慢性阻塞性肺疾病急性加重期患者外周血和诱导痰中肿瘤细胞因子的水平

目的观察慢性阻塞性肺疾病（COPD）急性加重期患者治疗前后诱导痰及血浆中肿瘤坏死因子α（TNF—α）和可溶性肿瘤坏死因子受体55、75（sTNF—R55、sTNF—R75）水平的变化。方法检测并分析48例COPD急性加重期患者治疗前后（A1组和A2组）及28例健康志愿者诱导痰及血浆中TNF—α、sTNF—R55、sTNF—R75水平及其肺功能。结果COPD急性加重期患者治疗前后诱导痰及血浆中TNF—α和sTNF—R55、sTNFR75的水平均高于健康组；治疗前后痰TNF—α浓度（0．82±0．34）μg/L和（0．48±0．27）μg/L，血（0．82±0．35）μg/L和（0．60±0．46）μg/L，均有明显下降（P〈0．01）；sTNF—R55、sTNF—R75浓度上升，血中浓度水平与肺功能无相关性（P〉0．05），诱导痰中浓度水平与肺功能呈正相关性（P〈0．05）；TNF—α浓度与第1秒用力呼气容积和其占预计值百分数呈负相关（P=0．000）。结论COPD患者急性加重与全身和局部炎性介质和抗炎介质的失衡有关。全身炎症反应与气流受限关系不大，而局部炎症反应与气流受限密切相关。     

帕金森病患者外周血TNF-α浓度和IL-6质量浓度的检测及分析

为观察肿瘤坏死因子 (TNF α)和白细胞介素 6(IL 6)在帕金森病 (PD)患者血清中的变化 ,采用放射免疫法测定PD组 ( 3 0例 ) ,其他神经系统免疫疾病组 (OND) ( 2 2例 ) ,正常对照组 (HC) ( 2 4例 )血清中TNF α的浓度和IL 6的质量浓度。结果 :PD患者血清中TNF α浓度〔( 1 3 .83± 4.47) pmol/L〕与OND组〔( 1 7.5 3± 7.2 5 )pmol/L〕、HC组〔( 1 6.5 7± 3 .0 5 )pmol/L〕比较均明显降低 (P <0 .0 5 )。PD患者血清中IL 6质量浓度〔( 1 1 2 .80± 2 5 .1 3 ) μg/L〕与OND组〔( 1 78.5 3± 42 .78) μg/L〕、HC组〔( 1 3 6.2 2± 1 7.40 ) μg/L〕比较均明显降低 (P <0 .0 0 1 )。PD组间比较 ,其结果与年龄、病程及分型无关。本研究结果表明PD患者存在外周血细胞因子的改变 ,提示免疫机制可能参与了PD的发病过程。     

PDTC对重症急性胰腺炎的抑制作用

目的　探讨抗氧化剂四氢化吡咯二硫代氨基甲酸脂 (PDTC)对重症急性胰腺炎 (SAP)的抑制作用。方法　Wistar大鼠 72只 ,随机分为 :假手术组 (shamoperation ,SO)、SAP组和SAP +PDTC组。术后分四个时段 ( 1、3、6、12h)分批进行下腔静脉采血后处死 ,取胰腺组织作病理切片。采用双抗体夹心ABC ELISA法测定血浆TNF α、IL 6。结果　SAP组血浆细胞因子TNF α和IL 6浓度较SO组增高 (P <0 .0 5 ) ,其中TNF α于术后 1h达到峰值 ( 871.6± 5 .9pg/ml) ,与SO组 ( 2 5 .2± 1.2 pg/ml)差异显著 (P <0 .0 0 1)。而IL - 6于术后 3h达到峰值( 5 9.2± 4 .1pg/m) ,与SO组 ( 2 5 .2± 1.2 pg/ml)差异显著 (P <0 .0 5 )。SAP +PDTC组的血浆TNF α和IL 6浓度较SAP组明显下降 (P <0 .0 5 ) ,胰腺局部炎症反应减轻。结论　细胞因子TNF α和IL 6是SAP炎症因子网络中重要的组成部分 ,可以作为判断AP严重程度和预后的预测指标 ;PDTC抑制NF κB的活化 ,不仅抑制了SAP时SIRS的过程 ,亦改善了胰腺本身的炎症过程     

巨细胞病毒肝炎患儿血清细胞因子水平测定及其临床意义

目的　研究巨细胞病毒 (CMV)肝炎患儿血清干扰素 α(IFN α)、白细胞介素 8(IL 8)和肿瘤坏死因子 α(TNF α)水平的变化及其临床意义。方法　应用ELISA法检测 35例CMV肝炎患儿血清中上述三种细胞因子的含量 ,并对其两两之间进行了相关性分析。结果　CMV肝炎组患儿IFN α、IL 8、TNF α的含量分别为 (770 .3± 2 0 5 .4 )ng/L、(41.9± 2 2 .5 )ng/L和 (10 33.2± 388.5 )ng/L ,非常显著高于正常对照组 (P <0 .0 1)。相关性研究发现IFN α与TNF α呈显著正相关 (r =0 .35 6 ,P <0 .0 5 )。结论　血清细胞因子明显增高与CMV肝炎的病理变化和病损程度有着密切的联系     

转化生长因子β1和肿瘤坏死因子α在门静脉高压症发病中的意义

目的　研究转化生长因子 β1 (TGFβ1 )和肿瘤坏死因子 α(TNFα)在门静脉高压症 (门脉高压 )发病中的作用。　方法　应用酶联免疫分析方法对 5 0例门脉高压患者 (其中 2 0例伴腹水形成 )、5 0例正常对照者进行TGFβ1 和 TNFα的检测。　结果　对照组血清 TGFβ1 和 TNFα为 12 .32± 3.2 9ng/ml,94.74± 49.30 pg/ml,门脉高压组分别为 19.2 1± 5 .87ng/ml,140 .85± 5 3.47pg/ml(P<0 .0 5 ) ;门脉高压伴腹水者为 18.44± 5 .89ng/m l,16 7.34± 38.6 2 pg/ml,不伴腹水者为 2 0 .6 8± 6 .73ng/ml,10 1.5 4± 2 8.2 4pg/m l,两者比较 TGFβ1 差异无显著性 ,而有腹水者 TNFα高于无腹水者 (P<0 .0 5 )。　结论　 TGFβ1 和 TNFα水平升高在肝硬化门脉高压发病的病理生理机制中起作用。     

肾衰冲剂抑制体外肾成纤维细胞增殖及分泌TNF-α的作用

目的　通过观察肾衰冲剂在体外对肾成纤维细胞增殖和分泌TNF α的影响和作用 ,阐释其减轻肾纤维化的机制。方法　制备肾衰大鼠毒素血清及肾衰冲剂含药血清 ,加入成纤维细胞培养液中 ,观测细胞增殖和分泌的变化。结果　大鼠体内用药后ET 1由 (30 5 5 74± 16 6 6 5 )ng/L降至(1184 90± 191 6 4)ng/L(P <0 0 1) ;体外用药后成纤维细胞的增殖由 (0 5 34± 0 0 37)降至 (0 4 99±0 0 5 0 ) (P <0 0 5 ) ,分泌的TNF α由 (8 33± 1 4 8)IU/mL降至 (5 70± 0 6 9)IU/mL(P <0 0 1)。结论　肾衰冲剂可以抑制成纤维细胞的增殖 ,其机制之一可能与降低ET 1从而减少成纤维细胞TNF α的分泌量有关     

糖尿病人血浆肿瘤环死因子α初步测定

目的 :探讨两型糖尿病人血浆肿瘤坏死因子 - α(TNF- α)水平的变化。方法 :选取正常对照 (正常组 )、 1型糖尿病(DM1组 )和 2型糖尿病 (DM2组 )共 3组研究对象 ,再将 2型糖尿病组按体质量指数 (BMI) <2 5的编为 DM2 a组 ,≥ 2 5的编为 DM2 b组 ;用酶联免疫法 (EL ISA)测定各组的 TNF- α水平并比较。结果 :正常对照组血浆 TNF- α为 (0 .90±0 .0 7) μg/L,1型糖尿病组为 (0 .86± 0 .0 6 ) μg/L,与正常组比较无差异 (P >0 .0 5 ) ;2型糖尿病组中 BMI<2 5者为 (1.0 2± 0 .2 8) μg/L,比正常组升高 (P <0 .0 5 ) ,BMI≥ 2 5者为 (2 .2 3± 0 .41) μg/L,与正常组比显著升高 (P <0 .0 1) ,与 BMI<2 5者比 ,两者差异亦有显著意义 (P <0 .0 1)。结论 :2型糖尿病人血浆 TNF- α水平显著高于正常人和 1型糖尿病人 ,并与肥胖有一定的关系。     

生长激素对全身麻醉肿瘤坏死因子的影响

目的　探讨生长激素对全身麻醉引起肿瘤坏死因子 (TNFα)增高的改善作用。方法　雄性成年Wistar大鼠 4 0只 ,平均分两组。一组生长激素 (Saizen) 1U/kg ,皮下注射 ,连续 3日 ;对照组生理盐水 1ml/kg。腹腔苯巴比妥麻醉后腹主动脉插管。测血TNFα0小时、1小时、2小时、4小时 4时相值。结果　对照组TNFα2 60 80±69 2 1ng/ml,2 4 0 4 1± 7 5 2ng/ml,2 4 5 2 8± 4 0 2 8ng/ml;生长激素组分别为 12 0 4 2± 3 0 72ng/ml,10 0 4 3±2 0 5 2ng/ml,13 0 5 2± 3 0 4 6ng/ml。均有明显统计学差异。 结论　生长激素对全身麻醉引起TNFα增高具有明显改善作用。     

电针足三里对溃疡性结肠炎大鼠TNF-α的下调作用

目的 :探讨电针足三里穴对溃疡性结肠炎 (ulcera tivecolitis,UC)大鼠肿瘤坏死因子 α(TNF α)的调节作用及机制 .方法 :将 32只SD大鼠随机分为 4组 :正常对照组 ,UC模型对照组 ,UC模型 +针穴组 ,UC模型 +非穴组 .在诱导产生UC大鼠模型的基础上 ,分别电针其相应部位 ,1 0d后同时处死 4组大鼠 ,观察其结肠质量、结肠组织髓过氧化物酶(MPO)活性及TNF αmRNA表达水平、血清TNF α含量的变化 .结果 :与正常对照组相比 ,UC模型对照组结肠质量 /体质量 (mC/mB)及MPO活性均显著增加 (8.5 3± 2 .5 9vs 2 .4 6± 0 .4 2 ,1 4 5 .2± 2 5 .3vs 2 4 .3± 7.8,P <0 .0 1 ) ;血清TNF α含量和结肠组织TNF αmRNA表达水平分别上升 2 .5倍及 4 .3倍 (2 2 78± 1 70vs 894± 2 4 8,0 .98± 0 .1 1vs 0 .2 3±0 .1 1 ,P <0 .0 1 ) ;电针足三里穴后 ,mC/mB 和MPO活性显著降低 (5 .2 9± 2 .0 4vs 8.5 3± 2 .5 9,1 0 3.5± 35 .7vs 1 4 5 .2± 2 5 .3,P <0 .0 1 ,0 .0 5 ) ;TNF α含量和TNF αmRNA表达水平也分别减少 1 6 %和 4 4 % (1 91 3± 2 32vs2 2 78± 1 70 ,0 .5 5± 0 .1 3vs0 .98± 0 .1 1 ,P <0 .0 1 ) .非穴组与UC模型对照组相比无统计学显著性差异 (P >0 .0 5 ) .结论 :电针足三里穴能够良性下调TNF α生成     

糖化血清蛋白和肿瘤坏死因子与2型糖尿病并发脑梗死的关系

目的　探讨糖化血清蛋白 (GSP)和肿瘤坏死因子 (TNF -α)水平与 2型糖尿病伴发脑梗死 (ACI)的关系。方法　用酮氨氧化酶法 (KAO)和放射免疫法 (RIA)分别测定 30例正常人和 32例 2型糖尿病无并发症患者 ,36例伴发脑梗死患者的血清GSP和TNF -α水平。结果　对照组血清GSP水平为 (2 5 2 2 0± 38 39) μmol/L ,TNF -α水平为 (1 12± 0 2 1) μg/L ;2型糖尿病无并发症患者GSP水平为 (333 6 7± 2 2 2 9) μmol/L ,TNF -α为 (1 77± 0 16 ) μg/L ,2型糖尿病伴发脑梗死患者GSP水平为 (4 17 6 6± 18 71) μmol/L ,TNF -α为 (2 5 9± 0 14) μg/L。统计学结果表明对照组、2型糖尿病无并发症组与伴有脑梗死组间血清GSP和TNF -α有显著差异 (P <0 0 1)。结论　高GSP和TNF -α水平与 2型糖尿病伴发脑梗死具有一定的相关性。     

The relationship between tumor necrosis factor-α gene polymorphisms and acute severe pancreatitis

Objective To investigate the relationship between the presence of the TNF2 allele and plasma concentrations of tumor necrosis factor-α (TNFα) and soluble TNF receptor (sTNF-R) with the development of acute severe pancreatitis (ASP) and severe sepsis.Methods Genomic DNA was prepared from peripheral blood leukocytes. The TNF1 and TNF2 biallelic polymorphisms were identified by analyzing NcoI-digested DNA fragments obtained from PCR products. Plasma levels of TNFα and sTNF-R were measured by EASIA.Results The overall TNF2 allele frequency in ASP patients was comparable to that found in healthy volunteers (29.2% vs. 29.3%, P&gt;0.05). Severe sepsis occurred in 26 of 72 patients. Patients with severe sepsis showed a significantly higher prevalence of TNF2 than those without (46.2% vs. 19.6%, P&lt;0.05). Plasma TNFα, sTNF-R Ⅰ, and sTNF-R Ⅱ levels were (36±31) pg/ml, (5.4±3.5) ng/ml, and (11.2±7.8) ng/ml, respectively, in patients with severe sepsis, and (31±25) pg/ml, (4.6±3.8) ng/ml, and (8.8±6.6) ng/ml in non-severe sepsis subjects. Differences in TNF levels were not statistically significant between patients with ASP and control group (P&gt;0.05). Moreover, there was no correlation between TNF2 allele frequency and TNFα levels ［(37±31） pg/ml vs. （31±25） pg/ml in TNF2 group and TNF1 group, respectively, P&gt;0.05］.Conclusions Our results suggest that there is no relationship between ASP and the TNF2 allele, but that the TNF2 allele is associated with a susceptibility to severe sepsis as a result of ASP.     

血清降钙素原和白细胞介素6检测在感染和非感染性全身性炎症反应鉴别诊断中的作用

目的　评价降钙素原 (PCT)和白细胞介素 6 (IL 6)对感染和非感染引起的全身炎症反应综合征 (SIRS)的鉴别作用。方法　共有 2 0例感染性全身性SIRS及 31例非感染性SIRS患者入选。患者临床出现炎症表现 2 4h内测定血清PCT、IL 6和C反应蛋白 (CRP)水平。同时记录白细胞计数 ,中性粒细胞比例 ,中性粒细胞绝对计数和最高体温。结果　全身性感染患者血清PCT[3 6(1 8,2 7 5)μg/L]、IL 6 (81 0ng/L± 51 6ng/L)、CRP(1 80g/L± 1 0 8g/L)水平及最高体温 (38 6± 1 2℃ )明显高于SIRS患者 [0 5(0 2 ,1 8) μg/L ,2 35ng/L± 1 77ng/L ,1 0 9g/L± 70g/L ,37 9± 0 9℃ ]。所有炎症指标中 ,IL 6和PCT的敏感性 (≥ 80 % )和特异性 (>70 % )最高。由IL 6和PCT构成的感染评分对全身性感染的辨别力最佳 (受试者工作特征曲线下面积为 0 92 3)。结论　与传统炎症指标相比 ,IL 6和PCT有助于鉴别全身性感染和SIRS。     

严重烧伤脓毒症患者骨骼肌蛋白分解代谢的临床研究

目的分析严重烧伤脓毒症患者骨骼肌蛋白降解变化及其生物学机制。方法收集同期收治的20例严重烧伤脓毒症患者(烧伤脓毒症组)和12例整形患者(对照组)的血、24h尿和股四头肌标本,通过放免法测定血浆皮质醇和肿瘤坏死因子(TNF)-α含量,高效液相-色谱分析法检测股四头肌内3-甲基组氨酸(3-MH)含量以及尿中3-MH排出量,核糖核酸印迹法检测股四头肌内编码泛素、E2-14k和蛋白酶体C2亚基的mRNA表达变化。蛋白免疫印迹法检测股四头肌内蛋白酶体C2亚基的蛋白表达变化。结果烧伤脓毒症组血浆内皮质醇含量(478±56)μg/L和TNF-α含量(22·4±3·8)μg/L均显著高于对照组血内皮质醇含量(72±12)μg/L和TNF-α含量(0·5±0·1)μg/L(均P<0·01)。烧伤脓毒症组股四头肌内3-MH含量(4·3±0·6)μmol/g及24h尿内3-MH排出量(456±25)μmol均显著高于对照组股四头肌内3-MH含量(2·5±0·4)μmol/g和24h尿内3-MH排出量(202±29)μmol(均P<0·01)。烧伤脓毒症组股四头肌泛素mRNA2·4kb条带和1·2kb条带的表达分别较对照组增强51%和32%,差异有统计学意义(P<0·01);E2-14k mRNA1·2kb条带的表达较对照组增强75%,差异有统计学意义(P<0·01);蛋白酶体C2亚基mRNA和蛋白表达分别较对照组增强39%和130%,差异有统计学意义(P<0·01)。结论重症烧伤脓毒症时骨胳肌蛋白降解显著增强,体内糖皮质激素及TNF-α含量增加,从基因水平激活细胞内蛋白降解途径-泛素系统是重症烧伤脓毒症患者骨胳肌蛋白降解增强的原因之一。     

冠脉搭桥围手术期肿瘤坏死因子和内皮素的动态变化及意义

目的观察冠状动脉搭桥手术(CABG)中肿瘤坏死因子-α(TNF-α)和内皮素1(ET-1)的动态变化,探讨其病理意义.方法对32例行冠状动脉搭桥术的病人,分别于术前、麻醉诱导期、阻断升主动脉后、开放升主动脉、手术结束时以及术后2、8、24 h等8个时相采集血样.TNF-α及ET-1血浆浓度应用放射免疫方法进行测定.结果 (1)TNF-α水平在阻断升主动脉后较术前明显升高(18.3 ng/L±3.4 ng/L vs 12.1 ng/L±2.0 ng/L,P<0.05),开放升主动脉后继续上升,并达到峰值(22.4 ng/L±3.6 ng/L),后呈下降趋势,但至术后24 h仍维持在较高水平(18.5 ng/L±4.1 ng/L P<0.05).开放升主动脉后心肺再灌注时TNF-α浓度显著高于阻断升主动脉后未开放前(22.4 ng/L±3.6 ng/L vs 18.3 ng/L±3.4 ng/L P<0.05).(2) ET-1血浆浓度在阻断升主动脉后较术前显著上升 (146 ng/L±20 ng/L vs 97 ng/L±14 ng/L,P<0.05).开放升主动脉后下降,术后2 h出现了第二个高峰,达134 ng/L±19 ng/L,后呈下降趋势,至术后24 h降为92 ng/L±18 ng/L.结论 CABG手术中,减轻TNF-α介导的炎症反应是围术期心肺保护的重要策略.CABG围术期血浆ET-1水平升高可能与手术操作和缺血再灌注损伤有关.     

Induction of type Ⅱ alveolar epithelial cells apoptosis in mouse by lipopolysaccharide does not require TNF-α

Objective To examine whether lipopolysaccharide (LPS)-induced apoptosis correlates with TNF-α release by type Ⅱ alveolar epithelial cells (AEC Ⅱ), whether TNF-α knockout (TNF KO) abrogates the induction of apoptosis by LPS and whether TNF-α is sufficient to induce apoptosis in this cell type.Methods AEC Ⅱ were isolated from wild type mice and TNF KO mice. Cells were stimulated with LPS or recombinant murine TNF-α for 24 h. TNF-α in culture supernatant was determined by ELISA following LPS stimulation. Apoptosis was determined by the terminal deoxynucleotidyl transferase end-labeling (TUNEL) assay after treatment with either LPS or TNF-α. Results LPS induced apoptosis in wild type AEC Ⅱ in a concentration-dependent manner. LPS-induced AEC Ⅱ apoptosis was accompanied by an 11-fold increase (from 0.073±0.065 ng/ml in control to 0.94±0.14 ng/ml in 50 μg/ml of LPS, P&lt;0.01) in TNF-α release. However, increasing concentrations (5 or 25 ng/ml) of recombinant murine TNF-α failed to induce AEC Ⅱ apoptosis. In addition, apoptosis did occur in AEC Ⅱ isolated from TNF KO mice following LPS stimulation.Conclusions This study confirms that LPS induces TNF-α release and apoptosis in murine AEC Ⅱ in vitro. Exogenous TNF-α failed to induce AEC Ⅱ apoptosis, and apoptosis occurred following LPS stimulation in cells lacking the ability to produce TNF-α. Taken together, these results suggest that LPS-induced AEC Ⅱ apoptosis occurs by a TNF-α-independent mechanism.     

清除循环炎症因子对体外循环心脏手术患者肾、肺功能的保护作用

目的观察清除循环细胞因子对体外循环心脏直视手术患者术后肾、肺功能的影响。方法30例接受换瓣术的风湿性心脏瓣膜病患者分成两组,每组15例,分别在体外循环(CPB)回路中安放具有吸附细胞因子功能的磺化聚丙烯腈膜(AN69)滤器(实验组),或不具有吸附功能的三醋酸纤维素膜(CT190G)滤器(对照组)。比较两组术前、术中和术后血浆肿瘤坏死因子(TNFα)、白细胞介素(IL)6、IL8、IL10、白细胞介素1受体拮抗剂(IL1ra)、C反应蛋白(CRP)水平并观察两组术后肾、肺功能的变化。结果(1)二组术后TNFα、IL6、IL8、CRP、IL10、IL1ra水平较术前均明显升高(均P<0.05)。CPB结束时,实验组TNFα(10ng/L±3ng/L)、IL6(115ng/L±22ng/L)水平均明显低于对照组TNFα(13ng/L±3ng/L)、IL6(134ng/L±29ng/L)(均P<0.05)。实验组IL10、IL1ra水平仅略低于对照组(均P>0.05)。(2)CPB术后24h,实验组与对照白细胞计数升高幅度分别为(17±3)×109/L和(22±3)×109/L,体温升高幅度1.6℃±0.2℃和2.1℃±0.2℃,心率升高幅度15次/min±4次/min和23次/min±6次/min,CRP升高幅度56mg/L±13mg/L和69mg/L±15mg/L,均明显低于对照组(均P<0.05)。(3)术后24h实验组、对照组尿蛋白分别为0.20g/d±0.08g/d、0.30g/d±0.14g/d,尿NAG酶分别为28U/L±11U/L、38U/L±13U/L,实验组均明显低于对照组(均P<0.05)。实验组内生肌酐清除率(68±7)ml·min-1·1.73m-2明显高于对照组(57±11)ml·min-1·1.73m-2(P<0.05)。(4)CPB结束后60min,实验组气道平台压和气道峰压增加幅度亦明显低于对照组(均P<0.01)。实验组术后停止机械辅助呼吸时间为4.9h±0.6h,明显早于对照组5.8h±0.8h(P<0.05)。结论在CPB中用AN69膜滤器吸附循环炎症因子,能明显改善CPB术后全身炎症反应,减少对肾、肺的损害。     

Serum procalcitonin and interleukin-6 levels may help to differentiate systemic inflammatory response of infectious and non-infectious origin

Objective To evaluate the efficacy of using procalcitonin (PCT) and interleukin-6 (IL-6) to differentiate sepsis from non-infectious systemic inflammatory response syndrome (SIRS). Methods We made a prospective study in a general intensive care unit at Peking Union Medical College Hospital. Twenty patients with sepsis and 31 patients with non-infectious SIRS were enrolled in this study. Serum concentrations of PCT, IL-6 and C-reactive protein (CRP) were determined within 24 h after clinical onset of sepsis or non-infectious SIRS. Leukocyte count, percentage of neutrophils, and absolute neutrophil count, as well as maximal body temperature were also recorded.Results Serum concentrations of PCT, IL-6, and CRP, as well as maximal body temperature, were significantly higher in septic patients ［3.6 (1.8, 27.5) μg/L, 810±516 ng/L, 180±108 g/L, 38.6±1.2℃］ than non-infectious SIRS patients ［0.5 (0.2, 1.8) μg/L, 235±177 ng/L, 109±70 g/L, 37.9±0.9℃］. IL-6 and PCT exhibited the best discriminative power between sepsis and non-infectious SIRS, with sensitivity above 80% and specificity above 70%. A sepsis score with combination of IL-6 and PCT showed the best discriminative power with the area under the receiver operating characteristic curve of 0.923.Conclusions Assessing IL-6 and PCT levels are more reliable ways to differentiate sepsis from non-infectious SIRS, compared with conventional inflammatory parameters.     

异丙肾上腺素对高血压患者单核细胞分泌白细胞介素6及肿瘤坏死因子α的影响

目的:观察异丙肾上腺素(isoproterenol, ISO)对高血压患者单核细胞分泌肿瘤坏死因子α(tumor necrosis factor-alpha ,TNF-α)及白细胞介素6(interleukin-6, IL-6)的影响.方法:选取17例健康志愿者和6例原发性高血压病患者(Ⅰ期)的静脉血样,分离得到单核细胞,用脂多糖(lipopolysaccharide,LPS)刺激细胞后,检测在有或无ISO存在条件下细胞上清液中TNF-α和IL-6含量.结果:(1)在LPS刺激下,高血压组单核细胞分泌TNF-α量较健康对照组显著增加[(1 897±393) ng/L vs. (975±473) ng/L, P＜0.01],但IL-6的分泌在两组间的差异无统计学意义[(5 532±796) ng/L vs. (6 092±2 249) ng/L];(2)在健康对照组和高血压组中,ISO能剂量依赖性抑制LPS引起的单核细胞TNF-α分泌,但对IL-6的分泌则无显著影响;(3)在Ⅰ期高血压患者的单核细胞中,ISO对TNF-α产生的抑制作用与健康对照组相比,差异无统计学意义(P》0.05),给予β肾上腺素受体拮抗剂普萘洛尔可拮抗这种效应.结论:β肾上腺素受体激动可抑制LPS引起单核细胞分泌TNF-α,而对IL-6的分泌无影响,这种抑制效应在Ⅰ期高血压病患者与健康志愿者之间差异无统计学意义.     

Association of TNF2, a TNF-alpha promoter polymorphism, with septic shock susceptibility and mortality: a multicenter study.

CONTEXT: Tumor necrosis factor alpha (TNF-alpha) is believed to be a cytokine central to pathogenesis of septic shock. TNF2, a polymorphism within the TNF-alpha gene promoter, has been associated with enhanced TNF-alpha production and negative outcome in some severe infections. OBJECTIVES: To investigate the frequency of the TNF2 allele in patients with septic shock and to determine whether the allele is associated with the occurrence and outcome of septic shock. DESIGN: Multicenter case-control study conducted from March 1996 to June 1997. SETTING: Seven medical intensive care units in university hospitals. SUBJECTS: Eighty-nine patients with septic shock and 87 healthy unrelated blood donors. MAIN OUTCOME MEASURES: Frequency of the TNF2 allele among patients with septic shock and among those who died and the level of corresponding TNF-alpha concentrations. RESULTS: Mortality among patients with septic shock was 54%, consistent with the predicted mortality from the Simplified Acute Physiologic Score (SAPS II) value. The polymorphism frequencies of the controls and the patients with septic shock differed only at the TNF2 allele (39% vs 18% in the septic shock and control groups, respectively, P =.002). Among the septic shock patients, TNF2 polymorphism frequency was significantly greater among those who had died (52% vs 24% in the survival group, P =.008). Concentrations of TNF-alpha were higher in 68% and 52% with the TNF2 and TNF1 polymorphisms, respectively, but their median values (48 pg/mL vs 29 pg/mL) were not statistically different (P = .31). After controlling for age and the probability of death, derived by the SAPS II score, multiple logistic regression analysis showed that, for the same rank of SAPS II value, patients with the TNF2 allele had a 3.7-fold risk of death (95% confidence interval, 1.37-10.24). CONCLUSION: The TNF2 allele is strongly associated with susceptibility to septic shock and death due to septic shock.     

BURDEN OF ABNORMAL HEMATOPOIETIC CLONE IN PATIENTS WITH MYELODYSPLASTIC SYNDROMES

MYELODYSPLASTIC syndromes (MDS) is agroup of clone hematopoietic stem cell diseasescharacterized by dysplasia and ineffective hem-atopoiesis in one or more of the myeloid cell lines·1Studiesindicated that recurring chromosomal abnormalities werefound in4…