It is hypothesized that H 2S is the third endogenous signaling gasotransmitter, after NO and CO. Endogenous H 2S may regulate some aspects of synaptic activity via cAMP mediated pathways and function as a neuromodulator or transmitter. H 2S is an endogenous vasorelaxant factor that activates K ATP channels and hyperpolarizes membrane potential of vascular SMCs. By directly acting on vascular SMCs, H 2S may reduce the extracellular calcium entry and relax vascular tissues.

Objective To investigate the effect of 50Hz magnetic field on the monoamine neurotransmitters contents in the hippocampus of rats. Methods 32 male SD rats were divided into 4 groups, exposed to 50 Hz magnetic field at the density of 0, 0.1, 1.2, and 1.6 mT, 2 h a day for a certain time. The contents of NE, E, DA and 5-HT were measured by HPLC. Results The contents of NE, DA and 5-HT in hippocampus were increased when the young rats were exposed to 1.2 and 1.6 mT for 10 days, the changes of monoamine neurotransmitters in 0.1 mT exposed group was not significant. The increase in monoamine neurotransmitters was disappeared when the 1.6 mT exposed group stop being exposed to the magnetic field for 30 days, while the monoamine neurotransmitters contents were decreased when the young rats were continuously exposed to 1.2 mT for 90 days. The contents of NE, DA and 5-HT, except E, in the old rats were decreased significantly when exposed to 0.1 mT intensity for 8 months. Conclusion Magnetic field exposure may affect the monoamine neurotransmitters content in the hippocampus, which may be responsible for the changes of learning and memory of rats induced by 50 Hz magnetic field exposure.

Aim To study the adaptive protection of H_2O_2 preconditioning against dopamine-induced damage in PC12 cells.Methods The apoptosis of PC12 cells was observed by electron microscope, PI stain flow cytometry (FCM) and Hoechst stain. The mitochondrial energy redox state was measured by MTT assay. The mitochondrial membrane potential(△?m) was investigated by the fluorescent probe of rhodamine 123.Results PC12 cells exposed to 50 ?mol?L -1 DA showed chromatin condensation and nucleus fragmentation observed by electron microscope. Exposure to DA (50 ?mol?L -1) for 24 h, the apoptosis of PC12 cells preconditioned by 10 ?mol?L -1 H_2O_2 for 90 min as measured by Hoechst stain was significantly decreased,compared with no-preconditioned cells. Exposure to 50,100,and 200 ?mol?L -1 H_2O_2 for 24 h, the proportion of apoptosis of PC12 cells was decreased from (20.9?1.8)%, (40.5?6.4)% and (88.1?3.9)% to (4.9?2.9)%, (12.0?1.4)%, (61.5?3.4)% after H_2O_2 preconditioning, respectively. By exposuring PC12 cells to 20,40,and 80 ?mol?L -1 DA for 24 h, the rates of MTT metabolism were reduced and the effect was prevented by H_2O_2 preconditioning. After 50 ?mol?L -1 DA exposure for 24 h,the mean fluorescence intensity of rhodamine 123 in no-preconditioned PC12 cells was decreased from (46.87?0.33) to (4.39?2.93),and that of preconditioned PC12 cells was decreased from (46.87?0.33) to (10.50?0.28). Conclusion H_2O_2 preconditioning possesses adaptive protection against dopamine-induced damage in PC12 cells.

Objective:To analyze the effect of endoscopic submucosal tunnel dissection on patients with large esophageal superficial neoplasms.Methods: Chosen patients with large esophageal superficial neoplasms in our hospital as research object, randomly divided into control group treated by endoscopic mucosal dissection (ESD) and observation group treated by endoscopic submucosal tunnel dissection(ESTD), compared surgery related indicators, complications and treatment outcomes.Results: 1)Observation group patients’ tumor stripping rate (23.17±4.73)/min was significantly higher than control group patients’ (12.65±2.19)/min; Intraoperative blood loss(9.14±0.67)ml, total length of hospital stay (7.34±1.89) d, were significantly less than control group patients with intraoperative blood loss(21.38±3.14)ml, total length of hospital stay (13.21±3.05)d, t value was 4.965, 5.395, 4.932, respectively(t=4.965,t=5.395,t=4.932;P<0.05); 2)Observation group patients esophageal bleeding ESTD rate(5.26%), esophageal stricture rate(31.58%), mediastinal emphysema rate(5.26%), esophageal perforation rate of 0, were significantly less than control group patients with esophageal bleeding rate(31.58%), esophageal stricture rate(5.26%), mediastinal emphysema rate(21.05%), esophageal perforation rate (26.32%), t value were 4.378, 4.378, 4.471, 5.758, (t=4.378,t=4.378,t=4.471,t=5.758;P<0.05); 3)Observation group patients with no recurrence during the follow-up period, control group patients with local recurrence rate of 21.05%, t value 8.623,P<0.05(t=8.623, P<0.05).Conclusion: Endoscopic tunnel mucosal stripping technique can effectively improve the complete tumor removal rate, during the process of optimization operation at the same time reduce the occurrence of complications, to the improvement of the prognosis of patients with positive clinical significance.

Objective To observe the effect of estrogen on H2O2-induced apoptosis and to explore the mechanism of protection by estrogen.Methods Setting up the experimental model of apoptosis induced by H2O2 in PC12 cells. The viability of cells was assessed by MTT assay. The activity of lactate dehydrogenase was detected by colorimetry. Hoechst 33258 was used as indicator of apoptosis. Apoptotic cells were measured by flow cytometry (FCM) with propidium iodide stain. The activity of caspase-3 was detected by colorimetry. Results H2O2 significantly decreased the viability of cell, increased LDH release and promoted apoptosis as well as caspase-3 activity in PC12. Estrogen markedly reduced these changes. Conclusion Estrogen reduces apoptosis induced by H2O2, and its mechanisms may be explained by inhibition of activation of caspase-3.

AIM To investigate the poteintation of adriamycin induced apoptosis by neferine in resistant human breast cancer cell line MCF 7/Adr. METHODS Apoptosis was detected by PI stain flow cytometry and Tunel assay. The intracellular adriamycin (ADR) accumulation was assayed by HPLC and the expression of P gp was determined by flow cytometry. RESULTS (1)MCF 7/Adr cells resisted the apoptosis induced by ADR while Nef augmented ADR medidated apoptosis; (2) Nef (10 ?mol?L -1 ) increased the accumulation of ADR up to 2 88 fold in MCF 7/Adr cells but not in sensitive cells MCF 7/S; (3) Nef(10 ?mol?L -1 ) reduced the expression of P gp in MCF 7/Adr cells. CONCLUSIONS Nef can overcome apoptosis resistance in MCF 7/Adr cells and its mechanisms are involved in the augment of ADR accumulation and the down-modulation of P gp expression in MCF 7/Adr cells.

Objective To study the effects of short-term and long-term exposure to extremely low frequency electromagnetic field(ELFEMF)on Morris learning and memory among rats. Methods Both younger(2-3 months old)and adult(18 months old)male SD rats were exposed to 50 Hz uniform ELFEMF with continuously adjusted intensities(0.1,1.2,1.6 mT) developed by Helmholtz coil pair for 10 days to 8 months. The levels of escape latency and the crossing annulus coefficients reflecting the behavioral changes in place navigation ability and spatial probe ability were examined by Morris water maze after exposure to ELFEMF among rats. Results The escape latency was shortened and the crossing annulus coefficients were increased compared with those of control group when the younger rats were exposed to 0.1,1.2 and 1.6 mT ELFEMF for 10 days respectively,and only revealed significant differences in 1.2 and 1.6 mT ELFEMF exposure groups compared with those of control group. In the younger rats of 1.6 mT ELFEMF exposure group with 10-day exposure ,their escape latencies were prolonged and the crossing annulus coefficients were decreased gradually and showed no significant differences compared with those of control group after the 30-day blank exposure period without ELFEMF.The younger rats of 1.2 mT ELFEMF exposure group showed significantly longer escape latency and lower crossing annulus coefficient compared those of control group after continuous 90-day exposure to 1.2 mT ELFEMF. The escape latency of adult rats in 0.1 mT ELFEMF exposure group showed no significant difference after 10-day exposure,was prolonged after 4-month exposure,and was significantly prolonged further more after 8-month exposure. Conclusion The learning and memory ability could be promoted by short-term ELFEMF exposure and impaired by long-term ELFEMF exposure for the young rats,and could be obviously inhibited by long-term ELFEMF exposure for the adult rats.

AIM To study the expression of brain-derived neurotrophic factor (BDNF) in lymphocytes modified by BDNF gene and its effect on the proliferation and the H 2O 2-induced apoptosis of PC12 cells for the transfer of ex vivo therapeutic gene into central nervous system (CNS) tissue with atraumatic means. METHODS Recombined BDNF cDNA plasmid was transfected by LipofectAMINE into the packing cell line PA317 and G418-resistant clones with highest titer was selected. Rat lymphocytes were infected repeatedly with virus supernatant. The expression of BDNF in rat lymphocytes was assayed by FCM and immunohistochemistry. The proliferation of PC12 cells was evaluated by MTT assay. H 2O 2-induced apoptosis of PC12 cells was determined by PI stain flow cytometry. RESULTS BDNF expressed in rat lymphocytes genetically modified and the concentration of BDNF in the conditioned medium of engineered lymphocytes had a linear correlation with the proliferation of the PC12 cells. The supernatant of lymphocytes modified by BDNF gene decreased the apoptosis of PC12 cells induced by H 2O 2. CONCLUSION Rat lymphocytes genetically modified can express and secret active BDNF in vitro.

AIM To study the protective effect of curcumin (Cur) on PC12 cells damage induced by oxidative stress. METHODS Using H 2O 2-induced PC12 cells damage as the model of neuron damage induced by oxidative stress, the proliferation of PC12 cells was observed by 3-[4,5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide(MTT)assay, the apoptosis of PC12 cells was detected by propidium iodide stain flow cytometry (FCM), the mitochondrial membrane potential (△?m) was analyzed by rhodamine123 stain FCM and the level of reactive oxygen species (ROS) in PC12 cells was analyzed by dihydrohodamine123 stain FCM. RESULTS In the presence of Cur (20 and 40 ?mol?L -1), the inhibitory rates of PC12 cells induced by H 2O 2 from 25 to 400 ?mol?L -1 and the apoptosis of PC12 cell induced by 100 and 200 ?mol?L -1 H 2O 2 for 24 h were decreased. The level of △?m was decreased significantly in PC12 cells after 100 and 200 ?mol?L -1 H 2O 2 treatment for 24 h, however, those decreases were significantly ameliorated by Cur (20 and 40 ?mol?L -1) treatment. The level of ROS was significantly increased in PC12 cells exposed to H 2O 2 (100 and 200 ?mol?L -1) for 12 h, whereas 40 ?mol?L -1 of Cur prevented the rise induced by H 2O 2. CONCLUSIONS Cur has protective effect on PC12 cells damage induced by oxidative stress and the effect might be attributed to its removal of ROS and increase of △?m level.

Objectives To investigate the risk factors of cardiorenal syndrome type 1 (CRS1) in patients with acute myocardial infarction (AMI).Methods The medical date of hospitalized patients with AMI from January,2013 to February,2014 in Hunan Provincial People~ Hospital were reviewed.A total of 265 patients with AMI was divided into CRS1 and non-CRS1 groups.The univariate comparison and multivariate Logistic regression analysis were performed to obtain the CRS1 risk factors.Results In the 265 AMI patients,CRS1 was found in 59 patients (22.3％).Age,history of diabetes,Killip classification,left ventricular ejection fraction (LVFF),baseline serum creatinine,blood urea nitrogen,uric acid,baseline evaluated glomerular filtration rate (eGFR),serum sodium,the left anterior descending artery lesion,emergency percutaneous coronary intervention (PCI),β-blocker,and angiotensin converting enzyme inhibitor/angiotensin receptor antagonist (ACEI/ARB) were statistically different between CRS1 and non-CRS1 groups (all P ＜ 0.05).Multivariate logistic regression showed that age,history of diabetes,Killip classification,reduced LVEF,reduced eGFR,hyponatremia,the left anterior descending artery lesionn,emergency PCI non-undergo,and β-blocker non-use were independent risk factors for CRS1 after AMI.Conclusions CRS1 is a common complication in AMI patients,which is associated with many factors.Our data suggest that patients with AMI should be more comprehensively assessed and monitored,thereby preventing the occurrence of CRS1.