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Beside its role as a neurotransmitter in the central nervous system, serotonin appears to be a central physiologic mediator of many gastrointestinal (GI) functions and a mediator of the brain-gut connection. By acting directly and via modulation of the enteric nervous system, serotonin has numerous effects on the GI tract. The main gut disturbances in which serotonin is involved are acute chemotherapy-induced nausea and vomiting, carcinoid syndrome and irritable bowel syndrome. Serotonin also has mitogenic properties. Platelet-derived serotonin is involved in liver regeneration after partial hepatectomy. In diseased liver, serotonin may play a crucial role in the progression of hepatic fibrosis and the pathogenesis of steatohepatitis. Better understanding of the role of the serotonin receptor subtypes and serotonin mechanisms of action in the liver and gut may open new therapeutic strategies in hepato-gastrointestinal diseases. Received 15 August 2007; received after revision 1 November 2007; accepted 5 November 2007  相似文献   
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L Soll  P Berg 《Nature》1969,223(5213):1340-1342
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M J Sanders  A Ayalon  M Roll  A H Soll 《Nature》1985,313(5997):52-54
The resistance of the gastric mucosa to acid and peptic injury is reflected by a resistance to the back-diffusion of H+ from gastric lumen to blood. The nature of this 'barrier', however, remains undefined. Using Ussing chambers, we have now studied the acid-barrier function of monolayers prepared from dispersed canine fundic chief cells. These monolayers secrete pepsinogen in response to stimulation. We found that, on acidification of the apical solution to pH 2, transepithelial resistance (R) increased 2.6-fold and the monolayers maintained this 1:100,000 H+ concentration gradient for more than 4 h. The addition of aspirin to the acidified apical solution caused a rapid decay in R, as did acidification of the basolateral solution to a pH less than 5.5. Ouabain-treated monolayers displayed the rise in R expected with apical acidification, while potential difference (V) and short-circuit current (Isc) decreased essentially to zero, indicating impermeability to H+. However, if the integrity of the ouabain-treated monolayers was disrupted by low apical pH, H+ permeation occurred, reflected by an Isc that was dependent on the H+ gradient across monolayers. These data indicate that the apical surface of chief cells is a very tight barrier to H+ diffusion and may be an important element resisting acid-peptic injury.  相似文献   
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INTRODUCTION India is among one of the ten most industrialized nations in the world. Increase in population has raised the urbar industrial, transport and agriculture demands which are major reasons for the degradation of the environmel condition. For India besides land and soil degradation, deforestation, low accessibility of water, ,industrial pollution and urban congestion are the major environmental issues of priority. The industries that generate huge quantities of waste are thermal power station, Iron and Steel Plants, Sugar, Paper and Fertilizer Industries.  相似文献   
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To study the mitosis-specific phosphorylation of caldesmon (CaD), we generated a mutant of the C-terminal fragment (amino acids 244–538) of human fibroblast CaD (CaD39-6F), as well as a mutant of the full-length CaD (CaD-6F), in which all six potential phosphorylation sites for Cdc2 kinase were abolished. The mitotic CaD39-6F-overexpressing cells required more time to progress from anaphase start to 50% cytokinesis, exhibited larger size, and abnormally formed numerous small blebs. In contrast, overexpression of the wild-type C-terminal fragment of CaD (CaD39) did not result in abnormal bleb formation, but led to larger size and prolonged the time requirement between anaphase start and 50% cytokinesis. Similar abnormal blebs were also observed in the CaD-6F-overexpressing cells. CaD-6F-overexpressing cells did not show larger size but required more time to progress from anaphase start to 50% cytokinesis. These results suggest that mitosis-specific phosphorylation of CaD plays a role in inhibiting bleb formation and that the N-terminal fragment of CaD is required for cell size determination. Received 4 September 2002; received after revision 25 November 2002; accepted 4 December 2002  相似文献   
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