Fellowship: Case Western Reserve University
Residency: Case Western Reserve University
Medical School: University of Pittsburgh
My laboratory focuses on two areas of research: (a) respiratory muscle dysfunction in critically ill patients, and (b) the mechanisms of organ failure and death from sepsis. Both topics are related to critical care medicine. The goal of our study of respiratory muscle dysfunction is to discover new treatments designed to improve weaning patients from mechanical ventilation, thereby reducing patient morbidity. The goal of our study of sepsis is to discover new treatments to prevent multiorgan failure, the leading cause of death in intensive care units in the United States. We use animal models of disease to establish disease mechanisms and to trial new therapies and we also study human patients in the ICU to allow us to translate basic science discoveries into clinical therapies. Our laboratory uses a mixture of techniques to accomplish these objectives, including proteomic assessments, physiological assessment of organ and cell function, biochemical assessment of enzyme pathways, cell culturing techniques, fluorescent microscopy, molecular techniques to alter gene expression, assessment of organ function in critically ill patients (muscle cardiac, vascular, lung), and muscle biopsy techniques in patients. Our work is currently funded by three NIH grants.
Supinski GS, Callahan LA. Double-stranded RNA-dependent protein kinase activation modulates endotoxin-induced diaphragm weakness. J Appl Physiol. 2011;110(1):199-205.
Callahan LA, Supinski GS. Diaphragm weakness and mechanical ventilation – what’s the critical issue? Crit Care. 2010;14(4):187.
Supinski GS, Vanags J, Callahan LA. Eicosapentaenoic acid preserves diaphragm force generation following endotoxin administration. Crit Care. 2010;14(2):R35.
Supinski GS, Ji XY, Callahan LA. p38 Mitogen-activated protein kinase modulates endotoxin-induced diaphragm caspase activation. Am J Respir Cell Mol Biol. 2010;43(1):121-7.
Supinski GS, CallahanLA. Calpain activation contributes to endotoxin-induced diaphragmatic dysfunction. Am J Respir Cell Mol Biol. 1020;42(1):80-7.
Callahan LA, Supiniski GS. Sepsis-induced myopathy. Crit Care Med. 2009;37(10 Suppl):S354-67.
Supiniski GS, Wang W, Callahan LA. Caspase and calpain activation both contribute to sepsis-induced diaphragmatic weakness. J Appl Physiol. 2009;107(5):1389-96.
Supinski GS, Murphy MP, Callahan LA. MitoQ administration prevents endotoxin-induced cardiac dysfunction. Am J Physiol Regul Integr Comp Physiol. 2009;297(4):R1095-102.
Supinski GS, Ji X, Callahan LA. The JNK MAP kinase pathway contributes to the development of endotoxin-induced diaphragm caspase activation. Am J Physiol Regul Integr Comp Physiol, 2009;297(3):R825-34.
Callahan LA, Supinski GS. Hyperglycemia and acquired weakness in critically ill patients: potential mechanisms. Crit Care. 2009;13(2):125.