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Faculty Detail     Name IRSHAD H CHAUDRY   Campus Address VH G094 Zip 0019 Phone 205-975-2195 E-mail IChaudry@uab.edu Other websites http://www.uab.edu/surgery/CenterforSurgicalResearch/

Faculty Appointment(s) Appointment Type Department Division Rank Primary  Surgery   Surgery - General Surgery Professor Secondary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor Secondary  Microbiology  Microbiology Professor Center  Arthritis & Musculoskeletal Diseases Center  Arthritis & Musculoskeletal Diseases Center Professor Center  Center for Metabolic Bone Disease  Center for Metabolic Bone Disease Professor Center  Medicine  Comprehensive Diabetes Ctr Professor Center  General Clinical Research Center  Ctr for Free Radical Bio Professor Center  Medicine  Ctr Cardiovasc Bio Professor

Graduate Biomedical Sciences Affiliations Immunology  Integrative Biomedical Sciences  Medical Scientist Training Program  Pathobiology and Molecular Medicine  Waiting to be Seated

Biographical Sketch  Irshad H. Chaudry was born on May 2, 1945. He received a B.S. as well as M.S. with honors from Sind University, and a Ph.D. from Monash University, Australia. After his postdoctoral training at Toronto University, Canada, he was an appointed as an Instructor and subsequently as an Assistant Professor at the Jewish Hospital and Washington University School of Medicine. He then moved to Yale University as an Associate Professor and subsequently became a Professor. He moved to Michigan State University in 1986 as Professor and Director of Research and in 1996 became the Director of the Center for Surgical Research at Brown University. In 2000, he became the Director of the Center for Surgical Research at the University of Alabama at Birmingham, and the Vice Chairman of the Department of Surgery. His has over 600 publications to his credit and is a recipient of the NIH MERIT award.

Society Memberships Organization Name Position Held Org Link International Federation of Shock Societies  President-elect 2004-2008  http://www.shocksocieties.org/international/shockjournal/  International Federation of Shock Societies  President 2008-2012  http://www.shocksocieties.org/international/shockjournal/  Surgical Infection Society  Treasurer 1994-1998  http://www.sisna.org/  Surgical Infection Society  President 1999-2000  http://www.sisna.org/

Research/Clinical Interest Title Cardiovascular/Immunological Alterations Following Trauma-Sepsis Description Current research interests include determining the mechanisms responsible for cellular and subcellular alterations following soft tissue trauma, bone fracture, hemorrhage and sepsis. Additionally, the use of novel, readily available, FDA approved inexpensive therapeutic agents to attenuate such alterations in patients following trauma is planned. Other areas include evaluation of: (1) gender dimorphism and the mechanisms responsible for producing cardiovascular and hepatocellular dysfunction and immunological alterations following trauma-hemorrhage; (2) trauma-induced changes in the hypothalamus-pituitary-adrenal axis; (3) apoptosis of immune cells; and (4) wound healing. Specific research interests include determining the mechanism of regulation of estradiol levels by hypothalamic/pituitary factors, adrenals and steroidogenic enzyme activity and how differences in estradiol levels or the estradiol: androgen ratio due to the estrus cycle, ovariectomy, and age affect immune responses after trauma. Studies of T lymphocytes, macrophages and Kupffer cell functions using molecular biological techniques are being conducted to determine why low estradiol fails to maintain immune functions in aged females after trauma. The use of estradiol, Raloxifene, prolactin, metoclopramide, or flutamide to restore immune/cardiovascular functions following trauma should yield novel information and provide an innovative approach for improving the host responses and reducing mortality from sepsis following trauma in postmenopausal and in surgically ovariectomized patients with low estrogen activity. Additional interests encompass the mechanisms by which androgen depletion/androgen antagonists improve cardiac performance and other organ functions after trauma. These studies also examine whether androgen depletion/androgen antagonists affect the adrenals and modify the response of the heart, liver and vascular smooth muscle to catecholamines. The hemodynamic parameters and organ functions being measured include blood flow, circulating blood volume, cardiac output, left ventricular performance, vascular reactivity, liver, gut, adrenal and pulmonary functions. The integration of cardiac function with other organ functions and detailed mechanistic studies at the cellular and subcellular levels using physiological, pharmacological and molecular biology techniques to identify targets for novel treatment modalities using sex steroid antagonists/agonists or hormones should provide new information for the improved treatment of trauma victims with major blood loss and for decreasing the susceptibility to sepsis following trauma.

Selected Publications  Publication PUBMEDID Zou L, Yang S, Hu S, Chaudry IH, Marchase RB, Chatham JC. The protective effecs of PUGNAc on cardiac function after trauma-hemorrhage are mediated via increased protein O-GlcNAc levels. Shock 2007  17414423  Moeinpour F, Choudhry MA, Kawasaki T, Timares L, Schwacha MG, Bland KI, Chaudry IH. 17beta-estradiol normalizes toll receptor 4, mitogen activated protein kinases and inflammatory response in epidermal keratinocytes following trauma-hemorrhage. Mol Immunol 2007  17403539  Hsieh YC, Yu HP, Frink M, Suzuki T, Choudhry MA, Schwacha MG, Chaudry IH. G protein-coupled receptor 30-ependent protein kinase a pathway is critical in nongenomic effects of estrogen in attenuating liver injury after trauma-hemorrhage. Am J Pathol 2007  17392161  Shimizu Y, Yu HP, Suzuki T, Szalay L, Hsieh YC, Choudhry MA, Bland KI, Chaudry IH. The role of estrogen receptor subtypes in ameliorating hepatic injury following trauma-hemorrhage. J Hepatol 2007  17336418  Yang S, Hu S, Choudhry MA, Rue LW 3rd, Bland KI, Chaudry IH. Anti-rat soluble IL-6 receptor antibody down-regulates cardiac IL-6 and improves cardiac function following trauma-hemorrhage. J Mol Cell Cardiol 2007  17313958  Hsu JT, Hsieh YC, Kan WH, Chen JG, Choudhry MA, Schwacha MG, Bland KI, Chaudry IH. Role of p38 mitogen-activated protein kinase pathway in estrogen-mediated cardioprotection following trauma-hemorrhage. Am J Physiol Heart Circ Physiol 2007  17293487  Suzuki T, Shimizu T, Yu HP, Hsieh YC, Choduhry MA, Chaudry IH. Salutary effects of 17 beta-estradiol on T-cell signaling and cytokine production after traumma-hemorrhage are mediated primarily via estrogen receptor-a. Am J Physiol Cell Physiol 2007  17287365  Hsieh YC, Frink M, Hsieh CH, Choudhry MA, Schwacha MG, Bland KI, Chaudry IH. Downregulation of migration inhibitory factor is critical for estrogen-mediated attenuation of lung tissue damage following trauma-hemorrhage. Am J Physiol Lung Cell Mol Physiol 2007  17277045  Frink M, Hsieh YC, Thobe BM, Choudhry MA, Schwacha MG, Bland KI, Chaudry IH. TLR4 regulates kupffer cell chemokine production, systemic inflammation and lung neutrophil infiltration following trauma-hemorrage. Mol Immunol 2007  17239439  Frink M, Pape HC, van Griensven M, Krettek C, Chaudry IH, Hildebrand F. Influence of sex and age on MODS and cytokines after multiple injuries. Shock 2007  17224789  First Prev   1 2 3 4 5 of  5  Next Last

Keywords trauma, hemorrhage, sepsis, gender dimorphism, immune functions, cardiovascular functions

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