PRIMARY FACULTY

Juliann G. Kiang, Ph.D.
Professor
Radiation Biology/Medicine
 
8901 Wisconsin Avenue
Bethesda MD 20889-5603
Office: 301-295-1076
Fax: 301-295-1731
kiang@afrri.usuhs.mil
 
More about Dr. Kiang's Research

My research interests are focused on the development of drugs and treatment approaches designed to prevent, mitigate, or reverse the health damage resulting from exposure to ionizing radiation. The potential for exposure to harmful doses of ionizing radiation exists in a wide variety of industries and professions. Many nations possess nuclear weapons whose purposeful or accidental use could expose many thousands to potentially lethal doses of radiation, and terroristic use of nuclear or radiological weapons remains a very real concern. The high radiation environment of space puts our astronauts at risk. Despite the real risk of exposure associated with these endeavors, there currently exist few drugs that address radiation health effects. Amifostine is currently approved by the FDA for ameliorating injury to normal tissues caused by radiation therapy, but its effectiveness is limited and the large doses required produce many undesirable side effects.
 
My effort to identify better radioprotectant drugs focuses on various signal transduction pathways activated by radiation, including the iNOS-caspases pathway, the iNOS-cytokines pathway, and the iNOS-autophagy pathway. My previous studies showed that HSP-70 inducers and iNOS inhibitors effectively block hemorrhage-induced multiple organ dysfunction syndromes (MODS) and multiple organ failure (MOF), both of which employ biochemical pathways known also to be active in the response to radiation. We are investigating agents that induce HSP-70 and inhibit iNOS as potential countermeasure in a project is supported by AFRRI intramural funding.
 
Radiation exposure combined with other trauma can occur under many of the circumstances mentioned above. Irradiation combined with trauma such as wounding, burning, bleeding, hypoxia, or sepsis can produce synergistic effects greater than either injury alone. We are investigating radiation exposure combined with wound trauma in vivo and radiation exposure combined with hypoxia in vitro to understand why the augmentation occurs. Using these models, we are exploring whether upregulation of HSP-70i and downregulation of iNOS can prevent, mitigate, or reverse combined injury. We are also investigating gene repair by ciprofloxacin that might block MODS and MOF. The combined injury project is supported by NIAID/NIH extramural funding.
 
The route of radioprotectant drug administration and its timing is often critical for drug efficacy. In mass casualty situations where many people need to be treated promptly, timing and the route of administration can be a limiting factor. We are thus exploring the effectiveness of oral administration of radioprotectant drugs as well as intraperitoneal, subcutaneous, intramuscular, and intravenous injection based on patient-operated injector approaches. The project is supported by DTRA extramural funding.

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