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.

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 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 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 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 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 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.

ObjectiveTo establish a rat model of nerve damage induced by intrathecal(IT) lidocaine.MethodsFifty-five adult male SD rats weighing 200-220 g were randomly divided into 5 groups (n =11 each):group normal control (group C); group dimethyl sulfoxide (DMSO)-the solvent(group D) and groups IT 5％,10％,15％ lidocaine (groups L5.10.15 ).IT catheter was successfully implanted without complication in groups D,L5,L1o,L15.DMSO,5％,10％ and 15％ lidocaine 20 μl were injected IT in groups D,L5,L10,L15 respectively.Motor dysfunction of hindlimb was assessed and scored (0 =normal,2 =complete block) and paw withdrawal threshold to mechanical stimulation (von Frey filaments) (MWT) and paw withdrawal latency to thermal nociceptive stimulus (TWL) were measured before (baseline) and at 1,2,3,4,5,7 d after IT administration in 8 animals in each group.Three animals in each group were sacrificed at 1 d after IT administration.The lumbar segment (L4-5) was removed for microscopic examination.ResultsThere was no significant difference in motor dysfunction score,MWT and TWL among groups C,D and L5.MWT was significantly increased and TWL prolonged at 1 and 2 d after IT administration in group L10,while in group L15 motor dysfunction score was significantly increased at 1,2 d after IT administration and MWT was significantly increased and TWL prolonged at 1,2,3 d after IT administration.There was significant histologic damage to spinal cord in groups L10 and L15.Conclusion Nerve damage can be induced by IT 10％ lidocaine.

Objective To investigate the variation of the thioredoxin system (Trx),and the role of it in transient out-ward potassium current (Ito) channels in left ventricular myocytes of diabetes mellitus (DM) in rats. Methods Forty-five SD rats were divided into DM group and control group. DM group were treated with streptozotocin (STZ) to induce DM model. The values of left ventricular end diastolic diameter (LVEDD), end-systolic diameter (LVESD), fractional shortening (LVFS), ejection fraction (LVEF) and heart rate (HR), QRS duration and corrected QT (QTc) interval were detected by echocardiogra-phy (UCG) and electrocardiogram (ECG) in two groups. The left ventricular myocardial tissue samples were taken to detect the Trx,glutaredoxin (GRX),thioredoxin reductase (TrxR) and glutathione reductase (GR) by using UV spectrophotometer. The level of free thiol (P-SH) of total cardiac protein was detected by 5, 5′-dithio-bis-2-nitrobenzoic acid method. Ito of the cardiomyocytes was recorded by whole-cell patch-clamp method. After being incubated in vitro with insulin(Ins), treated with TrxR inhibitor-auranofin(AF) and 13-cis-retinoic acid(RA), the changes of Ito of the cardiomyocytes were observed. Results Compared with control group, the values of heart rate (HR), left ventricular minor axis decurtaion rate (LVFS), left ventricular ejection fraction (LVEF) and TrxR were lower in DM group. The values of LVEDD, LVESD, QRS and QTc inter-vals, Trx, Grx and P-SH were higher in DM group than those of control group. Ito density was significantly higher in DM+Ins group than that of DM group, Ins+RA group and Ins+AF group when the stimulation voltage ≥ 0 mV (P ＜ 0.05). Conclusion The impaired Trx system in diabetic rat myocardium was the electrophysiological basis of the reduced ventric-ular function and arrhythmia. And Ins was able to reverse the decreased Ito of cardiomyocytes in DM rats.