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 investigate the effect of different doses of dexmedetomidine(Dex)on sevoflurane consumption in patients undergoing laparoscopic oophorocystectomy.Methods Eighty ASA Ⅰ or Ⅱ patients aged 25-50 yr with body mass index 18-25 kg/m2 undergoing laparoscopic oophorocystectomy were randomly divided into 4 groups (n =20): control group (group C),low dose Dex group(group DL),medium dose Dex group(group DM) and high dose Dex group(group DH).Normal saline 20 ml and Dex 0.3,0.6,0.9μg/kg was infused iv over 10 min at 10 min before skin incision in groups C,DL,DM and DH,respectively.End-tidal sevoflurane concentration (ETsev) was recorded before Dex administration(T1 ),skin incision(T2 ),immediately after pneumoperitoneum (T3 ),10 min of pneumoperitoneum(T4 ) and the end of surgery (T5 ).Duration of anesthesia,consumption of sevoflurane,emergence time,extubation time were recorded and restlessness at 10 min after extubation was also recorded.The concentrations of blood glucose and corticosteroid were measured by quickly by glucose analyzer and radio-immunity gefore anethesia induction (T0) and at T3,T4,T5 respectively.Results The consumption of sevoflurane per hour,ETsev at T2-5,concentrations of blood glucose and corticosteroid at T3-5 were decreased gradually in groups C,DL,DM and DH ( P ＜ 0.05).The emergence time and extubation time were shorter and the incidence of restlessness was lower in groups DL,DM and DH than in group C ( P ＜ 0.05 ).Conclusion Dexmedetomidine can reduce the consumption of sevoflurane in a dose-dependent manner in patients undergoing laparoscopic oophorocystectomy.

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.

BACKGROUND:Valgus knee deformity is rare in the clinic. The therapeutic effects of artificial knee arthroplasty are worse than varus knee deformity. There is no unified opinion for replacement approach, soft tissue release method and procedure and prosthetic choice at present.
OBJECTIVE:To summarize case data and to observe clinical effects of total knee arthroplasty for valgus knee deformity.
METHODS:Clinical data of 37 cases of valgus knee deformity (42 knees) undergoing total knee arthroplasty, who were treated by the same group of physicians in the First Department of Orthopedics, Gansu Provincial Hospital of Traditional Chinese Medicine from January 2010 to December 2012 were retrospectively analyzed. There were 11 males (13 knees) and 26 females (29 knees), at the age from 56 to 78 years, with an average age of 63.7 years. The differences in range of motion, femorotibial angle and Hospital for Special Surgery knee score were compared before and after replacement. Clinical effects of total knee arthroplasty for valgus knee deformity were evaluated.
RESULTS AND CONCLUSION:The postoperative fol ow-up lasted from 6 to 36 months. Knee joint range of motion increased from preoperative 68.5° to an average of postoperative 108.5°. Femorotibial angle reduced from preoperative 16.82° to postoperative 5.62° on average. The average Hospital for Special Surgery knee score increased from preoperative 39 points to postoperative 88 points (P<0.05). These results suggested that the curative effect of total knee arthroplasty for valgus knee deformity is proved. Total knee arthroplasty is an effective way to improve deformity.

Objective To preliminarily evaluate the role of Ras homolog gene (Rho)/Rho-associated coiled coil-forming protein kinase (ROCK) signaling pathway in propofol-induced inhibition of metastasis of human gastric cancer cells.Methods Human gastric cancer MKN-45 cells cultured in vitro,with the concentration of 1.0× 106 cells/ml,were seeded in culture plates,and incubated for 24 h.The plates were then randomly divided into 4 groups using a random number table:control group (group C),propofol group (group P),lysophosphatidic acid group (group L) and propofol + lysophosphatidic acid group (group PL).Group C received no administration.In group P,propofol at the final concentration of 16 μg/ml was given.In group L,lysophosphatidic acid at the final concentration of 1 μmol/L was administered.In group PL,propofol and lysophosphatidic acid were given with the final concentration of 16 μg/ml and 1 μmol/L,respectively.All the cells were then incubated for another 24 h.The migration of cells was determined by wound healing assay,and cell migration rates were calculated.The invasion of cells was determined by Transwell assay,and the invaded cells were counted.The expression of matrix metalloproteinases-2 (MMP-2),MMP-9,RhoA,and ROCK1 in cells was detected by Western blot.Results Compared with group C,cell migration rates and the number of invaded cells were significantly increased,and the expression of MMP-2,MMP-9,RhoA and ROCK1 was up-regulated in group L,and cell migration rates and the number of invaded cells were decreased,and the expression of MMP-2,MMP-9,RhoA and ROCK1 was down-regulated in group P.Compared with group L,cell migration rates and the number of invaded cells were significantly decreased,and the expression of MMP-2,MMP-9,RhoA and ROCK1 was down-regulated in group PL.Conclusion Inhibition of RhoA/ROCK1 signaling pathway is involved in the mechanism by which propofol decreases metastasis of human gastric cancer cells.

Objective To evaluate the effect of propofol on invasiveness of human gastric cancer MKN-45 cells.Methods Human gastric cancer cell line MKN-45 were seeded in culture plates.After being cultured for 24 h,the cells were randomly divided into 5 groups(n =12 each):control group (group C),intralipid group (group Ⅰ),4 μg/ml propofol group (group P1),8 μg/ml propofol group (group P2) and 16μg/ml propofol group (group P3).The cells were treated with 10％ intralipid and 4,8 and 16 μg/ml propofol for 24 h in I and P1-3 groups,respectively.The cells were then cultured for another 24 h.The migration of cells was determined by cell scratch test.The invasion of cells was determined by Transwell invasion assay.The expression of RhoA and ROCK1 was detected by Western blot.Results Compared with group C,the cell migration and invasion were significantly decreased,and the expression of RhoA and ROCK1 was down-regulated in P1-3 groups,and no significant changes were found in the parameters mentioned above in group Ⅰ.With the increasing concentrations of propofol,the cell migration and invasion were gradually decreased,and the expression of RhoA and ROCK1 was gradually down-regulated in P1-3 groups.Conclusion Propofol can inhibit the invasiveness of human gastric cancer MKN-45 cells cultured in vitro dose-dependently and inhibition of RhoA/ROCK1 signaling pathway may be involved in the mechanism.

Objective To evaluate the role of interleukin-4 receptor (IL-4R) in renal fibrosis following renal ischemia-reperfusion (I/R) injury in mice.Methods Twelve male wild type BALB/C mice and 12 IL-4Rα gene-knockout mice,aged 8-10 weeks,weighing 20-30 g,were used in the study.The mice of either type were divided into 2 groups (n =6 each) using a random number table:sham operation group (group S) and group I/R.In group I/R,renal I/R was induced by occlusion of the right renal artery for 1 h with atraumatic microclips followed by 2 weeks of reperfusion.The right renal artery was only isolated in group S.At 2 weeks of reperfusion,blood samples were taken from the orbital vein for determination of the concentrations of serum blood urea nitrogen (BUN) and creatinine (Cr).The renal tissues were obtained,and the renal fibrosis area was measured by Sirius Red staining.The expression of fibronectin (FN),collagen Ⅰ (COL-Ⅰ) and α-smooth muscle actin (α-SMA) in renal tissues was detected by immunofluorescence.The expression of signal transducer and activator of transcription 6 (STAT6) and phospho-STAT6 in renal tissues was determined by Western blot.The ratio of phoshop-STAT6 to STAT6 was calculated to reflect the phosphorylation of STAT6.Results Compared with group S of wild type mice,the serum BUN and Cr concentrations and renal fibrosis area were significantly increased,the expression of FN,COL-Ⅰ and α-SMA in renal tissues was significantly up-regulated,and the phosphorylation of STAT6 in renal tissues was significantly increased in group I/R of wild type and IL-4Rα KO mice (P＜0.05).Compared with group I/R of wild type mice,the serum BUN and Cr concentrations and renal fibrosis area were significantly decreased,the expression of FN,COL-Ⅰ and α-SMA in renal tissues was significantly down-regulated,and the phosphorylation of STAT6 in renal tissues was significantly decreased in group I/R of IL-4RαKO mice (P＜0.05).Conclusion The mechanism of renal fibrosis following renal I/R injury is partially related to IL-4R,and IL-4R results in renal fibrosis through promoting activation of STAT6 signaling pathway in mice.

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 dexmedetomidine on the cellular immune function of the rats with scald.Methods Seventy-two healthy male Sprague-Dawley rats,weighing 200-220 g,aged 120-150 days,were randomly divided into 3 groups (n =24 each):normal control group (group C),scald group (group S) and dexmedetomidine group (group D).Thirty percent of the total body surface was shaved and then exposed to 94 ℃ water for 12 s in S and D groups.The rats were resuscitated according to Parkland formula after scald in S and D groups,and in addition,dexmedetomidine 30 μg/kg was also intraperitoneally injected immediately after scald in D group.Before the model was established (T1) and at 12 and 24 h after scald (T2,3),blood samples from the inferior vena cava were collected for determination of T lymphocyte subsets CD3 +,CD4 + and CD8 +,NK cell,C-reactive protein (CRP),interleukin-6 (IL-6),IL-10 and tumor necrosis factor-alpha (TNF-α) level.CD4+/CD8+ was calculated.Arterial blood samples were collected for blood gas analysis.Results Compared with C,the CD3+,CD4+ and NK cell levels,CD4+/CD8+,pH value,PaCO2 and PaO2 were significantly decreased,and CD8+ levels,IL-6,IL-10,TNF-α,CRP and BE negative value were increased at T2,3 in S and D groups.Compared with group S,the CD3+,CD4+,NK cell and IL-10 levels,CD4+/CD8+,pH value,PaCO2 and PaO2 were significantly increased,and CD8+ levels,IL-6,TNF-α,CRP and BE negative value were decreased at T2,3 in group D.Conclusion Dexmedetomidine can improve the cellular immune function of the rats with scald.

Objective To investigate the effects of intrathecal(IT)CX3 CR1 neutralizing antibody(antiFKR)on morphine tolerance in rats with bone cancer pain(BCP)and the unlerlying mechanism.Methods Forty-eight adult female SD rats aged 3 months weighing 180-200 g were randomized into 4 groups(n =12 each):group I sham operation(S); group Ⅱ BCP + normal saline(NS); group Ⅲ BCP + IgG(IgG)and group ⅣBCP + anti-FKR.Bone cancer pain(BCP)was induced by injecting Walker 256 cancer cells 10 μl(400 cells/ μl)into the medullary cavity of right tibia in groups Ⅱ,Ⅲ and Ⅳ.Ten days later morphine 20 μg/kg was administered IT twice a day for 7 consecutive days.Starting from the 8th day NS,IgG and anti-KFR 10 μl was administered IT once a day for 3 consecutive days in groups Ⅱ,Ⅲ and ⅣⅣ respectively.Paw withdrawal threshold to yon Frey filament stimulation(MWT)and paw withdrawal duration(MWD)were determined bcfore(To,baseline)and at 3,6,9 day after intra-tibial cancer cell inoculation(T1.2,3),on the 3rd and 7th day of IT morphine(T4.5)and on the 3rd day of IT NS/lgG/anti-KFR(T6).The animals were killed at T6 after last pain behavior assessment.The lumbar segment(L4-6)of the spinal cord was removed for determination of the expression of CX3 CR1 protein(by Western blot),μ-opioid receptor and TRPV1 receptor(by immuno-histochemistry)in the dorsal horn of spinal cord.Results IT morphine significantly eased BCP at T4,but morphine analgesia was significantly reduced on the 7th day of IT morphine in the 3 groups indicating morphine tolerance which was significantly relieved by anti-KFR in group Ⅳ.IT anti-KFR significantly down-regulated CX3CR1 prolein and TRPVI receptor expression and up-regulated μ-opioid receptor in group Ⅳ as compared with IT NS and lgG in groups Ⅱ and Ⅲ.Conctusion IT anti-KFR can relieve morphine tolerance in the rats with bone cancer pain by up-regulating μ-opioid receptor and down-regulating CX3 CR1 protein and TRPVI receptor expression.