Objective To investigate the analgesic efficacy and spinal neurotoxicity of intrathecal (IT) different doses of dexmedetomidine in rats. Methods Sixty male SD rats weighing 180-220 g were randomly divided into 5 groups ( n = 12 each): groupnormal control (group C); group IT normal saline (group N); different doses of dexmedetomidine groups received IT dexmedetomidine 0.75, 1.50 and 3.00 μg/kg respectively (groups D1.3). Paw withdrawal threshold to mechanical stimulation (PWMT)with yon Frey filaments and tail flick latency (TFL) to a thermal nociceptive stimulus were measured before (To, baseline) and at 30 or60 rin after IT dexmedetomidine or normal saline administration (T1, T2 ) and the percentage of the maximum possible effect ( MPE ) was calculated. Lumbar segment of the spinal cord ( L4-6 ) was removed for microscopic examination and determination of c-Fos expression (by immuno-histochemistry) at 7, 24 and 48 h after IT dexmedetomidine or normal saline administration. Results PWMT, TFL and the percentage of MPE were significantly increased after IT dexmedetomidine as compared with the baseline values at T0 in groups D1-3 ( P ＜ 0.05). PWMT was significantly higher at T1 and TFL and the percentage of MPE were higher at T2 in groups D1-3 than in groups C and N,and in group D3 than in groups D1,2 ( P ＜ 0.05). At 7,24 h after IT dexmedetomidine c-Fos protein expression was significantly higher in group D3 than in groups C and N( P ＜ 0.05). There was no significant difference in c-Fos expression at 48 h after IT dexmedetomidine between group D3 and groups C and N ( P ＞ 0.05 ). At 24 h after IT dexmedetomidine c-Fos protein expression was significantly higher in group D3 than in other 4 groups( P ＜ 0.05). Slight spinal cord injury was observed at 24 h after IT dexmedetomidine in group D3. Conclusion IT dexmedetomidine has antinociceptive effect. High dose dexmedetomidine IT can produce transient reversible toxicity to the spinal cord.

Objective To investigate the effects of ischemic pre- and postconditioning on cerebral glycogen synthase kinase-3 beta (GSK-3β) activity in a rat model of global cerebral ischemia-reperfusion (I/R).Methods Forty male Wistar rats weighing 200-230 g were randomly allocated into 4 groups (n =10 each) : Ⅰ group sham operation (group S); Ⅱ group I/R; Ⅲ group ischemic preconditioning (group IPR) and Ⅳ group ischemic postconditioning (group IPO). The animals were anesthetized with intraperitoneal 10% chloral hydrate 0.4 ml/100 g. Global cerebral ischemia was induced by four-vessel-occlusion in group Ⅱ , Ⅲ and Ⅳ. Bilateral vertebral arteries were cauterized and bilateral carotid arteries were occluded for 10 min. In group IPR cerebral ischemia was preceded by 3 cycles of 10 s ischemia followed by 30 s reperfusion. The group IPO received 3 cycles of 30 s reperfusion followed by 10 s ischemia at the end of 10 min cerebral ischemia. The animals were killed 2 days later. The brains were immediately removed for determination of neuronal apoptosis in the cortex (by TUNEL), the infarct size (by TTC), p-GSK-3β activity (by spectrum assay) and the expression of Bcl-2, Bax and Caspase-3 (by SP). Linear correlation of p-GSK-3β activity with the number of apoptotic neurons in the cortex and cerebral infarct size was analyzed. Results Cerebral I/R significantly increased the number of apoptotic neurons in the cortex and infarct size, decreased p-GSK-3β activity, down-regulated Bcl-2 expression and up-regulated Bax and Caspase-3 expression in group I/R as compared with group S. Ischemic pre- and postconditioning significantly attenuated these cerebral I/R-induced changes. The p-GSK-3β activity was negatively correlated with the number of apoptotic neurons in the cortex and cerebral infarct size. Conclusion Ischemic pre- and postconditioning reduces cerebral I/R injury through inhibiting the activity of GSK-3β.

Objective To evaluate the effects of Janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT3) signaling pathway on the brain injury induced by myocardial ischemia-reperfusion (I/R) in diabetic rats.Methods Pathogen-free male Sprague-Dawley rats,weighing 200-220 g,were used in this study.Diabetes mellitus was induced by intraperitoneal 1％ streptozotocin 60 mg/kg and confirmed by blood glucose level ≥ 16.7 mmol/L 3 days later.Twenty-four rats with diabetes mellitus were randomly allocated into 3 groups (n =8 each) using a random number table:sham operation group (group S),I/R group,and myocardial I/R + AG490 (JAK inhibitor) group (group ⅠA).Myocardial I/R was induced by occlusion of the anterior descending branch of the left coronary artery for 30 min,followed by 120 min of reperfusion in the rats anesthetized with pentobarbital sodium.AG490 3 mg/kg was injected intravenously at 20 min before reperfusion in group IA.The rats were sacrificed at 120 min of reperfusion,and the brains were removed for determination of caspase-3 and nuclear factor kappa B (NF-κB) activities (using colorimetric method),cell apoptosis (by TUNEL),and expression of interleukin-1 (IL-1),IL-6,IL-8,Bax,Bcl-2,cytochrome C (Cyt c),phosphorylated JAK2 (p-JAK2),and phosphorylated STAT3 (p-STAT3) (by Western blot).Apoptosis index was calculated.Results Compared with group S,the expression of Bax,Cyt c,IL-1,IL-6,IL-8,p-JAK2 and p-STAT3 was significantly up-regulated,the expression of Bcl-2 was down-regulated,and NF-κB and caspase-3 activities and apoptosis index were increased in I/R and IA groups (P＜0.05).Compared with group I/R,the expression of Bax,Cyt c,IL-1,IL-6,IL-8,p-JAK2 and p-STAT3 was significantly down-regulated,the expression of Bcl-2 was up-regulated,and NF-κB and caspase-3 activities and apoptosis index were decreased in group IA (P＜0.05).Conclusion Inflammatory responses mediated by JAK2/STAT3 signaling pathway are involved in the brain injury induced by myocardial I/R in diabetic rats.

Objective To investigatc the role of phosphatidylinositol 3-kinase (PI3K)/protein-serine-threonine kinases (Akt) signal pathway in ginsenoside Rb1 pretreatment-induced attenuation of myocardial ischemiareperfusion (I/R) injury in diabetic rats.Methods Male SD rats weighing 250-300 g were used in this study.Diabetes mellitus was induced by intraperitoneal streptozotocin and confirmed by fasting blood glucose ≥ 16.7mmol/L.Eight weeks after diabetes mellitus was induced,48 rats were randomly divided into 4 groups ( n =12each):group myocardial I/R (group I/R); group ginsenoside Rb1 (group R); group ginsenoside Rb1 + wortmannin (PI3K inhibitor) (group RW) and group wortmannin (group W).Myocardial I/R was induced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 120 min reperfusion.Ginsenoside Rb1 40 mg/kg was injected iv at 10 min before ischemia in groups R and RW,while in groups RW and W wortmannin 15 μg/kg was injected iv at 20 min before ischemia.Arterial blood samples were collected at the end of 120 min reperfusion for determination of creatine kinase (CK) and lactate dehydrogenase (LDH) activities.The rats were then sacrificed.The infarct size was measured by tetrazolium method.Myocardial apoptosis was detected by TUNEL and apoptotic index (the number of apoptotic myocardial cells/the total number of myocardial cells) was calculated.The expression of Akt and phosphorylated Akt (p-Akt) was determined by Western blotting.Results Ginsenoside Rb1 pretreatment significantly reduced the infarct size,myocardial cell apoptotic index and serum CK and LDH activities and up-regulated p-Akt expression in group R as compared with group I/R.The protective effects of ginsenoside Rbl against myocardial I/R injury were significantly attenuated by wortmannin pretreatment in group RW compared with group R.Conclusion PI3K/Akt signal pathway is involved in the protective effects of ginsenoside Rb1 against myocardial I/R injury in diabetic rats.

This paper introduced the background, contents, methods and main results, as well as its strategic goals for the next decade and strategic development planning for the next five years. The authors believed that inherent logic, supports from the governments and other authorities as well as the executive power of the hospital in question were the basic factors for the success of its strategic planning and implementation. The authors also held that a package of actions would be conducive to correctly positioning tertiary hospitals and that medical services pricing ought to be rational for the costs, technology and policy guidelines of medical care.

AIM:To study the effects and mechanisms of ethanol on chloride channels in poorly differentiated nasopharyngeal carcinoma CNE-2Z cells.METHODS:The effect of ethanol on the cell growth was analyzed by MTT as-say.The technique of whole-cell patch-clamp was used to detect the chloride current .The characteristics of the chloride current were analyzed by using the chloride channel blockers .The siRNA technique was used to analyze the molecular basis of the ethanol-sensitive chloride channels .RESULTS: Under isotonic conditions , the background current was weak and stable.Ethanol at concentrations of 0.17~170 mmol/L activated a chloride current in a concentration-dependent manner (an inverted U-shape), with a maximum effect at the concentration of 17 mmol/L.The currents showed obviously outward rectification and were susceptible to extracellular hypertonicity and the chloride channel blocker , 5-nitro-2-(3-phenylpropyl-amino) benzoic acid ( NPPB) .ClC-3 siRNA obviously decreased the currents activated by ethanol .CONCLUSION:Ex-tracellular ethanol induces chloride currents through activating the ClC-3 chloride channels .

Objective To observe analgesia effect of morphine hydrochloride and hydromorphone hydrochloride in patients after transurethral resection of prostate. Methods Patients after transurethral resection of the prostate (TURP) were randomly divided into 2 groups, morphine hydrochloride group (n=45) and hydromorphone hydrochloride group (n=47). Analgesia, sedation efficacy and adverse reactions were evaluated at 6 and 24 h after they received epidural postoperative analgesia by using VAS score and Ramsay score. Results In 6 h, hydromorphone hydrochloride group had a better pain tolerance and feeling than morphine hydrochloride group (P<0.05) [(2.9±0.3) score vs.(1.3±0.2) score, (2.4±0.3) score vs. (0.9±0.2) score].However, in 6-12 h, the results were on the contrary (P<0.05) [(3.4±0.3) score vs.(5.4±0.3) score, (3.3±0.2) score vs. (5.7±0.4) score].After 24 h, there was no difference between the two groups (P>0.05).There were no differences in adverse reactions between the two groups ( P>0. 05 ) . Conclusion Hydromorphone has a better effect than morphine in epidural analgesia in 6 h.

Objective To observe the effect of telbivudine combined with adefuvir dipivoxil in the treatment of Hepatitis B patients with decompensated cirrhosis.Methods 56 Hepatitis B patients with decompensated cirrhosis were divided into two groups:treatment group (30 cases) and control group (26 cases).During 24 weeks,the control group received adefuvir dipivoxil( 10mg daily),supportive and symptomatic treatments,while the treatment group received telbivudine therapy(600mg daily) combiled with adefuvir dipivoxil ( 10mg daily) based on the regular treatments.After 24 weeks,the effect was observed and compared between the two groups.Results After treatment,the biochemical markers,Child-Pugh score of the treatment group was (33.2 ± 13.8) μmol/L,(44.5 ± 16.4) U/L,(36.1 ±1.5) g/L,(6.1 ± 1.8) points,respectively,and was better than those of the control group[ (71.8 ±18.6) μ mol/L,(89.9 ±44.9) U/L,(29.7 ± 1.3)g/L,(8.1 ±2.2) points] (t=15.32,15.20,23.37,6.09,all P＜0.05) ;HBV-DNA negative rate,HBeAg seroconversion rates of the treatment group was 93.3％ (28/30),43.3％(13/30),and was higher than that of the control group[76.9％ (20/26),7.6％ (2/26) ] (x2 =4.87,9.08,all P＜0.05).Conclusion Telbivudine combined with adefuvir dipivoxil was effective and safe for the treatment of Hepatitis B patients with decompensated cirrhosis.

AIM:To investigate the type of chloride channel activated by cisplatin in poorly differentiated na -sopharyngeal carcinoma cells (CNE-2Z cells).METHODS:The technique of whole-cell patch-clamp was used to investi-gate the role of Ca 2+in the activation of cisplatin-activated chloride currents and to analyze the effect of hypertonic stress on these currents in CNE-2Z cells.RESULTS:Chloride currents were induced when the cells were exposed to the calcium -free cisplatin solution , showing the similar density to the currents induced by cisplatin with the presence of extracellular cal -cium.However , the latency and the peak time of cisplatin-activated currents in the absence of extracellular calcium were prolonged.The activation of cisplatin-activated chloride currents was insensitive to the depletion of intra-and extracellular calcium.Calcium channel antagonist nifedipine had no effect on the cisplatin -activated chloride currents , while hypertonic solution completely inhibited those currents .CONCLUSION:The cisplatin-activated chloride currents are independent on intra/extracellular calcium .The chloride channels activated by cisplatin are not calcium-activated chloride channels , but are probably volume-sensitive chloride channels .

BACKGROUND:Bone marrow mesenchymal stem cel s transplantation can inhibit experimental emphysema inflammatory reaction and apoptosis, and has been experimental y confirmed to treat severe lung function impairment. OBJECTIVE:To explore the inhibitory effects of bone marrow mesenchymal stem cel s transplantation via different ways on inflammatory reaction and apoptosis due to experimental emphysema. METHODS:Female Wistar rats were randomly divided into control group, intravenous group and endotracheal group fol owing model establishment using fumigation plus intratracheal instil ation of porcine pancreatic elastase. In the latter two groups, bone marrow mesenchymal stem cel s from male rats were injected via the tail vein and the trachea, respectively. In the control group, rats were given PBS via he tail vein and trachea. At 14 days after transplantation, pathological changes of rat lung tissues were observed, cel apoptotic index in alveolar wal cel s and tumor necrosis factorαlevel in the bronchoalveolar lavage fluid were detected. RESULTS AND CONCLUSION:Compared with the control group, in the intravenous and endotracheal groups,the pathological changes of lung tissues were relieved, tumor necrosis factorαlevel and apoptosis index were reduced significantly (P<0.01);but there were no differences between the intravenous and endotracheal groups (P>0.05). These findings indicate that bone marrow mesenchymal stem cel s transplantation via the tail vein and trachea both can exert obvious therapeutic effects on emphysema. Moreover, cel transplantation via the tail vein is more convenient and easier than that via the trachea in the treatment of emphysema.