Glucocorticoids stimulate the maturation of H,K-ATPase in the infant rat stomach

The development of gastric H,K-ATPase from fetal to adult life was studied in the rat. The alpha and beta H,K-ATPase mRNA abundance, the protein abundance, and the enzyme activity increased postnatally. The sharpest increase in mRNA and enzyme activity was observed in the weaning period. Several intestinal enzymes are known to be stimulated by glucocorticoids at the time of weaning. To study the role of glucocorticoids in the maturation of gastric H,K-ATPase, we treated 10-d-old rats with a single injection of betamethasone. Twenty-four hours after betamethasone injection, the enzyme activity was significantly higher than in the control animals (2.6-fold, p < 0.05). The abundance of catalytic alpha H,K-ATPase protein was also increased (2.5-fold, p < 0.01). The time-dependent effect of betamethasone on alpha H,K-ATPase mRNA was determined from 6 to 24 h after treatment. Glucocorticoids did not significantly alter the mRNA abundance within 18 h. Twenty-four hours after injection, the gastric H,K-ATPase mRNA was significantly increased compared with controls (2.8- and 2.2-fold increase for alpha and beta subunits, respectively, P < 0.01 for both). In conclusion this study indicates that glucocorticoids may regulate the long-term maturation of gastric H,K-ATPase by indirectly stimulating enzyme synthesis.     

Outcome of coronary bypass surgery versus coronary angioplasty in diabetic patients with multivessel coronary artery disease

The coloration of cells of the cyanobacterium Synechococcus sp. PCC 7002 changed from normal blue-green to yellow-green when cells were grown at 15 degrees C in a medium containing nitrate as the sole nitrogen source. This change of coloration was similar to a general response to nutrient deprivation (chlorosis). For the chlorotic cells at 15 degrees C, the total amounts of phycobiliproteins and chlorophyll a decreased, high levels of glycogen accumulated, and growth was arithmetic rather than exponential. These changes in composition and growth occurred in cells grown at low (50 microE m-2 s-1) as well as high (250 microE m-2 s-1) light intensity. After a temperature shift-up to 38 degrees C, chlorotic cells rapidly regained their normal blue-green coloration and normal exponential growth rate within 7 h. When cells were grown at 15 degrees C in a medium containing urea as the reduced nitrogen source, cells grew exponentially and the symptoms of chlorosis were not observed. The decrease in photosynthetic oxygen evolution activity at low temperature was much smaller than the decrease in growth rate for cells grown on nitrate as the nitrogen source. These studies demonstrate that low-temperature-induced chlorosis of Synechococcus sp. PCC 7002 is caused by nitrogen limitation and is not the result of limited photosynthetic activity or photodamage to the photosynthetic apparatus, and that nitrogen assimilation is an important aspect of the low-temperature physiology of cyanobacteria.     

Teichoic acid content in the cell wall of Actinomyces rimosus LST-118 in the process of ontogeny

Polymeric compounds of the cell walls of Act. rimosus were studied during the actinomycete growth. It was found that the content of teichoic acid decreased 2 times by the end of development of Act. rimosus, while content of glycane polymer remained approximately at the same level. The molar ratios of teichoic acid and glycopeptide glycane were determined.     

A microtiter plate assay for cytochrome c oxidase in permeabilized whole cells

A new mouse retinal degeneration that appears to be an excellent candidate for modeling human retinitis pigmentosa is reported. In this degeneration, called rd-3, differentiation proceeds postnatally through 2 weeks, and photoreceptor degeneration starts by 3 weeks. The rod photoreceptor loss is essentially complete by 5 weeks, whereas remnant cone cells are seen through 7 weeks. This is the only mouse homozygous retinal degeneration reported to date in which photoreceptors are initially normal. Crosses with known mouse retinal degenerations rd, Rds, nr, and pcd are negative for retinal degeneration in offspring, and linkage analysis places rd-3 on mouse chromosome 1 at 10 +/- 2.5 cM distal to Akp-1. Homology mapping suggests that the homologous human locus should be on chromosome 1q.