运动干预对轻度认知障碍患者认知水平和脑脊液相关指标的影响

目的:探讨轻度认知障碍(MCI)患者给予运动干预对其认知水平、脑脊液Tau蛋白和Aβ_(1-42)水平产生的影响。方法:回顾分析我院2014年6月~2015年12月收治的70例MCI患者临床资料,随机将其分为观察组(n=35例)与对照组(n=35例),对照组不干预,观察组行6个月的运动干预,评估两组患者认知水平、脑脊液Tau蛋白及Aβ_(1-42)水平。结果:观察组患者实施6个月运动干预后,Mo CA评分明显升高、Aβ_(1-42)水平明显增加,与对照组比较差异显著,且观察组(488±186)pg/ml脑脊液Tau蛋白水平低于对照组(623±224)pg/ml,组间数据对比差异显著(P0.05)。结论:健身气功八段锦干预能有效提升轻度认知障碍患者认知水平,脑脊液Tau蛋白及Aβ_(1-42)水平是重要的可监控指标。     

新生儿术后镇痛对炎症反应和术后感染的影响

目的 探讨新生儿术后镇痛对感染发生率的影响.方法 120例行开腹手术新生儿随机均分为三组:A组术后输注芬太尼6-8μg/kg+0.9％氯化钠45 ml;B组舒芬太尼0.6-0.8tg/kg+0.9％氯化钠45 ml;C组给予0.9％氯化钠45 ml.持续输注24 h.记录术后新生儿疼痛评分(NIPS).检测术前及术后24 h时外周静脉血白细胞(WBC)计数、血清C-反应蛋白(CRP)及白细胞介素6(IL-6)含量;比较术后感染发生率.结果 A、B组术后镇痛效果均满意.术后感染发生率低于C组[15.0％、5.0％ vs.35.0％],抗生素使用时间短于C组[(10.68±1.13)d、(7.22±0.46)d vs.(13.87±3.79) d](P＜0.05).术后,A、B组WBC计数低于C组[(10.93±5.08)×109/L、(8.83±2.98)×109/L vs.(13.97±5.96)×109/L],血清CRP低于C组[(38.52±20.31) mg/L、(27.67±16.50) mg/L vs.(67.44±24.82) mg/L],IL-6低于C组[(198.46±35.16)pg/ml、(156.94±15.08)pg/mlvs.(379.47±54.35) pg/ml],B组WBC计数、血清CRP和IL-6表达明显低于A组,抗菌药物使用时间亦短于A组(P＜0.05).结论 新生儿术后用芬太尼和舒芬太尼,尤其是舒芬太尼镇痛,可减轻炎症反应和感染发生率.     

尼莫地平对急性脑梗死患者血浆内皮素1的影响

目的 探讨尼莫地平对急性脑梗死患者血浆内皮素1(ET-1)水平的影响。方法 83例急性脑梗死患者随机分为尼莫地平组(A组)42例和常规治疗组(B组)41例,并以35例健康体检人群作为正常对照组(C组)。采用放射免疫法测定血浆ET-1水平。结果 治疗前,A、B组患者血浆ET-1水平均高于C组[(89.45±12.75)pg/ml、(92.35±11.88)pg/ml vs.(68.99±10.03)pg/ml](P<0.01);治疗后,A、B组患者血浆ET-1水平均较治疗前降低[(72.29±8.46)pg/ml vs.(89.45±12.75)pg/ml、(83.01±10.51)pg/ml vs.(92.35±11.88)pg/ml](P<0.05),且A组较B组血浆ET-1降低更明显(P<0.01)。结论 尼莫地平可改善急性脑梗死患者的血管内皮功能,对急性脑梗死具有良好的治疗作用。     

氨甲环酸联合乌司他丁对心肺转流心脏手术患者出血量及IL-6的影响

目的 探讨氨甲环酸(TA)加乌司他丁(U)对心肺转流(CPB)术中出血量及白细胞介素6(IL-6)的影响.方法 60例CPB下行二尖瓣膜置换术患者随机均分为三组.切皮前,A组静注TA 20 mg/kg和U 1×10<'6>IU,B组静注TA 50 mg/kg和U 1×10<'6> IU,C组静注生理盐水作为对照.记录术中出血量和输血量、术后12 h心包及纵隔引流量,检测CPB前后血细胞压积和IL-6水平.结果 与C组比较,A、B两组术后12 h心包及纵隔引流量[(259.5±82.6)ml vs.(121.0±87.2)ml、(109.6±78.2)ml]、红细胞输入量[(1.2±0.3)U vs.(0.8±0.2)U、(0.8±0.1)U]及停机后IL-6水平[(54.8±15.5)pg/ml vs.(31.2±8.7)pg/ml、(32.1±9.0)Pg/ml]均明显减少(P<0.05).结论 瓣膜置换术患者CPB前联合应用TA和U可有效减少术中、术后的出血量和输血量,减轻炎症反应.     

慢性阻塞性肺疾病患者血清白细胞介素17的表达

目的探讨白细胞介17(IL-17)在慢性阻塞性肺疾病(COPD)发病机制中的作用。方法抽取100例COPD急性加重期(A1组)、100例稳定期患者(A2组)及100例健康人(C组)静脉血标本,采用双抗体ELISA法测定血清IL-17水平。并作肺功能检查,计算第1秒用力呼气容积比(FEV1%)。结果 A1组血清IL-17明显高于A2组[(73.1±58.4)pg/mlvs.(34.8±21.6)pg/ml](P<0.01),A2组血清IL-17高于C组[(16.4±7.6)pg/ml](P<0.01)。A1组血清IL-17与FEV1%呈负相关(P<0.05)。结论 IL-17可能参与COPD的发病。     

不同透析方式治疗尿毒症的临床效果

目的 探究不同透析方式治疗尿毒症的临床效果。方法 84例接受透析治疗的尿毒症患者,随机分为A组和B组,每组42例。A组以常规高通量血液透析方式治疗, B组在A组基础上联合血液透析滤过方式治疗。比较两组患者心血管不良事件(心力衰竭、心绞痛、心肌梗死)发生率及治疗前后血清炎症因子[超敏C反应蛋白(hs-CRP)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)]、血管内皮细胞损伤因子[血管性血友病因子(vWF)、可溶性血管细胞粘附分子1(sVCAM-1)]水平。结果 B组患者心血管不良事件发生率2.38%低于A组的14.29%,差异有统计学意义(P<0.05)。治疗后,B组患者血清hs-CRP(7.21±2.12)mg/L、IL-6(5.24±1.82)pg/ml、TNF-α(1.16±0.32)pg/ml均低于A组的(10.04±2.32)mg/L、(9.92±2.28)pg/ml、(1.62±0.46)pg/ml,差异有统计学意义(P<0.05)。治疗后, B组患者vWF(16.28±3.85)IU/dl、sVCAM-1(0.77±0.22)μg/ml均低于A组的...     

2型糖尿病患者泪液白细胞介素6的表达

目的 探讨泪液白细胞介素6(IL-6)表达与糖尿病及糖尿病视网膜病变的关系.方法 用ELISA法检测2型糖尿病(T2DM)无视网膜病变(A组,40例)、T2DM合并视网膜病变(B组,40例)和正常人(C组,40例)泪液和血清IL-6的表达.结果 A、B组泪液IL-6表达量明显高于C组[(12.21±3.88) pg/ml、(18.86±6.56) pg/ml vs.(4.29±3.27) pg/ml](P＜0.01),B组泪液IL-6表达量高于A组(P＜0.01).泪液IL-6与血清II-6表达水平呈正相关(r=0.731,P＜0.05).结论 泪液IL-6表达与T2DM及糖尿病视网膜病变的发生有关.泪液IL-6表达的测定有可能成为糖尿病病情评估的方法之一.     

川芎嗪在预防增殖性玻璃体视网膜病变中的作用及对肿瘤坏死因子水平的影响

目的：分析川芎嗪对增殖性玻璃体视网膜病变(PVR)的预防作用及对肿瘤坏死因子(TNF-α)浓度水平的影响。方法抽取本院2012年1月~2013年1月收治的42例PVR患者,均接受玻璃体手术,术后未给予药物干预20例(A组),行川芎嗪治疗22例(B组),抽取同期行健康体检的20例正常人群为对照组,通过酶联免疫吸附试验(ELISA)对所有研究对象的TNF-α、血管内皮细胞生长因子(VEGF)进行测定并比较。比较三组细胞黏附分子-1(ICAM-1)及白细胞介素-1β(IL-1β)水平。结果 B组患者TNF-α、VEGF分别为(157.90±53.04)、(81.24±40.23) pg/ml,明显低于A组患者的(658.81±190.56)、(108.18±74.26) pg/ml,差异有统计学意义(P<0.05);B组与对照组比较,差异无统计学意义(P>0.05);A、B组ICAM-1、IL-1β比较,差异有统计学意义(P<0.05)。结论川芎嗪能明显降低TNF-α、VEGF水平,减少ICAM-1、IL-1β表达,能有效防治PVR。     

替米沙坦联合阿托伐他汀对早期糖尿病肾病微炎症状态的影响

目的 替米沙坦联合阿托伐他汀对早期糖尿病肾病(DN)微炎症状态的影响.方法 早期DN患者40例均分为A组(替米沙坦80 mg/d,口服)、B组(替米沙坦80 mg/d+阿托伐他汀20mg/d,口服),疗程20周,采用ELISA检测核转录因子cB(NF-cB) p65亚基活性,生化检测仪检测血清炎症因子水平,RT-PCR和Western blot检测肾组织中NF-кBmRNA及蛋白表达情况.结果 治疗后,两组各项检测指标均较治疗前明显降低(P＜0.05),B组NF-кB p65亚基活性(0.56±0.03vs.1.31±0.05)、超敏C反应蛋白[(3.31±1.95) mg/L vs.(5.48±2.06) mg/L]、IL-1[(11.45±1.71) pg/mlvs.(14.48±1.75) pg/ml]、IL-6[(14.15±2.13) pg/mlvs.(16.19±2.15) pg/ml]、TNF-α[(20.69±4.45) pg/ml vs.(28.89±3.86) pg/ml]、NF-кBmRNA(0.546±0.013 vs.0.780±0.012)及蛋白(0.451±0.021 vs.0.743±0.031)表达水平改善均较A组更为明显(P＜0.05).结论 替米沙坦联合阿托伐他汀可延缓早期DN的进展.     

糖尿病和冠心病患者血清糖基化终产物与血管细胞黏附分子1浓度的变化

目的 研究糖基化终产物(AGEs)与血管细胞黏附分子1(VCAM-1)间的关系,探讨AGEs在动脉粥样硬化中的作用.方法 分别抽取30例健康人群(A组)、32例糖尿病患者(B组)及36例冠心病患者(C组)的外周血液,用ELISA法检测各组血清中AGEs与VCAM-1的水平.结果 B组AGEs和VCAM 1浓度均较A组明显升高[(12.43±0.52) U/ml vs.(8.82±0.36) U/ml和(735.50±55.75) pg/ml vs.(417.80±27.34) pg/ml](P＜0.01)；而C组AGEs和VCAM-1浓度为(9.04±0.38) U/ml和(417.80±27.34) pg/ml,均与A组相仿(P＞0.05).B组、C组血清中AGEs浓度与VCAM-1浓度均呈显著正相关(r=0.7347、0.6329,P＜0.01).结论 AGEs在体内可以促进VCAM-1的分泌,这可能是糖尿病患者易患动脉粥样硬化的重要机制之一.     

Quantitative in vivo and in vitro sex differences in artemisinin metabolism in rat

1. The pharmacokinetics of the antimalarial compound artemisinin were compared in the male and female Sprague-Dawley rat after single dose i.v. (20 mg.kg) or i.p. (50 mg.kg) administration of an emulsion formulation. 2. Plasma clearance of artemisinin was 12.0 (95% confidence interval: 10.4, 13.0) l.h. kg in the male rat and 10.6 (95% CI: 7.5, 15.0) l.h. kg in the female rat suggesting high hepatic extraction in combination with erythrocyte uptake or clearance. Artemisinin half-life was 0.5 h after both routes of administration in both sexes. Values for plasma clearance and half-lives did not statistically differ between the sexes. 3. After i.p. administration artemisinin AUCs were 2-fold higher in the female compared with male rat (p 0.001). Artemisinin disappearance was 3.9-fold greater in microsomes from male compared with female livers and it was inhibited in male microsomes by goat or rabbit serum containing antibodies against CYP2C11 and CYP3A2 but not CYP2B1 or CYP2E1. 4. The unbound fraction of artemisinin in plasma was lower (p 0.001) in plasma obtained from the male (8.8 2.0%) compared with the female rat (11.7 2.2%). 5. The possibility of a marked sex difference, dependent on the route of administration, has to be taken into account in the design and interpretation of toxicological studies of artemisinin in this species.     

Quantitative in vivo and in vitro sex differences in artemisinin metabolism in rat

1. The pharmacokinetics of the antimalarial compound artemisinin were compared in the male and female Sprague-Dawley rat after single dose i.v. (20 mg x kg(-1)) or i.p. (50 mg x kg(-1)) administration of an emulsion formulation. 2. Plasma clearance of artemisinin was 12.0 (95% confidence interval: 10.4, 13.0) 1 x h(-1) x kg(-1) in the male rat and 10.6 (95% CI: 7.5, 15.0) 1 x h(-1) x kg(-1) in the female rat suggesting high hepatic extraction in combination with erythrocyte uptake or clearance. Artemisinin half-life was approximately 0.5 h after both routes of administration in both sexes. Values for plasma clearance and half-lives did not statistically differ between the sexes. 3. After i.p. administration artemisinin AUCs were 2-fold higher in the female compared with male rat (p < 0.001). Artemisinin disappearance was 3.9-fold greater in microsomes from male compared with female livers and it was inhibited in male microsomes by goat or rabbit serum containing antibodies against CYP2C11 and CYP3A2 but not CYP2B1 or CYP2E1. 4. The unbound fraction of artemisinin in plasma was lower (p < 0.001) in plasma obtained from the male (8.8 +/- 2.0%) compared with the female rat (11.7 +/- 2.2%). 5. The possibility of a marked sex difference, dependent on the route of administration, has to be taken into account in the design and interpretation of toxicological studies of artemisinin in this species.     

休克时血中氧自由基的变化

本实验测定10名休克患者血浆和红细胞的丙二醛(MDA)、血浆总抗的氧化活性(AOA)的含量。结果表明:休克病人红细胞膜和血浆 MDA 含量(4.298±0.722;5.348±0.834)与对照组(3.235±0.682;4.356±1.081)比较明显增高(P<0.05);血浆 AOA(39.65±7.858)与对照组(48.21±10.81)比较明显降低(P<0.01)。提示:休克时,患者机体内自由基反应增强是引起组织细胞损伤的原因之一。     

Interindividual variability in metabolic activation in humans in vivo

In assessing interindividual variability in metabolic activation, the toxic metabolite is often too unstable for conventional analysis. Possible alternatives include a stable product of the reactive metabolite e.g. cysteinyl derivatives of N-acetyl-4-benzoquinoneimine, the toxic metabolite of paracetamol, adducts with DNA or protein, and indirect measurement of the activity of the enzyme(s) producing the active metabolite. An example of the last approach is the use of furafylline, a highly specific inhibitor of human CYP1A2, to determine the extent of the metabolic activation of the cooked food mutagens PhIP and MeIQx. The extent of inhibition, determined from levels of unchanged amine in urine, is an indirect measure of the activity of the activation pathway. Further refinement of this approach, allied to improved measures of the biological process of interest should prove of value in evaluating interindividual variability and its role in the risk assessment process.     

Theophylline kinetics in peripheral tissues in vivo in humans

Several biochemical and cellular effects have been described for methylxanthines under in vitro conditions. However, it is unknown, whether threshold concentrations required to exert these effects are attained in target tissues in vivo. We therefore employed the microdialysis technique for measuring theophylline concentrations in peripheral tissues under in vivo conditions.Following in vitro and in vivo calibration, microdialysis probes were inserted into the medial vastus muscle and into the periumbilical subcutaneous adipose layer of healthy volunteers. Following single oral dose administration of 300 mg or i.v. infusion of 240 mg theophylline, in vivo time courses of theophylline concentrations were monitored in tissues and plasma. Major pharmacokinetic parameters (c_max, t_max, AUC) were calculated for plasma and tissue time courses. The mean AUC_tissue /AUC_plasma-ratio was 0.56 (p.o.) and 0.55 (i.v.) for muscle and 0.55 (p.o.) and 0.72 (i.v.) for subcutaneous adipose tissue.We conclude that microdialysis provides important information on the distribution and the tissue pharmacokinetics of theophylline.Abbreviations FPIA Fluorescence polarisation immuno assay - AUC Area under the curve - t_max Time to peak concentration - c_max Peak concentration     

Changes in angiopoietin expression in glomeruli involved in glomerulosclerosis in rats with daunorubicin-induced nephrosis

AIM: To study the potential pathological role of endogenous angiopoietins in daunorubicin-induced progressive glomerulosclerosis in rats. METHODS: Seventy male Wistar rats were allocated randomly into a daunorubicin group (DRB; n=40) or a control group (n=30). The rats in the DRB group were injected with DRB (15 mg/kg), in their tails. Subsequently, at intervals of 1, 2, 4, 6, 8, and 12 weeks, 5 male Wistar rats in each group were chosen randomly for 24 h urinary protein quantitative measurements (24 h UPQM), and determination of plasma tumor necrosis factor alpha (TNF-alpha), angiopoietin-1 (Ang1), and angiopoietin-2 (Ang2) levels. Kidney sections were examined by electron microscopy, Periodic Acid Schiff (PAS) staining, immunohistochemical staining and in situ hybridization histochemistry. RESULTS: As glomerulosclerosis progressed in the DRB group, expression of Ang1 mRNA and protein in glomeruli decreased and expression of TNF-alpha protein, Ang2 mRNA and protein in glomeruli increased. Expression of Ang1 mRNA and protein in glomeruli were negatively correlated with 24 h UPQM, Fn protein expression, and mean area of extracellular matrix (MAECM). In comparison, expression of Ang2 mRNA and protein in glomeruli were positively correlated with 24 h UPQM, Fn protein expression and MAECM; furthermore, there was a positive correlation between plasma Ang2 and 24 h UPQM. Plasma TNF-alpha and expression of TNF-alpha in glomeruli were positively correlated with expression of Ang2 mRNA and protein in glomeruli. There was a negative correlation between Ang1 protein expression and Ang2 protein expression in glomeruli. CONCLUSION: During DRB-induced glomerulosclerosis, podocyte injury led to a shift in the balance of Ang1 and Ang2 in glomeruli. Increased TNF-alpha in plasma and glomeruli may upregulate Ang2 expression in glomeruli. Elevated Ang2 in both plasma and glomeruli may mediate protein permeability through the glomerular filtration barrier. Moreover, local expression of Ang2 may facilitate the progress of glomerulosclerosis by upregulating a component expression of extracellular matrix.