MARC Profiles

The MARC program is suported by a grant from the National Institutes of Health. This page is under construction.


Student: Taylor Brown
PI: Dr. Heather R. Christofk
Graduate Student Mentor: William J. Sullivan
Project Title: Towards an Understanding of Herpesvirus RRM2 and Host Cell Metabolism


Taylor Brown is a 4th year Microbiology, Immunology, and Molecular Genetics Major and Biomedical Research Minor at the University of California, Los Angeles. She began working in the Cell Metabolism laboratory of Dr. Heather R. Christofk in September 2012, and is studying mutant versions of ribonucleotide reductase small subunit (RRM2) and their potential effect on viral replication and cellular metabolism. She has also worked in the lab of Dr. Tyler Jacks for 10 weeks during the summer, studying the effects of mutated circadian rhythm genes on cancer progression. Her immediate goals include graduating from UCLA with a degree in MIMG and a minor in Biomedical Research, and pursuing a Ph.D in Cancer Biology or Immunology.
Taylor is studying viral ribonucleotide reductase small subunit (RRM2), which is conserved throughout the herpesvirus family, and its potential role in regulating host cell metabolism to meet the biosynthetic needs of viral replication. RRM2 is an enzyme encoded in both human and many viral genomes that catalyzes the reduction of ribonucleotides to deoxyribonucleotides, a rate-limiting step in de novo nucleotide synthesis. Although RRM2 is ubiquitously expressed in human cells, expression of the exogenous viral protein is needed for efficient viral replication. Her goal is to better characterize how specific amino acid differences between the human protein and its viral homolog lead to potentially altered enzymatic function, and how these differences promote viral replication in the host cell. To this end, the effects of overexpression of wild-type RRM2 and specific mutants on human cells will be assessed via proliferation assays, cell cycle analysis, and metabolic profiling. Through her work, she hopes to make progress towards more effective treatments for viral infection through further understanding of the way viruses metabolically reprogram the host cell.
Taylor plans to attend graduate school. She also plans to continue working in research laboratories outside of UCLA to gain more research experience, to better understand the scientific process, to gain more laboratory skills, and to acquire knowledge about cancer and the immune system through emerging research. She ultimately wants to become an effective researcher, acquire her own lab space, and apply the knowledge she has acquired through her research and schooling to mentor young scientists, develop antitumor drugs, and help those suffering from cancer. She would like to acknowledge the CAMP, LSAMP, and MARC program for funding.



Student: Swasty Chandra
Faculty Mentor: Daniel H. Geschwind, M.D./Ph.D.
Direct Mentors: Maria Lazaro and Dr. Olga Peñagarikano
Project Title: Alterations in excitatory neurotransmission of Cntnap2 knock-out mice, an ASD model.

Swasty Chandra is a third-year Neuroscience major at the University of California, Los Angeles. Swasty has been a member of the MARC program since the fall of 2014. She has been working in the lab of Dr. Daniel H. Geschwind in the department of Neurology since the summer of 2014. Her project is focused in elucidating the cellular and neuroanatomical mechanisms that give rise to the excitatory synaptic deficits in the Cntnap2 knock-out mouse, a model of autism.
Autism Spectrum Disorder (ASD) is a highly prevalent neurodevelopmental disorder affecting 1 in every 68 children. There is currently no treatment available that can alleviate the three core behavioral deficits associated with it: restrictive/repetitive behaviors, language and social impairments. Although autism etiology remains to a great extent elusive, several studies have shown that genetic components account for 20-30% of reported cases. The Cntnap2 knock-out (KO), a genetic mouse model of ASD, recapitulates the three hallmark behaviors associated with autism, as well as epilepsy and abnormalities in neuronal migration. Swasty will expand on these preliminary findings by first determining the neuronal cell-type specific expression of Cntnap2, using immunohistochemistry, which is yet unknown. In following experiments, she will be studying whether the reduction in excitatory neurotransmission in the KO mice results from a reduction in the number of excitatory neurons and/or excitatory neuron receptors in the cortex of the mouse brain.
Swasty is greatly appreciative of the MARC program, especially Dr. Dwayne D. Simmons and Dr. Diana Azurdia for their constant guidance. She would also like to thank Dr. Daniel H. Geschwind as well as Maria Lazaro and Dr. Olga Peñagarikano for being patient and supportive mentors.



Student: Abel Ferrel
Mentor: Dr. Rachelle Crosbie-Watson
Funding: UCLA Bridges Bridges Summer Undergraduate Research Program (BriSURP) NIH Grant R25 GM 050067, Maximizing Access to Research Careers (MARC), the NIH/National Institute of General Medical Sciences (NIH MARC T34 GM008563) to D. D. Simmons, the NIH (R01 AR048179) to R. Crosbie-Watson, and the NIH (UL1TR000124) to R. Crosbie-Watson.
Research Title: Investigating molecular responses of cardiac tissue to age- and adrenergic agonist-induced hypertrophy


Abel Ferrel is a 3rd year Microbiology, Immunology, and Molecular Genetics (MIMG) major at the University of California, Los Angeles (UCLA). Beginning June 2014, he joined Dr. Crosbie-Watson's laboratory in the Department of Integrative Biology and Physiology where he contributes to elucidating the function of sarcospan (SSPN) for its potential use as a therapeutic agent for children affected by Duchenne muscular dystrophy (DMD) and its associated cardiomyopathy.
SSPN is an integral membrane protein embedded in the sarcolemma of both cardiac and skeletal muscle. It is part of a protein complex known as the dystrophin-glycoprotein complex (DGC) that maintains muscle integrity during contraction. The DGC also includes dystrophin, which is the protein product of the DMD disease gene. Although loss of dystrophin causes DMD, SSPN is of interest due to its DGC-stabilizing capabilities and potential to be a therapeutic agent. Previous studies from the Crosbie-Watson group have shown that SSPN stabilizes the muscle membrane and alleviates symptoms associated with DMD in relevant mouse models. Mr. Ferrel is currently investigating the role of SSPN in cardiac muscle function. Specifically, he is investigating cardiac hypertrophy and the effects SSPN loss on cardiac function. The approach he is using measures changes in gene expression by (RT-qPCR) and examines whether SSPN-loss affects gene expression in SSPN-null hearts. He has found that genes involved in the cardiac hypertrophic response are affected by SSPN. Furthermore, studies will be conducted to determine whether SSPN deficiency exacerbates the response of the heart to aging or beta adrenergic induced stressors. Additionally, hematoxylin and eosin (H&E) staining will be complimented with RT-qPCR to reveal the morphological changes associated with age and beta adrenergic stimulation. More specifically, he will be working toward quantifying fibrosis in SSPN-null hearts relative to the wild type controls. Altogether, this data can then be established as a baseline for future investigations which will reveal SSPNs involvement in cardiac tissue.
Upon receiving his bachelor's in MIMG from UCLA, he plans on pursuing an MD/PhD degree in pathology. Ultimately, he is working toward becoming a scientific researcher and working in the field of medical pathology. Abel Ferrel would like to thank Dr. Crosbie-Watson, Dr. Parvatiyar, and the Crosbie-Watson lab for their help and support. He would also like to thank the UCLA Bridges Summer Undergraduate Research Program (BriSURP), Maximizing Access to Research Careers (MARC) program, California Alliance for Minority Participation Program (CAMP), and the NIH for their support.



Student: Richard Flores
Mentor: Christopher Colwell
Funding: MARC
Project Title: Treating circadian dysfunction in a mouse model of Huntington's disease (HD).


I'm Richard Flores. I am a 5th year neuroscience major, theater minor. I began working in Dr. Colwell's lab September of 2012.
Dr. Colwell's lab focuses on sleep and circadian rhythms and my project involves studying how circadian rhythms affect the progression of HD. Prior to the onset of motor dysfunction that are characteristic of the disease, HD patients experience difficulty sleeping at night and have a difficult time staying awake during the day, suggesting a disrupted circadian clock. Using two mouse models of HD (the BACHD and Q175 mouse), I am attempting to restore their circadian rhythms in hope that this will also help the mice with their motor difficulties.
My future plans are to apply to graduate school and earn a PhD in neuroscience. I have had the pleasure of working with many great scientist throughout my time here at UCLA. I plan to continue contributing to the growing body of knowledge. I would like to thank MARC at UCLA, the Colwell lab, the NIH, and the undergraduate resource center for guiding me all of these years.



Student: Ruben Galindo
Mentor: Eric Torres
Funding: 2T34GM008563-19 NIH Grant
Project Title: Pink1 Construct for Small Molecule Import Inhibition of Pink1 into Mitochondria


I am a 3rd year UCLA undergraduate student with a declared major in Biochemistry and minor in Biomedical Research. I have been a member of the NIH funded Bridges and Marc programs since June 2015 and September 2015 respectively. During the summer of 2015 I conducted research on protein purification of Fibromodulin from mammalian cell secretion in the lab of Dr. Kang Ting and Dr. Chia Soo. Since December 8, 2015 I have been working in the lab of Dr. Carla Koehler focusing on Pink1 import into mitochondria and its association with Parkinson's.
Mitochondria dysfunction is associated with many severe and prevalent diseases including Alzheimer's, Parkinson's, Lou Gehrig's, and diabetes. My project focuses on mitochondrial import of dysfunctional human PTEN induced putative kinase 1 (Pink1), a protein associated with autosomal recessive early-onset Parkinson's disease. Briefly, Pink1 alters its import pathway and arrests as a stable protein on the mitochondrial outer membrane when mitochondria become damaged. E3 ubiquitin ligase component Parkin, is subsequently recruited and downstream mitophagy events are induced. Utilizing a fusion construct of reporter gene Ura3 fused to the mitochondrial targeting sequence of Pink1, I will be able to screen for small molecule inhibitors of Pink1 mitochondrial import in Saccharomyces cerevisiae. Screened drugs that inhibit import will localize the Ura3 reporter in the cytosol. This allows growth on uracil deficient media and identifies potential small molecules probes for the Pink1 import pathway.
Upon graduation from UCLA my goal is to enroll in a Ph.D. or M.D./Ph.D. program to further my studies of biochemistry and conduct research in either an academic or industrial setting. As a budding scientist, I currently have a broad interest in my research interests that include disease mechanisms and cellular homeostasis. Ultimately, I aim to make valuable contributions to molecular biology and related fields. I would like to acknowledge the NIH for funding as well as my PI Dr. Carla Koehler and my direct mentor Eric Torres. I would also like to acknowledge the Marc and Bridges programs for helping me achieve these goals.



Student: Luis Gonzalez
Faculty Mentor: Paivi Pajukanta
Project Title: Targeted analysis of the Mexican hypertriglyceridemia locus on chromosome 18

Hello my name is Luis Gonzalez. I am a senior majoring in Biochemistry and minoring in Biomedical research. I started in my lab in June of 2013 through the Bridges to UCLA summer program. My lab is located in the department of Human Genetics and we study the role genetics plays in the development of cardiovascular diseases.
Mexican populations and populations of Amerindian heritage are more susceptible to developing dyslipidemias and coronary heart disease (CHD) than European populations. On average 31.5% of Mexicans have hypertriglyceridemia (HTG), 43.6% hypercholesterolemia, and 60.5% have a decrease in high-density lipoprotein cholesterol (HDL-C) levels. Previous epidemiological studies have demonstrated that increased serum triglyceride (TG) levels and decreased serum HDL-C levels increase an individual's risk to develop CHD. Elevated serum TGs have been linked to atherosclerosis and, by extension, the risk of heart disease and stroke, which can be partly accounted for by the strong inverse relationship between triglycerides and HDL-C levels. In the first Mexican GWA study of lipids, a novel locus for high TG levels was identified on chromosome 18 that includes the transmembrane 241 (TMEM241) gene, the function of which has not been discovered as of yet. We hypothesized that a part of this increased susceptibility is caused by population-specific genetic factors, such single nucleotide polymorphisms (SNPs), which are point mutations that may affect disease phenotypes through regulatory mechanisms. Our research goal is to characterize both the common noncoding variants responsible for the increase in TG levels in Mexicans on chromosome 18 and the rare coding variants found exclusively in the population extremes of serum TGs in Mexicans. We propose that the lead SNP (rs9949617) or variants in tight LD with it may control the expression of the TMEM241 gene or a surrounding gene in an allele-specific manner, which in turn influences serum TG levels. This will be verified through luciferase assays, additional functional studies and liver gene expression data. Therefore, if a specific variant can be identified, as the one responsible for an increase in TG levels, individuals can be informed about their increased susceptibility to cardiovascular disease, which should help delay or prevent the onset of the disease and ultimately treat it.
I am currently planning to participate in a 1-year PREP program after my graduation in June of 2015. Following the completion of the program, I plan to participate in an MD/PhD program in order to become a physician-scientist. I would like to focus on personalized medicine and conduct research in rare genetic disorders. I would like to acknowledge the members of the Pajukanta Lab as they have all been supportive during my research endeavors, as well as the MARC program for the funding and support provided.




Student: Shadia Hamideh
PI: Dr. David Glanzman
Mentor: Dr. Adam Roberts, Ronny Choe
Funding: UCLA Bridges Bridges Summer Undergraduate Research Program (BriSURP) NIH Grant R25 GM 050067, NIH/National Institute of General Medical Sciences (NIH MARC T34 GM008563) to D. D. Simmons
Project Title: Understanding the Role of the Mauthner Cell in Learning and Memory


Shadia Hamideh is a third year Molecular, Cell, and Developmental Biology student at UCLA. She has been working in the lab of Dr. David Glanzman in the Department of Neurobiology, Physiology, and Biology in the David Geffen School of Medicine since the summer of 2014.
The research goal of the Glanzman Lab is to better understand the cell biology of learning and memory and the changes that have to occur in the brain to facilitate this process. Experiments are designed to study the neural basis of nonassociative and associative behavioral modification of simple reflexes in small organisms. Ms. Hamideh is studying the Mauthner (M) cell and how it contributes to learning and memory in zebrafish. The M cell is a bilateral hindbrain neuron in the zebrafish brain and it is responsible for eliciting a signature reflex found in all teleosts: the C-start reflex response. Although zebrafish have a complex vertebrate nervous system, the C-start is a simple reflex mediated by a simple circuit and for that reason much research has gone into understanding the role of this neuron. The Glanzman Lab is interested in studying the possible modifications of circuits in the brain that may occur as a result of learning. Previous studies in the Glanzman Lab have shown that zebrafish are capable of learning that certain stimuli are not harmful and they eventually learn to cease startling in response to that stimuli. This simple form of learning is known as habituation and the process by which these zebrafish learn to habituate is of great interest in the Glanzman Lab. Ms. Hamideh hopes to uncover the role of the M cell in learning and memory by the time she earns her Bachelors degree here at UCLA.
Ms. Hamideh aspires to earn a dual M.D./Ph.D degree in Molecular Biology in the years to come with a research interest in learning and memory. She would like to acknowledge the Bridges to Summer Undergraduate Research Program (BriSURP) for preparing her in her endeavors as a MARC student and the MARC program for guiding her path to graduate school. Ms. Hamideh would also like to thank her faculty mentor, Dr. Glanzman, and her direct mentors Dr. Adam Roberts and Ronny Choe for supporting her growth as a researcher in the lab. With the help of the MARC Program, the generous NIH grants, UCLA faculty and direct mentors, Ms. Hamideh will achieve her goals of becoming a clinical researcher.



Student: Rachel Lopez
Mentor: Dr. Thomas M. Vondriska
Direct Mentor: Ms. Emma Monte


My name is Rachel Lopez and I am a transfer student from Antelope Valley College. I'm a 4th year at UCLA as an Ecology and Evolutionary Biology major. I started in Dr. Vondriska's lab in the summer of 2013 through the Bridges to UCLA program. Through this program, I received my first exposure to research in a field that I was interested in. I'm also involved in outreach through SACNAS at UCLA where I am currently the fundraiser manager.
For my research, I am focused on understanding how chromatin structure affects heart failure. More specifically, I am looking at proteins and post-translational modifications that can affect the chromatin structure. I am using a proteomics approach to study these proteins and using techniques such as Western blots and mass spectrometry.
I plan to pursue a career in cardiology with an MD/PhD that will allow me the flexibility of research and patient care. I am especially thankful for the lab experience I've had so far. My lab is completely supportive of my career and me. They have been a positive influence in my development as a person and researcher. I am grateful to have my Bridges, MARC, and SACNAS family. I'd like to especially acknowledge the MARC program and the NIH, their funding source as well as the summer fellowship I received from the American Heart Association.



Student: Roberto Naranjo
Mentor: Professor Louis Bouchard
Funding: UCLA Bridges Summer Undergraduate Research Program (BriSURP) NIH Grant R25 GM050067, Maximizing Access to Research Centers (MARC), the NIH/National Institute of General Medical Sciences (NIH MARC T34 GM008563) to D. D. Simmons.
Project Title: Studying Olefin Metathesis Reaction using Para-hydrogen Induced Hyperpolarization (PHIP)- Pt Nanoparticles as MRI Contrast Agents using Para-hydrogen Induced Hyperpolarization (PHIP)


Roberto Naranjo is a 3rd year Chemical Engineering major at the University of California, Los Angeles (UCLA) in the School of Engineering and Applied Science. He joined Professor Louis Bouchard's laboratory in the Department of Chemistry and Biochemistry in June 2014 during his participation in Bridges to the Baccalaureate Summer Research Program. He was under the direct mentorship of Dr. Stefan Gloeggler working on determining reaction mechanisms for metathesis reactions.
Since the beginning of summer, he was been working on studying metathesis reactions using para-hydrogen. Para-hydrogen is used to enhance NMR signals and provides unique quantum spin signatures that can help elucidate reaction mechanisms. His work leads to an entirely novel methodology that can be used to study most metathesis reactions in operating catalytic reactors. These metathesis reactions can be used as potential methods in producing longer hydrocarbon chains from smaller hydrocarbon chains. He is switching over to a new project; synthesizing platinum nanoparticles that will serve as MRI contrast agents. They will also use para-hydrogen that will enhance and heighten the MRI signal, thus obtaining a higher resolution.
Roberto plans to graduate with his B.S in Chemical Engineering and join a Ph.D program in Chemical Engineering. His research interests range from nanoscience, specific drug delivery systems, heterogeneous catalysis, and biotechnology. He would like to thank Dr. Dwayne Simmons, Dr. Diana Azurdia, Alfred Morales, and the MARC U*STAR program for all their support and guidance. He would also like to thank Professor Bouchard, Dr. Stefan Gloeggler, and every member of the Bouchard lab for their continuous assistance and guidance.



Student: Nancy Morones
Mentor: Dr. Karen Lyons
Funding: MARC U*STAR Program (NIH MARC T34 GM008563, PI: D.D. Simmons)
Project Title: CCN Protein Localization Patterns in Skeletal Tissues


My name is Nancy Morones and I am a fourth year UCLA undergraduate student and a second year transfer student from Cerritos College in Norwalk. I am currently completing a major in Molecular, Cell, and Developmental Biology with a minor in Biomedical Research. I have been working in Dr. Karen Lyon's laboratory since January 2014, studying various molecular and developmental aspects of bone development.
The CCN family consists of six matricellular proteins that serve regulatory rather than structural roles. Both CCN1 (Cyr61) and CCN2 (Connective Tissue Growth Factor) have been shown to be expressed in developing limbs and play a role in cartilage and bone formation; however, their roles in vivo are not clear because temporal and spatial expression patterns have not been characterized. For this study we are examining the spatial and temporal expression of CCN1 and CCN2 during limb development. Understanding their expression patterns in development can provide insight to understanding how loss or overexpression of these genes impacts cartilage formation as well as the onset and progression of diseases such as osteoarthritis, a leading cause of disability in the US.
Once I acquire my bachelor's degree, I plan to apply to an MD/PhD degree program. I am interested in continuing studies within molecular and developmental biology, particularly in degenerative diseases associated with aging. I am extremely thankful to the MARC U*STAR Program (NIH MARC T34 GM008563; PI: D.D. Simmons) for funding my academic endeavors. I have truly grown as a student and a scientist and look forward to all the challenges that will come.



Student: Tien Phan
Mentor: Dr. Karen Lyons
Funding: NIH 5R01AR052686-09
Project Title: Functions of Matricellular Proteins CCN1 and CCN2 in Embryonic Skeletal Development


Tien is a senior majoring in Molecular, Cell, & Developmental Biology and minoring in Biomedical Research. She transferred from Orange Coast College in Fall 2013. Since December 2013, she has been conducting research in Dr. Karen Lyons's lab, studying the functions of the matricellular proteins CCN1 and CCN2 in skeletal development.
CCN proteins reside primarily in the extracellular matrix and serve regulatory rather than structural roles. The absence of CCN2 results in a range of skeletal defects; however, the role of CCN1 has not been explored. We examine the skeletal phenotypes in CCN1, CCN2, and CCN1/CCN2 cartilage-specific conditional knockout mice during development to evaluate the roles of CCN1 and CCN2. Ablation of CCN2 is neonatal lethal because of severe skeletal dysplasia including bent limbs, kinked ribs, and misaligned spines. CCN1 mutants, on the other hand, survive to adulthood and display very subtle skeletal phenotype. The phenotypes seen in both mutants are due to defects in extracellular matrix deposition which lead to weakened cartilage structures. Due to the differential expressions of CCN1 and CCN2 in some parts of the skeletal system, the absence of both of these proteins results in augmented skeletal defects.
Cell proliferation and apoptosis assays showed that CCN1 inhibits proliferation and promotes apoptosis while CCN2 had the opposite functions. Presently, the gene expression profiles of the mutants are being examined to characterize the pathways by which CCN1 and CCN2 act to mediate cartilage development. This study not only enhances our current understanding of cartilage homeostasis but also holds promise for therapeutic treatments of diseased bone conditions.
Tien is pursuing a career in research. She appreciates the generous support and continued encouragement from the MARC Program. Additionally, she would like to thank Dr. Karen Lyons, Dr. Jie Jiang, and other members of the Lyons lab for their guidance and support.



Student: Lara Roach
Mentor: Dr. Eric Vilain, Matthew Bramble
Project Title: The Molecular Underpinnings of Gonadal Hormone-Influenced Gene Alterations through DNA Methylation Mechanisms in the Central Nervous System of Rodents and Humans


I am a third year Molecular, Cellular, and Developmental Biology major and Biomedical Research minor from Orange County, California. Prior to the MARC Program, I was a CARE Fellow and participated in the SMART Summer Program at the University of Colorado, Boulder. I started in the Vilain lab at the beginning of my third year, Fall 2014.
My current project is to investigate the affects of gonadal hormones on a developing central nervous system. There have been many previous studies done to understand the influence of gonadal hormones on sexual differentiation and brain masculinization, but none of these studies has unraveled the affects of these hormones on a molecular or cellular level. The goal of my project is to use mouse and human sex-specific neural stem cells to determine if gonadal hormones can permanently alter gene expression and through what possible mechanisms. Our hope is that these findings can be used to bridge the gap of unknown knowledge in the field with regards to molecular alterations, and may shed light on how sexual behavior can be altered from a cellular level through the role of androgenic compounds.
After graduating from UCLA, I plan to pursue a Ph.D. in cellular and molecular biology. I would like to thank and acknowledge all of my mentors who have helped me tremendously during my undergraduate career: Jeannie Barber-Choi, Dr. Paul Barber, Dr. Ira Clark, Dr. Leslie Leinwand, Dr. Eric Vilain, Matthew Bramble, Dr. Diana Azurdia, Dr. Patricia Quinones, and Dr. Dwayne D. Simmons. I would also like to acknowledge the NSF for funding the SMART Program and the NIH for funding the MARC Program.



Student: Benni Vargas
Mentor: Dr. Robert L. Modlin
Project Title: B Cells in the Cutaneous Immune Response against Leprosy


Benni Vargas is a fourth-year Microbiology, Immunology, and Molecular Genetics major. Benni's passion for biology and research flourished in UCLA's supportive undergraduate research environment. He had been working in the lab of Dr. Modlin in the department of Dermatology in the summer of 2014 investigating B-cell related disease-host mechanisms that contribute to resistance versus susceptibility in the immune response against leprosy.
The role B cells play in the cutaneous immune response is largely unknown. Leprosy, a chronic disease caused by Mycobacterium leprae, is a useful model to examine the immune response in the skin because lesions are easily accessible for study. Leprosy causes a spectrum of diseases in which we can observe differences in the immune response. B cells have been found to be present in leprosy skin lesions but their role in these lesions in unknown. We sought to gain insight into the role B cells play in the cutaneous immune response by using leprosy as a model system. We hypothesize that B cells, their products, or both help form the immune response against M. leprae. Specifically, we asked whether M. leprae or its products could activate B cells. We used cellular proliferation and expression of cell surface activation markers as measures of activation. To this end, we isolated B cells from peripheral blood mononuclear cells (PBMC) from donors and exposed these cells to products of M. leprae. We found that products of M. leprae did not directly activate B cells. Future studies include examining B cells from patients with leprosy, and examining other markers of cellular response including cytokine and Immunoglobulin production in the presence of M. leprae or its products. We hope that information gained about the role B cells play in the immune response to M. leprae may provide new possibilities for advancement of treatments for various human diseases.
Benni would like to get a Ph.D. in Microbiology, Immunology, and/or Infectious Diseases. In the future, he would like to apply his learned skills as a biomedical researcher for cures to infectious diseases such as AIDS, become a university professor, and/or as a researcher for private industry (biotech, pharmaceutical, food. It would be his dream to work for the Centers for Disease Control and Prevention (CDC). This work is funded in part by the National Institutes of Health/National Institute of General Medical Sciences training grant (NIH MARC T34 GM008563, PI: D.D. Simmons).