Regulation of protein synthesis in ventricular myocytes by vasopressin. The role of sarcoplasmic/endoplasmic reticulum Ca2+ stores

Protein synthesis in H9c2 ventricular myocytes was subject to rapid inhibition by agents that release Ca2+ from the sarcoplasmic/endoplasmic reticulum, including thapsigargin, ionomycin, caffeine, and arginine vasopressin. Inhibitions were attributable to the suppression of translational initiation and were coupled to the mobilization of cell-associated Ca2+ and the phosphorylation of eIF2alpha. Ionomycin and thapsigargin produced relatively stringent degrees of Ca2+ mobilization that produced an endoplasmic reticulum (ER) stress response. Translational recovery was associated with the induction of ER chaperones and resistance to translational inhibition by Ca2+-mobilizing agents. Vasopressin at physiologic concentrations mobilized 60% of cell-associated Ca2+ and decreased protein synthesis by 50% within 20-30 min. The inhibition of protein synthesis was exerted through an interaction at the V1 vascular receptor, was imposed at physiologic extracellular Ca2+ concentrations, and became refractory to hormonal washout within 10 min of treatment. Inhibition was found to attenuate after 30 min, with full recovery occurring in 2 h. Translational recovery did not involve an ER stress response but rather was derived from the partial repletion of intracellular Ca2+ stores. Longer exposures to vasopressin were invariably accompanied by increased rates of protein synthesis. Translational inhibition by vasopressin, but not by Ca2+-mobilizing drugs, was both preventable and reversible by treatment with phorbol ester, which reduced the extent of Ca2+ mobilization occurring in response to the hormone. Larger and more prolonged translational inhibitions occurred after down-regulation of protein kinase C. This report provides the first compelling evidence that hormonally induced mobilization of sarcoplasmic/endoplasmic reticulum Ca2+ stores is regulatory upon mRNA translation.     

Effect of the sulfonylurea glyburide on glycogen synthesis in alloxan-induced diabetic rat hepatocytes

1. The effect of glyburide (glibenclamide) treatment on the liver glycogen levels of diabetic rats have been studied. 2. 3 weeks treatment with glyburide (5 mg/kg, orally) increased liver glycogen and decreased blood glucose levels. 3. The results of this study demonstrated that the sulfonylurea, glyburide is capable of exerting direct insulin-like effects on liver glycogen values in vivo.     

可编程控制器在扩口成型机中的应用

扩口成型机在塑型管材生产线中属关键设备，本文探讨可编程控制器（PLC）及其温控模块在加热成型机中的实现技术，以及图示操作终端在加工设备中的应用。根据扩口成型机顺序控制的特点以及PLC及其组件齐全的硬件配置和软件功能，有针对性地具体研究扩口成型机的硬件配置和软件编制。     

Correlation of odontogenic soft tissue infection and thermal effects with special reference to temperature sense. Statistical analysis of 2,111 patients

Many persons are exposed to preservatives/biocides based on methylchloroisothiazolinone/methylisothiazolinone (MCI/MI), since toiletries and cosmetics, as well as products/water-based systems used occupationally, may all contain MCI/MI. In toiletries and cosmetics, the MCI/MI concentration is often below 15 ppm (0.0015%). In some industries, workers handle high concentrations of MCI/MI, which can cause chemical burns and induce sensitization if skin is exposed. Contact allergy to MCI/MI is common and reports on chemical burns have been published. Thus, there is a need for prevention of skin diseases caused by MCI/MI. The inactivation of MCI/MI by glutathione (GSH) in emollients, containing different amounts of lipids, was studied by HPLC. Various amounts of GSH were added to Fenuril, Essex, and Locobase, giving 3 preparations of each emollient containing 0.10%, 0.50% and 2.0% GSH, respectively. The inactivation of 15 ppm MCI/MI and the total inactivating capacity of GSH in these preparations, kept at room temperature and refrigerated, was studied over a period of 6 months. The inactivating capacity of GSH in the emollients was almost equivalent, regardless of the lipid contents of the emollients, type of storage and age. On the other hand, the GSH concentration in the emollients had a crucial importance on the inactivation of MCI/MI. Emollients containing 2% GSH were capable of inactivating up to 2400 ppm MCI/MI.     

Placental 11 beta-hydroxysteroid dehydrogenase activity in normotensive and pre-eclamptic pregnancies

Apparent mineralocorticoid excess and licorice induced hypertension, both hypertensive disorders, have been attributed to a defect in the enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD), which interconverts cortisol to cortisone. Therefore, we undertook this study to determine the role of human placental 11 beta-HSD activity in preeclampsia, which is a hypertensive disorder in pregnancy. 11 beta-HSD activities were determined in placentas of 17 normotensive and 11 preeclamptic patients matched for gestational age at 34-42 weeks. Cortisol levels in umbilical venous and arterial sera were also determined for both groups. Statistical analysis was performed using Student's t-test, significance at p < 0.05. 11 beta-dehydrogenase (oxidation activity of 11 beta-HSD) activity was significantly lower in placentas of preeclamptic compared to normotensive patients (0.19 +/- 0.09 vs. 0.26 +/- 0.08 mmoles/min/placenta, p = 0.02). Cortisol level in umbilical cord blood was significantly higher in the preeclamptic group (14.99 +/- 14.08 vs. 6.71 +/- 3.69 g/dL, p = 0.02). The decreased 11 beta-HSD activity is accompanied by an expected increase in umbilical cord blood cortisol level and decrease in fetal weight. This enzyme may play an important role in influencing fetal growth.