Jenny AguilarGraduate Student, Galli laboratoryBA, Princeton University (2011)
Disruptions in dopamine (DA) homeostasis are associated with several neuropsychiatric disorders, including attention deficit hyperactivity disorder, and drug addiction. The Galli Lab has recently identified several missense mutations in the human DA transporter (DAT) gene (SLC6A3) in individuals with autism spectrum disorder (ASD). These mutations result in aberrant DAT function, strongly implicating disruptions in DA transport as a risk factor in ASD. My Ph.D. work will focuses on understanding the contributions of altered or disrupted dopamine signaling mediated by variations in DAT to ASD risk.
Joseph BalsamoGraduate Student, Hong laboratoryBS, James Madison University (2015)
Hi, my name is Joe Balsamo and I grew up in Flemington, New Jersey before moving to Castle Rock, Colorado. I received my B.S. in Biotechnology from James Madison University in 2015. Following graduation, I worked for LabCorp performing clinical diagnostics for women’s health before attending Vanderbilt University. Currently, I work in the Hong lab studying zebrafish development, drug discovery, and cardiovascular biology. Outside of lab, I enjoy exploring Nashville’s food scene and attending hockey games.
Brian BenderGraduate Student, Meiler laboratoryBA, Colgate University (2011)
I use computational modeling and biophysical techniques to understand how proteins interact with their binding partners such as small molecules, peptides, or large proteins. The Meiler Lab actively develops the Rosetta software for protein structure prediction. I complement this software with biophysical techniques such as X-ray crystallography, nuclear magnetic resonance (NMR), and electron paramagnetic resonance (EPR). I have a particular focus on G-protein coupled receptors (GPCRs). I am interested in how ligand binding induces a conformational change in the receptor to lead to activation and signaling through cellular binding proteins such as heterotrimeric G-protein and arrestin.
Jordan BrownGraduate Student, Winder and Sweatt laboratoriesBA, Auburn University (2014)
I was born in Mobile, Alabama and received my Bachelor’s degree in Chemistry at Auburn University. Following graduation, I spent two years in a post-baccalaureate program at the University of Alabama in Birmingham (UAB) studying epigenetic modifications involved in learning and memory. I started my graduate career at Vanderbilt University in the Fall of 2016 and am co-mentored by Drs. David Sweatt and Danny Winder. My research project focuses on the role of DNA methylation on intrinsic neuronal excitability. Specifically, I am researching alterations in calcium gated potassium channels induced by changes in DNA methylation using epigenetic editing tools and electrophysiological recordings. When I am not in lab, I enjoy doing yoga, reading, cooking and exploring Nashville with my dog.
Jamal BryantGraduate Student, Blind laboratoryBS, Florida State University (2015)
I was born in Baltimore, Maryland and raised mostly in St. Petersburg, Florida. I attended Florida State University, where I studied Biochemistry and performed research in developmental genetics and gene regulation. Currently, I am a graduate student in Dr. Raymond Blind's lab, studying the signaling properties of non-membrane nuclear lipids. In my free time, I like to enjoy Nashville's vibrant music scene and play competitive sports.
Benjamin ColemanGraduate Student, Sweatt laboratoryBS, Virginia Polytechnic Institute (2015)
My name is Ben Coleman and I grew up in the small town of Abingdon Virginia. I did my undergraduate training at Virginia Tech, after which I worked as a lab technician in the Department of Psychiatry at UTSouthwestern for a year before coming to Vanderbilt in the fall of 2016. I recently joined the lab of Dave Sweatt where my research will focus on the epigenetics of memory. In my free time I love to hike, fish, and spend time with my wife and dog.
Mark CrowderGraduate Student, Blind laboratoryBA, Fisk University (2015)
It is established that the phosphatase and tumor suppressor PTEN (phosphatase and tensin homolog deleted on chromosome 10) is mutated in a variety of cancers, often resulting in PTEN loss of function. At cell membranes, PTEN opposes the activity of phosphatidylinositol 3-kinases (PI3Ks), which generate the signaling lipid PIP3. PI3K activation leads to the stabilization of key cell signaling complexes at the membrane via PH-domain mediated interactions with PIP3. This complex formation is required for proper signal transduction to occur; however, upregulated PI3K activity (overproduction of PIP3) is associated with several cancer types . However, drugs targeting membrane PI3Ks have widely failed. Our lab studies a nuclear PI3K called IPMK (inositol polyphosphate multikinase) that converts PIP2 to PIP3 while bound to a transcription factor, NR5A1. IPMK conversion of PIP2 to PIP3 while bound to NR5A1 increases the expression of NR5A1 target genes. PTEN, in an opposing manner, is able to dephosphorylate PIP3 to PIP2, causing repression of NR5A1 target genes. I hypothesize that a close NR5A1 homolog, NR5A2, is regulated by IPMK in the same way and that PIP3 stabilizes transcriptional complexes via PH-domain mediated interactions similar to its role at cell membranes. If proven, these results would implicate IPMK as a cancer drug target.
Claire DelBoveGraduate Student, Zhang laboratoryBS, Rhodes College (2011)
I study the impacts of secretase inhibition on the trafficking of amyloid precursor protein (APP) and its cleavage products. γ- and β-secretase inhibitors prevent the production of amyloid β from APP and have been investigated as possible treatments for Alzheimer’s disease. However, little is known about the potential consequences of disrupting the amyloidogenic cleavage pathway at the cellular level. I am using a dual-tagged fluorescent APP fusion protein (pH-APP-BFP2) to track APP’s subcellular distribution, endo/exocytosis and cleavage to investigate the effects of α-, β- and γ-secretase inhibitors in live primary neurons. My project aim is to increase understanding of Alzheimer’s disease pathogenesis and aid in the discovery of safer and more selective treatments for Alzheimer’s disease.
Andrew FeigleyGraduate Student, Davies laboratoryBS, York College of Pennsylvania (2015)
My research focuses on the lipid signaling molecules and how these are altered by obesity. Specifically, how obesity causes a reduction in circulation of N-acylethanolamines (NAE). NAEs have been shown to have anorexic effect and reduce feedings and alter weight gain. We investigate the cellular and molecular mechanisms responsible for production of NAEs which include precursor synthesis and enzymatic production, through a combination of cellular and animal models utilizing a range of molecular and instrumental techniques. In our laboratory we also develop recombinant bacteria to alter the gut microbiome as a potential therapeutic treatment for obesity
Eric FigueroaGraduate Student, Denton laboratoryBS, University of Arizona (2014)
Diabetes affects more than 9% of Americans and has a cost burden of $245 billion. Kir4.2 (KCNJ15) was recently identified as a type 2 diabetes mellitus (T2DM) susceptibility gene and that knock down of the gene stimulated insulin secretion, a function that is normally disrupted in diabetes patients. Together, these data show that Kir4.2 is a potential therapeutic target for T2DM. I will use pharmacological tools to investigate Kir4.2 and its role on insulin secretion in in vitro models, as well as in vivo models. My project will use a range of techniques from molecular biology to integrative physiology.
Rachel FischerGraduate Student, Sappington laboratoryBS, University of Saint Thomas, MN (2012)
The Sappington lab studies the impact of neuronal-glial signaling in glaucoma. My research focuses on understanding the causes of early glaucoma pathology. Glaucoma pathology begins with functional deficits in retinal ganglion cells prior to structural degeneration of the optic nerve. There is a potential therapeutic window after the onset of functional deficits, but prior to physical degeneration of retinal ganglion cells to interrupt optic nerve degeneration and prevent further vision loss. I am working to identify extracellular factors that mediate early functional deficits in retinal ganglion cells. We believe that one such factor may be a disruption in the potassium homeostasis within the retina that leads to altered retinal ganglion cell physiology.
Nicole FisherGraduate Student, Conn and Niswender laboratoriesBS, Miami University (2014)
My project focuses on validating novel treatment strategies for Rett syndrome and MECP2 Duplication syndrome. These are two debilitating neurodevelopmental disorders that are caused by either a loss-of-function mutation or duplication of the MECP2 gene, which codes for the transcriptional regulator Methyl-CpG-Binding Protein 2. We have shown that expression of the metabotropic glutamate receptor 7 (mGlu7) is altered downstream of changes in MECP2 gene dosage. I am particularly interested in understanding how mGlu7 function is altered in these disease contexts and to evaluate the therapeutic potential of fine-tuning mGlu7 activity with small molecule allosteric modulators. To do this, I perform genetic and pharmacological manipulations in mouse models of Rett syndrome and MECP2 Duplication syndrome using a combination of techniques that include biochemistry, brain slice electrophysiology and rodent behavior.
Oakleigh FolkesGraduate Student, Patel LaboratoryBA, Vanderbilt University (2013)
The Patel lab investigates the relationship between endocannabinoid signaling and stress-induced neuroadaptation. By understanding the molecular, structural, and physiological adaptations in endocannabinoid signaling that occur in response to stress, we hope to uncover novel bio-markers and pharmacological targets for drug development. My project will focus on investigating the role of endocannabinoid signaling in social interaction and social stress.
Breanne GibsonGraduate Student, Schoenecker laboratoryBS, Cedarville University (2012)
I’m a graduate student in the lab of Jonathan Schoenecker studying the physiologic changes that occur following a severe injury and how those changes impair healing of injured tissues. Specifically, I study the systemic loss of the regenerative enzyme plasmin after trauma and how it negatively affects the healing of wounds, muscle injuries, and fractures. My research uses both clinical and basic science elements to identify how the loss of plasmin occurs following severe injury and how this system can be targeted therapeutically in order to improve healing of injuries in patients.
Elizabeth GibsonGraduate Student, Osheroff laboratoryPharm.D., Lipscomb University (2014)BA, Reinhardt College (2010)
Fluoroquinolones, which target type II topoisomerases in bacteria, are one of the most widely prescribed antibacterials in the world; however, resistance is on the rise. My project focuses on characterizing two new classes of antibacterials that target type II topoisomerases in bacteria: Novel Bacterial Topoisomerase Inhibitors and Mycobacterium tuberculosis gyrase inhibitors. My work will aid in antibacterial drug development to help combat fluoroquinolone resistance in a wide range of bacteria including, Escherichia coli, Neisseria gonorrheoae, and Mycobacterium tuberculosis.
Yuanjun GuoGraduate Student, Force/Lal laboratoryBS, China Medical University
My research project is about the role of a novel protein-Homeodomain-interacting protein kinase 2 (HIPK2) in the heart. HIPK2 is a highly conserved nuclear serine/threonine kinase, which was first found to interact with NK homeodomain transcription factors. HIPK2 also acts as a tumor suppressor, and regulates cell death by p53-dependent and independent pathway. However, the role of HIPK2 in the heart is unknown. The goal of this project is to explore the major role that HIPK2 plays in the heart and identify the mechanism of how HIPK2 maintains the normal heart function. This study may lead to better understanding of the mechanism of heart failure and identification of therapeutic targets.
Christopher HofmannGraduate Student, Emeson laboratoryBS, Penn State (2012)
My current project focuses on the functional consequences of RNA editing on the Kv1.1 voltage-gated potassium channel. The α-subunit of the Kv1.1-subtype of voltage-gated potassium channel (Kv) plays an important role in regulating neuronal excitability. By dampening excitability at the axon initial segment and juxtaparanodal region, it can influence action potential initiation, propagation and reduce nerve terminal excitability, permitting fine-tuning of neurotransmitter release. Genetic knockout studies have revealed that mice lacking Kv1.1 expression develop spontaneous seizures, hyperalgesia, and neurogenic cardiac dysfunction. RNA transcripts encoding the Kv1.1 subunit are modified by a site-specific Adenosine to Inosine editing event in which a genomically-encoded isoleucine (ATT) is converted to a valine (ITT) codon, changing the identity of amino acid 400 within the S6 transmembrane domain lining the ion-conducting pore. Changes in Kv1.1 editing have been shown to affect the rate of channel recovery from inactivation.
Hussain JinnahGraduate Student, Emeson laboratoryBS, Vanderbilt University (2012)
The 2C-subtype of serotonin 2C receptor (5HT2C) is a member of the G-protein coupled receptor superfamily which is expressed in many brain regions and plays an important role in regulating appetite, metabolism, mood, and sleep. Transcripts encoding the 5HT2C receptor undergo up to five adenosine-to-inosine (A-to-I) RNA editing events to generate as many as 24 protein isoforms with unique signaling properties. Our research focuses on examining the differential expression and function of these edited 5HT2C isoforms, as well as clinical implications resulting from the dysregulation of normal 5HT2C editing patterns.
Krystian KozekGraduate Student, Weaver laboratoryBS, North Carolina State University
Substance abuse and overdose are sharply on the rise in the USA. To understand why drug abuse and addiction are so problematic in our society, our laboratory investigates ion channels in the brain and these channels’ role in addiction. If we can change the way in which these channels behave, we hypothesize that we may be able to stop addiction from developing. I specifically study the G protein-gated inwardly-rectifying potassium (GIRK) ion channels, which are found in neurons in the brain. GIRK channel behavior is difficult to alter with currently known molecules. I aim to create new drug-like molecules that will target the structures in the brain associated with addiction and alter the behavior of GIRK channels in these areas. With the discovery of such molecules, I will enable further investigation of GIRK channels’ role in the development, prevention, and treatment of addiction.
Kelvin LuongGraduate Student, Fesik laboratoryBS, California State University (2015)
I grew up in the San Fernando Valley of California. I obtained a B.S. in biochemistry from Cal State Northridge. After graduating, I spent a year working for a DNA sequencing company. Coming back to school, my research interest is in structure based drug discovery. In my free time, I enjoy exploring the food scene, especially Nashville's hot chicken.
James MaksymetzGraduate Student, Conn laboratoryBS, UCLA (2013)
Deficits in cortical-dependent executive function and working memory constitute core symptoms of schizophrenia and remain untreated by current antipsychotic medications. Positive allosteric modulators (PAMs) of both the M1 subtype of muscarinic acetylcholine receptors (mAChR) and the metabotropic glutamate receptor subtype mGlu5 improve cortical-dependent cognition in wild-type animals and rescue deficits in schizophrenia-like animal models. My project aims to investigate how M1 and mGlu5 interact to regulate neurotransmission and synaptic plasticity in the rodent medial prefrontal cortex (PFC) to understand how this interaction contributes to in vivo efficacy. I am using a combination of biochemical, genetic, electrophysiological, and behavioral methods to probe the roles of M1 and mGlu5 in different neuronal populations with the goal of ascertaining which of their actions at a cellular- and circuit-level are responsible for PAM-mediated cognition enhancement. Knowledge of how these two receptors interact to improve learning and memory will help us develop better, more targeted therapeutics to treat cognitive deficits in patients with schizophrenia and other brain disorders.
Annah MooreGraduate Student, C. Niswender and Sweatt laboratoriesBS, BA, University of Rochester (2015)
I was born in Michigan and raised in Massillon, Ohio. Once I received a BS in Neuroscience and a BA in Chemistry at the University of Rochester, I began post-baccalaureate IRTA in the National Institute for Neurological Disorders and Stroke (NINDS) at the National Institutes of Health (NIH) to study dopamine receptor modulation. Upon completion this fellowship, I knew I wanted to pursue a Ph.D. in Pharmacology. While out of the lab and classroom, I love exploring new hiking trails and getting creative in the kitchen.
Stephanie MooreGraduate Student, Schoenecker laboratoryBS, Ohio Northern University (2003)
Trauma-induced skeletal muscle calcification is a spectrum of disease, including dystrophic calcification and heterotopic ossification (HO), that may occur following severe injuries such as burn, blast, neurologic and musculoskeletal injuries, as well as certain orthopaedic procedures. Under normal physiologic circumstances, when the body undergoes injury, innate protection mechanisms inhibit the formation of calcification within skeletal muscle. Additionally, the body also possesses mechanisms to remove mineral deposits formed in damaged tissues, thereby allowing for proper tissue healing and regeneration. The goal of my project is to identify critical skeletal muscle protection mechanisms and the mechanisms by which calcification is regressed from damaged tissues. Through identifying the mechanism at work, I am now examining novel therapeutics aimed at enhancing these mechanism to better prevent soft tissue calcification.
Shan ParikhGraduate Student, Knollmann laboratoryMS, University of Connecticut (2011)BS, University of Connecticut (2010)
Shan is a mentee in the Bjorn Knollmann lab in VanCART. Here, he is growing his toolbox for studying calcium handling and its relevance to cardiomyocyte dysfunction in models which develop cardiomyopathy and/or arrhythmias. His main project involves developing the use of iPSC-CM for modeling cardiac laminopathy.
Brynna PaulukaitisGraduate Student, Sweatt laboratoryBS, University of Alabama at Birmingham (2015)
Long-lasting memories are underlied by changes in gene expression. The Sweatt laboratory focuses on neuroepigenetic mechanisms that provide a biological basis for the persistence of memories. One such mechanism is histone variant exchange, wherein canonical histones comprising nucleosomes are replaced with variant histones, which can alter the accessibility of DNA for transcription. We have previously shown that the incorporation of histone variant H2A.Z in the hippocampus is negatively associated with contextual fear memory in mice. We are currently working to further elucidate the mechanisms by which H2A.Z influences memory formation and consolidation.
Rafael PerezGraduate Student, Winder laboratoryBS, York College of Pennsylvania (2013)
My research focuses on understanding the role of adrenergic signaling within the extended amygdala in stress-induced relapse of cocaine seeking. Stress is often cited as a precipitating factor in cocaine relapse. Compounds that decrease stress and anxiety by targeting adrenergic receptors, such as beta-blockers and alpha 2a adrenergic receptor agonists, show some efficacy in clinical trials. However, the neuronal substrates responsible for the beneficial effects of these compounds remains unknown. To address this gap in knowledge I am using a combination of behavioral pharmacology, genetic, and biochemical approaches to investigate the role of adrenergic receptors in the extended amygdala in cocaine and stress-exposed animals treated with adrenergic ligands.
Nicole PerryGraduate Student, V. Gurevich and Iverson laboratoriesBS and BA, Wittenburg University (2014)
Nicki is under the co-mentorship of Dr. Gurevich and Dr. Iverson, whose labs she officially joined in April 2015. Her chosen thesis research, which is to elucidate the interaction of arrestin-3 with the mitogen-activated protein kinases (MAPKs), is based on evidence from both labs and current publications in the field. As a member of two labs, Nicki is presented with the unique opportunity to approach her scientific questions from two angles: biochemical assays, which allow her to conduct studies of arrestin function, and macromolecular X-ray crystallography, which she uses to determine different arrestin complex structures. This arrangement enables her to develop novel functional experiments with the help of solved crystal structures, a process that usually requires extensive collaboration. It also exposes her to a wide variety of experimental techniques, which range from basic molecular and cell biology to advanced instrumental study.
Kristin PetersonGraduate Student, Hasty laboratoryBS, University of Richmond (2013)
Our lab studies the intersection of metabolism and immunology, with an emphasis on how obesity-related inflammation impacts metabolic disease progression. For my project, I am studying relationship between complement factor 5 of the innate immune system and insulin receptor processing and resultant insulin signaling. We have evidence that this protein is necessary for proper insulin action, so I am working to determine how the pathways are connected to ensure metabolic homeostasis.
Francis J. (FJ) Prael, IIIGraduate Student, Weaver laboratoryBS, University of Michigan, Ann Arbor (2013)
An estimated 1 in 26 people are predicted to develop epilepsy at some point in their life. Epilepsy, a chronic neurological condition defined by recurrent seizures, is a tremendous burden on those afflicted with the disease. With nearly one-third of epilepsy patients being refectory to all treatments, novel approaches for the treatment of epilepsy are urgently needed. In the C. David Weaver laboratory, I work on discovering and developing chemical tools targeting transporters that are dysfunctional in epilepsy. We will use these chemical tools to evaluate the therapeutic potential of correcting dysfunction of these transporters in epilepsy and to further characterize fundamental characteristics of these proteins relevant to their dysfunctional state in epilepsy. If successful, our work could lay the foundation for novel approaches to the treatment of epilepsy.
Meagan QuinlanGraduate Student, Blakely laboratoryBS, University of Vermont (2012)
My research explores the molecular underpinnings of serotonin transporter (SERT) regulation. More specifically, I am building on the discovery of multiple, functional SERT coding variants in subjects with autism spectrum disorder (ASD) that display altered regulation through PKG and p38 MAPK-linked pathways. The availability of a mouse model expressing the most common of these variants, SERT Ala56, provides a key opportunity to examine how disrupted SERT function and regulation leads to risk for ASD and other disorders associated with perturbed serotonin signaling.
Jason RussellGraduate Student, Jones laboratoryDoctorate, University of Cambridge (2012)BA, University of Cambridge (2009)
Corey SeacristGraduate Student, Blind laboratoryMBA, College of Charleston (2015)
I am studying a promiscuous inositol kinase, IPMK, which has been linked to diabetes and cancer. Using traditional biochemistry techniques, I am determining how IPMK is integrated into classical signaling networks, and what substrates it has within mammalian cells. Furthermore, I am attempting to generate a molecular model of the enzyme using X-ray crystallography, which can be used in future structure-based drug design efforts. These studies may help validate IPMK as a viable drug target for the treatment of diabetes or cancer.
Melaine SebastianGraduate Student, Lopez laboratoryBS, Tulane University (2013)
Mabel SetoGraduate Student, Lindsley laboratoryBSLAS, University of Illinois @ Urbana (2015)
The Lindsley laboratory focuses on drug discovery with an emphasis on the development of allosteric modulators for the validation and investigation of novel targets and mechanisms for a variety of different diseases. My project is on the development of novel and selective positive allosteric modulators for the metabotropic glutamate receptor subtype 7 (mGlu7). My primary goals are the chemical synthesis and optimization of the modulator as well as the exploration of the role of mGlu7 in the neurological disorder, schizophrenia. These studies may not only lead to a better understanding of the biology of mGlu7 in schizophrenia, but also in other neurological disorders.
Aparna ShekarGraduate Student, Galli laboratoryB.Eng, VTU India, Sri Jayachemarajendra College of Engineering (2012)
During my Ph.D. training, I aim to understand the biophysical and functional properties of proteins with key roles in regulating dopamine signaling pathways, and how these properties are disrupted or altered in neuropsychiatric disorders. In Dr. Galli’s lab, I am learning and applying electrophysiological techniques (including whole-cell patch clamp and amperometry), as well as biochemistry and confocal imaging, to elucidate the underlying biophysical principles and molecular regulators of neurotransmitter transporter function. In addition, I am exploring and mastering how to translate these molecular discoveries in vivo using Drosophila melanogaster as an animal model.
Megan ShueyGraduate Student, N. Brown laboratoryMS, Northern Arizona University (2012)BS, University of Arizona (2009)
My research focuses on leveraging electronic health records and genetics to enhance our understanding and treatment of resistant hypertension. By identifying patients within Vanderbilt's BioVU that have resistant hypertension we intend to test specific genetic variants to potentially identify a novel antihypertensive therapeutic. I am also using the population to determine if there are genetic predictors that predispose patients to attenuated responses to specific antihypertensive therapies.
Kayla ShumateGraduate Student, Emeson laboratoryBS, University of North Carolina (2011)
Calcium-dependent activator protein for secretion 1 (CAPS1) serves as a priming factor for vesicular fusion associated with the regulated secretion of peptides, neurotransmitters and hormones from synaptic and dense core vesicles. The RNA encoding CAPS1 undergoes a site-specific adenosine-to-inosine RNA editing event which can alter a genomically-encoded glutamate to a glycine codon within the carboxyl-terminal domain previously shown to be responsible for interactions with large dense-core granules. CAPS1 is prevalent throughout the central nervous system and editing levels in the mouse brain reach 30% in the frontal cortex. I am interested in the physiological role(s) for CAPS1 editing and am currently examining the consequences of editing on the regulation of CAPS1-dependent modulation of synaptic vesicle release and recycling.
Brittany SpitznagelGraduate Student, Weaver laboratoryPharm.D., Lipscomb University(2016)
There is currently an unmet need to identify more selective drugs for Slack-induced epilepsies. In order to better understand the role Slack plays in childhood epilepsies we need to develop highly selective molecular probes. When identified, such probes will allow for the investigation of the hypothesis that selective small molecule modulators that normalize inhibitory interneuron based transmission will safely and effectively correct the epileptiform behavior caused by Slack mutations. Discovery and characterization of such compounds will provide a starting point for the development of new clinical tools for the treatment of Slack-induced epilepsies.
Bradley SteinerGraduate Student, Hadjfrangiskou laboratoryBS, Florida State University (2014)
My research is driven by an interest in antibiotics, infectious diseases, and cellular signaling. My thesis work focuses on understanding the signaling networks that Uropathogenic E. coli use throughout pathogenesis to acquire vital nutrients, respond to hazards, and to regulate virulence factors, with an overarching goal to develop new antimicrobial therapies targeting these systems.
David TaylorGraduate Student, Wang laboratoryBS, Texas Southern University (2012)
The primary goal of the Wang lab is to identify mechanisms of therapeutic resistance and to translate this knowledge into transformative and effective treatments for a variety of cancers. My cancer of interest, glioblastoma multiforme (GBM), is the most malignant form of primary brain cancer with a patient life expectancy of only 12-15 months. Knowing this, my long term goal is to identify novel combination therapies that suppress or inhibit the ability of GBM tumors to self-renew, proliferate rapidly, and resistant chemo-radiation.
Laura TealGraduate Student, Jones laboratory, BA, BS, Hope College (2017)
Sheryl Anne VermudezGraduate Student, C. Niswender laboratoryBS, Chaminade University of Honolulu, HI (2016)
I'm originally from the Philippines but grew up in the island of Oahu in Hawaii. I attended Chaminade University of Honolulu where I double majored in Biochemistry and Forensic Science. I’m interested in studying and targeting signaling pathways associated with neurodevelopmental disorders for therapeutic discovery. I have joined the lab of Colleen Niswender and Jeff Conn to pursue this interest, focusing on the implications of metabotropic glutamate receptors in the cognitive phenotypes observed in MeCP2-associated diseases, Rett Syndrome and MecP2-duplication syndrome. Outside of lab, I enjoy outdoor activities and sports, especially hiking and playing basketball.
Rebecca (Becca) WeinerGraduate Student, Sappington laboratoryBS, University of Tennessee-Knoxville (2014)
Laura WinalskiGraduate Student, Ihrie laboratoryBS, Georgia Institute of Technology (2017)
Nathan WintersGraduate Student, Denton laboratoryBS, University of Evansville (2016)
I was born and raised in Evansville, IN, where I received my BS in Neuroscience from the University of Evansville in 2016. Following graduation, I came directly to Vanderbilt the following fall. I am currently a graduate student in the laboratory of Dr. Jerod Denton, where I will be pursuing my interests in exploring the therapeutic potential of underexploited ion channel drug targets in the central nervous system. Outside of the lab, I enjoy fishing, hiking, and exploring the music scene.
Matthew WleklinskiGraduate Student, Knollmann laboratoryBS, University of Wisconsin-Madison (2015)
The Knollmann Lab is interested in studying various arrhythmias, their development, and how to treat them. One of the main arrhythmias they focus on is catecholaminergic polymorphic ventricular tachycardia (CPVT). My current research interest is to study CPVT and try to understand the calcium handling that causes these to form. We are looking at using various mouse models that have knock out mutations in calsequestrin from different patient populations to understand how these mutations affect calsequestrin and lead to the generation of these arrhythmias.
Yuantee ZhuGraduate Student, Elefteriou laboratoryBS, Tufts University (2011)
Osteoporosis is a bone metabolic disease affecting approximately 14 million Americans over the age of 50, resulting in increased risk of fractures and associated morbidities. The prevalence of the disease increases with age, independent of hormonal status (e.g. menopause). Understanding the pathology and developing clinical interventions for age-related osteoporosis depends on understanding bone remodeling – a process regulated by local and systemic signals – and how these signals are affected during aging. The sympathetic nervous (SNS) system controls bone remodeling via norepinephrine release, which directly inhibits bone formation by osteoblasts and promotes bone resorption by osteoclasts. The proposed project aims to determine whether NET in osteoblasts or neurons modulate bone remodeling, and whether a reduction in NE uptake by bone cells during aging contributes to bone loss. Results from this study will elucidate the interactions between endogenous SNS outflow and bone remodeling during bone mass accrual and aging. This research will ultimately expand the understanding of age-related osteoporosis, and open new avenues of research towards treatment of bone metabolic diseases.