|
William R. Law, Ph.D.
Professor and Chair
Department of Biological Sciences
Voice: (215) 596-8919
Fax: (215) 596-8710
E-mail: w.law@usip.edu
Training and Degrees
Post-Doctoral training: Loyola University Medical Center, 1986-1988
Ph.D. University of Illinois College of Medicine at Chicago 1985
B.A. Augustana College, Rock Island, IL 1979
B.A. Central High for Boys, Philadelphia, PA 1974
Prior Positions
Associate Professor of Physiology: University of Illinois at Chicago,
Chicago, IL 1991-2005
Senior Scientist I: Geo-Centers, Inc. under contract to Naval Medical
Research Institute, Bethesda, MD. 1989-1991
Assistant Professor, Department of Surgery, Loyola University Medical
Center, Maywood, IL 1988-1989
Instructor, Barat College, Lake Forest, IL 1987-1989
Visiting Professor, Gama Filho University, Rio de Janeiro, R.J.,
Brasil 1985-1986
High School Teacher (basic and advanced physics) Alleman High School,
Rock Island, IL 1979-1981
Membership in Professional Organizations
American Physiological Society (Full)
American Heart Association
American Diabetes Association (Professional)
International Society for Heart Research (Full)
Shock Society
Society for Critical Care Medicine (Full)
Research Interests
Our lab is exploring the hypothesis that a balance between enzymatic
and allosteric (non-enzymatic) influences of adenosine deaminase
on adenosine actions plays a major role in regulating macrophage
and cardiac cytokine signaling. This has implications in such diverse
arenas as sepsis, ischemic and non-ischemic heart failure, and diabetes.
Selected Recent Publications:
ROLE OF ADENOSINE IN SYSTEMIC INFLAMMATORY
RESPONSE SYNDROME
LAW, W.R., Conlon, B.A., and Ross, J.D. The Extracellular Cardiac
Purine Metabolome in Sepsis. Shock. (In Press), 2006
LAW, W.R. Transgenic approaches to reintegration: Adenosine deaminase
deficiency improves ischemic tolerance. Cardiovascular Research.
71: 8-9, 2006
LAW, W.R. Adenosine receptors in the response to sepsis: What do
receptor-specific knockouts tell us? American Journal of Physiology:
Regulatory, Integrative, and Developmental Physiology. (In Press),
2006
Conlon BA, Ross JD, LAW WR. Advances in understanding adenosine
as a plurisystem modulator in sepsis and the systemic inflammatory
response syndrome (SIRS). Frontiers in Bioscience 10:2548-65, 2005
Conlon BA, Law WR. Macrophages are a source of extracellular adenosine
deaminase-2 during inflammatory responses. Clin Exp Immunol. 138(1):14-20,
2004
LAW, W.R., Valli, V.E., and Conlon, B.A. Therapeutic Potential
for Transient Inhibition of Adenosine Deaminase in Systemic Inflammatory
Response Syndrome. Critical Care Medicine May, 2003.
Cohen, E.S, LAW, W.R., Easington, C.R., Cruz, K.Q., Nardulli, B.A.,
Balk, R.A., Parrillo, J.E., and Hollenberg, S.M. Adenosine Deaminase
Inhibition Attenuates Microvascular Dysfunction and Improves Survival
in Sepsis. Am. J. Resp. Crit. Care Med. (In Press), 2002.
Adanin, S.,Yalovetskiy, I.V., Narduli, B.A., Sam, A.D., II, Jonjev,
Z.S. and LAW, W.R. Inhibiting Adenosine Deaminase Modulates the
Systemic Inflammatory Response Syndrome in Endotoxemia and Sepsis,
American Journal of Physiology 282: R1324-R1332, 2002.
MECHANISMS OF PROTECTION DURING CARDIOPLEGIC ARREST
Law WR, Ross JD, Jonjev ZS. Adenosine attenuates C-terminal but
not N-terminal proteolysis of cTnI during cardioplegic arrest. J
Surg Res. 123(1):126-33., 2005
Jonjev ZS, Schwertz DW, Beck JM, Ross JD, Law WR. Subcellular distribution
of protein kinase C isozymes during cardioplegic arrest. J Thorac
Cardiovasc Surg. 126(6):1880-5, 200389:163-168, 2000.
Created by: Robert A. Smith
Last updated: September 2006
|