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No description available.

Cytoplasmic 15-hydroxyprostaglandin dehydrogenase from swine kidney was purified to specific activity of 1.2 U per mg protein, by chromatographic techniques. Native molecular weight of enzyme was estimated at 45,000. Enzyme was inhibited by sulfhydryls, diuretics, and various fatty acids. Substrate studies indicated NAD+ specificity and ability to catabolize prostaglandins, except prostaglandin B and thromboxane B. Initial velocity studies gave intersecting plots conforming to a sequential mechanism. 15-keto-prostaglandin exhibited linear noncompetitive production inhibition with respect to either prostaglandin or NAD+; NAD yielded linear competitive production inhibition with respect to NADH. Results, and those of dead-end inhibition and alternated substrate studies, are consistent with an ordered Bi-Bi mechanism: NAD+ is added first, then prostaglandin; then 15-keto-rostaglandin is released, then NADH.

D.Sc. / Please refer to full text to view abstract

Polymorphonuclear leukocytes infiltrate tissues in response to an inflammatory stimulus such as endotoxin or parasite products. Previous studies have shown an extensive cellular infilteration about the parasitized skeletal muscle of mouse infected with the nematode, Trichinella spiralis. Infection of the host with Trichinella pseudospiralis, on the other hand, is associated with a dramatic suppression of inflammatory cellular response. Prostaglandin Bi is a product of arachidonic acid metabolism and is synthesized by variety of cell types. Prostaglandins of the E series have been generally known to suppress inflammatory responses. In the present study, I have investigated the possible relation between plasma prostaglandin Bi levels and host cellular response in infected mice. Concentrations of prostaglandin Bi in mice plasma were measured at 5, 11, and 21 days after infection with larvae of either nematode species by enzyme immunoassay. There were noticeable elevations in the concentrations of prostaglanding Bi in samples of mice infected with Trichinella pseudospiralis compared to controls. Conversely, decreased levels of prostaglandin Bi were observed in samples from the mice infected with Trichinella spiralis. These results suggest that the differences observed in the host inflammatory response to infection with Trichinella spiralis versus Trichinella pseudospiralis might be associated with recognized properties of prostaglandin Bi· In this connection, I have suggested three possible mechanisms by which the differences of inflammatory response in relation to PGEi production may be explained.

Abstract not available

No description available.

No description available.

No description available.

Thesis (Ph. D. in Cancer Biology)--Vanderbilt University, May 2008. / Title from title screen. Includes bibliographical references.