Objective To evaluate the role of autophagy in apoptosis in cortical neurons of rats in the early phase of oxygen-glucose deprivation (OGD).Methods Female Sprague-Dawley rats at 16-18 days of gestation,weighing 350-400 g,were sacrificed after being anesthetized with pentobarbital sodium.The fetal rats were obtained and the primary cortical neurons were isolated and seeded in culture plates.The neurons were then divided into 4 groups (n =7 each) using a random number table:control group (group C),OGD 30 min group,OGD 1 h group,OGD 2 h group,and OGD 3 h group,OGD + autophagy inducer rapamycin group (OGD + R group),and OGD + autophagy inhibitor 3-methyladenine (3-MA) group (OGD + 3-MA group).The neurons were incubated in sugar-free DMEM medium containing 5％ CO2 and 95％ N2 for 30 min,1,2 and 3 h in OGD 30 min,1 h,2 h,and 3 h groups,respectively.Rapamycin (final concentration of 100 nmol/L) and 3-MA (final concentration of 10 mmol/L) were added to sugar-free DMEM medium in OGD + R and OGD + 3-MA groups,respectively,and the neurons were then incubated for 1 h.The CCK-8 assay was used to detect the neuronal viability after the end of OGD.The expression of caspase-3 and LC3 Ⅱ was measured by Western blot.Results Compared with C group,the survival rates of cortical neurons were significantly decreased in the other groups,the expression of LC3 Ⅱ was up-regulated in OGD 30 min,1 h,2 h and 3 h groups,no significant change was found in caspase-3 expression in OGD + R group,and the expression of caspase-3 was up-regulated in the other groups.Compared with OGD 1 h group,the survival rates of cortical neurons were significantly decreased in OGD2 h,OGD3 h and OGD + 3-MA groups,the survival rates of cortical neurons were increased,and the expression of caspase-3 was down-regulated in OGD + R group,the expression of LC3 Ⅱ was up-regulated in OGD + 3-MA group,and the expression of LC3 Ⅱ was down-regulated in OGD2 h and 3 h groups.Conclusion Autophagy initiated in the early phase of OGD can inhibit apoptosis in cortical neurons of fetal rats.

Immune response after blood transfusion is closely related to prognosis of the patients receiving blood productions. Thus, the safety and effectiveness are paid increasing attention.This article reviews immunological consequence and clinical manifesta-tions and response strategies after transfusion, which aims to provide reference for clinical transfusion decisions.

The effects of SHCDCT (selective head coolingdehydration combined therapy) on hypermetabolism, and its relation with thyroigenous hormones.The changes of glucose,phosphlipids,FT3 and TSH at 30, 180, 360 min of reperfusion following 30 min complete cerebral ischemia (four-vessel model ) in rabbits were observed.The effect of SHC (selective head cooling), DH(dehydration),SHCDCT on these changes were compared.SHC (28'C ) was induced by surface cooling methods.Compared with non-ischemia group,glouse, phospholipids decreased during reperfusoin,FT3 and TSH increased (P

Objective: To assess whether selective head cooling (SHC)could ameliorate the post-ischemie reperfusion injury. Method: Complete cerebral ischemia (CCI)was induced with the four vessel model for 30 min. 196 New Zealand rebbits were randomly allocated into three groups:group Ⅰ served as nonischemie control; animals in three subgroups of other groups had reperfused lasting 30,180 and 360 min respectively following CCI. Group Ⅱ served as normothermic reperfusion; group Ⅲ treated with selective head cooling(28℃,). Twenty-one endogenous parameters in brain were determined, and histomorphological assessment of neuronal chanes was observed. Neurons were classified respectively into type A(normal)and B(mild damage)etc. Result: As compared with group Ⅰ, the percentage of type A neurons was progressively decreased, while that of type B neurons increased sigmficantly in group Ⅰ (P

Objective To investigate the effects of ketamine on endotoxin-induced production of proinflammatory cytokines (IL-6, TNF-?) and activation of their modulating factor NF-?B in rat. Methods Thirty-six adult male Wistar rats weighing 250-300 g were randomly divided into 4 groups : (Ⅰ Ⅰ ) control group ( n = 6) ; (Ⅱ) endotoxin group received intravenous endotoxin ( Escherichia coli O111: B4)5mg?kg-1(n = 6); (Ⅲ) ketamine group received ketamine 50 mg?kg-1 ? h-1 i.v. (n = 6) and (Ⅳ) endotoxin + ketamine group received ketamine 0.5 or 5 or 50 mg?kg-1 ? h-1 after endotoxin ( n = 18 ) . The animals were anesthetized with urethane i. p. (1 g?kg-1) . Carotid artery was cannulated for BP and HR monitoring and jugular vein was cannulated for fluid or drug administration. Two hours after endotoxin administration the animals were sacrificed by exsanguination. Blood was collected and peripheral blood monocytes (PBMC) were isolated. NF-icB content in PBMC was measured by EMSA and plasma TNF-? and IL-6 concentrations were determined by ELISA. Results Progressive hypotension and tachycardia developed after endotoxin administration. Endotoxin also increased NF-icB content in PBMCs and plasma TNF-? and IL-6 concentrations. Ketamine 50 mg?kg-1 attenuated the endotoxin-induced hemodynamic response. Ketamine (0.5, 5, 50 mg?kg-1?h-1 ) suppressed NF-?B content in PBMC and inhibited plasma TNF-? level but plasma IL-6 level was not affected. Conclusion Ketamine can suppress endotoxin-induced NF-kappa B activation. Subanesthetic dose of ketamine has anti-inflammatory action.

Objective:To compare the cardiovascular effects of sufentanyl and fentanyl as combined with propofol in anesthesia during laparoscopic cholecystectomy(LC).Methods:Patients undergoing LC were randomly divided into two groups: 60 patients in the Sufentanyl group(group S,0.3 ?g/kg) and 53 patients in the Fentanyl group(group F,3 ?g/kg).The mean arterial pressure(MAP),heart rate(HR),cardiac output(CO),and cardiac index(CI) were recorded before induction,before pneumoperitoneum,after pneumoperitoneum and at the end of operation.Results:There was no difference in MAP,HR,CO or CI between the two groups before induction.The values of HR and CO increased significantly in group F after preumoperitoneum comparing with the values before preumoperitoneum(P

Esophageal cancer is the leading cause of cancer-related deaths worldwide.A single intraoperative intervention is unlikely to benefit the outcome.A multimodal management plan that includes the use of TEA seems to demonstrate improved results in high-volume centers.Anesthetic management may contribute to the containment of pulmonary morbidity and anastomotic leakage by the use of TEA,protective ventilation strategies during OLV,prevention of tracheal aspiration,and judicious fluid management.

Objective To evaluate the effects of different concentrations of hydroxyethyl starch (HES) 130/0.4 applied for different time periods on injury to human renal tubular epithelial cells.Methods Human renal kidney epithelial cells HK-2 at the logarithmic growth phase were seeded in 96-well plates at a density of 1 × 105 cells/ml (0.1 ml/well),in culture flasks (5 ml/flask) or in cluture dishes (5 ml/dish).HK-2 cells were randomly divided into 4 groups (n=49 each) using a random number table:control group (group C) and 0.3％,1.5％ and 3.0％ HES 130/0.4 groups (H1,H2 and H3 groups).In H1,H2 and H3 groups,HK-2 cells were incubated with 0.3％,1.5％ and 3.0％ HES 130/0.4,respectively.The equal volume of PBS was added to the culture medium in group C.At day 1,3,5 and 7 of incubation,the cell viability was measured.At day 3,5 and 7 of incubation,cell apoptosis was detected,and apoptosis rate was calculated.On day 7 of incubation,the cells were stained with toluidine blue for examination of intracellular HES deposition (under light microscope) and pathological changes (with transmission electron microscope).Results Compared with group C,the cell viability was significantly decreased on day 5 and 7 of incubation,and apoptosis rate was increased on day 3,5 and 7 of incubation in group H3,and no significant difference was detected in the parameters mentioned above in H1 and H2 groups.Microscopic examination showed that intracellular HES deposition was observed in H2 and H3 groups,and pathological changes were obvious,and apoptotic cells were also found in H3 group.Conclusion Application of high-concentration HES 130/0.4 for a long period can lead to injury to human renal tubular epithelial cells,however,application of high-or low-concentration HES 130/0.4 for a short period produces no influence on the cells.

BACKGROUND:Although the mechanism why neuronal cels wil die after transient cerebral ischemia has not been completely elucidated, many researches nowadays have investigated the pathological mechanism in the level of celular organs, such as mitochondria.
OBJECTIVE:To summarize and discuss the functions of neuronal mitochondria and apoptosis signaling pathways in transient cerebral ischemia.
METHODS: A computer-based online retrieval was performed to search papers in CNKI and PubMed databases using the key words of “cerebral ischemia, mitochondrion, apoptosis, reactive oxygen species, reperfusion, superoxide dismutase, nitric oxide synthase, Bcl-2 protein family, review” in Chinese and English, respectively. Papers published recently or in the prestigious journals were selected in the same field. After excluding objective-independent papers and repeated studies, 50 papers were included for further analysis.
RESULTS AND CONCLUSION:Recently mitochondria are found to play an important role after transient cerebral ischemia by producing a lot of reactive oxygen species to activate many kinds of signaling pathways and regulate mitochondria-mediated apoptosis. Reactive oxygen cannot only induce biomacromolecule injury but also induce apoptosis signal transduction. Deeply investigation is needed on the pathological mechanism after transient cerebral ischemia.

Objective To explore the possible mechanism for the neuroprotective effect of ifenprodil by investigating its effects on inducible nitric oxide synthase (iNOS) expression and activity and apoptosis in the ischemic penumbra following focal cerebral ischemia-reperfusion (I/R) in rats.Methods Fifty-four adult male SD rats weighing 280-320 g were randomly divided into 3 groups ( n = 18 each) : I sham operation group (group S) ; II focal cerebral I/R group (group I/R) and Ⅲ ifenpradil preconditioning group (group IF) received intraperitoneal ifenprodil 10 mg/kg before focal cerebral I/R. Focal cerebral I/R was induced by middle cerebral artery occlusion (MCAO) . A 3-0 nylon thread with rounded tip was inserted into right internal jugular vein and threaded cranially until resistance was met. MCAO was maintained for 2 h. At 48 h after reperfusion, the animals were assessed for neurological function which was scored (0 = no functional deficit, 4 = unable to crawl, unconscious) and then decapitated. The brains were immediately removed for microscopic examination and determination of iNOS protein expression and activity, NO content and apoptosis in the ischemic core (IC) and penumbra (IP). Results Ifenprodil pretreatment significantly decreased the cerebral infarct size and neurological scores in group IF as compared with group I/R. In group I/R the iNOS activity was increased compared with group S.The iNOS activity and NO content were significantly lower in IP than in IC in group IR and IF. The TUNEL-positive cells were also mainly confined to IP. Compared with group I/R, in group IF the iNOS protein expression was significantly down-regulated in IC and IP and the iNOS activity and NO content in IC and IP were suppressed and TUNEL-positive cells were significantly reduced in IP. Conclusion Ifenprodil pretreatment has protective effect against cerebral I/R injury by inhibiting iNOS protein expression in IP, suppressing iNOS activity and NO content and reducing apoptosis.