Faculty and Research Interests
Carl E. Hock, PhD
Assistant Dean
for Research
Associate Professor
Department of Cell Biology
Science Center 218
2 Medical Center Drive
Stratford, NJ 08084
856-566-6078 (office)
856-566-6195 (fax)
hock@umdnj.edu
Education:
University of Louisville School of Medicine,
Department of Physiology and Biophysics,
PhD, 1982
Research Interests:
Work in this laboratory is directed
toward the study of cardiovascular function
under both normal and pathophysiologic
conditions (i.e., circulatory shock,
myocardial ischemia, etc.). Animal models
of myocardial ischemia-reperfusion injury
and acute endotoxemia are currently
under investigation. Current work is
focused on the effect of humoral mediators
and inflammatory cells (i.e., angiotensin
II, nitric oxide, eicosanoids, leukocytes,
macrophages etc.) in the pathophysiology
of ischemic states. We are also interested
in the effect of modification of dietary
lipid on cardiovascular function under
both normal and pathophysiologic conditions.
Diet-induced modification of cell membrane
lipid structure can alter the cellular
response to humoral mediators, receptor
mediated processes, calcium binding
and fatty acid mobilization. Current
investigations include both nutritional
and pharmacological interventions aimed
at reducing both the formation and pro-ischemic
actions of mediators of cardiovascular
pathology.
Relevant Publications:
Liu, P., B. Xu and C.E. Hock.Inhibition
of nitric oxide synthesis by L-NAME
exacerbates acute lung injury induced
by hepatic
ischemia-reperfusion. (Accepted, Shock
2000).
Yin, K., C.E. Hock,
P-S. Lai, J.T. Ross and G. Yue.Role
of interferon-gamma in lung inflammation
following cecal ligation and puncture
in rats.Shock 12:215-221, 1999.
Liu, P., B. Xu, C.E. Hock,
R. Nagele, F.F. Sun, and P. Y-K Wong.NO
Modulates P-selectin and ICAM-1 mRNA
expression and hemodynamic alterations
in hepatic I/R.Am J. Physiol. 275:H2198,
1998.
Yin, K. C.E. Hock,
M. Tahamont and P. Y-K Wong. Time-dependent
cardiovascular and inflammatory changes
in acute endotoxemia. Shock 9:434-442,
1998.
Liu, P., C.E. Hock,
R. Nagele and P.Y-K Wong. Formation
of nitric oxide, superoxide and peroxynitrite
in myocardialschemia-reperfusion injury
in rats. Am. J. Physiol. 272:H2327-H2336,1997.
Hock, C.E., K. Yin,
G. Yue and P. Y-K Wong. Effects of inhibition
of nitric oxide synthase (NOS) by aminoguanidine
in acute endotoxemia. Am. J. Physiol
272:H843-H850,1997.
Forman, L.J., C.E. Hock,
M. Harwell and S. Estilow-Isabell. Comparison
of the effects of immobilization and
pressure overload induced cardiac hypertrophy
on immunoreactive beta-endorphin. Life
Sciences 57:2041-2047,1995.
Carsia, R.V., D. Forman, C.E.
Hock, R.G. Nagele and P.J.
McIlroy. Lead (Pb2+) alters growth and
reduces angiotensin II receptor density
of rat aortic smooth muscle cells. Proc.
Exp. Biol. Med. 210:180-190,1995.
Patel, J.P., L.D. Beck, F.A. Briglia
and C.E. Hock. Beneficial
effects of combined thromboxane and
leukotriene receptor antagonism in hemorrhagic
shock. Critical Care Medicine 23:231-237,1995.
Forman, L.J., C.E. Hock,
M. Harwell and S. Isabell-Estilow. The
results of exposure to immobilization,
hemorrhagic shock and cardiac hypertrophy
on -endorphin in rat cardiac tissue.
Proc. Soc. Exp. Biol. Med. 206:124-129,1994.
Hock, C.E., L.D. Beck
and L.A. Papa. Peptide leukotriene receptor
antagonism in myocardial ischemia and
reperfusion. Cardiovascular Research
26:1206-1211,1992.
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