Objective To investigate the effects of sevoflurane delayed preconditioning on caspase recruitment domain (ARC) expression during myocardial ischemia-reperfusion (I/R) in rats. Methods Sixty-four adult male SD rats weighing 270-350 g were randomly divided into 4 groups ( n = 16 each): sham operation (group S); myocardial I/R group; sevoflurane + sham operation group (group S-S) and sevoflurane delayed preconditioning + myocardial I/R group (group S-I/R) . Myocardial I/R was induced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 2 h of reperfusion in groups I/R and S-I/R. Group S-S inhaled 33% oxygen for 2 h, and sham operation was performed 24 h later. Group S-I/R inhaled 2.5% sevoflurane for 2 h, and then myocardial I/R was induced 24 h later. Eight animals were sacrificed at the end of 2 h reperfusion in each group and the hearts removed for determination of myocardial infarct size (IS) as a percentage of area at risk (AAR) by triphenyl tetrazolium chloride staining (IS/AAR) . Myocardial apoptosis was detected using TUNEL and apoptosis index was calculated. Another 4 animals were sacrificed immediately before ischemia and at the end of 2 h reperfusion to determine the expression of ARC and Caspase-8 in myocardium by Western blot. Results Compared with group S, the infarct size and apoptosis index were significantly increased in groups I/R and S-I/R, and ARC expression was up-regulated immediately before ischemia in groups S-S and S-I/R, and Caspase-8 expression was up-regulated at 2 h of reperfusion in group I/R ( P ＜ 0.05) . Compared with group I/R, the infarct size and apoptosis index were significantly decreased in group S-I/R, and ARC expression was up-regulated, while Caspase-8 expression was down-regulated at 2 h of reperfusion in groups S-S and S-I/R ( P ＜ 0.05) . Conclusion Sevoflurane delayed preconditioning can attenuate myocardial I/R injury through up-regulating the ARC expression and decreasing the myocardial apoptosis.

Objective To investigate the effect of sevoflurane (Sero) preconditioning (Precon) on cardiomyocyte apoptosis following myocardial ischemia-reperfusion (I/R) in rats. Methods Sixty-four adult male SD rats weighing 270-350 g were randomly divided into 4 groups ( n = 16 each): group Ⅰ sham operation (group S); group Ⅱ myocardial I/R; group Ⅲ Sero and group Ⅳ Sevo-Precon + myocardial I/R. The animals were anesthetized with intraperitoneal pentobarbital 50 mg/kg, intubated and mechanically ventilated. PET CO2 was maintained at 35-45 mm Hg. Myocardial I/R was induced by 30 min occlusion of the left anterior descending branch of coronary artery followed by 2 h reperfusion in group Ⅱ and Ⅳ . In group Ⅲ the animals inhaled 2.5 % sevoflurane for 30 min while in group Ⅳ the animals inhaled 2.5% sevoflurane for 30 min at 15 min before myocardial I/R. Eight animals were killed at the end of 2 h reperfusion in each group. The hearts were removed for determination of myocardial infarct size (IS) as a percentage of area at risk (AAR) (IS/AAR) by triphenyl tetrazolium chloride staining. Myocardial apoptosis was detected using TUNEL and apoptosis index (AI) was calculated. Another 4 animals were killed before ischemia and at the end of 2 h reperfusion for determining the expression of Bcl-2 and caspase-3 protein in myocardium by Western blot. Results Sevoflurane preconditioning significantly decreased infarct size and AI in group Ⅳ as compared with group Ⅱ (group I/R). Bcl-2 protein expression was significantly decreased and caspase-3 protein expression was significantly increased after 2 h reperfusion as compared with the expression before ischemia in group I/R (group Ⅱ ). Sevoflurane preconditioning significantly reversed the I/R-induced changes in Bcl-2 and caspase-3 protein expression. Conclusion Sevoflurane preconditioning can attenuate myocardial I/R injury by decreasing myocardial apoptosis.

Objective To evaluate nuclear factor (NF)-κB signaling pathway and autophagy in inhaled sevoflurane-produced delayed myocardial protection in rats.Methods Ninety-six adult male Sprague-Dawley rats,weighing 270-350 g,were randomly assigned into 6 groups (n =16 each):sham operation group (group S),ischemia-reperfusion (I/R) group,sevoflurane group (SEVO group),specific NF-κB inhibitor parthenolide (PTN)group,dimethyl sulfoxide (DMSO) group and PTN + sevoflurane group (PTN + SEVO group).The animals were anesthetized with intraperitoneal pentobarbital 50 mg/kg,intubated and mechanically ventilated.Myocardial I/R was induced by 30 min of occlusion of the left anterior descending branch of coronary artery followed by 2 h of reperfusion.In group I/R,33％ oxygen was inhaled for 2 h.In group SEVO,2.5％ sevoflurane was inhaled for 2 h.In groups PTN and DMSO,PTN 500 μg/kg and DMSO were administered intraperitoneally 15 min before oxygen inhalation respectively.In group PTN + SEVO,PTN 500 μg/kg was administered intraperitoneally 15 min before exposure to sevoflurane.Myocardial I/R was induced 24 h after intraperitoneal administration.Eight animals in each group were sacrificed immediately before ischemia and the hearts were removed to detect the NF-κB activity and expression of LC3-Ⅱ and cathepsin B.The left animals in each group were sacrificed at 2 h of reperfusion and the hearts were removed to determine the myocardial infarct size (by TTC staining).Results Compared with group S,the myocardial infarct size was significantly increased at 2 h of reperfusion in the other groups,and the NF-κB activity was significantly increased and the expression of LC3-Ⅱ and cathepsin B was up-regulated immediately before ischemia in group SEVO (P ＜ 0.05).Compared with group I/R,the NF-κB activity was significantly increased and the expression of LC3-Ⅱ and cathepsin B was up-regulated immediately before ischemia,and the myocardial infarct size was significantly reduced at 2 h of reperfusion in group SEVO (P ＜ 0.05).Compared with group SEVO,the NF-κB activity was significantly decreased and the expression of LC3-Ⅱ and cathepsin B was down-regulated immediately before ischemia,and the myocardial infarct size was significantly increased at 2 h of reperfusion in DMSO,PTN and PTN + SEVO groups (P ＜ 0.05).Conclusion NF-κB signaling pathway and autophagy are involved in inhaled sevoflurane-produced delayed nyocardial protection in rats.

Objective To evaluate the role of the mitochondrial ATP-sensitive potassium (mito-KATP)channel in sevoflurane preconditioning-induced delayed cardioprotection against ischemia-reperfusion (I/R) injury in isolated rat hearts.Methods Seventy-two adult male Sprague-Dawley rats were randomly divided into 6 groups (n =12 each):control group (group CON),I/R group,sevoflurane control group (group SEVO),sevoflurane preconditioning group (group SWO P),5-hydroxydeconoate (5-HD) + sevoflurane preconditioning group (group 5-HD+ SWOP) and 5-HD control group (group 5-HD).The rats were exposed to 33％ pure oxygen for 1 h in groups CON and I/R.The rats were exposed to 2.5％ sevoflurane for 1 h in groups SEVO and SWOP.5-HD (a mito-KATP channel inhibitor) 10 mg/kg was injected intraperitoneally 30 min before sevoflurane preconditioning in group 5-HD + SWOP.5-HD 10 mg/kg was injected intraperitoneally in group 5-HD.The hearts were immediately removed and perfused in a Langendorff apparatus.The hearts were made globally ischemic for 30 min followed by 120 min reperfusion in groups I/R,SWOP,5-HD + SWOP and 5-HD.The expression of phosphorylated protein kinase C-epsilon (p-PKC-ε) and caspase-8 was measured by Western blot immediately before ischemia (T0) and at 120 min of reperfusion (T1).The myocardial infarct volume was measured by TTC staining.Results Compared with group CON,the myocardial infarct volume was significantly increased at T1 in groups I/R,SWOP,5-HD +SWOP and 5-HD,p-PKC-ε expression was up-regulated at T0 in groups SEVO and SWOP and at T1 in groups I/R,SWOP,5-HD + SWOP and 5-HD,and caspase-8 expression was down-regulated at T1 in group SEVO (P ＜0.05).Compared with group I/R,the myocardial infarct volume was significantly decreased at T1 in groups SWOP and 5-HD + SWOP,p-PKC-ε expression was up-regulated at T0 in groups SEVO and SWOP,and caspase-8 expression was down-regulated at T1 in group SWOP (P ＜ 0.05).Compared with group SWOP,the myocardial infarct volume was significantly increased,p-PKC-ε expression was down-regulated at T0,and caspase-8 expression was up-regulated at T1 in group 5-HD + SWOP (P ＜ 0.05).Conclusion The mito-KATP channel is involved in sevoflurane preconditioning-induced delayed cardioprotection against I/R injury in isolated rat hearts through upregulation of p-PKC-ε expression before ischemia and inhibition of cell apoptosis during reperfusion.

Objective To study on the results of magnifying endoscopy in gastric atrophy, intestinal metaplasia (IM) and dysplasia, and evaluate their feasibility and accuracy for the diagnosis of these lesions. Methods One hundred patients were examined by magnifying endoscopy, Fujinon EG485 ZH modal, and stained with 0. 5% methylene blue. After defining magnifying endoscopic patterns of gastric pits as types A, B, C, D, and E, the diagnostic classification and endoscopic criteria were developed for the diagnosis of atrophy, IM and dysplasia. The results of 417 histopathological biopsy specimens taken from the corresponding areas of gastric mucosa under magnifying endoscopy were regarded as gold standard. Results Sparse and thick gastric pits mainly appeared in gastric atrophy, IM mainly appeared in gastric mucosa of type C, type D, and type E with positive stain, dysplasia appeared as depressed, slightly raised, or flat mucosa accompanied by loss of clear pattern, fine pits or coarse and irregular microstructure. The sensitivity and specificity of magnifying endoscopies in the diagnosis of atrophy, IM and dysphasia were 95. 85% , 95. 09% ; 88. 30% , 90.83% ; and 91.52% , 94. 41% respectively, all were higher than those of routine endoscopy. Conclusion The diagnostic accuracy significantly increased as depending upon the morphological features of gastric atrophy , IM, or dysplasia under magnifying endoscopy.

Objective To study the expression of collapsin response mediator protein 2 (CRMP-2) in the visual cortex of monocular form deprivation amblyopia rats.Methods Sixty-four 14-day-old rats were randomly divided into monocular deprivation amblyopia group and normal control group by random number table method.Right eyelid margin suture was performed at 14 days after birth in the monocular deprivation amblyopia group.Eight rats in the monocular deprivation amblyopia group and the normal control group were observed at 14,21,45 and 120 days after birth,respectively.Flash visual evoked potential (F-VEP) was used to dectect the latency and amplitude of P1 wave.The expression of CRMP-2 in visual cortex was observed by immunohistochemical method.The use and care of the animals complied with Regulations for the Administration of Affair Concerning Experimental Animals by State Science and Technology Commission.This study protocol was approved by Ethic Committee of the University of South China (No.20140228).Results F-VEP results showed that the amplitudes of P1 were decreased and latent periods of P1 were prolonged in the monocular deprivation amblyopia group compared with the normal control group (t=16.760,P =0.000;t =-22.919,P =0.000).CRMP-2 expression levels in the visual cortex of monocular deprivation amblyopia groups and normal control groups were compared at different time points after birth,and the differences were statistically significant (Fgroup =8.855,P =0.010;Ftime =63.091,P =0.000).Compared with normal control groups,the expressions of CRMP-2 at the postnatal 21,45 and 120 days were obviously decreased in the monocular deprivation amblyopia groups,the differences were statistically significant (all at P＜0.05).Conclusions CRMP-2 may be involved in the occurrence and development of amblyopia.

OBJECTIVESTo investigate the relationship between H. pylori infection, gastric cancer and other gastric diseases through the changes in gastric mucosa and the status of different gastric diseases within 5 years after H. pylori eradication in H. pylori-positive subjects in a high incidence region of gastric cancer.

METHODSOne thousand and six adults were selected from the general population in Yantai, Shandong province, a high incidence region for gastric cancer in China. Gastroscopy and Campylobacter-like organism (CLO) testing were performed on all subjects. Biopsy samples from the gastric antrum and body were obtained for histology and assessment of H. pylori infection. All H. pylori-positive subjects were then randomly divided into two groups: treatment group receiving Omeprazole Amoxicillin Clarythromycin (OAC) triple therapy and placebo as controls. These subjects were endoscopically followed up in the second and fifth year. We compared the endoscopic appearance and histology of the biopsy specimens from the same site obtained at the first and last visits.

RESULTSAll 552 H. pylori-positive subjects were randomly and evenly divided into treatment group or control group. During the five-year follow-up, the numbers of patients who continued to be negative or positive for H. pylori were 161 and 198, respectively. Statistical analysis revealed that: (1) At the initial visit, there were no significant differences in the severity and activity of inflammation, atrophy and intestinal metaplasia between the biopsy specimens from the antrum and body respectively in both groups. (2) The severity and activity of inflammation in both the antrum and body were markedly reduced after H. pylori eradication (P = 0.000). (3) Within five years after H. pylori eradication, intestinal metaplasia in the antrum either regressed or had no progression, while the proportion of intestinal metaplasia in the H. pylori-positive group increased significantly (P = 0.032). (4) After H. pylori eradication, the atrophy in both the antrum and body had no significant regression. The P value was 0.223 and 0.402, respectively.

CONCLUSIONSH. pylori eradication results in remarkable reduction in the severity and activity of chronic gastritis, marked resolution of intestinal metaplasia in the antrum. On the other hand, continuous H. pylori infection leads to progressive aggravation of atrophy and intestinal metaplasia.

Adult ; Aged ; Double-Blind Method ; Follow-Up Studies ; Gastric Mucosa ; pathology ; Gastritis ; etiology ; Helicobacter Infections ; complications ; drug therapy ; pathology ; Helicobacter pylori ; Humans ; Metaplasia ; Middle Aged ; Stomach Neoplasms ; etiology

This study was aimed to explore and summarize traditional Chinese medicine (TCM) syndrome differentiation of chronic bronchial asthma,in combination with characteristics of clinical TCM syndrome,clinical phenotype of asthma and the research of genomics in order to provide references.This study was conducted by the method of combining retrospective literature research and clinical epidemiological survey,designing and inducing the formation of chronic duration of bronchial asthma in TCM syndrome observation table,through literature research and analysis and pre-survey feedback information revision method.The four diagnostic data of 204 cases was collected and filled in the observation table.With the help of SPSS22 statistical analysis software,the database was established and the method of cluster analysis was applied to induce the basic TCM syndrome types of chronic bronchial asthma.The results showed that bronchial asthma chronic persistent period was divided into two basic syndromes,which were the cold-deficiency syndrome and heat-deficiency syndrome.It was concluded that the clinical phenotype of bronchial asthma chronic duration was explored for further research on the relationship between TCM syndrome differentiation of cold and heat as well as the modem medicine genomics to provide research data.