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.

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.

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 explore the roles of insulin in the early treatment of acute brain injury and its administration methods.Methods 253 patients were randomly divided into the intensive insulin therapy group and the conventional therapy group.Infection rates,the short-term effect (APACHE Ⅱ assessment),and long-term efficacy (GOS prognosis) was compared between two groups.Results The results of the strengthen treatment group in the rate of infection (25.95％ vs 39.34％,x2 =5.17,P ＜0.05),the short-term effect (11.33 ± 7.66 vs 16.49 ± 14.97,u =3.42,P ＜ 0.05) and the long-term efficacy (40.46％,55.73％,3.82％ vs 25.41％,68.85％,5.74％,x2 =7.62,P ＜0.05) were significantly better than the conventional therapy group with the statistically significant differences (P ＜ 0.05).Conclusions The hypoglycemic effect,neuroprotective effect,regulatory role,and nutrition role of insulin occurred in the early treatment of acute brain injury.After acute brain injury,patients with hyperglycemia should be treated early with an enough volume,continuous,and uniform insulin.

Forty one patients with esophageal carcinoma (T3N1 M0 or less) underwent video-assisted thoracoscopic surgery (VATS) in prone position for esophagectomy from September 2006 to September 2010.The postoperative outcome and survival of patients were retrospectively analyzed.The results confirmed the feasibility and safety of this minimally invasive esophagectomy performed by thoracoscopy in the prone position for patients with esophageal carcinoma.

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.

AIM To study the adaptive cytoprotection of H 2O 2 preconditioning against oxidative stress damage in PC12 cell and the relationships between brain derived neurotrophic factor (BDNF) and the adaptive cytoprotection of H 2O 2 preconditioning. METHODS The viability of PC12 cells was evaluated by MTT assay. Apoptosis was detected by PI stain flow cytometer. Expression of BDNF was analyzed by immuo flow cytometer. RESULTS After H 2O 2 preconditioning, the survival of PC12 cells exposure to H 2O 2 (20～60 ?mol?L -1 ) was increased and the apoptosis of PC12 cells induced by H 2O 2 (20 or 30 ?mol?L -1 ) was inhibited and the expression of BDNF in PC12 cells was enhanced. CONCLUSION H 2O 2 preconditioning is protective against the damage of PC12 cells induced by H 2O 2 and its mechanisms may involve up modulation of the expression of BDNF.

Objective To study the influence and solution of pseudothrom bocytopenia (PTCP) caused by anticoagulant EDTA-K2.Methods Sysmex-2100 hematology analyzer was used to analyze PTCP-positive patients' blood samples,count the platelet in samples anticoagulant with EDTA-K2,sodium citrate and heparin,and used the manual counting methods.Results Platelets counts in anticoagulant bood by EDTA-K2 was significantly lower than anticoagulant bood by sodium citrate and heparin.Lots of aggregated platelets were appeared in the EDTA-K2 anticoagulant samples stained by Wright-Giemsa,while there was no aggregated platelets observed in sodium citrate anticoagulant samples and heparin anticoagulant samples.Conclusion Platelet aggregation in patients with PTCP causes patelet counts false reducation.The patients with PTCP is determined by measuring the whole blood (no anticoagulant)by automatic hematology analyzer immediately or manual couting method.

Objective To investigate the dose-response relationship of the treatment temperatures and heating time on human cervical carcinoma hela cells,aiming at providing experimental evidences for clinical hy-perthermia. Methods Hela cells were heated at 37 ～ 70 ℃ in temperature-controlled water baths, the tempera-ture was divided into nine groups,each time was divided into eight subgroups (1 ～ 30 min). The morphology changes of cells after hyperthermia were detected by inverted microscope. Proliferation rates were measured by MTT colorimetric assay. The apoptesis rates were determined by flow eytometric analyse. The levels of prolifera-ring cell nuclear antigen (PCNA) were measured with immunohistochemistry. Results lnereaseing the heating time at the same temperature, or increaseing heating temperature at the same time, the cell proliferation, survival rates and PCNA expression decreased. There was no significant morphological change about cells ,but have small amount of apoptosis and a direct role of the suppression and destruction at 41 ℃ and 43 ℃ group. A large num-ber of cells shrinked to round and a major role for apoptosis at 46℃ group. Cell necrosis was major role at 50 ℃and 55 ℃ group. More than 55 ℃ for necrotic cells. Conclusion With the increase of heating temperature and heating time, its treatment of Hela cells gradually enhance. So combining dose-effect relationship of hyperthermia temperature and time can reach the best therapeutic effects.