Simian virus 40 (SV40) growth on rhesus kidney cells and on the T-22 line of SV40-transformed green monkey kidney (GMK) cells is largely limited by the low plating efficiency of SV40 on these cells. In addition, a fraction of the rhesus kidney and T-22 cells are resistant to infection by SV40. Nevertheless, 72-h viral yields per infected rhesus kidney and T-22 cell are nearly equivalent to that obtained on normal GMK cells and are independent of the multiplicity of infection. Despite the production of high viral yields, infected rhesus kidney and T-22 cells are killed slowly by SV40. Monolayers of these cells are also refractory to plaque formation by SV40. SV40 induces the release of lysosomal N-acetyl-,8glucosaminidase into the cytoplasmic fractions of rhesus kidney and T-22 cells to an extent equal to that observed during infection of rapidly killed normal GMK cells. In contrast, damage to the plasma membrane, as indicated by the release of the cellular enzymes lactic dehydrogenase and glutamic oxaloacetic transaminase into the overlay media, occurred to a much greater extent in the normal GMK cells than in the rhesus kidney or T-22 cells. Neither a lysosomal hydrolase mechanism nor viral release appear to be responsible for this phenomenon. The different rates and extents ofthe SV40 cytocidal process on these cells do not result from the differences in the viral plating efficiency on them.
In this model, losartan did not improve survival compared to placebo and quinapril and, if anything, increased mortality. Our results suggest that AT1 receptor antagonists and ACE inhibitors are not necessarily equivalent or interchangeable in terms of their effects on cardiac hypertrophy and survival in selected progressive heart failure models.
Reproductive tracts were collected on the eastern coast of Canada from adult female grey seals (Halichoerus grypus) during gestation and postparturition, and from adult female harp seals (Phoca groenlandica) during delayed implantation and postparturition. Reproductive tracts were fixed in 10% buffered formalin for light microscopy. The placental site and adjacent tissue were preserved in 2% glutaraldehyde – 1% paraformaldehyde for scanning electron microscopy. During the delay of blastocyst implantation, the endometria of the gravid and nongravid uterine horns were similar in microscopic appearance. During gestation, maternal septa were often surrounded by maternal epithelium deep into the placental labyrinth except distally, where the maternal cells were replaced by syncytium. Marginal hematomas increased in size and complexity throughout placentation. Following parturition, uterine regression occurred earlier in harp seals (10 days postpartum) than in grey seals (21–25 days postpartum). Postpartum changes were most pronounced in the placental site where the blood vessels underwent extensive reorganization. In some specimens, the extensively vascularized placental site of the previous pregnancy was still apparent 12 months later. Epithelial replacement in the uterus was complete in grey seals 21–25 days postpartum and sooner in harp seals. Cervical and vaginal stratification occurred in both phocids following parturition and increased towards estrus. A recently ovulated grey seal was obtained between 21 and 25 days postpartum. The vaginal stratification and the presence of sperm in their uterine horns indicated that grey seals began estrus about 12–17 days postpartum. In harp seals, estrus appeared to occur towards the end of the lactational period, about 10–12 days postpartum.
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