Dr Sarfraz Ahmad was born on April 25, 1961 in Tanda (Faizabad) in northern India. He obtained a BSc (Hons.) and an MSc degree from Aligarh Muslim University. He earned his MPhil and Ph.D. degrees in Biochemistry from the North-Eastern Hill University, Shillong, India. After a couple of years ('90-'92) of research work at the prestigious Indian Institute of Technology, New Delhi, Dr. Ahmad joined Loyola University of Chicago (USA) as a postdoctoral Research Associate in Physiology.
He spent a few years as Research Instructor at the University of Illinois at Chicago before returning to Loyola as a full-time research faculty in the Departments of Thoracic & Cardiovascular Surgery and pathology.
Dr. Ahmad's research interests include cellular and molecular hemostasis/thrombosis, particularly the pathogenic mechanism(s) in autoimmune disorders such as heparin-induced thrombocytopenia (HIT). He is also interested in anticoagulant, antithrombin, antiplatelet and thrombolytic drug development. In the past, his research interests were focused on protein/enzyme purification and characterization, lectin-glycoprotein interactions, pathophysiology and signaling mechanisms in sepsis/shock syndrome, interferon/cytokine-mediated tyrosine phosphorylation in hematopoietic cells, immune response in T-cell signaling, and skeletal muscle metabolism research.
Dr. Ahmad's current research program is funded by the American Heart Association in the form of a Grant-in-Aid to study the "Functional Consequences of Cellular Interactions with Heparin-PF4 Antibodies in Heparin-induced Thrombocytopenia".
Dr. Ahmad has obtained several research grants and published research articles, book chapters, and critical reviews. He has published some 70 peer-reviewed research articles in high impact journals and numerous conference abstracts. Dr. Ahmad has received several awards and honors from national and international organizations.
The award winning paper which Dr Ahmad and his colleagues published in EMJ deals with the functional anti-heparin-platelet Factor 4 antibody-mediated platelet activation associated with intraplatelet Ca2+ signaling.
Molecular heterogeneity in unfractionated heparin (UFH) and low-molecular-weight heparins (LMWHs) results in the formation of multiple complexes with platelet factor 4 (PF4) leading to the generation of heterogeneous group of anti-heparin-PF4 (AHPF4) antibodies involving multiple mechanisms, which are responsible for heparin-induced thrombocytopenia (HIT) syndrome. This study evaluated the differences between the ELISA-detectable AHPF4 antibodies present in patients treated with UFH and a LMWH (Clivarin; Reviparin,) and the functionality of these antibodies in terms of platelet activation (mainly 14C-serotonin release response) and its relationship with intraplatelet Ca2+ signaling in human platelets. Plasma samples were tested for their AHPF4 antibody titer and the functionality was ascertained utilizing the unctional assays of laboratory diagnosis of HIT.
Dr. Sarfraz Ahmed is awarded for his original article published in the Emirates Medical Journal from outside UAE for the year 2003-2004.
