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Student Alumni

This page is sparsely maintained and only students who have graduated since mid-2014 are listed. If you are a student alum and would like to be listed, please fill in this form.

Student Alumni

Kristie Aamodt, BS, Brigham Young University

MD PhD Student, Molecular Physiology and Biophysics

Powers laboratory.

    Kristie Aamodt

    Graduate Student 2011-2015

    PI: Alvin Powers, M.D.

    Erica Joan Pruett Anderson, BS

    Graduate Student, Cone laboratory, Molecular Physiology & Biophysics

    My research project is focused on advancing our understanding of the molecular and kinetic mechanisms of energy maintenance by elucidating if and when MC4R induced Kir7.1 signaling is required for regulation of food intake and energy expenditure.  We believe MC4R functions as a rheostat of energy maintenance by utilizing both tissue specific Gαs and Kir7.1 signaling modalities as well as unique kinetic aspects of these modalities.  I am using an in vivo  modeling system to test this hypothesis.

    Caleigh Mariko Azumaya, BS

    Alumna Graduate Student, Terunaga Nakagawa lab, Molecular Physiology and Biophysics

    AMPA receptors (AMPARs) are ligand-gated cation channels whose appropriate activity and regulation are integral to most central nervous system function. They mediate the majority of excitatory neurotransmission and their dysregulation has been implicated in many cognitive disorders. My research focuses on the molecular details of auxiliary subunit interactions with the AMPAR. Using biochemical and structural biology techniques, we hope to illuminate the molecular basis of interaction between these two proteins and how that relates to the auxiliary subunit’s modulation of AMPAR in vivo.

    • : 766 RRB (MRB I)

    Kayla Boortz, BS

    Graduate Student, O'Brien lab, Molecular Physiology & Biophysics

    I work in Richard O’Brien’s laboratory and I study glucocorticoid regulation of G6pc2 expression in islet β cells.

    Karin Janae Bosma

    Graduate Student, O'Brien laboratory, Molecular Physiology & Biophysics

    Elevated fasting blood glucose (FBG) levels have been associated with an increased risk of type 2 diabetes (T2D) development and cardiovascular-associated mortality (CAM). Genome-wide association studies (GWAS) have identified SNPs in G6PC2 associated with FBG. G6PC2 is an isoform of the glucose-6-phosphatase catalytic subunit expressed in pancreatic islet beta cells. Deletion of G6pc2 in mice results in reduced FBG, consistent with the human GWAS data, and islets from these mice have enhanced glucose-stimulated insulin secretion (GSIS) at sub-maximal glucose concentrations. I am using mouse models to explore the function of G6pc2 in islet beta cells and its potential as a therapeutic target for the prevention of T2D and CAM.

    Adrian Gabriel Cadar, BS

    Graduate Student, Hong laboratory, Molecular Physiology & Biophysics

    Titin, the largest known protein, is indispensable for the structural integrity and function of the cardiac sarcomere. Yet, how such a massive ~3 mDa structural protein is maintained within the highly ordered sarcomere complex, while under continuously alternating tension, is unknown. My thesis focuses on elucidating the mechanisms mediating sarcomere homeostasis in human induced pluripotent stem cell-derived cardiomyocytes. Using CRISPR/Cas9 gene editing, I generated a novel model in which I can directly visualize sarcomeric titin in order to address fundamental questions regarding titin turnover, which is critical for sarcomere homeostasis.

      Megan Elise Capozzi, BA

      Graduate Student, John Penn Laboratory, Molecular Physiology & Biophysics

      I am currently studying inflammation in diabetic retinopathy in Dr. John S. Penn‘s Laboratory.

        Bethany Carboneau, BA

        Graduate Student, Maureen Gannon laboratory, Molecular Physiology & Biophysics

        Prostaglandins are important modulators of an array of physiologic functions including insulin secretion and systemic inflammation. In the Gannon lab, I focus on the specific roles of the prostaglandin E2 receptors EP3 and EP4 and how they regulate processes involved in β-cell mass expansion. I am using pharmacological tools to examine the effects of EP3 and EP4 signaling in β-cell proliferation and β-cell survival in isolated mouse and human islets. I am also studying the effects of an EP3 antagonist and an EP4 agonist on β-cell proliferation and β-cell survival in the db/db mouse model of type 2 diabetes.

        Joseph Cleland

        Graduate Student, Neuert laboratory, Molecular Physiology and Biophysics

          Liz Conrad, BS, BA, University of Michigan

          Graduate Student, Roland Stein Laboratory, Molecular Physiology & Biophysics

          Courtney Copeland, BS

          Graduate Student, Kenworthy Lab, Molecular Physiology & Biophysics

          In the Kenworthy lab, my project focuses on understanding the role of Cav-1 mutants in the pathogenesis of pulmonary arterial hypertension.

          Bethany Lyn Dale

          Graduate Student, Madhur Lab

          I study the role of interleukin-21(IL-21) in hypertension associated end-organ damage and dysfunction using an IL-21 global knockout mouse. I am looking at the presence and effector function of IL-21 producing cells in Angiotensin II induced experimental hypertension.

          Ken James Drake, BS, Cal State

          Graduate Student, Wikswo laboratory, Molecular Physiology & Biophysics

          I am a graduate student in the Wikswo lab studying the role of amino acids in cardiac ischemia and hypoxia.

            Amicia Elliott, PhD

            Graduate Student, David Piston's laboratory 2014, Molecular Physiology & Biophysics
            Postdoctoral Fellow, Benjamin White & Hari Shroff at the NIMH and NIBIB

            Joseph Elsakr, BSE

            Graduate Student, Gannon Lab

            A mother’s diet and metabolic status during gestation has been shown to affect her offspring’s risk of developing metabolic disease later in life. In the Gannon Lab, I study the mediators of this increased disease risk using two animal models of maternal high fat diet during pregnancy. In a collaboration with multiple labs across the country, I obtain pancreata from non-human primates exposed to high fat diet in utero. Pancreatic endocrine cell mass, structure, and function are currently being investigated. In a mouse model, I study the effects of maternal high fat diet on the epigenetic profile of pancreatic beta cells in the offspring. Together, these studies will enhance our understanding of how high fat diet during pregnancy predisposes offspring to develop metabolic disease.

            Jordan Taylor Feigerle, BS

            Graduate Student, Peter Weil laboratory, Molecular Physiology & Biophysics

              Liz Anne Ferrick, BS

              Graduate Student, Ron Emeson Laboratory, Molecular Physiology & Biophysics

              In Ron Emeson‘s lab, I am characterizing the physiological impact of Kv1.1 RNA editing in mice.

              Andrew Young Gordon, BA

              Graduate Student, Penn laboratory, Molecular Physiology & Biophysics

              I research and create novel nanoparticles for molecularly targeted imaging of the eye. My project involves using gold nanorods as exogenous contrast agents in the eye that are compatible with optical coherence tomography systems. My research includes the construction of gold nanorods and their modification for stability and biocompatibility. I collaborate with researchers outside my lab to perform work related to photothermal optical coherence tomography. Additionally, my research focuses on methods of drug delivery to the eye. As this is imaging research, I use a variety of imaging modalities relevant to in vivo imaging of the eye, notably optical coherence tomography.

                Sarah C. Graff

                Graduate Student, Jacobson laboratory, Molecular Physiology & Biophysics

                Our lab studies the function of potassium channels in electrically excitable endocrine cells within the pancreas. We are particularly interested in the β-cell specific potassium channel, TALK-1. TALK-1 is the most abundant potassium channel in the β-cell, and a polymorphism within TALK-1 has been associated with an increased risk for Type-2 diabetes. Our lab has previously shown that TALK-1 channels regulate the β-cells ability to release insulin in response to glucose. My work focuses on characterizing this regulation so that we can better understand the function that the channel plays in diabetes.

                Rachana Haliyur

                MD PhD Student, Al Powers laboratory, Molecular Physiology & Biophysics

                Recent observations have challenged long held concepts in the pathophysiology of type 1 diabetes. By implementing an integrative approach to study both the native pancreas and isolated islets from the same human donor, I work to characterize the function and morphology of T1D pancreatic islets using in vitro and in vivo functional studies and immunohistochemistry. My primary project focuses on the glucagon-producing alpha cells in the T1D islet and identifying the mechanisms behind disordered glucagon secretion in T1D.

                  Nick Harris, BS

                  MD PhD Student, Winder laboratory, Molecular Physiology & Biophysics

                  Drug dependent patients trying to maintain abstinence often relapse to their chosen of drug of abuse, with many citing stress as an antecedent to use and a lack of effective treatment to control the urge to use. Guanfacine is an α2A-adrenergic receptor agonist that targets receptors for the brain stress neurotransmitter norepinephrine and has been used in both preclinical and clinical trials for addiction, often showing positive results such as reduced craving but not producing changes in ultimate rates of relapse. We hypothesize that the ineffectiveness on relapse is due to competition among the myriad effects of this drug and aim to study a non-canonical neuronal activating effect in the bed nucleus of the stria terminalis, an area of the brain known to be implicated in both stress and addiction disorders, through the complementary use of whole cell electrophysiology and neuroanatomical methods in the hopes that uncovering the mechanism underlying this effect will aid in future treatment of patients dependent on drugs of abuse.

                  Andrea Alyssa Hill, BS, Clark Atlanta University

                  Graduate Student, Alyssa Hasty laboratory, Molecular Physiology & Biophysics

                  I work in Alyssa Hasty‘s laboratory where we study inflammation and obesity.

                  Merla Hubler, MS

                  MD PhD Student, Hasty laboratory, Molecular Physiology & Biophysics

                  I am studying the role of macrophages in maintaining iron homeostasis in adipose tissue. Specifically, we have identified a subset of resident macrophages that compensate for excess iron in the tissue. We are currently interested in depleting this population of macrophages in order to assess their importance in maintaining the health of adipocytes. In future studies we will address the importance of iron handling by macrophages in obesity, and the temporal distribution of iron in adipose tissue and liver tissues.

                  Nora Kayton, BS, University of Virginia

                  Graduate Student, Powers laboratory, Molecular Physiology & Biophysics

                  My thesis in the Powers laboratory addresses basic questions of diabetes pathology, specifically (1) the functional consequences of chronic hyperglycemia on human pancreatic islets in vivo, and (2) the effects of ErbB growth factors on islet growth and function

                    Peter Allerton Kropp, BA

                    Graduate Student, Gannon laboratory, Molecular Physiology & Biophysics

                    I am interested in understanding the role of the transcription factor Oc1 (Onecut1) in pancreas development and disease. Oc1 is essential for development of the endocrine pancreas, so I am investigating its interaction its cofactor Pdx1 in that role. I have thus far determined that proper dosage of both Oc1 and Pdx1 is necessary for endocrine cell differentiation and that defects established during development persist into adulthood. I am further interested in identifying the direct targets of Oc1 during pancreas development since so little is known about its direct regulatory role.

                    • : 7435 MRB IV

                    Michael Joshua Litt, BA

                    MD PhD Student, Cone laboratory, Molecular Physiology & Biophysics

                    In the Cone lab, I study the pathophysiology associated with deletion of the MC4R, the most common monogenetic obesity syndrome in man (1/5000 allele frequency). Using the mouse as a model organism, I am characterizing the cardiovascular, metabolic and energetic consequences that result from MC4R deletion. Observations from my research have furthered the need to identify and monitor patients with this distinct obesity syndrome.


                    More broadly, my research interests include: energy metabolism, mitochondrial physiology, cardiovascular pathophysiology, pharmicogenomics, and gene environment interactions.

                    Roxanna Loperena, BS

                    Graduate Student, Harrison laboratory, Molecular Physiology & Biophysics

                    In the past 20 years, two new mechanisms of hypertension have been defined: one is oxidative injury and the second is inflammation. Our lab has shown that dendritic cells (DCs) from hypertensive mice accumulate isolevuglandins that adduct to proteins and promote T cell activation. In hypertension, the endothelium is activated to produce reactive oxygen species and to express adhesion molecules and chemokines that attract inflammatory cells. In my project, we hypothesized that human endothelial cells exposed to mechanical stretch will promote conversion of human monocytes into activated DCs. Therefore, I study this conversion when monocytes co-cultured with human aortic endothelial cells exposed to either normal cyclical stretch (5%) or hypertensive cyclical stretch (10%) using the Flexcell® Tension System. I also study the different signaling molecules that could potentially be facilitating this process in hopes of understanding the mechanism of action.

                      Tammy Michelle Lundblad, BS, Centre College

                      Graduate Student, McGuinness laboratory, Molecular Physiology & Biophysics

                      In the McGuinness lab, my long-term research objective involves elucidating the mechanisms whereby neuroendocrine function can be regulated by alterations in the inflammatory environment.

                        Christian Randal Marks, BA

                        Graduate Student, Colbran laboratory, Molecular Physiology & Biophysics

                        Calcium/calmodulin-dependent kinase II (CaMKII) is a highly abundant serine/threonine kinase in the brain. Direct interactions between activated CaMKII and its substrates play a number of important roles within the cell such as feedback regulation of channels/receptors, and normal synaptic plasticity. Relatively few CaMKII-associated proteins are known to preferentially interact with inactive CaMKII, and their functional roles are poorly understood. Moreover, molecular mechanisms underlying the coupling of CaMKII to the G-protein coupled receptors (GPCRs) that stimulate the release of intracellular calcium are poorly characterized. An interaction between inactive CaMKII and the metabotropic glutamate receptor 5 (a Gq-coupled GPCR) was recently reported. I am currently investigating how CaMKII interactions with mGlu5 can change mGlu5 signaling. Understanding the physiological importance of this interaction may lead to novel treatments of neurological disorders linked to dysfunction of mGlu5 such as Parkinson’s Disease, addiction, schizophrenia, and autism spectrum disorder.

                        Brian Douglas McKenna, BS, James Madison University

                        Graduate Student, Stein laboratory, Molecular Physiology & Biophysics

                        In the Stein lab, I work on identifying co-regulators of Pdx-1 and their regulation of critical β-cell genes.

                        • : 723 Light Hall

                        Amanda Meyer, BA

                        Graduate Student, Weil Laboratory, Molecular Physiology & Biophysics

                        RNA Polymerase II transcriptional activation contributes importantly to the regulation of gene expression by controlling mRNA biosynthesis. A central driving force of the activation process is provided by the concerted action of a DNA-binding transfactor and at least one coactivator. I am interested in defining the transfactor-coactivator interactions required for activation. The specific goal of my current work in the Weil lab is to determine the specific domains the Rap1 transcriptional activator uses to interact with the general transcription factor TFIID to drive activation of the budding yeast S. cerevisiae ribosomal protein genes.  I combine genetic, biochemical, and biophysical approaches to accomplish this goal.

                        Sanjay Mishra

                        Graduate Student, Molecular Physiology & Biophysics

                        I work in Hassane Mchaourab‘s lab on the structure and function of small heat shock proteins, particularly their function in the lens.

                        Allison Elizabeth Norlander, BS

                        Graduate Student, Madhur laboratory, Molecular Physiology & Biophysics

                        My thesis project in Dr. Harrison’s laboratory is centered on the role of T cells in hypertension.

                          Brian T. Palmisano, BS, BA

                          MD PhD Student, Stafford lab, Molecular Physiology & Biophysics

                          • : 7445 MRB IV

                          Tyler L. Perfitt, BA

                          Graduate Student, Colbran lab, Molecular Physiology & Biophysics

                          Brain function relies on the formation and stabilization of synapses, and many neurological disorders are associated with disruptions in synaptic signaling. Scaffolding proteins play a critical role in maintaining spine morphology and bringing receptors and ion channels in close proximity to their downstream signaling molecules. In the Colbran lab, I study protein-protein interactions between CaMKII and scaffolds in the postsynaptic spines of neurons, and how they regulate downstream signaling. I am also interested in how neurons signal from the synapse to the nucleus in order to initiate gene transcription, an important process in learning and memory.

                          BA, DePauw University

                          Marquicia R. Pierce, PhD

                          Graduate student and Postdoctoral Fellow with James May 2008-2014, Michigan State University
                          Currently: Industrial Postdoctoral Fellow

                          Richard L. Printz, PhD

                          Research Assistant Professor, Molecular Physiology and Biophysics

                          Christopher Alan Reissaus, BS

                          Graduate Student, Piston laboratory, Molecular Physiology & Biophysics

                          Diane Caitlin Saunders, BS, BA

                          Graduate Student, Powers laboratory, Molecular Physiology & Biophysics

                          In the Powers Lab, I am investigating the role of pancreatic endothelial cell populations in the islet microenvironment, by determining their role in macrophage recruitment and beta cell regeneration. I am also isolating subpopulations of human islet cells, ultimately characterizing how gene expression varies during developmental stages and in disease states.

                          • : 8435 MRB IV

                          Leslie Roteta Sedgeman, BA

                          Graduate Student, Vickers laboratory, Molecular Physiology & Biophysics

                          Communication by HDL-miRNAs in Type 2 Diabetes

                          MicroRNAs (miRNAs) are small non-coding RNAs that post-transcriptionally repress gene expression and are found in both cells and extracellular fluids, including plasma. Extracellular miRNAs are protected from circulating nucleases through their association with lipid and protein carriers, specifically exosomes and lipoproteins.. Currently, I am studying the role of high-density lipoproteins (HDL)-miRNAs as cell-to-cell messengers in a novel endocrine-like communication pathway within Type 2 diabetes. We found that many of the most abundant miRNAs on HDL are also enriched in insulin-producing β-cells in the islets of Langerhans. Additionally, we found that the miRNA signature on HDL is significantly altered in rat models of Type 2 diabetes; therefore, the goal of my project is to investigate the molecular mechanisms by which the β-cell-originating miRNAs control gene expression in distal tissues and how this pathway regulates systemic lipid and glucose metabolism. Using high-throughput genomics, I aim to decode and control miRNA intercellular communication to better understand and treat type 2 diabetes, including developing biomarkers to predict pre-diabetes.

                          • : 358 RRB

                          Kristen Syring, BS

                          Graduate Student, O'Brien laboratory, Molecular Physiology & Biophysics

                          The prevalence type 2 diabetes (T2D) continues to increase worldwide. Multiple SNPs associated with altered risk of T2D have been identified through genome wide association studies including rs13266634 in the SLC30A8 locus, which encodes zinc transporter 8 (ZnT8). In addition, rare mutations resulting in SLC30A8 haploinsufficiency are protective against T2D. Using several mouse models, we are investigating the role that ZnT8 plays in beta cell function and the potential of ZnT8 as a therapeutic target for T2D.

                          • : 8415 MRB IV

                          Elijah Trefts

                          Graduate Student, Wasserman laboratory, Molecular Physiology & Biophysics

                          Liver is a primary site of macronutrient metabolism. Obesity linked diseases of the liver such as nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) result in ECM expansion, defective hormonal responses, and disrupted transcriptional networks. Integrin receptors and their immediate post-receptor pathways convert sensory inputs from the ECM to biochemical processes within the cell. Altered expression of several integrin signaling components accompanies the metabolic dysregulation that occurs in high fat (HF)-fed mice. The mechanisms linking ECM expansion and integrin signaling to metabolic disease are a primary focus of our lab. My research utilizes hepatocyte specific knockout of several integrin signaling components (e.g. integrin α5, integrin β1, and Integrin-linked kinase) in mice to fully characterize these pathways and their involvement in pathologic responses of the liver to high fat feeding.

                          Alessandro Ustione, PhD

                          Research Fellow / Piston Lab, Molecular Physiology and Biophysics

                          Research Interest:  I am currently investigating the function of dopamine in the pancreatic islets with the goal of understanding how observed dopaminergic feedback regulates glucose stimulated insulin secretion.

                          Nicholas Catin Vierra, BS

                          Graduate Student, Jacobson laboratory, Molecular Physiology & Biophysics

                          The deterioration of pancreatic islet function is a hallmark of type 2 diabetes mellitus (T2DM). In the Jacobson lab, I study the physiological functions of an islet potassium channel, TALK-1. TALK-1 is the most transcriptionally abundant potassium channel in insulin-secreting β-cells, and polymorphisms in TALK-1 are associated with an increased susceptibility for T2DM. However, the molecular mechanisms underlying TALK-1’s contributions to T2DM pathogenesis remain unclear. Using a variety of experimental approaches, including electrophysiology, calcium imaging, hormone secretion, and mouse models, we have recently found that TALK-1 channels regulate islet calcium homeostasis and insulin secretion. These findings suggest that TALK-1 could serve as a therapeutic target in T2DM.

                          Carrie Beth Wiese, BS

                          Graduate Student, Vickers laboratory, Molecular Physiology & Biophysics

                          Extracellular microRNAs have been identified in plasma, and our laboratory has identified these extracellular microRNAs are carried by lipoproteins including high-density lipoprotein (HDL). The goal of our laboratory is to characterize the role of these extracellular microRNAs, particularly to elucidate whether extracellular microRNAs may function as a novel cell-to-cell communication pathway. Within cells, microRNAs are small non-coding RNAs that post-transcriptionally regulate gene expression. Specifically, I study the myeloid-derived microRNA, miR-223, to understand to what tissue and cell types receive microRNA-223 after being exported from myeloid cells. To do this, I utilize bone marrow transplants between wild-type and miR-223 knockout mice to restore or deplete the myeloid (miR-223 donor cell) population. After restoring or depleting the myeloid population (miR-223 donor cell) I examine variety of tissue types and pure cell isolations to map out the delivery of extracellular miR-223 in vivo. My second project focuses on the role of endothelial microRNAs in the progression of Chronic Kidney Disease-associated atherosclerosis. I have found that complexing two microRNA inhibitors to HDL, allows me to effectively reduce endothelial microRNA levels. The decreased microRNA levels result in a dramatic reduction in atherosclerosis in vivo, which may be mediated through altered FAM220a regulation of STAT3 activation causing less inflammation.

                          • : 358 PRB

                          Ashley Silberman Williams, BS, Appalachian State University

                          Graduate Student, Wasserman laboratory, Molecular Physiology & Biophysics

                          • : 823 Light Hall

                          Ian Miller Williams, BS

                          Graduate Student, Wasserman laboratory, Molecular Physiology & Biophysics

                          Impaired insulin-stimulated muscle glucose uptake is a hallmark of insulin resistance and Type 2 diabetes. Before insulin can stimulate the muscle to take up glucose, it must first cross the endothelial barrier that separates the plasma from the interstitial fluid that bathes myocytes. I have developed an intravital microscopy technique which allows us to directly visualize and quantitate the trans-endothelial efflux of insulin in skeletal muscle. I am using this technique to 1) determine the mechanism by which insulin crosses the endothelium (i.e. receptor-mediated transport or passive diffusion) and 2) determine if impaired trans-endothelial movement of insulin may contribute to muscle insulin resistance.

                          • : 823 Light Hall

                          Lukasz Szczepan Wylezinski, BA

                          Graduate Student, Hawiger laboratory, Molecular Physiology & Biophysics