Publications

Department of Medicine faculty members published more than 3,000 peer-reviewed articles in 2022.

Filter by

Journal of general internal medicine

Efficacy of treating hypertension in women.

1999

Authors: Quan A, Kerlikowske K, Gueyffier F, Boissel JP

Gastroenterology

AGA technical review on the epidemiology, diagnosis, and treatment of pancreatic ductal adenocarcinoma. American Gastroenterological Association.

1999

Authors: DiMagno EP, Reber HA, Tempero MA

Clinical genetics

Human renin gene BglI dimorphism associated with hypertension in two independent populations.

1999

Authors: Frossard PM, Lestringant GG, Malloy MJ, Kane JP

Metabolism: clinical and experimental

Plasma platelet-activating factor acetylhydrolase activity in human immunodeficiency virus infection and the acquired immunodeficiency syndrome.

1999

Authors: Khovidhunkit W, Memon RA, Shigenaga JK, Pang M, Schambelan M, Mulligan K, Feingold KR, Grunfeld C

Endocrinology

Expression and signal transduction of calcium-sensing receptors in cartilage and bone.

1999

Authors: Chang W, Tu C, Chen TH, Komuves L, Oda Y, Pratt SA, Miller S, Shoback D

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

Vacuolar H+-ATPase activity and expression in mouse bone marrow cultures.

1999

Authors: Lee BS, Holliday LS, Krits I, Gluck SL

Journal of molecular and cellular cardiology

Pro-inflammatory cytokines stimulate mitogen-activated protein kinase subfamilies, increase phosphorylation of c-Jun and ATF2 and upregulate c-Jun protein in neonatal rat ventricular myocytes.

1999

Authors: Clerk A, Harrison JG, Long CS, Sugden PH

The American journal of gastroenterology

Management of Barrett's esophagus: a national study of practice patterns and their cost implications.

1999

Authors: Gross CP, Canto MI, Hixson J, Powe NR

Obstetrics and gynecology

Factors affecting prophylactic oophorectomy in postmenopausal women.

1999

Authors: Gross CP, Nicholson W, Powe NR

Volume 123 of Issue 12 | Archives of pathology & laboratory medicine

Higher prevalence of GPIIIa PlA2 polymorphism in siblings of patients with premature coronary heart disease.

1999

Authors: Goldschmidt-Clermont PJ, Coleman LD, Pham YM, Cooke GE, Shear WS, Weiss EJ, Kral BG, Moy TF, Yook RM, Blumenthal RS, Becker DM, Becker LC, Bray PF

View Abstract

BACKGROUND

The Pl(A2) polymorphism of GPIIIa has been associated with unstable coronary syndromes in some studies, but the association has remained debated. None of the previous studies have focused on families at high risk. Risk factors tend to cluster within kindreds with high prevalence of premature coronary heart disease (CHD). Therefore, a heightened prevalence of the Pl(A2) polymorphism among siblings of patients with CHD would support the hypothesis that Pl(A2) is linked, directly or indirectly, to CHD.

OBJECTIVES

To measure the prevalence of the Pl(A2) polymorphism among siblings of patients with CHD before the age of 60 years and to seek an association between the Pl(A2) polymorphism and established atherosclerotic and thrombogenic risk factors.

METHODS

From January 1994 to April 1996, we genotyped 116 asymptomatic siblings (60 Caucasians, 56 Afro-Caribbeans) of patients with CHD manifestations before the age of 60 years for the Pl(A) polymorphism (also called HPA-1). A control cohort was used for comparison, consisting of individuals that were matched for race and geographic area but were free of CHD (n = 268, 168 Caucasians and 100 Afro-Caribbeans). In addition, we have characterized the sibling cohort for other atherogenic and thrombogenic risk factors.

RESULTS

The prevalence of Pl(A2)-positive individuals (Pl(A2)[+], Pl(A1/A2) heterozygotes plus Pl(A2/A2) homozygotes) in the sibling cohort was high: 41.4%. When analyzed separately, the prevalence of Pl(A2)(+) siblings was 53.3% among Caucasians and 28.6% among Afro-Caribbeans. There was no association between Pl(A2) and other established atherogenic or thrombogenic risk factors. Interestingly, the clustering of other risk factors was lesser among Pl(A2)(+) siblings than their Pl(A1) counterparts.

CONCLUSIONS

This study supports the hypothesis that the prevalence of Pl(A2)(+) individuals is high in kindreds with premature CHD. Hence, like the established risk factors that tend to cluster in families with premature CHD and contribute strongly to the accelerated atherosclerotic process affecting these individuals, the Pl(A2) polymorphism of GPIIIa may represent an inherited risk that promotes the thromboembolic complications of CHD. That these asymptomatic Pl(A2)(+) siblings had overall less established risk factors than their Pl(A1) counterparts might represent an explanation for why they remained asymptomatic despite their Pl(A2) positivity.

View on PubMed