ObjectiveTo investigate the role of T-type calcium channel in the spinal neurotoxicity of intrathecal (IT) lidocaine in rats.MethodsForty-eight adult male SD rats in which IT catheter was successfully implanted,weighing 230-270 g,were randomly divided into 4 groups ( n =12 each):dimethyl sulfoxide (DMSO)group (group D),lidocaine group (group L),mibefradil + lidocaine group (group M),normal saline + lidocaine group (group N).Another 12 rats served as control group (group C).DMSO and 10％ lidocaine 20μl were injected intrathecally in groups D and L respectively.After mibefradil 200 μg/10μl and normal saline 10 μl were injected intrathecally in groups M and N respectively,10％ lidocaine 20 μl was injected intrathecally in the two groups.The mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were measured before IT injection and at 2,4,8 and 12 h and 1,2,3,4 and 5 d after IT injection (T0-9).Four rats were sacrificed at T6 in each group and their lumbar enlargements were removed for microscopic examination.ResultsCompared with group C,no significant change in MWT and TWL was found at each time point in group D,MWT was significantly increased at T1-8 and TWL was significantly prolonged at T1-7 in groups L and N,and MWT was significantly increased at T1-6 and TWL was significantly prolonged at T1-6 in group M ( P ＜ 0.05 ).Compared with groups L and N,MWT was significantly decreased at T1-4 and TWL was significantly shortened at T1-4 in group M ( P ＜ 0.05).Pathological injury was significantly reduced in group M as compared with groups L and N.ConclusionT-type calcium channel is involved in the spinal neurotoxicity of IT lidocaine in rats.

Objective To compare the quality of emergence from TCI of sufentanil and remifentanil supplementing propofol-sevoflurane anesthesia in patients undergoing radical colo-rectal cancer resection.Methods Forty ASA Ⅰ or Ⅱ patients of both sexes aged 40-64 yr undergoing elective radical colo-rectal cancer resection were allocated into 2 groups ( n =20 each):sufentanil group (group S) and remifentanil group (group R).Anesthesia was induced with propofol TCI at plasma concentration (Cp) of 4.0 μg/ml in both groups and sufentanil TCI (effect-site concentration Ce =0.4 ng/ml ) or remifentanil TCI ( Cp =4.0 ng/ml).Tracheal intubation was facilitated with vecuronium 0.1 mg/kg.The patients were mechanically ventilated (VT =8-10 ml/kg,RR =12-16 bpm).PErCO2 was maintained at 30-40 mm Hg.Anesthesia was maintained with propofol TCI-sevoflurane supplemented with sufentanil (Ce=0.25 ng/ml) or remifentanil (Cp=2.5 ng/ml).The depth of anesthesia was maintained at Narcotrend index of 37-56 by adjusting Cp of propofol TCI and sevoflurane concentration.The infusion of sufentanil was discontinued at 40 min before the conclusion of the operation while remifentanil was administered until the end of surgery.The incidence of postoperative adverse events,the time from the end of operation to eye openg and the time to extubation were recorded.Reesults The two groups were comparable with respect to demographic data.Neither group developed prolonged emergence and respiratory depression but the time from the end of operation to eye opening and the time to extubation were significantly longer in group S than in group R.The incidence of hypertension and tachycardia,agitation,shivering aad coughing were significantly lower in group S than in group R.Conclusion The quality of emergence from sufentanil supplementing propofol-sevoflurane anesthesia is higher than that from remifentanil.

Objective To study the effect of IL-8 on cell proliferation and invasion,and to analyze the correlations between chemokine and epidermal growth factor receptor(EGFR)signaling pathways in breast carcinoma cells.Methods IL-8 secretion responded to treatment with rhEGF and anti-EGFR and expression of its receptors CXCR1,CXCR2 in MDA-231 cells were measured by ELISA and immunocytochemistry,respectively.Effect of rhIL-8 and neutralizing antibody on cell proliferation and invasion were analyzed by using MTT and matrigel invasion assay.EGFR transactivation stimulated with rhIL-8 and neutralizing an tibody was assessed by Western blot using anti-phosphotyrosine antibody.Results MDA-231 cells released hish level of IL-8 and two receptom of IL-8(CXCR1 and CXCR2)both expressed on cell membrane.Exogenous IL-8 and its neutralizing antibody did not significantly influence the proliferation of breast carcinoma cells,but rhIL-8 stimulated invasive activity in MDA-231 cells and its neutralizing antibody inhibited the in vasive activity(P＜0.05).EGF and anti-EGFR both inhibited the secretion of IL-8 in breast carcinoma cells,and IL-8 had no effect on EGFR phosphorylation,but anti-IL-8 induced transactivation of EGFR after 24h.Conclusion IL-8 contributes to tumor progression in breast carcinoma through its enhancement of in vasive activitv but not act as an autocrine growth factor.The correlation of competitive inhibition rather than cross-talk is found between G protein coupled receptor(GPCR)-mediated IL-8 signaling pathway and EGFR pathway in breast carcinoma.

Objective To evaluate the use of laparoscopic operation in gynecological acute disease. Methods 56 cases of gynecological acute disease patients were treated with different laparoscopic operation according to pathogenetic condition. Results All were exelcymosised urinary canal, liquid diet, out-of-bed actived 6h post operation, ambulation 10h later,no infective fever,postoperative hospital stay 3～5d[mean (3.3?1.1d)] and incisal opening healing well. Conclusion Laparoscope is an effective and safe operation in gynecological acute disease.

Objective To evaluate the effects of the right stellate ganglion block on the expression of β3adrenoceptor (β3-AR) in rabbits with heart failure.Methods Forty-eight Japanese white rabbits of both sexes,weighing 2.5-3.0 kg,were randomly divided into 3 groups (n =16 each):sham operation group (group S),heart failure group (group HF) and right stellate ganglion block group (group RSGB).Heart failure was induced by occlusion of left anterior descending branch of coronary artery and confirmed by ultrasonic cardiography 4 weeks later.A PE-10 catheter was inserted into the right stellate ganglion for administration of drugs.0.25％ bupivacaine 2 ml was injected through the catheter once a day for 2 weeks in group RSGB,while the equal volume of normal saline was injected instead of bupivacaine in S and HF groups.The left ventricular end-diastolic diameter (LVEDD),left ventricular end-systolic diameter (LVESD),ejection fraction (EF) and left ventricular fractional shortening (LVFS) were measured at 1 day before ligation (T0),before catheter insertion (T1),before 8th administration (T2),and 1 day after the last administration (T3).Eight rabbits were sacrificed at T1 and T3 in each group and myocardial specimens were obtained from the apex of the left ventricle for determination of the expression of β3-AR by Western blot.Results Compared with group S,the LVEDD and LVESD were significantly enlarged and LVEF and LVFS were decreased at T1-3,and the expression of β3-AR was up-regulated at T1,3 in groups HF and RSGB (P ＜ 0.05).Compared with group HF,the LVEDD and LVESD were significantly decreased,LVEF and LVFS were increased,and the expression of β3-AR was significantly down-regulated at T3 in group RSGB (P ＜ 0.05).Conclusion The right stellate ganglion block can improve the cardiac function of rabbits with heart failure through down-regulating the expression of β3-AR in myocardium.

Objective To evaluate the effects of curcumin preconditioning on the activity of xanthine oxidase (XOD) during intestinal ischemia-reperfusion (I/R) in rats.Methods Thirty female Sprague-Dawley rats,aged 180-220 g,were randomly divided into 3 groups (n =10 each) using a random number table:sham operation group (S group),intestinal I/R group (I/R group),and curcumin preconditioning group (Cur group).Intestinal I/R was induced by clamping the superior mesenteric artery for 75 min followed by reperfusion.Curcumin 200 mg/kg was given everyday for 5 days before intestinal I/R in Cur group and the equal volume of normal saline was given instead of curcumin in S and I/R groups.The rats were sacrificed at 4 h of reperfusion and the intestinal specimens were obtained for microscopic examination of pathologic changes which were graded using Chiu scoring system and for determination of XOD activity,content of malondialdehyde (MDA),and superoxide dismutase (SOD) activity.Results Compared with S group,the Chiu score,activity of XOD and content of MDA were significantly increased,while the activity of SOD was decreased in I/R and Cur groups (P ＜ 0.05).Compared with I/R group,the Chiu score,activity of XOD and content of MDA were significantly decreased,and the activity of SOD was increased in Cur group (P ＜ 0.05).Conclusion Curcumin preconditioning can attenuate intestinal I/R injury in rats,which may be due to inhibition of XOD activity and decreased oxidative stress in intestinal tissues.

Objective To evaluate the role of C-Jun N-terminal kinase (JNK) signal transduction pathway in spinal neurotoxicity induced by lidocaine in rats.Methods Seventy-two adult male Sprague-Dawley rats,weighing 220-260 g,were randomly divided into 6 groups (n =12 each):control group (group Ⅰ),sham operation group (group Ⅱ),JNK inhibitor group (group Ⅲ),dimethyl sulfoxide (DMSO) group (group Ⅳ),lidocaine group (group Ⅴ),and JNK inhibitor and lidocaine group (group Ⅵ).Group Ⅰ received no treatment.Intrathecal catheter was placed in the subarachnoid space in group Ⅱ.SP600125 25 μg and DMSO 20 μl were injected intrathecally in Ⅲ and Ⅳ groups,respectively.In group Ⅴ,10％ lidocaine 20 μl was intrathecally injected.SP600125 25 μg was injected intrathecally and 30 min later 10％ lidocaine 20 μl was injected intrathecally in group Ⅵ.Paw withdrawal threshold to yon Frey filament stimulation (PWT) and paw withdrawal latency to nociceptive thermal stimulation (PWL) were measured before intrathecal catheter was implanted (T0),before intrathecal administration (T1) and at 4,8 and 12 h and on 1,2,3,4,5 and 6 days after intrathecal administration (T2-10).At 24 h after intrathecal administration,4 rats were randomly chosen from each group and sacrificed.Their lumbar enlargements were removed for determination of phosphorylated JNK (p-JNK) expression (using Western blot) and neuronal apoptosis (by TUNEL).The apoptotic index was calculated.Results Compared with group Ⅰ,no significant difference was found in MWT and TWL in Ⅱ,Ⅲ groups and expression of p-JNK in Ⅱ and Ⅳ groups (P ＞ 0.05),MWT at T2-4,6-8 and TWL at T2-4,7 in group Ⅴ and MWT at T2-6 and TWL at T2-5 in group Ⅵ were significantly increased,the expression of p-JNK was down-regulated and the apoptotic index was decreased in group Ⅲ (P ＜ 0.05),and the expression of p-JNK was up-regulated and the apoptotic index was increased in Ⅴ and Ⅵ groups (P ＜ 0.05).Compared with group Ⅴ,MWT and TWL were significantly decreased,the expression of pJNK was down-regulated and the apoptotic index was decreased in group Ⅵ (P ＜ 0.05).Conclusion Activation of JNK signal transduction pathway is involved in spinal neurotoxicity induced by lidocaine in rats possibly through promoting neuronal apoptosis in the spinal cord.

Objective To evaluate the effects of intrathecal TRESK gene recombinant adenovirus on inflammatory responses mediated by chemokine in the spinal cord of rats with neuropathic pain ( NP ) . Methods Thirty?six male Sprague?Dawley rats, weighing 200-250 g, were randomly divided into 6 groups (n=6 each) using a random number table: control group (group C); sham operation group (group S);NP group; TRESK?overexpressed adenovirus group ( group TRESK ); negative adenovirus group ( group Virus); normal saline group ( group NS) . Spinal nerve injury was produced by exposing the sciatic nerve and its branches and ligation and transection of tibial nerve and common fibular nerve in anesthetized rats. In TRESK, Virus and NS groups, pAd∕CMV∕V5?DEST?TRESK 25 μl (109IU∕ml), negative adenovirus 25 μl and normal saline 25 μl were intrathecally injected, respectively. At 1 day before operation ( base?line, T0 ) and 1, 3, 7 and 14 days after operation ( T1-4 ) , the mechanical paw withdrawal threshold ( MWT) and thermal paw withdrawal latency were measured. Six rats in each group were sacrificed after measurement of pain threshold at T3 . The L4,5 segments of the spinal cords were removed for determination of monocyte chemotactic protein?1 ( MCP?1) , MIP?2, tumor necrosis factor?alpha ( TNF?α) , interleukin?1 beta ( IL?1β) and IL?6 mRNA expression by real?time PCR. Results There was no significant difference in thermal paw withdrawal latency at each time point between groups. Compared with C and S groups, MWT at T1-4 in NP and TRESK groups and at T1-3 in Virus and NS groups were significantly decreased, and the expression of MCP?1, MIP?2, TNF?α, IL?1βand IL?6 mRNA was up?regulated in NP, TRESK, Virus and NS groups. Compared with group NP, MWT was significantly increased at T1-4, and the expres?sion of MCP?1, MIP?2, TNF?α, IL?1β and IL?6 mRNA was down?regulated in group TRESK. Conclusion The mechanism by which intrathecal TRESK gene recombinant adenovirus reduces NP is re?lated to inhibition of inflammatory responses mediated by chemokine in the spinal cord of rats.

Objective To evaluate the effects of sufentanil and morphine on cisplatin-induced acute kidney injury in rats.Methods Thirty-two healthy Sprague-Dawley rats, aged 8-10 weeks, weighing 220-280 g, were randomly divided into 4 groups (n =8 each) using a random number table: control group (group C);cisplatin group (group Cis);sufentanil group (group S);morphine group (group M).Cisplatin 16 mg/kg was injected intraperitoneally in group Cis.In group S, cisplatin 16 mg/kg was injected intraperitoneally, followed by injection of sufentanil 2 μg/kg over 5 min via the caudal vein for 3 consecutive days.In group M, cisplatin 16 mg/kg was injected intraperitoneally, followed by injection of morphine 2 μg/kg over 5 min via the caudal vein for 3 consecutive days.The equal volume of normal saline was given in group C.After the end of administration on 3rd day, blood samples were collected from the orbital venous plexus for measurement of serum blood urea nitrogen (BUN) and creatinine (Cr) concentrations.The animals were then sacrificed, and the left kidney specimens were obtained for examination of the pathological changes (under the light microscope) and for determination of the tumor necrosis factor-alpha (TNF-α) , interleukin-1 beta (IL-1β) and interleukin-6 (IL-6) concentrations (by enzyme-linked immunosorbent assay) , and expression of X-linked inhibitor of apoptosis protein (XIAP) , suvivin and caspase-3 (by Western blot).Periodic acid-Schiff's staining was used to evaluate the pathological changes of the renal tubule.Results Compared with group C, the serum BUN, Cr concentrations and renal tubule injury score were significantly increased, the contents of TNF-α, IL-1β and IL-6 were increased, the expression of XIAP and suvivin was down-regulated, and the expression of caspase-3 was up-regulated in Cis,S and M groups (P＜0.05).Compared with group Cis, the serum BUN and Cr concentrations and renal tubule injury score were significantly decreased, the contents of TNF-α, IL-1β and IL-6 were decreased, the expression of XIAP and suvivin was up-regulated, and the expression of caspase-3 was down-regulated in S and M groups (P＜0.05).There were no significant differences in the indexes mentioned above between group S and group M (P＞0.05).Conclusion Both sufentanil and morphine can reduce cisplatin-induced acute kidney injury in rats with similar efficacy, and the mechanism may be related to the inhibition of the inflammatory responses and cell apoptosis.