Former PSTP Scholars
- BA: Duke University, Chemistry (2003)
- PhD: University of Alabama at Birmingham, Molecular and Cellular Pathology (2010)
- MD: University of Alabama at Birmingham (2011)
My graduate work was in the laboratory of Joanne Murphy-Ullrich, PhD, who concentrated on the role of the extracellular matrix on fibrosis and wound healing. My work was focused on the molecular regulation of fibrillar collagens and their interactions with a chaperone protein called calreticulin. We found that calreticulin levels positively correlate with transcription and processing of fibrillar collagens in a cell culture model. Here at Northwestern, I have joined John Varga's laboratory in Rheumatology. His lab investigates pathways and molecular expression patterns in scleroderma. My research focus will be on morphea, a fibrotic skin disease that is thought to have a similar pathogenesis to scleroderma, although little is known. In the future, I am also interested in wound healing of the skin and the pathogenesis behind the increased risk of malignant transformation in the setting of chronic inflammation.
- BS: University of Illinois at Chicago, Bioengineering (2002)
- MD: University of Iowa, Doris Duke Clinical Research Fellow (2008)
- Subspecialty interest: Cardiology
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.
- BS: Villanova University, Comprehensive (1999)
- MD: Thomas Jefferson University (2004)
- Subspecialty Interest: Cardiology
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.
- BS: Tulane University, Cell and Molecular Biology/Physics (2001)
- PhD: Northwestern University, Cell and Molecular Biology (2007)
- MD: Northwestern University, Feinberg School of Medicine (2009)
- Subspecialty interest: Endocrinology
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.
- BS: Truman State University, Chemistry (1996)
- PhD: University of Kansas, Pharmaceutical Chemistry (2001)
- MD: Northwestern University (2007)
- Subspecialty Interests: Gastroenterology, Hepatology, Hematology/Oncology
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.
- BS: University of Wisconsin-Madison
- MD/PhD: University of Iowa
- Subspecialty Interest: Cardiology
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.
- MD: Beijing Medical University (1998)
- PhD: Northwestern University, Neuroscience (2007)
- Subspecialty Interest: Endocrinology
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.
- BSc: University of British Columbia, Physics and Computer Science (2000)
- MD: Columbia University (2004)
- MS: Northwestern University (2009), Epidemiology and Biostatistics
- Subspecialty Interest: Cardiology
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.
- BS: Northwestern University
- MD: Northwestern University (2009)
- Subspecialty interest: Cardiology
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.
During my residency and fellowship training, I have also enrolled in the Graduate School at Northwestern and will complete a Master of Science degree in Clinical Investigation. I believe that the excellent clinical training, superb mentorship, and limitless opportunities make the Northwestern PSTP program the ideal place to build my foundation to develop a successful career as an independent physician-scientist.
- BS: Ohio State University, Biology (2004)
- MD: Ohio State University College of Medicine (2009)
- Subspecialty interest: Rheumatology
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.
- BS: Loyola University
- PhD: Loyola University
- MD: University of Illinois at Chicago
- Current Position: Instructor of Medicine in Endocrinology
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.
- BS: Morehouse College, Biology (1996)
- PhD: University of Illinois, Physiology & Biophysics (2001)
- MD: Northwestern University (2005)
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.
R. Kannan MutharasanEducation:
- BS: Northwestern University, Biomedical Engineering (1999)
- MD: Northwestern University (2003)
- Subspecialty Interest: Cardiology
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.
- BS: St. Cloud State University, Biotechnology (2000)
- MD/PhD: University of Iowa, Molecular Biology (2006)
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.
- BS: University of Miami, Psychology (1999)
- PhD: University of Miami, Immunology (2005)
- MD: University of Miami (2007)
- Subspecialty Interest: Rheumatology
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.
- BS: Johns Hopkins University, Biology (2002)
- MS: Johns Hopkins University, Cellular and Molecular Biology (2002)
- PhD: University of Virginia, Microbiology/Immunology (2008)
- MD: University of Virginia (2010)
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.
- BA: University of Pennsylvania, Biology & Psychology
- MD: Rush University Medical College
- Neurology Residency: Harvard Medical School, Mass General Hospital and Brigham & Women's Hospital
- Associate Director, Neurology Residency Program
- Subspecialty interests: Neurology, Movement Disorders
I earned my medical degree at Rush University Medical College in 2009. I then completed residency in Neurology through Harvard Medical School (Massachusetts General Hospital and Brigham & Women’s Hospital). I now see patients with movement disorders as part of a 2-year clinical fellowship at Northwestern. My primary research interest is the study of Complementary and Alternative Medicine (exercise, meditation, acupuncture, Chinese medicine, and other modalities) for Parkinson’s disease and other movement disorders. With quality-of-life as a major end-point, I expect to find new and innovative ways of improving the health and daily lives of my patients. I hope to expand the field of neurology beyond the boundaries of Western science, and I am confident that significant progress with regards to disability can be achieved through integration of philosophical principals found in many alternative medicine modalities. Through my pursuit of a Master's of Science in Clinical Investigations I plan to approach these modalities with scientific rigor and improve the quality of life of patients with movement disorders in measurable ways.
- MBBS: Maulana Azad Medical College, University of Delhi, India (2003)
- MPH: Harvard School of Public Health (2004)
- PhD: Johns Hopkins School of Medicine (2014)
I did medical school at the University of Delhi (Maulana Azad Medical College), India. During medical school I did research work in tuberculosis (TB), studying health seeking delay by patients as well as delay in correctly diagnosing TB by physicians. Interestingly we found this delay varies based on the site of TB i.e. pulmonary Vs extrapulmonary as well as the fact whether it is a private clinic or a city hospital. This small study helped me realize that an in-depth knowledge of evidence based medicine will be essential if I hope to contribute in finding better treatments. I came to US to do an MPH at Harvard School of Public Health where I concentrated in quantitative methods. This involved an in-depth study of epidemiology, biostatistics and clinical trials.
This was also the time when I learnt about the MD-PhD programs and wished I was part of one but they are non-existent in my country. I felt that the rigorous curriculum and the depth of focus of a PhD would provide me with a strong foundation in neuroscience research. My doctoral research with Professor Craig Montell focused on using the fruit fly, Drosophila melanogaster, as a genetic model to elucidate mechanisms of phototransduction. We identified a novel pathway through which Rhodopsin couples with a small G-protein Rac2 to mediate arrestin translocation. This pathway assists in photoreceptor adaptation when an organism moves from a dimly-lit to brightly-lit environment. I later studied the visual pigment metabolic pathway by creating gene knockouts in two novel retinal dehydrogenases mutations of which have been found in hereditary forms of retinal degeneration. In addition, I conducted a very productive genetic screen using RNA interference (RNAi) to identify novel genes involved in retinal- and neuro-degeneration.
I remain interested in continuing basic science research in a neurological disease area during my residency and one of the reasons why I decided to come to Northwestern was the Physician-Scientist Training Program that nurtures physicians to help them transition into independent investigators as well as academic physicians. This dual track of a physician and scientist is longer than a conventional MD track and has its unique challenges. I am confident that the structured and supported environment that the program offers will be crucial for my success.
- MD: University of Milan (1994)
- PhD: University of Milan, Neuroscience (2003)
The basic question that has driven my career as a clinician scientist is the understanding of the molecular mechanisms underlying hereditary demyelinating and acquired peripheral neuropathies. I had several years of experience in basic science research, at Wayne State University and at Harvard Medical School, studying the biology of myelin and the pathogenesis of demyelinating disease in the Central and Peripheral Nervous System.
In order to be able to pursue translational research, I started the Neurology Residency Program at Northwestern University. During this time, I acquired the clinical skills and the knowledge required to become a Neurologist. I had particular interest in Neuromuscular Diseases and Peripheral Neuropathies including Painful Peripheral Neuropathies. In the Foundation for Peripheral Neuropathy Comprehensive Care Clinic at Northwestern University, I had the possibility to see many patients affected by painful diabetic neuropathy and I realized how little I could help with the current therapies. Given my background in molecular biology of peripheral nerve it was evident that only a better understanding of the molecular mechanisms underlying neuropathic pain in diabetes can lead to a potential treatment for this prevalent affliction.
In the rich academic environment of Northwestern University, I cultivated my interest in chemokine and neuropathic pain in diabetes. I learned about the role of chemokines in the pathogenesis of pain, when listening to a seminar of Dr. Richard Miller, a pioneer in the field. The extremely supportive Neurology Department Chairman, Dr. Kessler and Neurology Residency Program Director, Dr. Simuni, allowed me to start to investigate these questions during my residency program. In fact the National Institute of Neurological Disorders and Stroke recognized the importance of physician scientist education and Northwestern Memorial Hospital ’s leadership in this area by awarding the Department of Neurology the highly competitive NINDS Neuroscience Research Education Program at Northwestern (R25 grant) for 5 years. The R25 grant is designed to foster the development of clinician neuroscientists in the Departments of Neurology at Northwestern University’s Feinberg School of Medicine (NUFSM) to ensure that highly trained scientists will make future advances that lead to a reduction in the burden of neurological disease.
I was the first R25 grant awardees and in the PGY-3 of my Neurology Residency program I started to work in Prof. Richard Miller’s laboratory. My interest in painful diabetic neuropathy, inspired me to explore the role of chemokines in the pathogenesis of neuropathic pain in diabetes.
Diabetes affects 25.8 million people in the USA and neuropathic pain is present in 3 of 10 individuals with diabetes with a substantial impact on the quality of life. Despite this significant impact and prevalence, current therapies for neuropathic pain are only partially effective in diabetic patients. Moreover, the pathogenesis and the molecular mechanisms underlying neuropathic pain associated with diabetes are not well understood.
We hypothesized that chemokine and in particular stromal-derived-factor-1 (SDF-1) and its receptor (CXCR4) signaling has a role in the pathogenesis of neuropathic pain in diabetes. In our preliminary results, we demonstrated that intra-peritoneal administration of the specific CXCR4 antagonist, AMD3100, reverses neuropathic pain in a mouse model of diabetes type-II, the High-Fat-Diet (HFD)-induced diabetic mouse demonstrating that SDF-1/CXCR4 signaling is necessary for induction and maintenance of neuropathic pain in this animal model of diabetes. Following these observations we were interested to investigate the consequences of CXCR4/SDF-1 signaling on HFD-induced diabetic DRG sensory neurons excitability.
Dr Miller’s laboratory and others have already shown that activation of chemokine receptors CXCR4 by its ligand chemokine SDF-1 results in excitation of DRG sensory neurons and in an increase in intracellular calcium concentration in animal models of neuropathic pain. Therefore we, acutely isolated DRG sensory neurons from HFD-induced diabetic mice and performed calcium imaging studies as previously described. We were able to show that application of SDF-1 chemokine increases intracellular calcium concentration in HFD-induced diabetic DRG sensory neurons, demonstrating the functional significance of CXCR4 receptor expression in DRG sensory neurons in neuropathic pain in diabetes.
My experience as R25 fellow and PTSD scholar was extremely important as it allowed me to obtain these exciting preliminary results, which I have presented at international meetings and will provide the basis for a publication but also for the application for independent mentored research awards (K08 grant). This will facilitate my transition from resident to clinician-scientist. Most importantly, the results which I found in these years of research fellowship will shed light on the molecular mechanisms of neuropathic pain and open interesting avenues for translational research.
- BS: University of Illinois at Urbana-Champaign, Electrical Engineering
- PhD: Northwestern University, Biomedical Engineering (2000)
- MD: Northwestern University Medical School (2002)
This is my 18th year at Northwestern. My first eight years here were spent in the Medical Scientist Training Program. My dissertation research with David Mogul, PhD, examined the application of nonlinear dynamical systems theory to characterization and control of epileptiform activity in the rat hippocampus. The ultimate goal of this research was to investigate whether more sophisticated stimulation paradigms might allow us to stop epileptic seizures via electrical stimulation of the seizure focus. I showed first that in vitro epileptiform bursting had both deterministic and stochastic (random) features. I also showed that application of small, precisely-timed electrical stimuli to the hippocampus could modify the bursting pattern from a chaotic one to a (nearly) periodic one. In doing this, I implemented a novel technique for adaptively tracking the system’s “fixed point” in state space, and also developed two novel methods (state-point forcing and short time expansion) to assess for determinism in time-series data.
I chose to stay at Northwestern for my neurology residency in large part because of the support and flexibility the program provided to do research during residency. Although neurology was not affiliated with the PSTP during my residency training, I benefited greatly from the flexible scheduling and advice from our program director and chairman. During my residency training, I worked with Dr. Lee Miller for a total of eight months, and I have continued to work in his lab as an Instructor and now an Assistant Professor in Neurology. We are interested in the field of neural engineering, specifically in brain-machine interface (BMI). The ultimate goal of this research is to enable locked-in or tetraplegic patients to communicate and interact with their environment. Cortical signals are recorded, decoded using various signal processing techniques, and then used to control a computer cursor, and eventually will be used to electrically stimulate muscles so that patients can use their own arms again. The large amount of research time I spent during residency enabled me to successfully apply for an NIH K08 award for this work. Ultimately I plan to transition this bench research into translational work, and I hope it will vastly improve the quality of life of motor impaired individuals. It is gratifying to finally achieve my aspirations of a combined career in clinical medicine and research. I am grateful to the neurology department at Northwestern for facilitating my career path to physician-scientist.
- BS/MD: Peking University (2000)
- PhD: Albert Einstein College of Medicine (2006)
- Subspecialty Interest: Hematopathology
I am a MD/PhD tenure track assistant professor of pathology. I have extensive training in molecular and cell biology from Albert Einstein College of Medicine and the Whitehead Institute for Biomedical Research, as well as clinical hematopathology training at Northwestern Memorial Hospital. I started my independent research career in January 2011 after I finished my postdoctoral training in Dr. Harvey Lodish's laboratory at the Whitehead Institute. The research in my laboratory focuses on the characterizations of novel genes in the regulation of mammalian erythropoiesis; and studies of mDia formin proteins in the engraftment and homing of the hematopoietic stem cells. Our major focuses are erythroid cell terminal differentiation and hematopoietic stem cell biology using various genetic, molecular and cell biology techniques.
Kristina A. MatkowskyjEducation:
- BS: University of Illinois at Urbana-Champaign, Specialized Chemistry (1997)
- PhD: University of Illinois at Chicago, Pathology (2002)
- MD: University of Illinois at Chicago (2007)
- Subspecialty Interest: GI Oncology
I conducted my graduate research in the laboratory of Dr. Richard V. Benya, MD. The major research focus of the laboratory concerns the processing and regulation of heptaspanning, G protein-coupled receptors; specifically, the receptors for gastrin-releasing peptide and galanin.
Prior to the start of graduate and medical school, my investigations focused on the gastrin-releasing peptide receptor (GRP-R). My efforts focused on developing a novel algorithm for true quantitative immunohistochemistry (Q-IHC) based on calculating the cumulative signal strength, or energy, of the digital file encoding an image and to determine the absolute amount of chromogen present per pixel. Our efforts enabled us to use Q-IHC to accurately determine the amount of peptide hormone receptor in archived tissues. To this end, we set out to determine the expression and role of the GRPR protein in the gastrointestinal tract. This receptor is known to cause the proliferation of many, but not all cells in which it is expressed. Our studies identified that this receptor is not normally expressed by epithelial cells lining the GI tract, but is aberrantly expressed by many GI malignancies. Additional studies support GRPR acting as a mitogen, and recent data supports that in vivo it may behave as a morphogen.
The primary focus of my graduate research work was investigating the role of the galanin-1 receptor (Gal1R) in the context of infectious diarrhea. It is known that galanin is widely expressed in the central nervous system and in the GI tract by enteric nerves. In in the GI tract, galanin receptors are expressed by smooth muscle cells which when activated modulate intestinal transit. We have shown that epithelial cells lining the human GI tract express only GalR1 and when activated results in chloride secretion from these cells. Gal1R expression is transcriptionally regulated by the inflammation-associated transcription factor NF-kappa B, a factor activated in a number of inflammatory states. We have shown that an increase in Gal1R expression is observed in various infalmmatory conditions such as Crohns disease, ulcerative colitis, and infectious colitis. It is thus hypothesized that Gal1R expression and activation represents a common, unifying pathway accounting for the diarrhea associated with inflammatory conditions affecting the colon.
My current research interests focus on the chemoprevention of inflammation-associated malignancies of the gastrointestinal and pancreatico-biliary systems.
- BS/MD: Medical University of Warsaw
- PhD: Medical University of Warsaw
- Subspecialty interest: Pathology
I received my MD and PhD degrees from the Medical University of Warsaw, Warsaw, Poland. I joined the Wellman Center for Photomedicine at Massachusetts General Hospital, Harvard Medical School as a postdoctoral research fellow in the laboratory of Dr Michael R. Hamblin in 2005. In 2008 I was appointed as an Instructor at HMS and Assistant in Immunology at MGH and Wellman Center. I have been investigating a variety of anti-tumor immune responses after photodynamic therapy; in particular I have been investigating the role of T regulatory cells and tumor antigens in this process. Additionally, I have been involved in several projects evaluating the applications of new photosensitizers for PDT of cancer. I have been fortunate to receive two independent research grants and several awards for my research.
Since the beginning of my medical training, my professional life has been characterized by a rich balance of clinical and scientific interests. My significant research experience allowed me to familiarize myself with majority of current laboratory techniques used nowadays in Pathology while my clinical rotations helped me to better understand the profound role of Pathology in contemporary medical practice. These experiences have offered me insight into the responsibilities, challenges, joys and fulfillment ahead as a pathologist. I strongly believe that the ultimate goal of the Physician-Scientist Training Program is to train academic pathologists to become subspecialist pathologists and independently-funded principal investigators in biomedical research. I believe that with my versatile research and clinical background I perfectly fit that role and my goal is to excel in furthering the mission of this extraordinary specialty.
- BS: Iowa State University, Biology (1997)
- MD/PhD: University of Iowa (2005)
My research during graduate school focused on the regulation of the germinal center B cell response in an autoimmune setting. Currently, my clinical interest is in hematopathology and my main research interest is to begin to understand the link between autoimmune disease and the development of hematopoietic malignancies. I am starting to approach my research questions from both a clinical and basic science perspective. I am beginning projects which identify the signaling molecules involved in the development and regulation of malignant cells as well as projects focused on the dysregulation of the immune system during the development of autoimmunity.
- BS: Elizabethtown College (2004)
- MD/PhD: University of Connecticut (2012)
I did my undergraduate research with Dr Jane Cavender, investigating the reactivation of previously silenced genes in the nucleolar organizing region by SV40 T-Antigen. I completed my PhD under Dr Linda Shapiro. Her lab investigates the role of two transmembrane peptidases in various disease processes, including inflammation, angiogenesis and cancer. I focused on a protein called Prostate Specific Membrane Antigen (PSMA), a transmembrane peptidase which is virtually absent on normal prostate epithelium and on low grade prostate tumors, but highly up-regulated on metastatic and high grade prostate cancer, where its expression is correlated with poor prognosis. In addition, it has also been shown to be present on the vasculature of virtually all solid human tumors, but absent on normal and quiescent vessels. I investigated the relative contribution of tumor vs. endothelial PSMA expression to prostate tumor angiogenesis, and showed that PSMA expression on endothelial cells is necessary for tumor angiogenesis and that it’s absence cannot be compensated for by tumor expressed PSMA. PSMA contribution to pathologic angiogenesis is not restricted to tumor angiogenesis; inhibiting PSMA in a mouse model of retinopathy of prematurity nearly abrogates the pathologic neovascularization and allows a more normal vascularization of the retina. Interestingly, PSMA plays a VEGF-independent role in pathologic retinal angiogenesis; combined, these findings indicate that the inhibition of PSMA may represent a novel therapeutic strategy for treatment of angiogenesis-based ocular diseases.
- BS: University of Texas at Austin (1997)
- MD/PhD: Northwestern University, Neurophysiology (2007)
- Subspecialty Interest: Radiation Oncology
During college I conducted research on a potassium activated calcium channel in Drosophila which is required for the proper function of the nervous system in the laboratory of Dr. Nigel Atkinson. I identified the structural elements of the gene fundamental for expression of the gene during Drosophila development. My graduate research was conducted in the laboratory of Dr. Heidi Hamm. I studied the mechanism of how thrombin mediates changes in endothelial cell function through activation of the protease activated receptor-1 using novel small molecule peptide inhibitors of the G protein-receptor interface developed in our laboratory. In this phase of my training as a resident physician in radiation oncology; I have been looking at the clinical outcomes of treating patients with later stage mycosis fungoides with palliative radiation. We have developed a unique schedule for treating these patients which limits overall treatment time. In the long term I am interested to find ways to impact the types of treatment available for patients suffering from cancer with radiation.
- BA: Northwestern University (2002)
- MD: Northwestern University, Feinberg School of Medicine (2006)
- MS: Northwestern University, Feinberg School of Medicine (2011)
- Subspecialty Interest: Interventional Oncology
Under the direction of Drs. Robert Lewandowski and Andrew Larson, I am investigating novel loco-regional image-guided approaches to treating unresectable hepatocellular carcinoma (HCC). In the majority of patients, HCC remains confined to the liver, deriving its blood supply from the hepatic artery. Healthy liver tissue is predominantly supplied by the portal vein. My research involves minimally invasive image-guided techniques that exploit this anatomy. The goals of my research involve developing catheter-based and ablative techniques to: 1) increase intratumoral therapeutic delivery, 2) reduce off-target effects to healthy tissues, and 3) provide real-time feedback of treatment success. Utilizing animal models of HCC, I am developing novel high-resolution imaging and therapeutic strategies to treat this disease.
- BS: Duke University (2003)
- MD: Northwestern University (2008)
- MBA & MEM: Northwestern University (2013)
My research is focused on understanding the complex scientific, social, and economic factors that govern the translation of clinical ideas into novel medical technologies. Working with Dr. David Mahvi, we created a curriculum in surgical innovation. The curriculum was shaped to provide the skills necessary to lead multidisciplinary teams in the invention, design, and commercialization of medical technologies. The training began with an industry immersion experience to learn how a major medical device company manages their innovation process. At Cook Medical I participated in business development, regulatory strategy, reimbursement analysis, and clinical assessments of active device design projects. After this internship I worked with faculty within our department to identify unmet clinical needs. The immersive, real-world activities were supplemented by formal coursework through a dual-degree program in management and design. My research culminated in the submission of several patents and the formation of a startup company to develop and commercialize a unique radiofrequency ablation probe. Our company was founded by a team of students and faculty involving the Northwestern schools of medicine, business, law, and engineering. We have successfully obtained funding through multiple grants as well as angel investments and competition winnings. Follow our progress on Twitter (@innoblative).
- BS: Carnegie Mellon University (2003)
- MD: University of Pittsburgh (2007)
- Subspecialty Interests: General Surgery, Pediatric Surgery
Neuroblastoma (NB) is a common pediatric tumor that often presents at a late stage, with only a 20-35% survival in this group. Although most high-risk neuroblastomas show an initial response to chemotherapy, the majority of such patients eventually develop progressive disease that is refractory to chemotherapy. Therefore, drug resistance poses a major obstacle in the clinical treatment of NB. Our lab has discovered a novel mechanism of drug resistance involving a molecule known as midkine. Midkine is a cytokine that was found to be expressed in doxorubicin resistant neuroblastoma cell lines and whose directed inhibition results in loss of drug resistance. The goal of our current line of research is to confirm the function of midkine in neuroblastoma cells, investigate whether midkine is active in allowing drug resistance in other cancers, such as Wilms’ tumor, osteosarcoma and breast cancer, and to identify the receptor(s) for midkine that are important for drug resistance. As midkine has been shown to be expressed in other cancers such as Wilms’ tumor, esophageal, pancreatic lung, breast, and prostate cancer, the results of these studies have the potential for broad implications in cancer care and in understanding the deadly mechanisms behind drug resistance.
- Subspecialty Interest: Surgery
My research focuses on lung cancer and the growth and dissemination of cancer cells, specifically inflammation and the immune response to cancer by mast cells and regulatory T-cells (Treg). Mast cells have been observed to infiltrate a variety of human tumors and recently have been shown to be an independent predictor of poor prognosis in prostate cancer. However, there are conflicting findings regarding their significance in lung cancer. The interaction of mast cells and Treg in the tumor microenvironment is a burgeoning area of research. In the lab, I am working to further characterize human lung cancer infiltrating mast cells and Tregs and their clinicopathological significance. Specifically, I am investigating the density of mast cells and Tregs, mast cell expression profiles, Treg expression profiles, and the cytokine milieu of the human non-small cell lung cancer microenvironment and correlating this information with recurrence and survival in an effort to generate a novel prognostic tool, and possibly a novel therapeutic target for the treatment of lung cancer.
- BS: Johns Hopkins University, Biomedical Engineering (2003)
- MD: Johns Hopkins University (2007)
- Subspecialty interest: Surgery
Chronic wounds are a complex, burdensome disease process that often requires intervention by a plastic surgeon. Along with common conditions such as ischemia-reperfusion injury, diabetes, and venous insufficiency, bacterial biofilm, defined by bacteria embedded within a self-secreted matrix, has been implicated as a significant part of the development and maintenance of non-healing wounds. Biofilm bacteria, possessing protective mechanisms that make treatment difficult, have to date been studied mostly within synthetic, in vitro models, providing useful knowledge but with little clinical applicability. Meanwhile, published in vivo, animal models remain limited in their capabilities. Our group has developed a novel biofilm model that utilizes our established, FDA-recognized rabbit ear dermal wound healing model. Through rigorous testing, we have created a model that is both reproducible and highly quantitative. However, the majority of wound biofilms involve multiple bacterial species, a critical aspect that has never been studied in an in vivo setting. To address this deficiency, we aim to adapt our current work into a polybacterial biofilm wound healing model. We plan to initially inoculate wounds with equal amounts of fluorescent protein-labeled Staphylococcus aureus and Pseudomonas aeruginosa, verifying the presence of a mixed-species biofilm with wound bacterial counts, as well as fluorescence and scanning electron microscopy. Following model validation, we will quantify both wound healing parameters and genetic expression of host inflammatory mediators, which will be compared to data previously generated from their single-species counterparts. In addition, utilizing well-characterized biofilm-mutants, we will work towards identifying molecular mechanisms important to biofilm pathogenesis. Through our proposed experiments, we hope to develop new avenues for plastic surgery research, with potential to improve our understanding and management of chronic wounds.
- BA: Kalamazoo College (2003)
- MD: Loyola University (2008)
- MS: Health Services and Outcomes Research, Northwestern University (2013)
- Subspecialty Interest: Surgery
Dr. Sherman’s research focuses on surgical outcomes in oncology and patient safety and quality improvement. Her research is primarily focused on identifying predictors of deviation from guideline-recommended oncologic treatment in gastric adenocarcinoma. In addition, she is defining predictors of overtreatment in stage IV gastric cancer and under treatment in stage I gastric adenocarcinoma. Additional projects include redefining the classification system for complications following pancreatic resection and a review of key drivers for postoperative mortality at Northwestern Memorial Hospital.
- BS: University of Illinois at Urbana-Champaign, Finance (2004)
- MD: Northwestern University, Feinberg School of Medicine (2008)
- Subspecialty interest: Surgery
My primary research objective is to investigate treatment options and outcomes in endocrine surgery under the guidance of Dr. Cord Sturgeon, Associate Professor of Surgery and Director of Endocrine Surgery at Northwestern University. We are actively investigating techniques for resolving clinical decision-making controversies in the areas of thyroid cancer, hyperparathyroidism, and Graves’ disease through the use of decision analysis and cost-effectiveness analysis. I am expanding my knowledge base in clinical research by completing a Master of Science in Health Services and Outcomes Research through the Graduate School at Northwestern University. I seek to expand my focus to the acquisition of primary data in measuring the quality of life for various health states of the endocrine disorders that I am researching. To that end, I am working with Drs. Zeeshan Butt and David Cella at the Northwestern Institute for Healthcare Studies to develop quality of life metrics for administration to endocrinology and endocrine surgery clinic patients.
- MD/PhD: University of Ulm, Ulm, Germany (2002)
- Post-doctoral research fellowship at the Brigham and Women's Hospital/Harvard Medical School
- Residency in Anatomic Pathology at the Brigham and Women's Hospital
After graduating from medical school in 2002 I started my residency in Urology at the University Hospital of Ulm in Ulm, Germany, and transferred to Brigham and Women's Hospital/Harvard Medical School for a post-doctoral fellowship focused on biomarkers of aggressive prostate cancer. Combining tissue-based and patient cohort-based approaches, I was working on finding biomarkers at the DNA and protein level to identify those patients that were at risk of rapid progression. After 4 years of fellowship I joined the Department of Pathology at the Brigham and Women's Hospital for my residency in Anatomic Pathology from which I graduated in 2009. Wanting to return to my original field, Urology, I started my Urology residency at Northwestern University in 2009. My research interests remain in biomarkers of prostate cancer progression, technological and research advancement over the past decade and further insights in the heterogeneity of prostate cancer making research in this field ever more challenging.
- Harvard College
- Stanford University School of Medicine