Dr. Jane Salmon is Professor of Medicine and Professor of Obstetrics and Gynecology at Weill Cornell Medical College and the Collette Kean Research Professor at Hospital for Special Surgery.
Dr. Salmon graduated magna cum laude from New York University and earned a medical degree in 1978 from the College of Physicians and Surgeons of Columbia University, where she was the first woman enrolled in their Medical Scientist Training Program. She completed training in internal medicine at The New York Hospital and in rheumatology at Hospital for Special Surgery, and has been an HSS faculty member since 1983. Dr. Salmon has served on the Board of Directors of the American College of Rheumatology and as Councilor of the Clinical Immunology Society. She has served on the NIH Advisory Boards for the North American Rheumatoid Arthritis Consortium and the Lupus Multiplex Registry and was co-editor of Arthritis and Rheumatism. At Hospital for Special Surgery, she is a co-Director of the Mary Kirkland Center for Lupus Research, Director of the SLE APS Center of Excellence, Director of the FOCIS Center of Excellence, and Director of the Lupus Registry and Repository.
Dr. Salmon’s research has focused on elucidating mechanisms of tissue injury in lupus and other autoimmune diseases. Her basic and clinical studies have expanded our understanding of pregnancy loss and organ damage in SLE and the determinants of disease outcome in lupus patients with nephritis, pregnancy, and cardiovascular disease.
Industry Relationships |
One of the goals of Hospital for Special Surgery (HSS) is to advance the science of orthopedic surgery, rheumatology, and related disciplines for the benefit of patients. Physicians at HSS may collaborate with outside companies for education, research and medical advances. HSS supports this collaboration in order to foster medical breakthroughs; however HSS also believes that these collaborations must be disclosed.
As part of the disclosure process, this website lists physician collaborations with outside companies if payments were received during the prior year, or if the HSS physician currently receives payment. The disclosures are provided by information provided by the physician and other sources and are updated regularly. Further information may be available on individual company websites.
Below are the healthcare industry relationships reported by Dr. Salmon as of March 18, 2013.
By disclosing the collaborations of HSS physicians with industry on this website, HSS and its physicians make this information available to their patients and the public, thus creating a transparent environment for those who are interested in this information. Further, HSS’ Conflicts of Interest Policy does not permit physicians to collect royalties on products developed by him/her that are used on patients at HSS.
Patients should feel free to ask their HSS physicians questions about these relationships.
Qing X, Redecha PB, Burmeister MA, Tomlinson S, D’Agati VD, Davisson RL, Salmon JE. Targeted Inhibition of Complement Activation Prevents Features of Preeclampsia in Mice. Kidney Intl, 79: 331-9, 2011.
Lynch AM, Salmon JE. Dysregulated Complement Activation as a Common Pathway of Injury in Preeclampsia and Other Pregnancy Complications. Placenta 31: 562-567, 2010
Roman MJ, Crow MK, Lockshin MD, Devereux RB, Paget SA, Sammaritano, L, Levine DM, Davis A, Salmon JE. Rate and Determinants of Progression of Atherosclerosis in Systemic Lupus Erythematosus. Arthritis Rheum 56: 3412-19, 2007.
Roman MJ, Salmon JE. Cardiovascular Manifestations of Rheumatologic Diseases. Circulation 116: 2346-2355, 2007.
Girardi G, Yarilin D, Thurman JM, Holers VM, Salmon JE. Complement Activation Induces Dysregulation of Anglogenic Factors and Causes Fetal Rejection and Growth Restriction. J Exp Med 203: 2165-2175, 2006.
Roman M, Moeller E, Davis A, Paget SA, Crow MK, Lockshin MD, Sammaritano L, Devereux RB, Schwartz JE, Levine DM, Salmon JE. Preclinical Carotid Atherosclerosis in Patients with Rheumatoid Arthritis: Prevalence and Associated Factors. Ann Intern Med 144: 249-256, 2006.
Girardi G, Redecha PB, Salmon JE. Heparin Prevents Antiphospholipid Antibody-induced Fetal Loss by Inhibiting Complement Activation. Nat Med 10: 1222-6, 2004.
Roman, MJ, Shanker B-A, Davis A, Lockshin MD, Sammaritano L, Simantov R, Crow MK, Schwartz JE, Paget SA, Devereux RB, Salmon JE. Prevalence and Correlates of Accelerated Atherosclerosis in Systemic Lupus Erythematosus. New Engl J Med 349: 2399-406, 2003.
Girardi G, Berman J, Redecha P, Spruce L, Thurman JM, Kraus D, Hollmann TJ, Casali P, Caroll MC, Wetsel RA, Lambris JD, Holers VM, Salmon JE. Complement C5a Receptors and Neutrophils Mediate Fetal Injury in the Antiphophospholipid Syndrome. J Clin Invest 112: 1644-54, 2003.
Salmon JE, Millard SS, Schachter LA, Arnett FC, Ginzler EM, Gourley MF, Ramsey-Goldman R, Kimberly RP: FcgRIIA alleles are heritable risk factors for lupus nephritis in African Americans. J Clin Invest 97: 1348-1354, 1996.
For more publications, please see the PubMed listing.Lockshin MD, Salmon JE, Erkan D. Pregnancy and Rheumatic Diseases. In: Maternal-Fetal Medicine (6th edition), edited by RK Creasy and R Resnik Elsevier Health Sciences, Philadelphia, pp1079-1087, 2009.
Erkan D, Salmon JE, Lockshin MD. Antiphospholipid Syndrome. In: Kelley’s Textbook of Rheumatology, 8th Edition, edited by Ruddy S, Harris ED, Jr., Sledge C. Elsevier Saunders, Philadelphia, pp1301-1310, 2008.
Salmon JE. Mechanisms of Immune-mediated Injury. In: Cecil Textbook of Medicine (23rd edition), edited by L Goldman and D Ausiello, Saunders, Philadelphia, pp 266-270, 2008.
Salmon JE, Pricop L, D’Agati V: Immunopathology of SLE. In: Rheumatology 4th Edition, edited by MC Hochberg, AJ Silman, JS Smolen, ME Weinblatt, M Weisman. Mosby, London, pp 1217-1235, 2008.
The goal of our research is to identify determinants of disease phenotype in systemic lupus erythematosus (SLE) and related diseases, and to thereby identify targets for therapy. Our laboratory approach is to study effector function and mechanisms of tissue injury. In SLE and other autoimmune diseases, autoantibodies and immune complexes trigger inflammation and organ damage through receptors for Ig (FcgR) and complement activation products. These mechanisms are currently studied in three projects.
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