Medicine PSTP Scholars

Research Interests:

Research Interests:

I completed my thesis work in Molecular Biology at Loyola University under the direction of Dr. Mitchell Denning. I am interested in studying the epithelial to mesenchymal transition and developing novel therapies that target this process. To this end, I studied the tyrosine kinase Fyn, a member of the Src family kinases. Fyn is an oncogene in murine epidermis and is upregulated in multiple tumor types, including human cutaneous squamous cell carcinoma (cSCC). Increased Fyn expression levels following either the transduction of active Ras (HaCaT-Ras) or Fyn (HaCaT-Fyn) into HaCaT cells induced an epithelial-to-mesenchymal transition and inhibition of this protein using the clinical SFK inhibitor Dasatinib blocked this process by increasing the stability of cell-cell adhesions at the adherens junction through stabilization of F-actin. This inhibition blocked the keratinocyte's ability to migrate in culture, as well as undergo malignant transformation in a mouse model studying UV-induced skin damage. I look forward to continuing my clinical and research training at Northwestern University as it has a strong tradition of supporting physician-scientists and advancing the field of medicine.

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My long-term research interests lie within the realm of immunology. As a field, it has exciting potential. Our ever-increasing understanding of immunologic pathways are constantly changing clinical management of diseases that span every organ system. During graduate school, I studied innate immune dysfunction after severe burn injury and how being intoxicated at the time of injury leads to a detrimental immune response, which has both immediate sequelae and long-term consequences in both animal models and humans. Furthermore, specifically targeting signaling pathways altered by alcohol and burn can reverse the increased morbidity and mortality of the dual insult. As a part of Northwestern’s Physician-Scientist Training Program, I look forward to excellent clinical training and the many opportunities for immunologic research across the institution.

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I joined Dr. Scott Budinger’s laboratory as a post-doctoral research fellow in February 2015.  In his lab I had the opportunity to learn and study the cellular drivers of common disease.  I was focused on understanding alveolar macrophage heterogeneity in the aging human lung, and their contribution to pulmonary fibrosis.  We recently found that lung fibrosis is attenuated when monocyte-derived alveolar macrophages undergo necroptosis, but whether these cells retain an epigenetic “memory” of their origins as inflammatory monocytes and respond differently to a second injury is not yet known.  This led me to study alveolar macrophage ontogeny, and how these cells contribute to enhanced susceptibility to lung injury after repeated Influenza A infections. I created over 250 bone marrow chimeric mice, and exposed them to multiple injuries. I learned advanced research techniques such as flow cytometry and the use of fluroesence-activated cell sorting to obtain purified cellular populations for use in high-throughput gene expression studies using RNA-Seq.  I completed a Python Big Data Bootcamp where I increased my programming knowledge, which will help me in current and future research that require analysis of complex transcriptional data sets.  Working on this project has helped increase my knowledge of molecular biology, immunology and bioinformatics. I currently have two first author manuscripts that will soon be submitted to major journals related to this work, and look forward to the back and forth of the publication process over the next year.

Research Interests:

During my research fellowship, I worked in the labs of Dr. Scott Budinger and Dr. Gokhan Mutlu in the Division of Pulmonary and Critical Care Medicine at Northwestern. My research focused in understanding the role played by bone marrow-derived macrophages in response to lung injury and their contribution to the development of pulmonary fibrosis. We found that mice with a tissue-specific deletion of caspase-8 in lung macrophages are resistant to both bleomycin and TGF-β-induced fibrosis. More specifically, we showed that caspase-8 is required for the differentiation of bone marrow-derived monocytes into alveolar macrophages. Despite being phenotypically similar, both bone marrow-derived macrophages and tissue-resident macrophages, exhibit a very different inflammatory and fibrotic response during lung injury and fibrosis. Thus, potentially targeting recruited macrophages represents a novel approach in the treatment of pulmonary fibrosis.

Also, with Dr. Mutlu I extended on our previous published work, which showed that stimulation by β2-adrenergic agonists contribute to the development of a prothrombotic state in response to particulate matter air pollution. It is widely known that despite their beneficial effects on alveolar fluid clearance, the administration of β2-agonists to patients with the acute respiratory distress syndrome failed to demonstrate a beneficial effect in randomized clinical trials. Recently, we have shown that the loss of β2-adrenergic receptors (β2AR) specifically in the macrophages improves survival in a murine model of influenza A infection. Mechanistically, signaling through β2AR on monocytes and macrophages negatively regulates the recruitment of monocytes to the lung during influenza A infection and worsens survival. We think that strategies that act independently of the β2AR to enhance alveolar fluid clearance without the unwanted effects on monocyte-derive macrophage recruitment to the lung may prove effective for the treatment of patients with ARDS.

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I completed my PhD in the laboratory of Dr. Robert Lamb, PhD, on the Evanston campus of Northwestern University. My work in Dr. Lamb’s lab focused primarily on biophysical studies of the mechanics behind viral protein refolding in Paramyxoviruses, a family of enveloped, negative-stranded RNA viruses. Specifically, I worked with the fusion (F) protein of Parainfluenza virus 5 (PIV5). PIV5 F is a large timeric glycoprotein that sits on the surface of the viral membrane in a metastable conformation. When the virus particle binds to a target host cell, F is triggered to undergo a large-scale, ATP-independent, irreversible conformational rearrangement that physically fuses the viral membrane to that of the target cell. This allows the viral genetic material to infect the cell. My research interests primarily revolve around the intersection of biophysical and structural understanding of infectious diseases.

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I conducted my graduate research in the laboratory of Dr. Hossein Ardehali, MD, PhD, in cardiac iron metabolism. My work focused on the regulation of heme iron in cardiac ischemic injury and identified delta-aminolevulinic acid synthase (ALAS)-2 induction with resultant heme accumulation as novel pathologic features of failing hearts. I also worked on projects investigating the role of mitochondrial non-heme iron in cardiac ischemia/reperfusion injury, sirtuin proteins in cellular iron homeostasis and RNA-binding proteins in lipid metabolism. My long-term research interests involve understanding how alterations in genetic regulatory programs affect cellular metabolism and mitochondrial function in the developing, normal and diseased heart and developing methods to target these metabolic pathways as novel therapeutic agents. My overall career goal is to be a productive physician-scientist in academic cardiology by contributing to the advancement of cardiovascular research, facilitating the translation of research from the bench to bedside and using precision medicine approaches to provide the best possible clinical care for my patients. Northwestern has a strong tradition of supporting physician-scientists and being a national leader in cardiology, and I am excited to continue my career here as part of the PSTP.

Research Interests:

During graduate school, I completed a PhD in the Cancer Biology department, in the laboratory of Eric Brown at the University of Pennsylvania. For my thesis work, I investigated the regulation and function of novel factors involved in the senescence-associated secretory phenotype (SASP). The SASP has been implicated in multiple biological processes, including tissue regeneration, maintenance of senescence and aging, and cancer development.

My long-term research interests involve the intersection between aging and cancer, and how damaged cells can affect both tissue aging and tumorigenesis. I plan to continue studying the molecular mechanisms of cancer development and work towards developing novel therapeutics for cancer treatment.

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My interest in research began as an undergraduate student in the laboratory of Peter Armbruster at Georgetown University. I studied circadian rhythms in the invasive species of mosquito Aedes albopictus, a vector for several diseases, including dengue fever, to better understand how this tropical organism adapts to temperate climates as it spreads. After graduation, I enrolled in the Medical Scientist Training Program at Northwestern University’s Feinberg School of Medicine. For my doctoral thesis in the laboratory of Fred Turek, I examined how disruption of sleep and circadian rhythms impacts gastrointestinal function and contributes to inflammation and damage to the intestinal epithelial barrier in mouse models of colitis and alcoholic liver disease. My long-term interest as a member of the Physician-Scientist Training Program in the Department of Medicine at Northwestern University is to combine my passion for research in circadian biology with clinical medicine in the field of Gastroenterology. This affords the opportunity to conduct procedures as well as establish and maintain long-lasting relationships with patients. I look forward to this next phase in my career at Northwestern University, where I continue to benefit from working with excellent colleagues and mentors.

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For my PhD, I studied obesity and metabolic syndrome, joining the lab of Philipp Scherer, the director of the Touchstone Center for Diabetes Research at UT Southwestern. For my thesis research, I investigated the function of ceramides, a type of signaling lipid, and their role in the development of hepatic insulin resistance and non-alcoholic fatty liver disease. I developed acute, genetic means to modulate ceramide levels in the adult mouse that revealed novel insights into the understanding of the regulatory mechanisms linking nutrient sensing to metabolic regulation.

​My research interests focus on understanding the pathogenesis of diabetes and obesity-associated comorbidities. Lipotoxicity, which results from the accumulation of lipids in non-adipose tissues, is a common cause of obesity-related complications. I plan to investigate the mechanism of lipotoxicity-induced organ dysfunction, which ultimately results in the metabolic syndrome that complicates diabetes and cardiovascular disease. Furthermore, I also intend to identify and study key lipid mediators of insulin resistance in different tissues, ranging from adipose tissue to the liver and heart. I plan to do this through both disease- and patient-oriented research.

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I completed my PhD in the department of Bioengineering at Rice University with Dr. Rebekah Drezek and worked on several inter-departmental and inter-institutional collaborative projects. Part of my thesis work was to design and engineer gold nanoparticles for photothermal therapy in combination with magnetic resonance or fluorescence imaging to improve satellite cancer detection and real-time tumor margin detection. In addition, I have investigated other potential medical uses of gold nanoparticles for delivery of cancer vaccines, adjuvants, plasmids and chemotherapeutic agents. My overall goal is to utilize my nanoengineering knowledge to improve cancer treatment, including immunotherapy and intra-op diagnoses technologies.

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I completed my PhD in Biomedical Engineering at Stony Brook University under the mentorship of Dr. Ira Cohen. My work focused on cellular therapies for cardiac disease, specifically regeneration of contractile cardiomyocytes. The heart is estimated to have lost over one billion cardiomyocytes by the time it goes into heart failure. A growing body of evidence suggests that the heart is capable of replacing lost myocytes, but at a rate inadequate to reverse the damage from an insult such as myocardial infarction. Working with adult cardiac tissue, we investigated the origins of resident cardiac progenitor cells and produced quantitative evidence of differentiation along cardiac and other lineages in vitro. In addition, acellular extracellular matrix patches were used in a full thickness cardiac defect model to demonstrate native regeneration of contractile function specifically within the patch area. Furthermore, augmentation of this recovery was accomplished when human mesenchymal stem cells committed to a cardiac lineage were seeded on the patch. Other work focused on efforts to stimulate adult cardiomyocytes to re-enter the cell cycle and proliferate as another means of replacing myocytes. I am interested in continuing to work in the advancing field of cardiac regeneration and repair, including approaches utilizing cellular, genetic and deliverable pharmaceutical technologies.

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Prior to medical school I completed a Ph.D. in Pharmaceutical Chemistry and a short post-doctoral fellowship in Cancer Biology. During medical school, my interest in clinical epidemiology grew and I worked on various projects within the Department of Preventive Medicine. Although I was no longer doing basic science, the cognitive and writing skills I developed during my graduate and post-doc work proved invaluable. I am currently a Gastroenterology Fellow within the Department of Medicine and also a Fellow in the Institute for Health Care Studies, Integrated Fellowship in Health Services and Outcomes Research. My research interests are currently focused on patients with gastroesophageal reflux disease. Specific research projects include a telephone nursing intervention in patients referred to Northwestern for refractory GERD symptoms, the determination of PPI prescribing patterns in Veterans with GERD, and the incorporation of web based tools (in collaboration with NUBIC) within the Esophageal Center to develop an infrastructure to meet the challenges associated with patient enrollment, data collection, and tracking for comparative effectiveness research.

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My long-term research interest is the development of a comprehensive understanding of key pathways in the heart and kidney that are activated as a pathophysiological response to chronic kidney disease (CKD). I have had the opportunity to work in a number of labs within the fields of cardiology and nephrology. Prior to entering college, I was able to partake in research at Temple University under Dr. Steven Houser that involved pharmacologic interventions that affect the parameters of cardiac output, blood pressure and flow. At the University of Illinois at Chicago, I managed a research initiative with Dr. R. John Solaro to dissect the molecular mechanisms underlying changes in cardiac contractile proteins following acquired heart failure. As an undergraduate student, I worked with Dr. James Potter at the University of Miami to elucidate the effects of troponin mutations on molecular motors in congenital heart disease. As a visiting research scientist, I conducted research with Dr. Bruce McManus at the University of British Colombia to determine the role of integrin-linked kinase in coxsackie virus B3 infection and replication. I also participated in a study with Dr. Maggie Alonso-Galicia at Merck Pharmaceuticals to characterize a novel thiazide diuretic.

As a graduate student with Drs. Christian Faul and Myles Wolf, my research focused on defining the effects of fibroblast growth factor 23 (FGF23) on target organs (i.e., the heart and kidney). FGF23 levels are strongly linked to mortality and cardiovascular disease in all stages of CKD; we sought to define a potential underlying mechanism of this relationship. Our work was the first to establish a direct effect of FGF23 on cardiac myocytes via a novel signaling pathway. We demonstrated that FGF23 directly activates pro-hypertrophic signaling pathways in cardiac myocytes and induces left ventricular hypertrophy (LVH) in animal models. Furthermore, we confirmed that circulating FGF23 levels are increased in CKD and are independently associated with LVH and that elevated FGF23 is associated with increased risk of new-onset LVH. I am excited to join the PSTP at Northwestern and enhance my training experience by working with experts in multiple medical disciplines and contribute to dynamic research efforts that will continue to alter the course of disease progression and translate into manageable practices that improve patient health outcomes.

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As an undergraduate student at the University of Arizona, I conducted research in several different areas of biochemistry ranging from the biosynthesis of deazapurine metabolites to the mechanism of signal transduction in the FGF23/VitD pathway. After college, I spent a year in South Korea at Seoul National University, where I elucidated the mechanism of Hepatitis B virus activation of the Wnt signaling pathway and how this contributed to the development of hepatocellular carcinoma. During medical school at Johns Hopkins University, I worked with Joshua Mendell to study how miRNAs, a class of ~22 nt RNA molecules that regulate messenger RNAs (mRNA), are regulated in human diseases. My work undercovered a previously underappreciated role of the miRNA biogenesis machinery at the chromatin in cancer cells and embryonic stem cells. Being part of the PTSP program is a crucial step in my medical training to build upon the necessary skillset required for me to become both an excellent clinician and independent investigator. Although I intend to continue seeing patients throughout my career, research will ultimately forward the understanding of our patients' diseases and open the doors for future therapies. Currently, I am interested in both the fields of Hepatology and Oncology and look forward to being able to apply my experiences in basic research to patient-oriented problems.

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I completed my PhD in cell signaling and pharmacology at UT Southwestern in the laboratory of Dr. Melanie Cobb. My dissertation research focused on how scaffolding proteins facilitate cross-talk between MAP kinase and PKA pathways and how these signaling cascades elicited site-specific action within the cell, specifically in the context of cilia-related diseases (e.g., polycystic kidney disease, Kartagener, Bardet-Biedl syndromes). I became interested in cardiology during medical school, through didactic and clinical experiences in heart failure and interventional cardiology as well as through research examining stroke events after atrial fibrillation surgery under the mentorship of Dr. Richard Lee. Within cardiology, I am interested in examining the pathogenesis of heart failure through the myriad of underlying molecular mechanisms and signaling pathways that lead to the onset and progression of the disease. Given its significant clinical burden, there exists a burgeoning potential in developing therapeutics to not only reverse myocardial changes and damage that lead to decompensation in heart failure, but also to prevent the disease at its onset. Other areas of interest in cardiology include examining vascular endothelial function and repair, particularly after thromboembolic events. I am excited to begin my career as a physician-scientist in the vibrant clinical and research environment at Northwestern.

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I completed my PhD studies in Molecular Physiology at Iowa under the supervision of Dr. Mark E. Anderson. The Anderson laboratory studies cellular signaling mechanisms in heart with a principle focus on the multifunctional Ca2+ and calmodulin-dependent protein kinase II (CaMKII). CaMKII mediates excitation-contraction coupling in cardiomyocytes and launches pro-arrhythmic and cardiomyopathic cellular responses. My research focused on the interplay between CaMKII and aldosterone. Aldosterone is elevated in patients after myocardial infarction (MI), and aldosterone receptor antagonist drugs are clinically valuable for the treatment of patients with heart failure. I studied CaMKII oxidation and activation in mice models following MI and with elevated aldosterone levels. I have a clinical interest in treating patients with heart failure, in particular to identify patients most at risk to develop heart failure, before the onset of decompensation. In the future, I hope integrate my research and clinical interests by investigating the molecular signals that manifest in subclinical disease. I’m excited to become a member of the PSTP community at Northwestern and look forward to the next phase of training.

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I have a longstanding interest in immunity and autoimmunity. My research has focused on trying to better understand the mechanisms by which the immune system attacks the body, most recently through investigating the genetic basis of autoimmunity in the laboratory of Dr Daniel Kastner at the National Institutes of Health. I hope eventually to do clinical and translational research which will help make these types of studies more clinically relevant. As a scientist, I want to continue to do work which will provide fundamental insights into the etiology of complex rheumatic diseases. Furthermore, as a physician, I hope to utilize this new knowledge to elucidate novel treatments and individually tailor treatment regimens that will maximize efficacy and minimize potential side effects.

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My research focuses on identifying and exploring novel drug targets for type 2 diabetes. In type 2 diabetes, the insulin resistance observed in the setting of obesity leads to pancreatic islets adapting by increasing insulin secretion and production. Identifying the pathways that mediate the response of islets to insulin resistance is needed. Because of the importance of G-protein coupled receptors (GPCRs) as major drug targets and their known role in islet function, research during my fellowship focused on identifying novel GPCRs that may mediate this response in islets. From this research, we observed two novel GPCRs, free fatty acid receptor-2 and -3 (FFAR2 and FFAR3) that may have a role in this process. Importantly, little is known about the biology of these receptors. Because of this, the focus of my research now is to explore the role of these receptors in diabetes.

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My previous work sought to enlarge our understanding of the role of the cardiac troponin regulatory complex in physiologic myocardial function (with Dr. R. John Solaro), in hypertrophic and dilated cardiomyopathies, as well as in the eventual progression to end-stage pump failure (with Dr. Peter M. Buttrick).   Now, my research interests have been broadened to include investigation of the cardiovascular system as a whole, with particular focus on translational questions.  Under the tutelage of Dr. Douglas Vaughan, I will study the role of the plasminogen activator inhibitor (PAI-1), a key regulator of the fibrinolytic system, and its role in ischemic cardiovascular disease.  In particular, I plan to contribute to our understanding of how PAI-1 modulates the vascular and myocardial housekeeping processes (i.e., myocardial scar formation) that occur after ischemic injury.

My overall goal for training in cardiology is to merge my clinical and research interests.  To this end, I will focus my clinical cardiology fellowship on the cardiac patient with atherosclerotic coronary and peripheral artery disease.  As a clinical cardiologist, I will specialize in percutaneous, as well as novel medical approaches to this common disease entity.  Ultimately, my career goal is to help advance our state of thinking on critical issues in cardiovascular medicine through innovative patient care and translational research.

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I completed my PhD in Biomedical Engineering at Northwestern University in the laboratory of Dr. Phillip Messersmith. The main objective of my dissertation was to investigate the role that sacrificial coordination bonds could have on hydrogel mechanical properties. This work was motivated by the lack of biocompatible soft synthetic materials that can stand up to long-term cyclic strains for applications such as small vessel grafts or heart valve replacements. To address this need, we took inspiration from the chemistry that the marine mussel employs to produce tough, self-healing threads that anchor the mussel to coastal rocks. Specifically, by studying different metal-ligand hydrogel systems, we were able to show how small molecule kinetic and thermodynamic properties connect to bulk material properties. With these insights, we were able to toughen hydrogels by incorporation of sacrificial coordination bonds. I came to the Northwestern PSTP because of the strength of its clinical cardiology and the research opportunities available. During the research phase of this experience, I plan to develop new skills in cell and stem cell biology. I ultimately hope to connect this experience with my biomaterials background.

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I conducted my graduate research in the laboratory of Dr Joseph Zabner, MD. The primary focus of my research was the prevention of Pseudomonas aeruginosa biofilm formation in the lungs of cystic fibrosis patients. I directed my efforts at blocking Pseudomonas quorum sensing, a process whereby Pseudomonas and other bacteria regulate their gene expression in response to chemical signaling molecules, acyl-homoserine lactones secreted and detected by the bacteria. In P. aeruginosa, quorum sensing controls the expression of genes necessary for effective biofilm formation. Pseudomonas biofilms are colonies of bacteria within a self-secreted polysaccharide matrix that are highly resistant to biocides and antibiotics. Pseudomonas biofilms are medically relevant as they are shown to form in the lungs of cystic fibrosis patients and contribute to significant morbidity and mortality in this population. My hypothesis was that degradation of P. aeruginosa acyl-homoserine lactones by mammalian tissues would interrupt quorum sensing and prevent biofilm formation. During my research I discovered that human airway epithelia and other mammalian tissues possess an innate ability to degrade acyl-homoserine lactones. I further characterized this as an enzymatic activity and traced the activity to a family of proteins, the paraoxonases. I further found that mammalian paraoxonase activity was both necessary and sufficient to both degrade quorum sensing molecules as well as prevent Pseudomonas biofilm formation and that common polymorphisms within one member of this family, paraoxonase 2, had significant effects on the ability of the enzyme to block quorum sensing. My future research goals include further study into interactions between hosts and pathogens, as well as molecular mechanisms by which humans are able to protect themselves from infection.

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I did research in Dr. Nancy C. Andrews' lab at Children's Hospital Boston/Harvard Medical School (her lab is now at Duke), where I assisted Dr. Cindy N. Roy a postdoctoral fellow at the time (currently at Johns Hopkins) in making a mouse model for Anemia of Inflammation. We studied the role of hepcidin (hepc), a regulator of iron transport in iron homeostasis. ACI is caused by inflammatory diseases like cancer or rheumatoid arthritis. The inflammation may increase the level of hepc in the body. Hepc blocks iron absorption by the intestine, thereby contributing to the anemia seen in these patients. We successfully created a mouse with an extra copy of hepc. The transgenic mice anemia is associated with iron deficiency and iron-restricted erythropoiesis. The mice serve as a useful model by reiterating key features of anemia of inflammation seen in human patients.

While in medical school, as an American Society of Hematology Scholar and a UIC Craig Research Fellow in Dr. Joseph DeSimone’s lab, I studied the relative roles of transcription and translation in the mechanism responsible for increased fetal hemoglobin levels following decitabine (a DNA methyl transferase inhibitor) administration in the baboon model and investigated whether decitabine requires erythropoietic stress in order to increase HbF in vivo. We concluded that decitabine increases fetal Hb in vivo by transcriptional activation of the gamma globin gene and that decitabine does not require erythropoietic stress in order to induce a substantial increase in fetal hb levels. The findings in this study are interesting because the mechanism of decitabine’s ability to increase HbF has remained controversial so understanding the mechanism that DMNT inhibitors reactivate HbF is critical for the design of future pharmacological drugs for patients with sickle cell disease and β-thalassemia.

I remain interested in epigenetic mechanism of gene expression, clinical trials and improving the treatment for various cancers/blood disorders. I’m very excited about the PSTP at Northwestern and look forward to doing more research here because it will enable me to gain insight into some difficult clinical cases. I will make diagnoses not only based on familiar symptoms but also based on a solid grasp of concrete scientific concepts.

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During my PhD training, I worked with Dr. Lou Laimins and focused on studying the role of the E5 protein in Human Papillomavirus pathogenesis. Human papillomaviruses have been shown to be the causative agent of cervical cancer with over 99.7 percent of cases showing the presence of the viral sequence. My studies focused on elucidating the role of E5, which is poorly understood at this time. Using yeast two hybrid analysis, I identified B-cell associated protein 31 (Bap31) and differentiation dependent A4 protein (A4) as novel binding partners of the HPV16 and HPV31 E5 proteins and performed mutational analysis to identify the domains necessary for the interaction. Using siRNAs to reduce the levels of Bap31, the proliferative ability of HPV-positive keratinocytes upon differentiation was also reduced implicating Bap31 as a regulator of this process. I continue to be very interested in hematology/oncology and immunology research.

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During my dissertation work with Harinder Singh, PhD, I used the immune system as a tool to investigate gene regulatory networks that control cell fate choice. These networks are comprised of interconnected signaling molecules and transcription factors that regulate the developmental transitions that are critical for lineage determination. Using genetic, molecular and mathematical modeling approaches, I was able to demonstrate a novel molecular mechanism whereby lineage specific transcription factors feedback to alter the epigenetic DNA binding landscape of non-specific transcriptional regulators leading to cell specification and commitment. These efforts were aimed at being able to manipulate these regulatory networks to engineer stem cells to adopt particular immune cell fates in the future.

After completing my PhD and returning to medical school, I combined my scientific background in next generation sequencing, immunology and molecular biology with my clinical interests in gastroenterology. I joined Dr. Eugene Chang’s lab at the University of Chicago, which focuses on host microbe interactions in the gastrointestinal tract. My work focused on the role of viruses in the pathogenesis of inflammatory bowel disease. I look forward to being able to continue pursuing my interests in molecular biology and immunology within the field of gastroenterology during my training as a physician-scientist at Northwestern.

Research Interests:

I completed my thesis work in Genetics and Development at Columbia in the lab of Dr. Lori Sussel. Her lab is focused on understanding the transcriptional regulation of the development of the islets of Langherhan in the pancreas. I focused on one of the major transcription factors of islet cell development, Nkx2.2. I discovered that one of the conserved regions of the protein, the SD domain, was required for differentiating a single islet endocrine progenitor cell into five distinct monohormonal islet cell types. By knocking in a mutant SD domain into the native Nkx2.2 gene in mice, we showed that the iselts of these mice contained fewer insulin producing beta cells as well as many polyhormonal cells. We also showed that the SD domain interacts with a dna methyltransferance, DNMT1, and through this interaction, successfully regulates gene expression via methylation, to differentiate progenitor cells into single hormonal islet cells. As a result, mutation of the SD domain, leads to loss of this interaction and production of polyhormonal cells. I am excited to continue my research and clinical studies at Northwestern and look forward to many new exciting opportunities here.

Research Interests:

I performed my PhD research in the laboratory of Dr. Sarah Rice, studying how the molecular motor kinesin-5 provides the pushing force required to separate dividing cells in mitosis. By determining the structural steps that allow kinesin-5 to push on the microtubule-based mitotic spindle, we identified key differences between the first and subsequent steps of the motor, illustrating an example of molecular memory. We also found that phosphorylation of kinesin-5 substantially alters its affinity for a small molecule inhibitor. This novel regulatory mechanism opens doors to new therapeutic strategies to inhibit not only kinesin-5 in particular, but protein-based drug targets in general. 

I was fascinated by kidney physiology in medical school. Nephrology as a specialty combines the basic science of disease mechanism and the applied physiology of engineered kidney replacement therapies with long-term physician-patient relationships focused on preventative care. I hope to apply my background in biochemistry and biophysics to develop improved in vitro systems to model kidney function and better understand the cytoskeleton of glomerular cells. The supportive environment within Northwestern’s Physician-Scientist Training Program is allowing me to lay the groundwork of a career at the intersection of basic science and clinical care.

Research Interests:

After completing medical school at Maastricht University School of Medicine in the Netherlands, I decided to join the Duke Cardiovascular Magnetic Resonance Center (DCMRC) as a post-doctoral research fellow from July 2010 until July 2013. Under the mentorship of Raymond J. Kim, MD (co-director of the DCMRC), I focused on using cardiovascular MRI as a tool to study the physiology of coronary artery disease and acute coronary syndromes. 

My research has focused on three specific projects. The first focuses on physiologic processes in a large animal model of ischemic myocardial injury. Specifically, I am studying the time course and size change of myocardial edema after acute myocardial infarction (AMI). In the same animal model, I developed a new MRI protocol to investigate the three-dimensional characteristics of the area at risk and myocardial salvage during AMI. The main goal was to create three distinct myocardial contrast concentrations delineating viable area at risk (AAR), infarcted AAR and remote myocardium. This technique can be used to more accurately assess the effect of new therapies aimed at reducing infarct size. My second project focuses on the clinical and imaging predictors of microvascular obstruction (MO), a marker of poor prognosis in AMI. In a population of over 300 patients, I correlated infarct age with a decrease in MO prevalence and found that characteristics of infarct morphology were important predictors of MO. Finally, I am studying patients with AMI to ascertain the cardiac magnetic resonance imaging characteristics associated with LV thrombus. 

Research Interests:

I have long been interested in the full spectrum of cardiovascular disease as well as the seemingly endless opportunities within cardiology to advance the field through original research and its translational applications. As an undergraduate studying the relationship between behavior patterns and health status, I conducted independent research toward a thesis in a large, multinational database and found that more religious people may be less likely to seek preventive health care. During medical school, I continued to explore the complex relationship between religion and cardiovascular disease with the guidance of my research mentor, Dr. Donald Lloyd-Jones. Using data collected from the Multi-Ethnic Study of Atherosclerosis, we found that highly religious older adults are significantly more likely to be obese than their non-religious counterparts, even after adjustment for demographics and baseline cardiovascular risk factors. Subsequently, we used data from the Coronary Artery Risk Development in Young Adults study and found that frequent religious participants in young adulthood are particularly likely to become obese between young adulthood and middle age, even after adjustment for demographics and baseline cardiovascular risk factors. In light of these results, I collaborated on developing and piloting a cardiovascular risk education and prevention model at a local African-American church that has initially proven effective at decreasing BMI, waist circumference and systolic blood pressure. I have now begun working with Dr. Lloyd-Jones on various projects that use a relatively novel statistical application to examine competing risks for first occurring cardiovascular and non-cardiovascular events. The first project, in which we examined racial disparities in first incident cardiovascular disease in three large multi-center cohorts, revealed that our competing risks framework yields estimates of cardiovascular risk that may differ from those of traditional statistical models. This is potentially significant for clinicians and patients because we can simultaneously estimate risks for cardiovascular events and potential superceding non-cardiovascular events (i.e. cancer death), and may therefore obtain a "real life" contextual assessment of one's risk for cardiovascular events. We have also begun to examine competing risks for next events following different first cardiovascular events (e.g., most likely subsequent event following a stroke versus MI) and, in a separate project, are re-analyzing clinical trials of statins in populations with significant co-morbidities (systolic heart failure, end-stage renal disease) to determine if accounting for competing risks stemming from these substantial co-morbidities alters the estimated benefit of statins in preventing coronary events. I consider myself fortunate to have had such stimulating clinical and research experiences at Northwestern and am thrilled to be able to continue to do population-based cardiovascular epidemiology research here with the support of the PSTP program.

Research Interests:

My dissertation research was completed in the laboratory of Dr. Mary Hunzicker-Dunn at Northwestern University. In her lab, I studied the actions of luteinizing hormone (LH) to induce ovulation and luteinization of ovarian follicles. Particularly, I characterized LH receptor signal transduction in a rat primary granulosa cell culture model. My work described a rapid and targeted phospho-regulation of the AKAP microtubule-associated protein (MAP)2D via the cAMP/PKA pathway in granulosa cells. I found that the MAP2D protein performs a critical scaffolding function for signaling and regulation by kinases and phosphatases in this pathway. Through this research, I developed a strong background in cell culture and signal transduction which I hope to use in my future research endeavors.

Research Interests:

I conducted my undergraduate research in tissue and bone regeneration in the lab of Dr. Jeremy Mao at the University of Illinois at Chicago. In medical school, as a Doris Duke Clinical Research Fellow, I worked in the labs of Drs. Francois Abboud, William Haynes, and Allyn Mark at the University of Iowa examining the autonomic control of blood pressure in animal models and humans. Currently, I am exploring the use of biomaterials (nitric oxide releasing citrate polymers) for use as arterial stents and endovascular drug delivery vehicles using novel endovascular devices, and the development of targeted nanotherapeutics for atherosclerosis regression in the labs of Drs. Melina Kibbe and Guillermo Ameer. My ultimate goal is to become an interventional cardiologist specializing in the development and application of novel biomaterials and devices for the treatment of a range of cardiovascular diseases.

Research Interests:

Throughout my medical education, I have always been interested in immunology and its role in the pathogenesis of disease. I completed my PhD training at Penn State in the lab of Dr. Diane Thiboutot. My dissertation research focused on the mechanism of action of isotretinoin (13-cisretinoic acid; brand name Accutane) in inducing long-term remissions of acne. I designed a clinical study investigating the effects of isotretinoin therapy on acne patients’ peripheral immune cells and found that isotretinoin normalizes exaggerated immune responses to the commensal organism P. acnes through down-regulation of TLR-2 on monocytes. After completion of my PhD, I continued to do research during medical school on hereditary angioedema and asthma. My research experiences have cemented my desire to pursue a fellowship in Allergy/Immunology. I am very excited to join the PSTP program and look forward to the opportunity to work with some of the exceptional clinicians and scientists at Northwestern.

Research Interests:

During college and graduate school, I performed research in molecular and cellular biology. In addition, I gained an appreciation for the intricacies and importance of research to the fields of biology and medicine. During medical school, I again performed research in molecular biology, this time, molecular cardiology. This experience though was different. I was interacting with patients and subsequently performing research in the lab. This is the essence of the newly evolving field of translational medicine: to be able to move from bench to bedside and back with the goal of more rapidly integrating the rapid advances in the basic sciences with clinical advances for our patients. I plan on performing research in molecular cardiology with the ultimate goal of establishing a career in translational medicine.

Research Interests:

My career interests focus on the use of interdisciplinary methodologies to develop novel therapeutics for cancer. Early in my career, I investigated everything from the use of quantum dots as molecular sensors to the role of the nervous system in bone remodeling.  My interest in precision medicine led me to the laboratory of Stephen Fesik, PhD, where I worked to discover novel protein-protein interaction inhibitors targeting the Ras-signaling pathway for the treatment of cancer.

Ras is a small-GTPase that functions as a molecular switch to drive cell proliferation and survival, ultimately leading to cancer. Despite its clinical significance, the scientific community has been unable to develop a clinically efficacious Ras inhibitor since the discovery of Ras as one of the first oncogenes over 30 years ago. Within this context, I sought to apply novel methodologies to identify unique, functionally active small-molecules to provide a path forward for the discovery of Ras-targeted therapeutics. As part of an interdisciplinary team, I was able to show that by employing fragment-based approaches and structure-based drug design it was possible to target Ras with molecules that bind directly to Ras and inhibit Son of Sevenless (SOS)-catalyzed nucleotide exchange in a competitive manner. While conducting this work, I also made the observation that a specific set of small molecules had the ability to modulate the Ras-SOS protein-protein interaction in an unexpected manner. This led to the discovery that it was possible to target the Ras:SOS:Ras complex, an intermediate of nucleotide exchange, with small molecules. I worked to characterize this functionally important small molecule binding site on the Ras:SOS:Ras complex and showed that molecules that bound to it were capable of inhibiting MAPK and PI3K signaling downstream of Ras. These findings revealed a new approach to inhibit this highly validated oncology target and these molecules represent promising starting points for the discovery of compounds capable of inhibiting Ras-driven tumors.

I am excited to be a part of the Northwestern PSTP program, which combines high-quality clinical training with multidisciplinary research opportunities. I plan to pursue a career in hematology and oncology. By focusing on precision medicine, immuno-oncology and understanding the mechanisms that drive cancer, I hope to discover novel treatments and provide new therapeutic options to my patients with cancer not responsive to standard chemotherapy.

Research Interests:

I completed my PhD in Cell Biology at Northwestern University in the laboratory of Dr. Navdeep Chandel. My research focused on hypoxia signaling responses and used the nematode C. elegans as a genetic model organism. Specifically, we identified a novel hypoxia signaling response that, when activated, extended lifespan in C. elegans. This response was tissue-specific and was mediated by an intestinal transcription factor that was activated by increased reactive oxygen species generated under hypoxia. I chose to stay at Northwestern and enroll in the PSTP because of the University’s continued focus on physician-scientist training and the continued growth of the hematology/oncology program. My current research interests include studying the metabolic mechanisms of carcinogenesis and developing therapeutic strategies to target these pathways in human cancer.

Research Interests:

I joined the PSTP program at Northwestern in 2004-2005 as an intern, completing two years of internal medicine followed by three years of general cardiology, one year of interventional cardiology training, and one year of dedicated cardiac PET research. During my residency and fellowship, I also completed a master's degree from the Department of Preventive Medicine. Overall I enjoy applying my background in physics, mathematics, and computer science to medical problems.

My academic focus is clinical non-acute atherosclerotic coronary disease, from patient to pill to perfusion to PCI. This year I joined my long-term mentor Lance Gould as an Assistant Professor of Medicine at the Weatherhead PET Center of the University of Texas Medical School in Houston. The PSTP program at Northwestern gave me complete and rigorous training for a career in academic cardiology.

Research Interests:

As an undergraduate student at the Illinois Institute of Technology (IIT), I undertook research projects studying fundamental aspects of muscle physiology, studying the role of the androgen receptor in prostate cancer and synthesizing bifunctional compounds for targeted cancer therapies. In the laboratory of Hyun-soon Chong, PhD, I worked in the areas of organic synthesis and medicinal chemistry generating bimodal compounds for antibody-targeted radiation therapy, for MRI contrast enhancement and for metal chelation. In the laboratory of Nancy Zeleznik-Le, PhD, at the Loyola University Medical Center, I conducted dissertation work studying molecular aspects of mixed lineage leukemia (MLL) and evaluated novel therapeutics. My research aimed to understand how specific amino acids within a DNA-binding domain of MLL contribute to the leukemogenic capacity of MLL fusion proteins. Retroviral constructs expressing point mutations were generated to study the roles of specific residues in cell proliferation, colony formation, cell morphology, gene expression and in vitro protin binding.  Additional studies focused on post-translational modification of and novel epigenetic therapies for MLL-associated leukemias.

I have been drawn to the field of Hematology-Oncology through complementary research and clinical experiences at IIT and in Loyola’s MD/PhD program. The clinical experiences have demonstrated how our current knowledge of modern medicine can be effectively applied to the skills of diagnosis, treatment and prevention to alleviate patient suffering while the research experiences have demonstrated how we can advance this current understanding to address unanswered clinical questions and ultimately improve human health. During fellowship training, I look forward to acquiring specialized knowledge of human malignancies and to exploring the biochemical and epigenetic mechanisms of cancer while trying to identify new drug targets and developing novel cancer therapeutics. Through participation in the Physician-Scientist Training Program in the Department of Internal Medicine with subspecialty training in Hematology-Oncology, I will be prepared to transition into a successful career as an academic physician-scientist.

Research Interests:

I completed my graduate training in Pharmacology at UIC under the supervision of Dr. Xiaoping Du. In our lab, we investigated many of the signaling mechanisms involved in platelet activation and thrombosis. My work focused on several of the molecular aspects integrins signaling, specifically, the major platelet integrin, αIIbβ3. We sought to elucidate how integrins are activated by different agonists and determine the role of integrin signaling in platelet aggregation, secretion, spreading and clot retraction Study of the latter functions (spreading and retraction) also led us to investigate how integrin signaling controls and regulates the directions of cell membrane movement not only in platelets, but other cell types as well. As a physician, I am most interested in the pathophysiology and clinical aspects of cardiovascular disease, as well as the growing area of therapeutic interventions. Though my research interests will evolve throughout my training, I would like to investigate the role of platelets in multiple aspects of cardiovascular disease and explore novel anti platelet agents for the prevention and treatment of acute coronary syndromes. Other areas of scientific interest include vascular endothelial function, myocardial viability, angiogenesis and oxidative signaling in atherosclerosis.

Research Interests:

My long-term research goal is to better understand the mechanisms that lead to heart failure.  Heart failure's prevalence makes it an important problem; its growing prevalence makes it an urgent one.  This all appeals to the clinician in me. The scientist in me is fascinated by the complexity of the biology—a failing heart evokes hypertrophy, fibrosis, apoptosis, and myriad other events we have only begun to piece together. How does the heart fail, and how much of that failure can we undo so that our patients may live long, healthy lives? These are the types of "big picture" questions I want to spend my career investigating.

Research Interests:

I completed my undergraduate studies from the McCormick School of Engineering at Northwestern University with a Bachelors of Science degree in Biomedical Engineering. I subsequently completed my graduate medical education at the Feinberg School of Medicine as part of the Honors Program in Medical Education. My current research interests are focused on the protein, plasminogen activator inhibitor-1 (PAI-1) and its potential role in obesity and cardiometabolic diseases (eg. coronary artery disease, heart failure). Plasma PAI-1 levels significantly increase with increasing weight and burden of cardiovascular disease. In addition to its prognostic value, the accumulation of PAI-1 in human arterial walls of patients with diabetes and atherosclerotic plaques suggest the biologic plausibility of PAI-1 as a fundamental contributor to the development of cardiovascular disease, particularly in the obese. In addition, animal data have demonstrated that inhibition of PAI-1 with a small molecule antagonist prevents the development of obesity and associated vascular aging suggesting that this may be a promising novel preventive strategy to modulate and protect against aging-related cardiometabolic diseases. As part of the PSTP program, I have been very fortunate to develop this research project with the mentorship of Douglas E. Vaughan, MD, Chair, Department of Medicine, an international expert in vascular biology and PAI-1, and Donald Lloyd-Jones MD, ScM, Chair, Department of Preventive Medicine, a thought-leader in cardiovascular epidemiology. In addition, to help support my research endeavors, I have successfully competed for and received funding through career development awards from the Heart Failure Society of America and the Northwestern Woman’s Board.

Research Interests:

The burden of cardiovascular disease amongst patients with rheumatic diseases is striking. I am interested in modeling atherosclerosis in transgenic mice that are predisposed toward autoimmunity.

The logical next step will be to use molecular profiling to validate our animal specimens against samples from human patients. Ultimately, I hope to identify new biomarkers and therapeutic targets for reducing atherosclerosis in humans.

Research Interests:

My PhD dissertation research was investigating the role of the hypothalamic glucose-sensing ATP sensitive (KATP) channels in the regulation of GnRH secretion by ovarian steroids and negative energy balance. I found out that estrogen and progesterone up-regulate KATP channel expression in the mediobasal hypothalamus, and central inhibition of these channels restore the GnRH pulses, thus providing a novel mechanism for the negative feedback actions of the ovarian steroids on GnRH secretion likely by hyperpolarizing the GnRH neurons. I also found out that although the hypothalamic KATP channels can serve as central glucose sensor, they are not involved in the inhibition of GnRH pulsatile secretion by fasting. Currently, I am interested in the regulation of energy and glucose homeostasis by circadian rhythm. Recent studies have shown that disruption of the molecular clocks leads to hyperglycemia, hyperleptinemia, obesity and hypertriglyceridemia, reminiscent of the so called metabolic syndrome. Since the molecular clocks are present in almost all tissues, my current research is to pinpoint the tissue specificity and the molecular mechanisms underlying the adverse metabolic effects resulting from disruption of the molecular clock system.

Research Interests:

I am interested in the clinical application of basic immunology, particularly with regards to asthma and allergic disease.  My undergraduate and master’s training analyzed the distribution of histamine receptors on inflammatory and structural cells.  My doctorate dissertation examined memory CD8+ T cell regulation of Respiratory Syncytial Virus vaccine-enhanced disease.  Currently, my research focuses on investigating the clinical characteristics as well as the underlying cellular and molecular mechanisms of Aspirin Exacerbated Respiratory Disease.