A dose-response relation was established between prostaglandins and formation of adenosine 3',5'-monophosphate in the mouse ovary. The prostaglandin antagonist, 7-oxa-13-prostynoic acid, blocked the stimulatory effect of prostaglandin E(1), prostaglandin E(2), and luteinizing hormone on adenosine 3',5'-monophosphate formation in a competitive manner. Kinetic studies made it possible to suggest that there is a single luteinizing-hormone-related prostaglandin receptor in mouse ovaries, and that activation of this prostaglandin receptor is an essential requirement in the action of luteinizing hormone to stimulate adenosine 3',5'-monophosphate formation and steroidogenesis.

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Endogenous uterine prostaglandin levels were monitored in the cycling rat and prostaglandins of the F-type were found to rise at proestrus when estrogen levels have been shown to be maximal. Evidence that this is an estrogen-induced event is furnished by the finding that estradiol-17fl caused a similar rise in prostaglandin F levels in uteri of ovariectomized rats, an action blocked by coadministration of progesterone. Examination of in vitro prostaglandin synthetase by uterine microsomal fractions from cycling rats and estrogen-treated ovariectomized rats revealed that the action of estrogen to control prostaglandin synthesis in a directional manner is accomplished, at least in part, by regulation of the prostaglandin synthetase complex, resulting in a patterned alteration in the ratio of prostaglandin F to prostaglandin E. These results demonstrate that prostaglandins are involved in the expression of estrogen action in the rat uterus.Estrogen administration has been shown to effect the release of prostaglandin F2a (PGF2a) into uterine fluids of the guinea pig (1) and monkey (2). This prostaglandin, which has a potent contractile effect on the isolated uterus, has been identified in sheep as the luteolytic agent produced by the uterus which subsequently acts on the ovary to bring about luteal regression (3). Estrogen administration has also been shown to be associated with uterine hyperemia (4). Such hyperemia has been related to elevations in prostaglandin E (PGE) levels (5, 6). These findings, plus new data demonstrating the existence of receptors unique to PGE1 and PGF2, in the uterus (7) and corpus luteum (8, 9), pose the possibility that PGEs and PGF2a,, produced in the uterus as a consequence of estrogen action, play distinctly different roles in the reproductive processes.Recently, the action of estrogen on the uterus of the ovariectomized rat has been shown to be associated with a rise in guanosine 3': 5'-cyclic monophosphate (cyclic GMP) (10), an observation strengthened by the finding that cyclic GMP is maximal in the normal cycling rat at proestrus (10), a time when estrogen levels reach their peak value (11). Although there is evidence that the contractile effect of PGF2a on the uterus (N. D. Goldberg et al., personal communication and ref. 21) as well as on the canine saphenous and lung veins is associated with a rise in cyclic GMP levels (12, 13), estrogen itself exhibits no such acute contractile action on the isolated uterus. Thus, in view of the demonstrated ability of estrogen to trigger the production of both cyclic GMP and PGF by this organ, we were prompted to examine these events in more detail.Emphasis was placed on the estrogen-regulated biosynthesis of prostaglandins E and F, as well as the interrelationships between these prostaglandins and adenosine 3': 5'-cyclic monophosphate (cyclic AMP) and cyclic GMP. The results of these studies are the substance of this report. Female Charles River rats (150-250 g) were used throughout these studies. The stages of their estrus cycle wer...

Throughout America's first 145 years of war, far more of the country's military personnel perished from infectious diseases than from enemy action. This enduring feature of war was finally reversed in World War II, chiefly as a result of major medical advances in prevention (vaccines) and treatment (antibiotics). Safeguarding the health of a command is indispensable for the success of any campaign. Wars are lost by disease, which causes an enormous drain on the military's resources and affects both strategy and tactics. Disease and combat mortality data from America's principal wars (1775–present) fall into two clearly defined time periods: the Disease Era (1775–1918), during which infectious diseases were the major killer of America's armed forces, and the Trauma Era (1941–present), in which combat-related fatalities predominated. The trend established in World War II continues to the present day. Although there are currently more than 3,400 U.S. military fatalities in Iraq, the disease-death toll is so low that it is exceeded by the number of suicides.

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