问几句英语1.I small a 2.今天去哪吃饭怎么翻译?_百度作业帮
问几句英语1.I small a 2.今天去哪吃饭怎么翻译?
我感到不妙where shall we go to have dinner?
1.I small a rat
1。我的小老鼠
2. 今天去哪吃饭
2. Today where they eat
我感觉不妙where shall we go for dinner today?
1.我的小老鼠2.Today，where to eat其实我的英语也不太好啦，答案好牵强哦。。。。
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):79-87. doi: 10.1097/MAJ.0b013e3.Small volume resuscitation in a rat model of heatstroke.1, , , .1Department of Cosmetic Science, Chia-Nan University of Pharmacy and Science, Tainan, Taiwan.AbstractBACKGROUND: Herein, we compared the effectiveness of different small volume resuscitation in a rat model of heatstroke.METHODS: Anesthetized rats, immediately after the onset of heatstroke, were randomly divided into 5 groups and given the following: (a) (b) 0.9% NaCl (1-10 mL/kg of body weight, i.v.); (c) hydroxyethyl starch (HAES) (6%, 1-10 mL/kg of body weight, i.v.); (d) 7.2% NaCl (1-10 mL/kg of body weight, i.v.); and (e) hyper-HAES (6% HAES plus 7.2% NaCl, 1-10 mL/kg of body weight, i.v.).RESULTS: When the untreated or 0.9% NaCl (1-5 mL/kg of body weight)-treated rats underwent heat stress, their survival time values were found to be 20 to 22 minutes. Resuscitation with 10 mL/kg of body weight of 0.9% NaCl, 6% HAES, 7.2% NaCl, or hyper-HAES, their survival time values, respectively, are 93+/-6, 101+/-12, 154+/-18, or 286+/-21. Apparently, the order of effectiveness in resuscitation of heatstroke is hyper-HAES&7.2% NaCl&0.9% NaCl or 6% HAES. The heatstroke-induced hypotension, cerebral ischemia and hypoxia, hypercoagulable state, activated inflammation, and hepatic and renal dysfunction can be significantly reduced by hyper-HAES.CONCLUSIONS: Our results suggest that hyper-HAES seems superior to 7.2% NaCl or HAES alone in resuscitation of heatstroke. The benefit of hyper-HAES during heatstroke is related to restoration of normal multiorgan function.PMID:
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External link. Please review our .Localization of smg p25A/rab3A p25, a small GTP-binding protein, at...
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1992 Aug 14;186(3):1345-52.Localization of smg p25A/rab3A p25, a small GTP-binding protein, at the active zone of the rat neuromuscular junction.1, , , , , , , .1Department of Anatomy, Kobe University School of Medicine, Japan.Abstractsmg p25A is a small G protein which has been suggested to regulate neurotransmitter release from the synapses. We investigated here the ultrastructural localization of this small G protein in the rat neuromuscular junction by an immunoperoxidase method. The results showed that smg p25A was distributed non-uniformly on the presynaptic plasma membrane and among the synaptic vesicles with the focal accumulation on the discrete presynaptic sites which corresponded to the active zones, the regions of the presynaptic plasma membrane specialized for the exocytosis of the synaptic vesicles. This unique distribution of smg p25A suggests that it plays an important role in the attachment and fusion of the synaptic vesicles with the active zones.PMID: 1324664
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External link. Please review our .A small-molecule glucokinase activator lowers blood glucose in the ...
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2010 Aug 25;640(1-3):250-6. doi: 10.1016/j.ejphar.. Epub
2010 May 11.A small-molecule glucokinase activator lowers blood glucose in the sulfonylurea-desensitized rat.1, , , , , , , .1Tsukuba Research Institute, Banyu Pharmaceutical Co., Ltd., 3 Okubo, Tsukuba, Ibaraki 300-2611, Japan. sumika_AbstractGlucokinase activators increase insulin release from pancreatic beta-cells and hepatic glucose utilization by modifying the activity of glucokinase, a key enzyme in glucose-sensing and glycemic regulation. Sulfonylureas are antihyperglycemic agents that stimulate insulin secretion via a glucose-independent mechanism that is vulnerable to secondary failure through beta-cell desensitization. The present study determined whether glucokinase activator treatment retains its glucose-lowering efficacy in male, adult, non-diabetic Sprague-Dawley rats desensitized to sulfonylurea treatment and whether glucose-lowering during chronic glucokinase activator treatment is subject to secondary failure. Animals were given food containing either glimepiride (a sulfonylurea), Compound B (3-[(1S)-2-hydroxy-1-methylethoxy]-5-[4-(methylsulfonyl)phenoxy]-N-1,3-thiazol-2-ylbenzamide, an experimental glucokinase activator), or no drug for up to 5 weeks. Food containing 0.04% of either drug produced acute (within 4-8 h) and significant (P&0.05) reductions in blood glucose to approximately 50% of control levels. Chronic treatment with either 0.01% or 0.04% glimepiride resulted in complete failure of glucose-lowering efficacy within 3 days whereas the efficacy of Compound B was sustained throughout the entire study. Glipizide, also a sulfonylurea, had no glucose-lowering effect when given by gavage (3mg/kg) to glimepiride-desensitized animals whereas Compound B retained full glucose-lowering efficacy in glimepiride-desensitized animals. Oral glucose tolerance was significantly impaired, compared with controls, in animals treated with glimepiride for two weeks but was enhanced to a small extent in animals treated with Compound B. Compound B also significantly increased pancreatic insulin content, compared with controls. These findings suggest that Compound B has sustained glucose-lowering effects in a rat model of sulfonylurea failure.Copyright (c) 2010 Elsevier B.V. All rights reserved.PMID:
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External link. Please review our .cDNA cloning of a rat small-intestinal Na+/SO4(2-) cotransporter.
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-4):217-23.cDNA cloning of a rat small-intestinal Na+/SO4(2-) cotransporter.1, , , , , .1University of Zürich, Institute of Physiology, Switzerland.AbstractWe have isolated a cDNA (ileal NaSi-1) from rat small intestine by homology screening with a cDNA (renal NaSi-1) encoding rat kidney cortex Na(+)-SO4(2-) cotransport. Ileal NaSi-1 cRNA specifically stimulates Na(+)-dependent SO4(2-) uptake in a time- and dose-dependent manner in Xenopus laevis oocytes, with kinetic parameters almost identical to those of the renal NaSi-1. Ileal NaSi-1 cDNA contains 2722 base pairs (bp), almost 500 bp more than the renal NaSi-1 cDNA; however, it encodes a protein of 595 amino acids identical to the renal NaSi-1 protein. Northern blot analysis shows strong signals in rat lower small intestine and kidney cortex (2.9 x 10(3) and 2.3 x 10(3) bases), with the ileal NaSi-1 corresponding to the longer transcript. We conclude that we have identified a rat ileal cDNA that encodes a membrane protein most likely involved in brush-border Na(+)-SO4(2-) cotransport. It differs to the renal NaSi-1 only in the length of the 3' untranslated region, suggesting that the major difference lies in the differential use of polyadenylation signals.PMID: 7816544
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