Vaginal vault prolapse after nonsurgical and surgical treatment of MAAdullerian agenesis.

Background: Women with Mayer-Rokitansky-Küster-Hauser syndrome fail to develop müllerian ducts, present with primary amenorrhea, and an absent or rudimentary uterus and vagina. After creation of a neovagina, vaginal vault prolapse may occur because of lack of support to the artificially created vagina.

Cases: The first patient presented with vaginal vault prolapse 10 years after her vagina was mechanically dilated.

Atherosclerosis induced by infection with Marek's disease herpesvirus in chickens.

Background: This research was suggested after crystals that we observed in herpesvirus-infected cell cultures were identified as cholesterol. Other reports and the development of defined reagents led us to select the use of Marek's disease herpesvirus (MDV) infection of chickens to demonstrate a potential role of herpesviruses in the pathogenesis of atherosclerosis. Available for our use were a clone-purified strain of MDV of known virulence, genetically selected, specific pathogen-free chickens, and appropriate isolation facilities to design controlled experiments to fulfill Koch's postulates.

Sensitivity to nitrate and other oxyanions further distinguishes the vanadate-sensitive osteoclast proton pump from other vacuolar H(+)-ATPases.

The osteoclast proton pump (OC H(+)-ATPase) differs from other vacuolar H(+)-ATPases (V-ATPases) in its sensitivity to vanadate and in the subunit composition of its catalytic domain, where isoforms of subunits A and B are expressed [Chatterjee et al. (1992) Proc. Natl.

Viruses: causal factors in atherosclerosis.

Herpesvirus infections may lead to atherosclerosis by altering arterial cell lipid metabolism. In a pathogen-free animal model, the virus-induced arterial disease closely resembled human atherosclerosis. These and other experimental findings may eventually lead to the control of human cardiovascular disease.

Virus-induced atherosclerosis. Herpesvirus infection alters aortic cholesterol metabolism and accumulation.

Infection of normocholesterolemic, specific-pathogen-free chickens with Marek's disease herpesvirus (MDV) has been shown histologically to lead to chronic atherosclerosis like that in humans. The development of herpesvirus-induced atherosclerosis in vivo and the presence of specific Marek's antigen within aortic cells suggested that MDV infection may modify lipid metabolism and lead to significant lipid accumulation. Experiments reported herein were designed to determine the types and quantity of lipid present in aortas from MDV-infected and uninfected chickens between 2 and 8 months of age following infection and assess one possible mechanism of lipid accumulation by evaluating the effect of MDV infection on aortic cholesterol and cholesteryl ester (CE) metabolism.