Objective To investigate the effects of remifentanil postconditioning and combined remifentanil-prupofol postconditioning on liver ischemia-reperfusion (I/R) injury in rats.Methods Thirty male SD rats weighing 220-280 g were randomly divided into 5 groups ( n =6 each):group sham operation (group Ⅰ ) ; group I/R (group Ⅱ ) ; group propofol postconditioning (group Ⅲ ) ; group remifentanil postconditioning (group Ⅳ ) and group combined propofol-remifentanil postconditioning (group Ⅴ ).In groups Ⅱ- Ⅴ the hepatic arteries and veins of middle and left were occluded for 30 min.In groups Ⅲ-Ⅴ propofol ( at 30 mg· kg- 1 · h - 1 ) and/or remifentanil (at 1 μg· kg- 1 · min- 1 ) were infused iv at the onset of reperfusion for 1 h.Blood samples were taken at the end of 1 h reperfusion for determination of serum AST,ALT activities and IL-8,IL-10 concentrations.The animals were sacrificed after blood sampling.Liver specimens were obtained for determination of c-fos and c-jun expression in liver cells by immuno-histochemistry and microscopic examination with scanning electron microscope.Results Liver I/R significantly increased serum AST and ALT activities and IL-8 and IL-10 concentrations and c-fos and cjun expression in liver ceils in group Ⅱ as compared with group Ⅰ.The serum AST and ALT activities,IL-8 concentration and the c-fos and c-jun expression in liver cells were significantly lower.and the serum IL-10 concentration was significantly higher in groups Ⅲ- Ⅴ than in group Ⅱ,but there were no significant differences among the groups Ⅲ - Ⅴ.The histo-pathological changes in the liver tissue were significantly attenuated in groups Ⅲ- v as compared with group Ⅱ.Conclusion Postconditioning with remifentanil and/or propofol can attenuate liver I/R injury by inhibiting inflammatory response and apoptosis in the liver cells,but there is no significant difference in the protective effects induced by postconditioning with remifentanil or propofol alone or in combination.

Objective To investigate the effects of propofol combined with remifentanil on he-patic ischemia-reperfusion injury in cirrhotic rats.Methods Sixty male SD rats of 260 to 300 grams were randomly divided into five groups(n=12):the sham-operated group(group S);the model con-trol group (group M);propofol group (group P);remifentanil group (group R);propofol combined with remifentanil group (group PR).In group M,P,R,PR,the hepatic arteries and veins of middle and left lobes were occluded for 20 min after 1 w hepatocirrhosis by using four principal factors,and group S went through an open surgery only.In groups P,R,and PR,porpofol (at a rate 20 mg·kg-1 ·h-1 for 1 h)、remifentanil (at a rate 1 μg·kg-1·min-1 for 1 h)and porpofol (at a rate 20 mg·kg-1· h-1 )combined with remifentanil(at a rate 1 μg·kg-1·min-1 for 1 h)was infused iv at 10 min before is-chemia,respectively.In group M,normal saline was infused iv at the same rate.Blood samples were taken at the end of 4 h reperfusion to determine serum AST,ALT activity.Meanwhile liver specimens were collected to assess Bcl-2 and Bax protein expression in liver cell and measuring the apoptosis in-dex(AI)of hepatic cell.The pathological change of liver was also examined.Results Compared with group S,the activity of AST,ALT,the expression of Bcl-2 and Bax and the apoptosis index(AI)of hepatic cell of the other groups all increased significantly(P <0.05);Compared with group M,the expression of Bcl-2 of groups P,R,PR significantly increased,and the activity of AST,ALT,the ex-pression of Bax and the apoptosis index(AI)of hepatic cell significantly decreased(P <0.05 );Com-pared with groups P and R,the expression of Bcl-2 of group PR significantly increased,and the activ-ity of AST,ALT,the expression of Bax and the apoptosis index(AI)of hepatic cell significantly de-creased(P <0.05);Microscopy and scanning electron microscopy showed that,for groups P,R,PR, pathological injury of liver tissue significantly reduced compared with group M.Conclusion Propofol combined with remifentanil can reduce the hepatic ischemia-reperfusion injury in cirrhotic rat by regu-lating Bcl-2 and Bax protein expression and inhibiting apoptosis.The effect is much more enhanced when they are used in combination than individuals.

BACKGROUND:Diabetic cystopathy is one of the most common chronic diabetic complications. The establishment of animal models of diabetic cystopathy wil provide experimental animal platform for relevant research.
OBJECTIVE:To establish a guinea pig model of diabetic cystopathy and to evaluate its urodynamic characteristics.
METHODS:Fifty short-hair Britain female guinea pigs were randomly divided into two groups, 42 as the experiment group and the other 8 as the control group. The experiment group was intraperitoneal y injected with streptozotocin to induce diabetes. The control group received injection of blank citric acid buffered solution. Diabetic guinea pigs were detected by urinary dynamics test at 9 and 12 weeks. Diabetic guinea pigs were further assigned into diabetic cystopathy subgroup and compensated subgroup. The urodynamic parameters of three groups were compared.
RESULTS AND CONCLUSION:Twenty of 42 guinea pigs were successful y induced diabetes by the injection of streptozotocin. At 9 weeks after the injection, bladder function compensation was present in six diabetic guinea pigs while bladder function was decompensated in another three diabetic guinea pigs. At 12 weeks, bladder function compensation was present in one diabetic guinea pig, while another eight guinea pigs were confirmed with diabetic cystopathy (88.89%). In the diabetic cystopathy subgroup, the residual urine volume was increased (0.72±0.08) mL, maximal detrusor pressure was decreased (0.63±0.05) kPa, maximum bladder capacity was increased (2.01±0.05) mL, and bladder compliance was increased (0.34±0.04) mL/kPa. There were significant differences compared with the compensated subgroup and the control group (P<0.001). Diabetic cystopathy occurs at 12 weeks after diabetic models are successful y established in guinea pigs, and urodynamic changes are mainly the increase of residual urine volume.

Strokes due to atrial fibrillation (AF) are common and frequently devastating.While oral anticoagulant agents are the mainstay in the prevention of embolic events,they have several limitations and not all patients can tolerate them long term.The left atrial appendage (LAA) has been identified as the source of thrombus formation in nonvalvular AF.Several LAA closure devices have been developed,they have been successful in stroke prevention in patients with nonvalvular AF and fewer periprocedural complications.This article reviews the application of percutaneous left atrial appendage closure for stroke prevention in patients with nonvalvular AF.

The cultivation of research ability can promote eight-year medical students to explore the uncharted academic fields and solve complex clinical problems. One of the firts pilot universities to provide eight-year programs, Xiangya Medical College of Central South University builds on its profound experience in medical education, and establishes a curriculum structure aiming at improving the students' research ability. In the general education stage, cross-disciplinary courses are set up. In the core medical education stage, basic medical innovation experiment extracurricular research courses are set up, and a two-year overseas exchange program is set up in the postgraduate training stage. Different evaluation methods are also designed to meet the specific needs in each stage. This program has achieved preliminary effects.

OBJECTIVE: To explore the effect of hepatocyte growth factor (HGF) on inducible nitric oxide synthase (iNOS), NO and interleukin-1β (IL-1β) in the cerebrum of rats subjected to cerebral ischemia/reperfusion (I/R). METHODS: Sprague-Dawley rats were randomly divided into 5 groups: a sham group, an I/R group,an HGF1 group, an HGF2 group, and an HGF3 group. The latter 3 groups were respectively injected 15, 30 and 60 μg/kg HGF. The focal cerebral I/R model was established by sutureoccluded method. After 1.5 h ischemia followed by 24 h reperfusion, the iNOS activity and NO content in the ischemic cerebral tissue were assessed. The expression of iNOS mRNA and IL-1β mRNA was detected. The level of iNOS protein and IL-1β content were determined. In addition, cultured cerebral cortical neurons in vitro were exposed to I/R. Then the expression of iNOS and IL-1β protein in the neurons was detected, and NO content was assessed. RESULTS: The iNOS activity and NO content in the ischemic cerebral tissue were increased. The expression of iNOS mRNA and IL-1β mRNA was upregulated. The level of iNOS protein and IL- 1β content were increased. Administration of HGF decreased the iNOS activity and NO content, and downregulated the expression of iNOS mRNA, IL-1β mRNA, iNOS protein and IL-1β content in the ischemic cerebral tissue. HGF decreased the expression of IL-1β, iNOS protein and NO content in the cortical neurons exposed to I/R in vitro. CONCLUSION HGF can inhibit the expression of IL-1β and decrease the expression of iNOS and content of NO, which is probably one of the mechanisms mediating the protection of HGF against cerebral ischemia injury.
Animals ; Brain Ischemia ; metabolism ; Cerebrum ; metabolism ; pathology ; Down-Regulation ; Hepatocyte Growth Factor ; pharmacology ; Interleukin-1beta ; metabolism ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase Type II ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; Up-Regulation

Objective To investigate the current status of urinary incontinence (UI) at the third trimester of pregnancy among primiparas in Guangdong Province.Methods The convenience sampling method was adopted to conduct the retrospective analysis on 714 primiparas in 3 hospitals of Guangdong Province from June 2015 to March 2016.International Consultation on Incontinence Questionnaire Urinary Incontinence Short-Form Chinese was used to investigate the occurrence status of UI at the third trimester of pregnancy among primiparas.And its influencing factors were analyzed.Results Among 714 primiparas,192 cases (26.9％) developed UI during the third trimester of pregnancy,in which stress UI accounted for 67.2％ (129/192).The prepregnancy BMI and abortion had statistical difference between.the UI patients and non-UI patients (P＜0.05).The multivariate Logistic regression results showed that pre-pregnancy BMI was correlated with UI at the trimester stage of pregnancy (OR =1.077,P＜0.05).Conclusion Pre-pregnancy BMI might be an independent risk factor of UI occurrence at the third trimester of pregnancy.

To explore the effect of epigallocatechin gallate (EGCG) on oxidative stress and Nrf2/HO-1 pathway in neurons subjected to oxygen-glucose deprivation/reperfusion (OGD/R).
 Methods: Primary cultured cerebral cortical neurons were prepared from Sprague-Dawley rats, and the OGD/R cell model was established. After pretreatment with EGCG at different concentrations (12.5, 25.0, 50.0 or 100.0 μmol/L), the neurons were subjected to OGD/R. The cell viability, reactive oxygen species (ROS) level and malondialdehyde (MDA) content were assessed after reperfusion. The superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were measured. The expression of Nrf2 protein in nucleus, HO-1 mRNA and protein were detected.
 Results: OGD/R treatment reduced the cell viability, elevated ROS level and MDA content, decreased SOD and GSH-Px activities. The expression of Nrf2 protein in nucleus, HO-1 mRNA and protein were increased (P<0.01). Pretreatment with EGCG promoted the survival of neurons exposed to OGD/R, decreased ROS level and MDA content while increased SOD and GSH-Px activities. The levels of Nrf2 protein in nucleus, HO-1 mRNA and protein were upregulated (P<0.01).
 Conclusion: EGCG can reduce the oxidative stress of neurons subjected to OGD/R, which may be related to activation of Nrf2/HO-1 signal pathway and enhancement of the antioxidant ability of neurons.
Animals ; Catechin ; analogs & derivatives ; pharmacology ; Cell Survival ; drug effects ; Cells, Cultured ; Gene Expression Regulation ; drug effects ; Glucose ; Heme Oxygenase-1 ; genetics ; metabolism ; NF-E2-Related Factor 2 ; genetics ; metabolism ; Neurons ; drug effects ; Neuroprotective Agents ; pharmacology ; Oxidative Stress ; drug effects ; Oxygen ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; prevention & control

Detailed knowledge on tissue-specific metabolic reprogramming in diabetic nephropathy (DN) is vital for more accurate understanding the molecular pathological signature and developing novel therapeutic strategies. In the present study, a spatial-resolved metabolomics approach based on air flow-assisted desorption electrospray ionization (AFADESI) and matrix-assisted laser desorption ionization (MALDI) integrated mass spectrometry imaging (MSI) was proposed to investigate tissue-specific metabolic alterations in the kidneys of high-fat diet-fed and streptozotocin (STZ)-treated DN rats and the therapeutic effect of astragaloside IV, a potential anti-diabetic drug, against DN. As a result, a wide range of functional metabolites including sugars, amino acids, nucleotides and their derivatives, fatty acids, phospholipids, sphingolipids, glycerides, carnitine and its derivatives, vitamins, peptides, and metal ions associated with DN were identified and their unique distribution patterns in the rat kidney were visualized with high chemical specificity and high spatial resolution. These region-specific metabolic disturbances were ameliorated by repeated oral administration of astragaloside IV (100 mg/kg) for 12 weeks. This study provided more comprehensive and detailed information about the tissue-specific metabolic reprogramming and molecular pathological signature in the kidney of diabetic rats. These findings highlighted the promising potential of AFADESI and MALDI integrated MSI based metabolomics approach for application in metabolic kidney diseases.