Objective To evaluate the anatomical factor and risk assessment of right internal jugular vein (IJV) puncture-related damage to the vertebral artery (VA) at different neck planes in pediatric patients.Methods Two hundred and ten pediatric patients of both sexes,aged 6 months-10 yr,with body mass index less than 28 kg/m2,undergoing elective surgery,were enrolled in this study.At the cricoid cartilage plane,supraclavicular area plane and intermediate plane,the right IJVs and VAs were examined using ultrasound.The VA position relative to the IJV,diameters of IJVs and VAs (the diameter ratio of VAs to IJVs was calculated),extent of overlap between IJVs and VAs,and horizontal and vertical distance from VAs to IJVs were recorded,and the risk coefficient of accidental VA puncture was calculated.Results Ninety-seven percent of VAs lay deep and lateral to right IJVs.There was no significant difference in each parameter of VA position relative to IJVs between the three planes (P＞0.05).The diameter ratio of VAs to IJVs was decreased with the decreasing neck plane,the horizontal and vertical distance from VAs to IJVs was significantly shortened,the overlapping rate between VAs and IJVs was increased,and the risk coefficient of accidental VA puncture was increased (P＜0.05 or 0.01).The vertical distance from VAs to IJVs was not correlated with age,body weight or height (P＞0.05).The risk coefficient of VA damage was not correlated with age,body weight or height at the cricoid cartilage plane and intermediate plane (P ＞ 0.05).The risk coefficient of VA damage was positively correlated with the weight of pediatric patients at the supraclavicular area plane (P＜0.05,r=0.215).Conclusion Right VAs come nearer IJVs with the decreasing neck plane;the risk of VA damage increases gradually with the lowering of neck planes in pediatric patients.

Objective To evaluate the effect of resveratrol on the cognitive function after isoflurane anesthesia in obese rats.Methods Sixty SPF healthy male Sprague-Dawley rats,aged 4 weeks,weighing 70-80 g,were divided into 4 groups (n=15 each) using a random number table:normal diet plus 30％ O2 group (group N+O),high-fat diet plus 30％ O2 group (group H+O),high-fat diet plus 2％ isoflurane group (group H+I),and reveratrol plus high-fat diet plus 2％ isoflurane group (group R+H+I).Rats were fed a normal diet for 8 weeks in N+O group,while animals were fed a high-fat diet for 8 weeks in H+O,H+I,and R+H+I groups.Starting from 9th week,reveratrol 40 mg · kg-1 · d-1 was given into the stomach through a gastric tube for 7 consecutive days in group R+H+I,while the equal volume of 1％ carboxymethyl cellulose sodium was given instead of reveratrol in the other groups.After the end of drug intervention,animals were exposed to the mixture of 70％ nitrogen and 30％ oxygen for 4 h in N+O and H+O groups or to 2％ isoflurane for 4 h in H+I and R+H+I groups.Ten rats were randomly selected on 2nd day after inhaling isoflurane,and Morris water maze test was performed to assess the cognitive function.Five rats were randomly sacrificed on 3rd day after inhaling isoflurane,brains were removed,and hippocampi were isolated for determination of the expression of brain-derived neurotrophic factor (BDNF),tyrosine kinase B receptor (TrkB) and phosphorylated TrkB (p-TrkB) in hippocampal tissues by Western blot.The p-TrkB/TrkB ratio was calculated.Results Compared with group N+O,the escape latency was significantly prolonged on 3rd and 4th days,the exploration time spent on the original target quadrant was shortened,the expression of BDNF and p-TrkB in hippocampal tissues was down-regulated,and the p-TrkB/TrkB ratio was decreased in group-H+O (P＜0.05).Compared with group H+O,the escape latency was significantly prolonged on 2nd-5th days,the exploration time spent on the original target quadrant was shortened,the expression of BDNF and p-TrkB in hippocampal tissues was down-regulated,and the p-TrkB/TrkB ratio was decreased in group H+I (P＜0.05).Compared with group H+I,the escape latency was significantly shortened on 2nd-5th days,the exploration time spent on the original target quadrant was prolonged,the expression of BDNF and p-TrkB in hippocampal tissues was up-regulated,and the p-TrkB/TrkB ratio was increased in group R+H+I (P＜0.05).Conclusion Resveratrol can mitigates the cognitive dysfunction after isoflurane anesthesia in obese rats,and the mechanism may be related to promoting the activation of BDNF/TrKB signaling pathway.

Objective To evaluate the role of adenosine A1 receptors in hippocampal neurons in the cognitive dysfunction caused by isoflurane anesthesia in aged mice.Methods Sixteen male adenosine A1 receptor gene knockout homozygote mice (gene knockout mice) and 16 male wild-type mice,aged 18-22 months,weighing 27-32 g,were studied.Each type of mice was randomly divided into 2 groups (n=8 each) using a random number table:control group (group C) and isoflurane anesthesia group (group Ⅰ).Mice inhaled 1.4％ isoflurane in 100％ O2 for 2 h in group Ⅰ,and 100％ O2 for 2 h in group C.All the mice underwent Morris water maze test at 24 h after isoflurane or O2 inhalation.After the test,the mice were sacrificed and the hippocampal tissues were harvested to determine the number of β-amyloid1-42 (Aβ1-42) plaques (using immunohistochemistry) and expression of phosphorylated tau (p-tau) protein,and 2B subunit-containing N-methyl-D-aspartate receptors (NR2B) (by Western blot analysis).Results Compared with group C of wild type mice,the escape latency was significantly prolonged,the number of Aβ1-42 plaques was enlarged,the expression of p-tau protein was up-regulated,and the expression of N R2B was down-regulated in group Ⅰ of wild type mice.Compared with group Ⅰ of wild type mice,the escape latency was significantly shortened,the number of Aβ1-42 plaques was decreased,the expression of p-tau protein was down-regulated,and the expression of NR2B was up-regulated in group Ⅰ of gene knockout mice.There was no significant difference in the parameters mentioned above between group Ⅰ and group C of gene knockout mice.Conclusion Adenosine A1 receptors in hippocampal neurons mediate isoflurane anesthesia-induced cognitive dysfunction in aged mice,and the mechanism may be related to promotion of deposition of Aβ,phosphorylation of tau protein and inhibition of activities of NR2B.

AIM:To evaluate the effect of curcumin on impaired learning-memory ability and the expression of high mobility group box protein 1 ( HMGB1 ) and c-Jun N-terminal kinase ( JNK ) in a rat model of Alzheimer disease (AD).METHODS:Male Sprague-Dawley rats, weighing 250~270 g, were randomly divided into 4 groups (n=9):blank control group (group A), model group (group B), curcumin treatment group (group C, curcumin injected intraper-itoneally at 100 mg· kg-1· d-1 for 6 consecutive days) and solvent control group (group D).The rats of AD model were induced by injection of ibotenic acid into the nucleus basalis of Meynert ( NBM) bilaterally.All rats were trained in Morris maze to assess the ability of learning and memory .The expression of HMGB1 and JNK in the hippocampus was detected by the methods of immunohistochemistry and Western blotting .RESULTS:Compared with group A , the average escape laten-cy (AEL) in groups B and D were obviously longer (P<0.05), while AEL in group C in the 5th and 6th days were signif-icantly shorter (P<0.05).The releases of HMGB1 in the CA1 and CA3 areas in groups B and D from the nucleus were a-bundant.Compared with groups B and D , HMGB1 in hippocampal CA1 and CA3 areas in group C secreted out of the nu-cleus decreased obviously (P<0.05).No significant difference of the release of HMGB1 between group A and group C was observed (P>0.05).No significant difference in the expression of HMGB1 in the hippocampus among the 4 groups was found (P>0.05).However, compared with groups B and D , the expression of JNK in group C was decreased obvi-ously (P<0.05).CONCLUSION: Curcumin significantly improves the learning and memory ability of AD rats .The probable mechanisms may be related to inhibiting the release of HMGB 1 from the nucleus of hippocampal neurons and de-creasing the expression of JNK in the hippocampus .

Objective To evaluate the effects of curcumin on the activity of NR2B and NR1 in the spinal dorsal horn in a rat model of diabetic neuropathic pain (DNP).Methods Diabetes mellitus was induced by high-sucrose and high-fat diet and intraperitoneal streptozotocin 35 mg/kg,then confirmed by fasting blood glucose level ≥ 16.7 mmol/L 3 days later in male Sprague-Dawley rats.DNP was confirmed by the mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) measured on day 14 after streptozotocin administration ＜ 80％ of the baseline value.The rats were then randomly divided into 3 groups (n =27 each) using a random number table:DNP,DNP+ curcumin group (group DCur)and DNP + solvent control group (group DSC).Curcumin 100 mg· kg-1 · d-1 and corn oil 4 ml· kg-1 · d-1 were injected intraperitoneally for 14 consecutive days starting from 14 days after administration of streptozotocin in DCur and DSC groups,respectively.Another 27 normal male Sprague-Dawley rats served as control group (group C) and were fed with normal forage.At 3,7 and 14 days after curcumin injection,MWT and TWL were measured and the lumbar segments (L4-6) of the spinal cord were removed.The expression of pTyr1472-NR2B and pSer896-NR1 in the spinal dorsal horn was determined by immunohistochemistry and Western blot.Results Compared with group C,MWT was significantly decreased,TWL was shortened,and the expression of pTyr1472-NR2B was up-regulated at each time point in group DNP.Compared with group DNP,MWT was significantly increased,and TWL was prolonged at 7 days after curcumin injection,and the expression of pTyr1472-NR2B was down-regulated at 3 days after curcumin injection in group DCur.There was no significant difference in each parameter between DNP and DSC groups,and in the expression of pSer896-NR1 between the four groups.Conclusion The mechanism by which curcumin mitigates neuropathic pain in type 2 diabetic rats may be related to inhibition of up-regulation of pTyr1472-NR2B expression,while unrelated to pSer896-NR1 expression in the spinal dorsal horn.

Objective To evaluate the effects of propofol on apoptosis and invasiveness of human lung cancer cell line A549 cells.Methods Human lung cancer cell line A549 were seeded onto 96-well plates (100 μl/well) and 6-well plates (2 000 μl/well) at a density of 2× 105 cells/ml,and cultured for24 h at 37 ℃ in 5％ CO2.The cells were randomly divided into 2 groups (n =60 each) using a random number table:dimethyl sulfoxide (DMSO) group and propofol group (group P).In group P,propofol with the final concentration of 100 μmoYL was added.In group DMSO,0.5％ DMSO with the final concentration of 0.5％ was added.At 24 h of incubation with drugs,caspase-3 expression was detected by high content screening (HCS); the expression of matrix metalloproteinase (MMP-2) was detected by Western blot analysis.At 0.5,1 and 5 h of incubation,ERK1/2 expression was also measured using Western blot analysis.Results Compared with group DMSO,the expression of caspase-3 was up-regulated,the expression of MMP-2 was down-regulated,ERK1/2 expression was up-regulated at 0.5 of incubation and down-regulated at 1 h of incubation,and no significant change was found in ERK1/2 expression at 5 h of incubation in group P.Conclusion Propofol can promote apoptosis in A549 cells and inhibit invasiveness of human lung cancer cell line A549 cells.

Objective To evaluate the effects of different concentrations of parecoxib sodium on the rat sperm motility,capacitation and acrosome reaction in vitro.Methods The sperm samples from Sprague-Dawley rat epididymis were collected by Klinefelter diffusion method and randomly divided into 4 groups (n =18 each) using a random number table:control group (group C),and parecoxib sodium 100,500,1 000 μmol/L groups (P1-3 groups).Parecoxib sodium with the final concentrations of 100,500 and 1 000 μmol/L was added to the culture medium.The samples were then incubated for 5 h in an airtight container filled with 5 ％ CO2 at 37 ℃.Then sperm motility was examined in vitro at 37 ℃ and analyzed by the computer-assisted sperm analysis,including the sperm motility ((a + b)％),average path velocity (VAP),straight line velocity (VSL),curvilinear velocity (VCL) and amplitude of lateral head displacement (ALH).The capacitation effect was assessed by using the chlortetracycline staining and phase-contract microscopy.The acrosome reaction was evaluated by coomassie brilliant blue staining.Results The VAP,VSL,VCL and capacitation ability of the sperm were gradually decreased in C and P1-3 groups (P ＜ 0.05).Compared with group C,(a + b)％ in P2,3 groups and ALH in P2 group were significantly decreased (P ＜ 0.05).There was no significant difference in the acrosome reaction between groups (P ＞ 0.05).Conclusion Parecoxib sodium has significant inhibitory effects on the rat sperm motility and capacitation in a dose-dependent manner,while has no effect on the acrosome reaction in vitro.

Objective To evaluate the effects of lipoxin A4 (LXA4) administered at different time points on the expression of connexin43 (Cx43) during myocardial ischemia-reperfusion (I/R) in rats.Methods Seventytwo healthy male Sprague-Dawley rats,weighing 200-250 g,wcre equally and randomly divided into 6 groups:groups sham operation Ⅰ (group S1) and Ⅱ (group S2),groups myocardial I/R Ⅰ (group Ⅰ/R1) and Ⅱ (group I/R2),and groups LXA4 administered before chest opening (group LX1) and at 30 min of reperfusion (group LX2).Myocardial I/R was produced by 30 min occlusion of left anterior descending branch (LAD) of coronary artery followed by 120 min reperfusion.LXA4 100μg/kg was injected via femoral veins before chest opening and at 30 min of reperfusion in groups LX1 and group LX2,respectively.While normal saline 2 ml/kg was injected via the femoral vein at the corresponding time points in the other four groups.In groups S1 and S2,LAD was only threaded,but not ligated.Blood samples were taken from the femoral vein before chest opening and at 120 min of reperfusion for measurement of serum IL-8,TNF-α and cardiac troponin Ⅰ (cTnI) concentrations.The rats were then sacrificed after blood samples were taken at 120 min of reperfusion and hearts were removed for determination of Cx43 protein (by immunohistochemical SP method) and Cx43 mRNA expression (by real-time quantitative PCR),SOD activity and MDA content in myocardial tissues.The development of arrhythmia was observed from occlusion of LAD to 120 min of reperfusion.Duration of ventricular tachycardia (VTd) and ventricular fibrillation (VFd) was recorded.Scores of ventricular arrhythmias were calculated.Results The expression of Cx43 protein and mRNA was significantly down-regulated,and scores of ventricular arrhythmias,VTd,serum IL-8,TNF-α and cTnI concentrations,SOD activity and MDA content were increased in groups I/R1 and LX1 as compared with group S1,and in groups I/R2 and LX2 as compared with group S2 (P ＜ 0.05).The expression of Cx43 protein and mRNA was significantly up-regulated,SOD activity was increased,and scores of ventricular arrhythmias,VTd,VFd,serum IL-8,TNF-α and cTnI concentrations,and MDA content were decreased in group LX1 as compared with group I/R1,and in group LX2 as compared with group I/R2(P ＜ 0.05).The expression of Cx43 protein and mRNA was significantly lower,scores of ventricular arrhythmias,VTd and SOD activity were higher,and the serum IL-8,TNF-α and cTnI concentrations and MDA content were lower in group LX2 than in group LX1 (P ＜ 0.05).Conclusion LXA4 administered before myocardial ischemia and at 30 min of reperfusion can up-regulate the expression of Cx43 and reverse remodeling of Cx43,thus reducing myocardial I/R-induced arrhythmia in rats,and LXA4 administered before ischemia can provide better efficacy.

Objective To evaluate the effects of curcumin on the expression of phosphorylated extracellular signal-related kinase (p-ERK) and phosphorylated cAMP response element binding protein (p-CREB) in the spinal dorsal horn and dorsal root ganglion (DRG) in type 2 diabetic neuropathic pain (DNP) in rats.Methods Type 2 diabetes mellitus was induced by high-fat and high-sucrose diet and intraperitoneal streptozotocin (STZ) 35mg/kg,and confirmed by fasting blood glucose level≥ 16.7 mmol/L in male Sprague-Dawley rats.Type 2 DNP was confirmed by the mechanical withdrawal threshold (MWT) and thermal withdraw latency (TWL) measured on day 14 after STZ administration ＜ 80％ of the baseline value,and the rats with type 2 DNP were randomly divided into 3 groups (n =27 each):type 2 DNP group (group DNP),curcumin group (group Cur) and solvent control group (group SC).Curcumin and corn oil 100 mg/kg (25 mg/ml) were injected intraperitoneally once a day for 14consecutive days starting from 14 days after administration of streptozocin in Cur and SC groups,respectively.Another 27 normal rats were served as control group (group C) and were fed with common forage.MWT and TWL were measured at 3,7 and 14 days after curcumin injection (T1 3),and the lumbar segment 4-6 of the spinal cord and DRGs were removed at the same time for determination of the expression of p-ERK and p-CREB (by Western blot).Results Compared with group C,MWT was significantly decreased,TWL was shortened,and the expression of p-ERK and p-CREB in spinal dorsal horn and DRGs was up-regulated at T1-3 in DNP and SC groups,and at T1 in Cur group (P ＜ 0.05).Compared with group DNP,MWT was significantly increased,TWL was prolonged,and the expression of p-ERK and p-CREB in spinal dorsal horn and DRGs was down-regulated at T2,3 in Cur group (P ＜0.05).There was no significant difference in the MWT,TWL and expression of p-ERK and p-CREB between DNP and SC groups (P ＞ 0.05).Conclusion Curcumin can attenuate type 2 diabetic DNP by inhibiting up-regulation of the expression of p-ERK and p-CREB in the spinal dorsal horn and DRG in rats.

ObjectiveTo investigate the effects of curcumin on type 2 diabetic neuropathic pain (DNP)and expression of inositol-requiring enzyme 1α (IRE1α) in spinal dorsal horn and dorsal root ganglia (DRG) in rats.MethodsType 2 diabetes mellitus was induced by high-fat and high-sucrose diet and intraperitoneal streptozotocin (STZ) 35 mg/kg,and confirmed by fasting blood glucose level ＞ 16.7 mmol/L in male SD rats.Type 2 DNP was confirmed by the mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWI.) measured on day 14 after STZ administration ＜ 80％ of the baseline value.The rats were then randomly divided into 3 groups ( n =27 each):DNP group,curcumin group (group Cur) and solvent control group (group SC).Curcumin and corn oil 100 mg/kg (25 mg/ml) were given intraperitoneally once a day for 14 consecutive days starting from 14 days after administration of streptozocin in Cur and SC groups respectively.Another 27 rats were chosen and served as control group (group C) and fed with common fodders.MWT and TWL were measured at 3,7 and 14 day after curcumin administration.The expression of IRE1α in spinal dorsal horn and DRG was detected by Western blot.ResultsCompared with group C,MWT was significantly decreased and TWL was significantly shortened,and the expression of IRE1α was up-regulated in DNP,Cur,and SC groups (P ＜ 0,05),Compared with group DNP,MWT were significantly increased,TWL was significantly prolonged,and the expression of IRE1α in spinal dorsal horn and DRG was down-regulated in group Cur (P ＜ 0.05).There was no significantdifference in the parameters mentioned above between DNP and SC groups (P ＞ 0.05).ConclusionCurcumin can attenuate type 2 1)NP and inhibition of the expression of IRE1α in spinal dorsal horn and DRG is involved in the mechanism.