D. Hasday, M.D.
Professor of Medicine
Head, Division of Pulmonary and Critical Care Medicine
Medicine: Pulmonary and Critical Care Medicine
Special Interests: Interstitial Lung Disease; Asthmas; Acute Lung Injury/
Medical Degree: University of Rochester
Residency: University of Rochester
Fellowship: University of Michigan Medical Center, Pulmonary and Critical Care Medicine; University of Rochester, Clinical Pharmacology
Certification: Internal Medicine; Pulmonary Diseases; Critical Care Medicine
Dr. Hasday is internationally recognized for work on the immunomodulatory effects of physiologically-relevant changes in temperature. His bedside-to-bench-to-bedside research on the basic mechanisms through which febrile-range hyperthermia (FRH) modulates host defenses has produced a substantial body of work in this area in the last decade.
He recently reported that FRH dramatically increases pulmonary oxygen therapy. This work spans the range from the basic molecular and cell biology to whole animal models and clinical trials. If confirmed in humans, this will lead to a practice-altering ARDS study to originate from the Division. Drs. Hasday and Singh have advanced a concept that fever borrows some heat shock mechanisms, including the central heat-shock-activated transcription factor, Heat Shock Factor-1 (HSF-1), which act in different ways at febrile- and heat-shock-temperatures. His studies in HSF-1 knockout mice showing that heat shock increases lung inflammation and injury may lead to new therapeutic modalities.
Dr. Hasday has also showed that clinically-relevant hypothermia prolongs expression of the proinflammatory cytokines TNF and IL-1ß in monocyte cultures and blocks apoptosis in epithelial cells. He has recently shown that this effect is even more global in that activation of the pivotal transcription factor, NFkappaB, is prolonged in hypothermic cell. Since NFkappaB activates both proinflammatory cytokine genes and anti-apoptosis genes, this exciting finding may explain both the cytoprotective effects of hypothermia as well as its association with higher circulating cytokine levels and inreased mortality in patients with sepsis.
Dr. Hasday has also that the bronchoalveolar compartment of the lung is converted from an endotoxin-insensitive to an endotoxin-sensitive environment by the leak of the endotoxin accessory molecule, LPS-Binding Protein from the circulation. Dr. Hasday also showed that cigarette smoke contains large amounts of biologically active endotoxin, representing a potential link between COPD and smoking and other environmental lung diseases attributable to inhaled endotoxin. He is currently extending these studies with Drs. Matthew Fenton and Stefanie Vogel.
Current Research Funding:
1-800-373-4111 (physicians only)
1-800-492-5538 (patients only)
1-410-328-8919 (news media only)
1-410-605-7198 or 410-706-5502 (academic office only)