Medicine

Dr. Langlais graduated from Texas Tech University in 1997 with the realization that he enjoyed his Cell Biology class, so he got lucky and ended up as a Research Assistant in an insulin signaling lab that Fall, all of which led to a PhD in biochemistry from the University of Texas Health Science Center at San Antonio. Dr. Langlais met his boss, Dr. Lawrence Mandarino, when he interviewed for grad school and they both left UTHSCSA for Arizona State University together in 2005, Dr. Mandarino as the Chair of Kinesiology, Dr. Langlais as a Post-Doctoral Fellow. Spent too long there before taking an Assistant Professor position at the Mayo Clinic in Arizona in 2012 and shortly after had the excellent fortune of obtaining an NIH R01 grant. Dr. Langlais joined the Endocrinology Division in the Department of Medicine at the University of Arizona College of Medicine in the Fall of 2016. Dr. Langlais has enjoyed his time at the UA, so good to be back at a health science center and an institution that has a passion for basic biomedical research. Dr. Langlais is also a member of the Physiological Sciences Graduate Interdisciplinary Program at the UA. Dr. Langlais started his career as a scientist in an era where radiation was the main approach to study protein phosphorylation. Luckily he met the right people and got an early introduction to mass spectrometry. As a result, his training incorporated basic molecular biology, traditional signaling techniques, microscopy, and eventually mass spectrometry and proteomics. During this scientific journey, he became self-proficient as an end user capable of running mass spectrometers to study proteins. This led to a lot of collaboration, so much so, that together with Dr. Lawrence Mandarino, they developed numerous proteomics facilities, all of which cumulated to create the University of Arizona College of Medicine Quantitative Proteomics Laboratory, a collaborative resource designed to offer UA investigators a chance to use quantitative proteomics to answer their own personal research questions, of which Dr. Langlais is the Director.

Dr Tara Carr is a board certified Allergist/Immunologist physician with subspecialty training and experience in the evaluation and treatment of allergic and immunologic diseases in both children and adults. She is focused on studying the impact of environmental exposures on development and heterogeneity of allergic disease, with an emphasis on asthma. She has significant clinical research experience in pediatric and adult allergic disease and asthma within the Asthma & Airway Disease Research Center at the University of Arizona. She has led multiple industry trials at the research center as primary investigator, in areas of severe asthma, nasal polyps, and food allergy. She has also been a sub-investigator within three large NHLBI-funded clinical research networks in asthma (PrecISE, AsthmaNet, American Lung Association-Airway Clinical Research Centers), and served as a clinical core co-director for the Dysfunction of Innate Immunity in Asthma U19 program. Her roles include leadership of the research team, recruitment of participants, and oversight of procedures and adverse reactions among those participants. At Bio5, Dr Carr leads the immunology and genetics laboratory responsible for receiving all samples collected as part of these studies, processing those samples for future use, biobanking those samples in a longitudinal repository, and running various experiments on those samples as necessary for the planned study. A sub-investigator in the Tucson Children’s Respiratory Study, Dr Carr is contributing to longstanding efforts toward understanding early life risk factors of lung disease by leading metabolic, allergic, and immunologic analyses of longitudinally collected samples. As co-investigator for the Binational Early Asthma and Microbiome Study, Dr Carr leads the scientific effort to collect, transport, and store human and environmental samples from Nogales Mexico and Tucson. Dr Carr is responsible for describing the immunology of pregnant women and the immunological development of their babies, with a goal of understanding which maternal and environmental factors influence allergic (asthma-prone) and non-allergic immune development.
To this end, Dr Carr’s lab utilizes a broad range of experimental methods- often in collaboration with other Bio5 researchers- to describe the biological characteristics of asthma and allergic disease, including DNA and RNA sequencing, protein measurement by ELISA, Immulite and Luminex, culture and stimulation of peripheral blood mononuclear cells with cellular phenotyping, and metabolomics.

Post medical training in Iran, she obtained a Ph.D. at Gifu University in Japan. Her research focused on candida albicans and its interaction with the human host with development of specific expertise in protein purification, molecular biology, and gene manipulation techniques to further identify C. albicans virulence factors. During post-doctoral work in the US, she focused on Coccidioides species, and was able to purify the urease protein, constructed a urease knockout strain of the fungus with lesser virulence in the animal model. The knockout strain showed promise as a potential vaccine candidate. This work remains an active area of Valley fever research. Later she broadened the research to the genetic manipulation of histoplasma capsulatum and the immune interaction in the animal model. Subsequently by the completion of her internal medicine residency and infectious disease fellowship as a natural extension of her research, she put into clinical practice her research interests and findings. In 2017 she was recruited to the University of Arizona at the Valley Fever Center for Excellence, to continue her Valley fever research and improve the prevention, diagnosis, and treatment of Valley fever.

Dr. Ruslan Rafikov, Ph.D. is an internationally recognized scientist in the field of pulmonary hypertension, vascular biology, and acute respiratory distress syndrome. He has four primary research interests: 1) metabolic reprogramming events in vascular cells, 2) mitochondrial dysfunction due to impairment of oxidative phosphorylation and anaplerosis, 3) proliferative signaling in vascular cells due to activation of Akt and 4) free heme as a signaling molecule that regulates inflammation, endothelial barrier function and p38 MAPK-regulated pathways. Dr. Rafikov's laboratory works in a wide range of applications from protein structure-function studies to novel genetic models of pulmonary hypertension and acute lung injury. He is also interested in translational studies related to using metabolic reprogramming and machine learning for the diagnosis of chronic disease.

Dr. Rachna Shroff is the Chief of GI Medical Oncology at the University of Arizona Cancer Center (UACC) where she also serves as the Director of the Clinical Trials Office. Within the UA College of Medicine Tucson, she is the Associate Dean for Clinical and Translational Research. Dr. Shroff is a clinical and translational investigator focused on dveloping novel targeted therapies and immunotherapies for pancreatic and hepatobiliary cancers. She is an internationally recognized expert in these cancers and has led multiple clinical trials in these spaces. She serves on the NCI Hepatobiliary Task Force and has served on multiple commitees for the American Society of Clinical Oncology (ASCO). Dr. Shroff served as the national PI for SWOG 1815, the first randomized phase 3 trial in biliary cancers in the US.

Dr Parthasarathy has a broad background in translational and clinical-translational research that is focused on the following areas as PI or co-investigator: (a) sleep disturbances and the relationship to inflammation and patient-outcomes in critically ill patients receiving mechanical ventilation and (b) health-services research with emphasis on patient-centered approaches and dissemination and implementation aspects of interventions for sleep apnea. He continues to receive extramural funding as PI or Co-investigator from NIH, PCORI, Health Services Research & Development (HSR&D) portfolio of the Department of Veterans Affairs, Department of Defense, American Lung Association, as well as funds from industry and private foundations which have enabled him to make contributions to sleep and critical care research.

The research focus of my lab focuses on the molecular mechanisms underlying normal and pre-neoplastic epithelial cell growth in the luminal gastrointestinal tract. My recent studies involve the use of animal and cell culture models to dissect the pathways through which chronic inflammatory processes, generally from bacterial colonization, leads to mucosal alterations of the luminal GI tract sets the stage for neoplastic transformation (pre-neoplasia). Ongoing projects in my laboratory include the role of sonic hedgehog in gastric homeostasis, e.g., acid secretion and chronic gastritis leading to metaplasia/dysplasia; the role of the nuclear protein menin in the genesis of neuroendocrine tumors, e.g., gastrinomas, carcinoids, and the role of the Krüppel-like transcription factor ZBP-89 (ZNF148) in mucosal restitution from infection to neoplastic transformation. We have used mouse models to dissect the role of Hedgehog signaling in the stomach during chronic inflammation. Over the past 18 years, my lab has established a major role for Hedgehog signaling in normal gastric physiology and during gastric preneoplasia. My initial studies demonstrated that parietal cells and therefore acid secretion requires sonic hedgehog signaling. More recently, studies from my lab have revealed that myeloid-derived suppressor cells (MDSCs) require Hedgehog signaling to create a permissive environment that supports the development of gastric metaplasia, a mucosal lesion preceding cancer.

Stern lab research aims to understand the role of glucagon signaling in the pathogenesis of obesity, type II diabetes mellitus, and aging. Glucagon Signaling in Obesity and Type II Diabetes: Insulin resistance and elevated insulin are key to the metabolic disturbances in type II diabetes mellitus (T2DM). Yet, elevated glucagon, common to diabetes, may be equally important in the metabolic abnormalities in T2DM. Dr. Stern has shown that nutritional state differentially affects glucagon secretion in obesity. In turn, the glucagon:insulin ratio is dysregulated in obesity. Current Stern lab research aims to understand the metabolic consequences of a dysregulated glucagon response to fasting and re-feeding. Glucagon Signaling and Aging: More than 25% of the U.S. population greater than 65 years old has Type II diabetes mellitus, representing the highest prevalence of diabetes of any age group. Most research aimed at understanding the consequences of obesity in aging have focused on insulin and downstream signaling cascades, overlooking a potential role for glucagon. Given that many prominent diabetes treatments target glucagon or glucagon signaling pathways, it is essential to understand the role of glucagon in aging. Stern lab research examines 1) the tissue specific effects of glucagon signaling, 2) the role of glucagon signaling in obesity-accelerated aging, and 3) the role of glucagon signaling in healthspan extension promoted by calorie restriction. This work will close a significant gap in our understanding of how glucagon alters aging, while allowing us to assess the potential risks associated with inhibition of glucagon signaling. Other Stern Lab Research Foci: Sleep disturbance and metabolic dysfunction Obesity related cancer development and progression

Jil C. Tardiff, M.D., Ph.D. is a Professor of Medicine and Cellular and Molecular Medicine at the University of Arizona College of Medicine and is a member of the Clinical and Translational Institute at the BIO5 Institute. She attended the University of California at Berkeley where she completed her B.A. in Genetics in 1984. She subsequently completed her M.D. and a Ph.D. (in Cell Biology) at the Albert Einstein College of Medicine in New York City in 1992. Dr. Tardiff pursued her housestaff training at Columbia-Presbyterian Medical Center in New York City. As one of the first participants in the ABIM Clinician-Scientist pathway as a Markey Fellow, she completed an internal medicine residency coupled to a combined clinical-research fellowship in cardiovascular medicine at Columbia. In 2001 she joined the faculty at the Albert Einstein College of Medicine as an Assistant Professor of Medicine and Physiology and Biophysics. She remained on faculty at Einstein, achieving the rank of Associate Professor. In 2012, Dr. Tardiff joined the faculty at the University of Arizona College of Medicine, where she currently holds the Steven M. Gootter Endowed Chair for the Prevention of Sudden Cardiac Death. As a physician-scientist, Dr. Tardiff’s work focuses on the molecular mechanisms that underlie the development of the most common form of genetic cardiomyopathy, those caused by mutations in proteins of the cardiac sarcomere, hypertrophic cardiomyopathy (HCM). These complex disorders affect one in 500 individuals of all ages and represent the most common cause of sudden cardiac death in young people in the field. Her studies detailing the mechanisms of disease pathogenesis at the level of individual cells using transgenic mouse models has been continuously funded by the NIH since 2002 and her findings regarding disruptions in myocellular Ca2+ handling and energetics work has been cited in support of new clinical trials to evaluate novel treatment modalities for this challenging cardiomyopathy. She is a founding member of the International Thin Filament Consortium, a group of physician-scientists from many of the major academic centers in the world that focuses on bench-to-bedside studies using large, genotyped HCM cohorts. More recently, in collaboration with Professor Steven Schwartz in the Department of Chemistry at the University of Arizona, her lab has developed computational approaches to modeling and eventually predicting disease severity based on protein structure. To fully translate these basic research findings to the clinical realm, Dr. Tardiff has established a referral center for HCM (and other genetic cardiomyopathies) at the University of Arizona where patients from all over the southwest can obtain lifelong cutting edge medical care for this complex and often devastating disorder.

Dr. Marvin "Marv" J. Slepian has significant experience in converting concept to reality. Over his career he has developed and brought to the clinic a number of innovative technologies, using his unique and creative approach to biomedical problem solving. He has designed a number of stents, or scaffolds, for arteries, with unique properties that make them more responsive to the clinical situation – essentially "smart stents." Slepian is quick to point out that "all this occurred by virtue of vision in combination with collaboration and team building."