like to express his deepest appreciation for the generosity and support of the Wasserman family.

Back to top


Ms. JoJo Yang
Mentor: Dr. Judith Berliner
Funding: Sparks Scholar
Title: Investigating the role of rhoA-family small G-proteins in the regulation of gene expression by Ox-PAPC in human aortic endothelial cells

Dr. Judith Berliner, JoJo Yang and Dr. Sangderk Lee

JoJo Yang is a fourth year student completing her double major in Molecular, Cell, Developmental Biology and Comparative Literature, with a focus on English and Spanish language literatures. JoJo has been conducting research since her first year at UCLA and joined the Berliner lab at the beginning of her third year. Since then, she has been working in this area of atherosclerosis research. Atherosclerotic lesions obstruct the arterial lumen, leading to cardiovascular disease and stroke. In examining the progression of atherosclerotic lesions, the Berliner lab focuses on the initial event of endothelial cell activation. It has previously been shown that Ox-PAPC, a mixture of oxidized phospholipids present in minimally modified low density lipoprotein (mm-LDL), can mimic mm-LDL’s effect on human aortic endothelial cells (HAECs) in recruiting monocytes. In doing so, Ox-PAPC alters gene expression levels of over 1000 genes, including pro-inflammatory genes such as IL-8. To further investigate the mechanisms of Ox-PAPC’s effect on gene expression, JoJo is studying the rho-A family small G-proteins for a possible role in this pathway. Since small G-proteins, specifically rac1, are so ubiquitous and essential in various intracellular signal transduction pathways, this project hypothesizes that they do play some role in the pathways of Ox-PAPC-induced changes in gene expression. Rac1 may be involved in Ox-PAPC-mediate expression changes in pro-inflammatory genes via VEGFR2 and increased oxidative stress within the cell. Results from this work would generate a postulated mechanism for rac1 participation in the Ox-PAPC pathway, elucidating the significance of small G-proteins in the oxidation hypothesis of atherosclerosis.

JoJo is currently applying to medical schools and hopes to obtain a dual MD/MBA degree. She is interested in healthcare management and working with the urban underserved. She hopes to contribute to nonprofit healthcare providers dedicated to increasing access to care for these underserved populations, whether they are at home or abroad. She would like to thank her research mentors Dr. Judith Berliner and Dr. Sangderk Lee for their continued support and guidance. She is extremely grateful to the Hale S. Sparks scholarship and the URSP program for this opportunity in undergraduate science research.

 

Back to top


Ms. Sophia Yang
Mentor: Dr. Yung-Ya Lin
Funding: Wasserman Scholar
Title: Spin Engineering in MRI to enhance contrast through the Active Feedback Nutation Method

Sophia Yang and Dr. Yung-Ya Lin

Sophia is a fourth year student in the departmental scholars program under the field of physical chemistry. Since her freshman year, she has worked with Dr. Yung-Ya Lin in the Department of Chemistry and Biochemistry, studying the spin dynamics occurring within magnetic resonance imaging (MRI) experiments in order to develop new techniques with better contrast.

MRI has shown to be useful in a wide variety of applications, but it continues to be elusive in the area of early cancer detection. The difficulty lies in the ability to distinguish between magnetically similar components. While tumor growth is marked by a high level of angiogenesis, early stage tumors remain almost identical to their healthy tissue counterparts, causing differentiation to be almost impossible. Dr. Lin’s group has developed an external circuit that can artificially create a magnetic feedback field to alter the nuclear spin evolution. By locking the direction of the magnetic spin for healthy tissue, the small tumor region can be highlighted. The theory for this method, “Active Feedback Nutation” has been developed by Sophia, and she is currently conducting experiments with early tumor mice to test its feasibility.

Sophia would like to thank the Wasserman Family for their generous support, the URC/CARE staff, as well as her graduate students and Dr. Lin for their support and guidance in the tempest of scientific uncertainty.

Back to top

 

 

 

 

 

 

 

 

 

Profiles of Students