High crystallinity of TiOwas prepared by a modified alcohothermal method, in which titanium isopropoxide was used as the titania precursor, absolute ethanol as the reaction medium, and NHHCOas the raw materials for re...High crystallinity of TiOwas prepared by a modified alcohothermal method, in which titanium isopropoxide was used as the titania precursor, absolute ethanol as the reaction medium, and NHHCOas the raw materials for release of water, ammonia and carbon dioxides via in-situ decomposition. The X-ray powder diffraction（XRD） and transmission electron microscope（TEM） measurements showed that water and ammonia from the in-situ decomposition of NHHCOplayed an important role in conducting the size, shape, crystallinity and microstructure of TiO. The photoluminescence spectroscopy and photocurrent measurements indicated that enhanced crystallinity could hinder the recombination and promote the separation of electron-hole pairs in TiO, which contribute to the improvement of photocatalytic activity.Methyl orange photodegradation under UV light confirmed that high crystallinity of TiOdid present a high photocatalytic activity due to the effective separation of photoinduced charges.展开更多
AIM To examine whether nizatidine stimulatesduodenal HCO<sub>3</sub><sup>-</sup> secretion in rats by inhibitingAChE activity.METHODS Under pentobarbital anesthesia,aproximal duodenal loop was ...AIM To examine whether nizatidine stimulatesduodenal HCO<sub>3</sub><sup>-</sup> secretion in rats by inhibitingAChE activity.METHODS Under pentobarbital anesthesia,aproximal duodenal loop was perfused withsaline,and the HCO<sub>3</sub> secretion was measuredat pH 7.0 using a pH-stat method and by adding10mM HCI.Nizatidine,neostigmine,carbacholor famotidine was administered i.v.as a singleinjection.RESULTS Intravenous administration ofnizatidine（3-30 mg/kg）dose-dependentlyincreased duodenal HCO<sub>3</sub><sup>-</sup> secretion,and theeffect at 10mg/kg was equivalent to thatobtained by carbachol at 0.01 mg/kg.Thisnizatidine action was observed at the same doserange that inhibited acid secretion and enhancedgastric motility,mimicked by i.v.injection ofneostigmine（0.03 mg/kg）,and significantlyattenuated by bilateral vagotomy and prior s.c.administration of atropine but not byindomethacin,a cyclooxygenase inhibitor,orN<sup>G</sup>-nitro-L-arginine methyl ester,a NO synthaseinhibitor.The HCO<sub>3</sub><sup>-</sup> secretory response toacetylcholine（0.001 mg/kg）was significantlypotentiated by the concurrent administration ofnizatidine（3mg/kg,i.v.）.The IC<sub>50</sub>of nizatidine for AChE of rat erythrocytes was1.4×10<sup>-6</sup>M,about 12 times higher than that ofneostigmine.Neither famotidine(】10<sup>-3</sup>M,30mg/kg,i.v.)nor cisapride(】 10<sup>-3</sup>M,3mg/kg,i.v.)had any influence on AChEactivity or duodenal HCO<sub>3</sub><sup>-</sup> secretion.Duodenaldamage induced by acid perfusion（100 mM HCIfor 4 h）in the presence of indomethacin wassignificantly prevented by nizatidine andneostigmine,at the doses that increased theHCO<sub>3</sub><sup>-</sup> secretion.CONCLUSION Nizatidine stimulates duodenalHCO<sub>3</sub><sup>-</sup> secretion,in both vagal-dependent andatropine-sensitive manners,and the action isassociated with the anti-AChE activity of thisagent.展开更多
基金support of the National Natural Science Foundation of China(No.21163008,No.21366020)Jiangxi Collaborative Innovation Center for in vitro diagnostic reagents and instruments,the Natural Science Foundation of Jiangxi Province(No.20114BAB203009)+1 种基金Scientific & Technological Project of Jiangxi Science and Technology Normal University(No.2013ZDPYJD01,No.2015CXTD003)Graduate Innovation Foundation of Jiangxi Science and Technology Normal University(No.YC2014-X2)
文摘High crystallinity of TiOwas prepared by a modified alcohothermal method, in which titanium isopropoxide was used as the titania precursor, absolute ethanol as the reaction medium, and NHHCOas the raw materials for release of water, ammonia and carbon dioxides via in-situ decomposition. The X-ray powder diffraction（XRD） and transmission electron microscope（TEM） measurements showed that water and ammonia from the in-situ decomposition of NHHCOplayed an important role in conducting the size, shape, crystallinity and microstructure of TiO. The photoluminescence spectroscopy and photocurrent measurements indicated that enhanced crystallinity could hinder the recombination and promote the separation of electron-hole pairs in TiO, which contribute to the improvement of photocatalytic activity.Methyl orange photodegradation under UV light confirmed that high crystallinity of TiOdid present a high photocatalytic activity due to the effective separation of photoinduced charges.
文摘AIM To examine whether nizatidine stimulatesduodenal HCO<sub>3</sub><sup>-</sup> secretion in rats by inhibitingAChE activity.METHODS Under pentobarbital anesthesia,aproximal duodenal loop was perfused withsaline,and the HCO<sub>3</sub> secretion was measuredat pH 7.0 using a pH-stat method and by adding10mM HCI.Nizatidine,neostigmine,carbacholor famotidine was administered i.v.as a singleinjection.RESULTS Intravenous administration ofnizatidine（3-30 mg/kg）dose-dependentlyincreased duodenal HCO<sub>3</sub><sup>-</sup> secretion,and theeffect at 10mg/kg was equivalent to thatobtained by carbachol at 0.01 mg/kg.Thisnizatidine action was observed at the same doserange that inhibited acid secretion and enhancedgastric motility,mimicked by i.v.injection ofneostigmine（0.03 mg/kg）,and significantlyattenuated by bilateral vagotomy and prior s.c.administration of atropine but not byindomethacin,a cyclooxygenase inhibitor,orN<sup>G</sup>-nitro-L-arginine methyl ester,a NO synthaseinhibitor.The HCO<sub>3</sub><sup>-</sup> secretory response toacetylcholine（0.001 mg/kg）was significantlypotentiated by the concurrent administration ofnizatidine（3mg/kg,i.v.）.The IC<sub>50</sub>of nizatidine for AChE of rat erythrocytes was1.4×10<sup>-6</sup>M,about 12 times higher than that ofneostigmine.Neither famotidine(】10<sup>-3</sup>M,30mg/kg,i.v.)nor cisapride(】 10<sup>-3</sup>M,3mg/kg,i.v.)had any influence on AChEactivity or duodenal HCO<sub>3</sub><sup>-</sup> secretion.Duodenaldamage induced by acid perfusion（100 mM HCIfor 4 h）in the presence of indomethacin wassignificantly prevented by nizatidine andneostigmine,at the doses that increased theHCO<sub>3</sub><sup>-</sup> secretion.CONCLUSION Nizatidine stimulates duodenalHCO<sub>3</sub><sup>-</sup> secretion,in both vagal-dependent andatropine-sensitive manners,and the action isassociated with the anti-AChE activity of thisagent.
