John A Nestler

US Patent:

51108100, May 5, 1992

Filed:

Feb 8, 1991

Appl. No.:

7/652518

Inventors:

David M. Eich - Suffolk VA
Robert Jesse - Richmond VA
John Nestler - Richmond VA

Assignee:

Virginia Commonwealth University - Richmond VA

International Classification:

A61K 3156

US Classification:

514178

Abstract:

Treating human beings with pharmacological quantities of DHEA results in their blood having increased serum DHEA and DHEA-S and lower rates of platelet aggregation. Reducing the rate of platelet aggregation can significantly reduce the incidence or morbidity and mortality from vascular events such as myocardial infarction and stroke, as well as reduce the occurrence of restenosis following vascular interventions. The concentration of DHEA and DHEA-S in the blood and the pre-incubation time of DHEA and DHEA-S with the blood will affect its impact on platelet aggregation. Hence, prior treatment of patients who are at risk with DHEA may produce the most beneficial affects. In addition, treatment of blood with DHEA-S reduces thromboxane production. Thromboxane is produced after platelets are subjected to many different types of agonists and is responsible for recruiting other platelets to aggregate and form a thrombus; therefore, blocking the production of thromboxane will reduce or prevent platelet aggregation.

US Patent:

49201158, Apr 24, 1990

Filed:

Dec 28, 1988

Appl. No.:

7/291149

Inventors:

John E. Nestler - Richmond VA
Cornelius O. Barlascini - Columbus GA
John N. Clore - Richmond VA
William G. Blackard - Richmond VA

Assignee:

Virginia Commonwealth University - Richmond VA

International Classification:

A61K 3156

US Classification:

514178

Abstract:

Therapeutic amounts of DHEA are administered to human patients for the treatment and prevention of such disorders as atherosclerosis, angina, diabetes, obesity and congestive heart failure. Administering therapeutic quantities of DHEA to human patients has been found to reduce body fat mass and increase muscle mass, lower serum LDL cholesterol levels, lower serum apoB levels, and not affect tissue sensitivity to insulin.

US Patent:

51621983, Nov 10, 1992

Filed:

Sep 25, 1991

Appl. No.:

7/765368

Inventors:

David M. Eich - Richmond VA
Robert Jesse - Richmond VA
John Nestler - Richmond VA

Assignee:

Virginia Commonwealth University - Richmond VA

International Classification:

A01N 102
A61K 3156

US Classification:

435 2

Abstract:

Treating human beings with pharmacological quantities of DHEA results in their blood having increased serum DHEA and DHEA-S and lower rates of platelet aggregation. Reducing the rate of platelet aggregation can significantly reduce the incidence of morbidity and mortality from vascular events such as myocardial infarction and stroke, as well as reduce the occurrence of restenosis following vascular interventions. The concentration of DHEA and DHEA-S in the blood and the pre-incubation time of DHEA and DHEA-S with the blood will affect its impact on platelet aggregation. Hence, prior treatment of patients who are at risk with DHEA may produce the most beneficial affects. In addition, treatment of blood with DHEA-S reduces thromboxane production. Thromboxane is produced after platelets are subjected to many different types of agonists and is responsible for recruiting other platelets to aggregate and form a thrombus; therefore, blocking the production of thromboxane will reduce or prevent platelet aggregation.