RESEARCH INTERESTS:
- Mechanisms of antioxidants, antiinflammatory agents, apoptosis and
apoptosis associated genes, catecholamines, cytokines, gene expression,
interleukin-1, ischemia reperfusion, signal transduction, tumor necrosis
factor, and transcription factors in neutrophils and lymphocytes within
murine models of acute lung injury, ARDS, and sepsis.
- The molecular basis for aging and age-related diseases, including
mitochondrial DNA deletions.
UNIQUE TECHNIQUES/EQUIPMENT:
- Gel Mobility Shift Assays
- PCR (Polymerase Chain Reaction)
- RT PCR
- Sequencing
- Southern Blot
- Western Blot
RECENT REPRESENTATIVE RESEARCH PUBLICATIONS:
- Shenkar, R.
and E. Abraham. Mechanisms of lung neutrophil activation
after hemorrhage or endotoxemia: roles of reactive oxygen intermediates,
NF-kappa B, and cyclic AMP response element binding protein. J. Immunol.
163:954-962, 1999.
- Abraham, E., J. Arcaroli, and R. Shenkar. Activation of
extracellular signal-regulated kinases, NF-kappa B, and cyclic adenosine 5’-monophosphate
response element-binding protein in lung neutrophils occurs by differing
mechanisms after hemorrhage or endotoxemia. J. Immunol. 166:522-530, 2001.
-
Shenkar, R.
, H.-K. Yum, J. Arcaroli, J. Kupfner, and E. Abraham.
Interactions between CBP, NF-k B, and CREB in the
lungs after hemorrhage and endotoxemia. Am. J. Physiol. (Lung Cell. Mol.
Physiol.) In Press, 2001.
LAY SUMMARY OF RESEARCH OBJECTIVES:
Our laboratory is investigating the events following blood loss or treatment
with bacterial toxins, which lead to acute lung injury. In particular, our basic
research focuses upon the molecular mechanisms and genes that produce acute lung
injury following blood loss or treatment with bacterial toxins.
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