Using the blind patch-clamp technique with the whole-cell mode, we have studied the modulation of pre-synaptic receptor on postsynaptic g-aminobutyric acid (GABA) receptor measuring miniature inhibitory postsy-naptic ...Using the blind patch-clamp technique with the whole-cell mode, we have studied the modulation of pre-synaptic receptor on postsynaptic g-aminobutyric acid (GABA) receptor measuring miniature inhibitory postsy-naptic currents (mIPSCs) in optic tectum of Xenopus during critical peroid. It was demonstrated that compared with mature neurons, mIPSCs recorded from immature neurons had smaller amplitude and longer decay time. mIPSCs are mediated by GABAa receptor. The nicotinic acetylcholine receptor agonists (carbachol, cytisine, nicotine, DMPP and so on) could increase the frequency of mIPSCs. The enhance-ment of mIPSCs frequency induced by nAChR agonists was calcium-dependent. However, the choline, a product of hy-drolyzed acetylcholine, could not increase the frequency of mIPSCs. DH-b-E, a competitive antagonist of nAChR, blocked the increase of mIPSCs frequency induced by car-bachol. Mecamyllamine, an a3b4 subtype of nAChR antago-nist, also blocked the carbachol-induced enhancement of mIPSCs. On the other hand, MLA, a7 subtype of nAChR antagonist, had no effect on it. Thus, it seems that nAChR could presynaptically modulate the mIPSCs and a3b4 sub-type of nAChR might be involved. But a7 nAChR subtype of nAChR would not be involved. The modulation is calcium- dependent. Meanwhile, we found that Ca2+-free solution could elicit giant PSCs. The frequency of mIPSCs also is related with the level of HP.展开更多
丝氨酸蛋白酶HtrA（The high temperature requirement factor A）家族最早在大肠杆菌中发现,随后在人类也发现,从细菌到人类一直进化保守。该家族显著结构特征就是包含一个和经典的丝氨酸蛋白酶胰蛋白酶类似的催化胰蛋白酶样结构域和...丝氨酸蛋白酶HtrA（The high temperature requirement factor A）家族最早在大肠杆菌中发现,随后在人类也发现,从细菌到人类一直进化保守。该家族显著结构特征就是包含一个和经典的丝氨酸蛋白酶胰蛋白酶类似的催化胰蛋白酶样结构域和一个或多个C端PDZ（突触后密度蛋白95-盘状大闭锁小带1）结构域。展开更多
AIM: To explore the etiology, pathogenesis, diagnosis, and treatment of postsurgical gastroparesis syndrome (PGS) after pancreatic cancer cryotherapy (PCC) or pancreaticoduodenectomy (PD), and to analyze the correlati...AIM: To explore the etiology, pathogenesis, diagnosis, and treatment of postsurgical gastroparesis syndrome (PGS) after pancreatic cancer cryotherapy (PCC) or pancreaticoduodenectomy (PD), and to analyze the correlation between the multiple factors and PGS caused by the operations.METHODS: Clinical data of 210 patients undergoing PD and 46 undergoing PCC were analyzed retrospectively.RESULTS: There were 32 (67%, 32/46) patients suffering PGS in PCC group, including 29 with pancreatic head and uncinate tumors and 2 with pancreatic body and tail tumors.Ten patients (4.8%, 20/220) developed PGS in PD group,which had a significantly lower incidence of PGS than PCC group (x = 245, P<0.001). In PCC group, 9 patients with PGS were managed with non-operative treatment (drugs,diet, nasogastric suction, etc.), and one received reoperation at the 16th day, but the symptoms were not relieved. In PD group, all the patients with PGS were managed with non-operative treatment. The PGS in patients undergoing PCC had close association with PCC,tumor location, but not with age, gender, obstructive jaundice, hypoproteinemia, preoperative gastric outlet obstruction and the type and number of gastric biliary tract operations. The mechanisms of PGS caused by PD were similar to those of PGS following gastrectomy. The damage to interstitial cells of Cajal might play a role in the pathogenesis of PGS after PCC, for which multiple factors were possibly responsible, including ischemic and neural injury to the antropyloric muscle and the duodenum after freezing of the pancreatico-duodenal regions or reduced circulating levels of motilin.CONCLUSION: PGS after PCC or PD is induced by multiple factors and the exact mechanisms, which might differ betweent hese two operations, remain unknown. Radiography of the upper gastrointestinal tract and gastroscopy are main diagnostic modalities for PGS. Non-operative treatments are effective for PGS, and reoperation should be avoided in patients with PGS caused by PCC.展开更多
基金the Na-tional Natural Science Foundation of China (Grant No.39670774)
文摘Using the blind patch-clamp technique with the whole-cell mode, we have studied the modulation of pre-synaptic receptor on postsynaptic g-aminobutyric acid (GABA) receptor measuring miniature inhibitory postsy-naptic currents (mIPSCs) in optic tectum of Xenopus during critical peroid. It was demonstrated that compared with mature neurons, mIPSCs recorded from immature neurons had smaller amplitude and longer decay time. mIPSCs are mediated by GABAa receptor. The nicotinic acetylcholine receptor agonists (carbachol, cytisine, nicotine, DMPP and so on) could increase the frequency of mIPSCs. The enhance-ment of mIPSCs frequency induced by nAChR agonists was calcium-dependent. However, the choline, a product of hy-drolyzed acetylcholine, could not increase the frequency of mIPSCs. DH-b-E, a competitive antagonist of nAChR, blocked the increase of mIPSCs frequency induced by car-bachol. Mecamyllamine, an a3b4 subtype of nAChR antago-nist, also blocked the carbachol-induced enhancement of mIPSCs. On the other hand, MLA, a7 subtype of nAChR antagonist, had no effect on it. Thus, it seems that nAChR could presynaptically modulate the mIPSCs and a3b4 sub-type of nAChR might be involved. But a7 nAChR subtype of nAChR would not be involved. The modulation is calcium- dependent. Meanwhile, we found that Ca2+-free solution could elicit giant PSCs. The frequency of mIPSCs also is related with the level of HP.
文摘丝氨酸蛋白酶HtrA（The high temperature requirement factor A）家族最早在大肠杆菌中发现,随后在人类也发现,从细菌到人类一直进化保守。该家族显著结构特征就是包含一个和经典的丝氨酸蛋白酶胰蛋白酶类似的催化胰蛋白酶样结构域和一个或多个C端PDZ（突触后密度蛋白95-盘状大闭锁小带1）结构域。
基金Supported by the Research Foundation of Department of Health of Sichuan Province,No.000050
文摘AIM: To explore the etiology, pathogenesis, diagnosis, and treatment of postsurgical gastroparesis syndrome (PGS) after pancreatic cancer cryotherapy (PCC) or pancreaticoduodenectomy (PD), and to analyze the correlation between the multiple factors and PGS caused by the operations.METHODS: Clinical data of 210 patients undergoing PD and 46 undergoing PCC were analyzed retrospectively.RESULTS: There were 32 (67%, 32/46) patients suffering PGS in PCC group, including 29 with pancreatic head and uncinate tumors and 2 with pancreatic body and tail tumors.Ten patients (4.8%, 20/220) developed PGS in PD group,which had a significantly lower incidence of PGS than PCC group (x = 245, P<0.001). In PCC group, 9 patients with PGS were managed with non-operative treatment (drugs,diet, nasogastric suction, etc.), and one received reoperation at the 16th day, but the symptoms were not relieved. In PD group, all the patients with PGS were managed with non-operative treatment. The PGS in patients undergoing PCC had close association with PCC,tumor location, but not with age, gender, obstructive jaundice, hypoproteinemia, preoperative gastric outlet obstruction and the type and number of gastric biliary tract operations. The mechanisms of PGS caused by PD were similar to those of PGS following gastrectomy. The damage to interstitial cells of Cajal might play a role in the pathogenesis of PGS after PCC, for which multiple factors were possibly responsible, including ischemic and neural injury to the antropyloric muscle and the duodenum after freezing of the pancreatico-duodenal regions or reduced circulating levels of motilin.CONCLUSION: PGS after PCC or PD is induced by multiple factors and the exact mechanisms, which might differ betweent hese two operations, remain unknown. Radiography of the upper gastrointestinal tract and gastroscopy are main diagnostic modalities for PGS. Non-operative treatments are effective for PGS, and reoperation should be avoided in patients with PGS caused by PCC.
