Tel (sec’y): 513.558-5244
Tel (office): 513.558-3944
Tel (lab): 513.558-3943
Fax: 513.558-1744
M.L.: 0595

Swarthmore College, B.A., 1981
Harvard Medical School, M.D., 1985

Office: Medical Sciences Building - Room 6555
Laboratory: Medical Sciences Building - Room 6459

Research Summary
The primary focus of the laboratory of Dr. Zucker is on elucidating the physiological and pathophysiological effects of bilirubin, which is the main breakdown product of heme catabolism. The primary areas of research center on elucidating the mechanism(s) underlying the anti-inflammatory and chemopreventive properties of bilirubin. An additional series of investigations are examining how bilirubin is able to enter the newborn brain and induce injury to nerve cells (kernicterus).

1. Wang WW, Smith DLH, Zucker SD. Bilirubin inhibits iNOS expression and nitric oxide production in response to endotoxin in rats.  Hepatology 2004; 40: 424 - 433.

2. Keshavan P, Schwemberger SJ, Smith DLH, Babcock GF, Zucker SD. Unconjugated bilirubin induces apoptosis in colon cancer cells by triggering mitochondrial depolarization.  Int. J. Cancer 2004; 112: 433 - 445.

3. Zucker SD, Horn PS, Sherman KE.  Serum bilirubin levels in the U.S. population: gender effect and inverse correlation with colorectal cancer.  Hepatology 2004; 40: 827 - 835.

4. Keshavan P, Deem TL, Schwemberger SJ, Babcock GF, Cook-Mills JM, Zucker SD. Unconjugated bilirubin inhibits VCAM-1-mediated transendothelial leukocyte migration. J. Immunol. 2005; 174: 3709 - 3718.

5. Smith DLH, Shire NJ, Watts NB, Schmitter T, Szabo G, Zucker SD. Hyperbilirubinemia is not a major contributing factor to altered bone mineral density in patients with chronic liver disease. J. Clin. Densitom. 2006; in press.