Inflammatory biomarkers in blood of patients with acute brain ischemia

Although many failed surrogate markers are provided in the literature, inflammation may contribute to the outcome of ischemic stroke. In 50 consecutive patients with acute ischemic stroke, in the absence of symptoms and signs of concomitant infection, we evaluated a panel of biomarkers reported to be variably associated with brain ischemia, and correlate their serum level with the brain lesion volume and clinical outcome. Infarct size was calculated on computed tomography (CT) scans by means of the Cavalieri's method. Neurological impairment was scored by using the Glasgow Coma Scale, Glasgow Outcome Scale and National Institutes of Health (NIH) scales at stroke onset and 3-month follow-up. Some markers showed a direct significant correlation with both initial and final NIH scale and with infarct size, particularly tumor necrosis factor alpha (TNF-alpha) (P=0.002), intercellular adhesion molecule-1 (P<0.01) and matrix metalloproteinase-2/9 (P=0.001). In contrast to previous reports, interleukin-6 (IL-6) serum level showed a significant inverse correlation with both final neurological impairment and infarct size (P<0.001). This novel finding allows us suggesting that IL-6, in the context of a complex pro-inflammatory network occurring during stroke, is associated with neuroprotection rather than neurotoxicity in patients with ischemic brain injury.     

IL-6对人精子顶体反应影响机制的初步探讨

目的:探讨IL-6对人精子顶体反应(AR)的影响机制。方法:采用BAEE/ADH法测定精子顶体酶的活性,以及通过FITC-PSA法检测精子顶体反应。结果:IL-6可诱导精子顶体酶及超氧化物歧化酶(SOD)的活性,促进精子顶体反应;胞外Ca2+单独不能诱导精子顶体反应,且没有胞外Ca2+的参与,IL-6也不能诱导精子顶体反应;蛋白激酶C(PKC)抑制剂calphC能逆转IL-6诱导的精子顶体反应。结论:IL-6对精子顶体反应有一定的促进作用,可能通过诱导精子的顶体酶和SOD活性等途径来实现,在此作用中,也涉及了PKC的激活,且还需要外源性Ca2+的参与。     

rhIL－1α对小鼠骨髓细胞长周期培养中造血细胞增殖的影响

应用小鼠骨髓细胞长周期培养（ＬＴＢＭＣ）体系，观察重组人白细胞介素－１α（ｒｈＩＬ－１α）对造血细胞增殖的影响。结果显示，经ｒｈｌＬ－１α作用后，小鼠ＬＴＢＭＣ中悬浮细胞数增多，其中粒单系祖细胞（ＣＦＵ－ＧＭ）数量也明显增加，维持时间延长。表明ｒｈＩＬ－１α能促进小鼠造血细胞在体外ＬＴＢＭＣ中增殖并分化，而且与剂量有关系。ｒｈＩＬ－１α加入的时间，以骨髓细胞２次接种时同时加入为好，延迟加入则作用减弱。本实验对骨髓干、祖细胞体外扩增和自体骨髓移植等方面的研究有一定意义。     

Fever and feeding in the rat: Actions of intrahypothalamic interleukin-6 compared to macrophage inflammatory protein-1β (MIP-1β)

The chemokines, macrophage inflammatory protein-1 (MIP-1) and its subunit MIP-1β, induce an intense fever in the rat when they are injected directly into the anterior hypothalamic, pre-optic area (AH/POA), a region containing thermosensitive neurons. The purpose of this study was to compare the central action on body temperature (T_b) of MIP-1β with that of interleukin-6 (IL-6), which also has been implicated in the cerebral mechanism underlying the pathogenesis of fever. Following the stereotaxic implantation in the AH/POA of guide cannulae for repeated micro-injections, radio transmitters which monitor T_b continuously were inserted intraperitoneally in each of 15 male Sprague-Dawley rats. Each micro-injection was made in a site in the AH/POA in a volume of 1.0 μl of pyrogen-free artificial CSF, recombinant murine MIP-1β, or recombinant human IL-6. MIP-1β in a dose of 25 pg evoked an intense fever characterized by a short latency, a mean maximum rise in T_b of 2.4 ± 0.21°C reached by 3.7 ± 0.42 hr, and a duration exceeding 6.5 hr. Injected into homologous sites in the AH/POA, IL-6 induced a dose dependent fever of similar latency and a mean maximal increase in T_b of 1.2 ± 0.25°C, 1.8 ± 0.15°C, and 2.1 ± 0.22°C and duration of 6.2 ± 1.28 hr, 6.7 ± 0.49 hr, and 6.8 ± 0.65 hr when given in doses of 25, 50, and 100 ng, respectively. These results show that MIP-1β and the highest dose of IL-6 induce a fever of comparable intensity, but MIP-1β exerts its action in a much lower concentration. Thus, the de novo synthesis and subsequent action of the MIP-1 family of cytokines on neurons of the AH/POA in response to a pyrogen challenge apparently play a functional role in the pathogenesis of fever. Further, the endogenous activity of IL-6 in the hypothalamus which is enhanced in response to a lipopolysaccharide also may reflect its essential part in the acute phase response to a bacterial challenge. Copyright © 1994 Wiley-Liss, Inc.     

短波紫外线照射对小儿肺炎及中性粒细胞吞噬功能和IL－2的影响

用短波紫外线照射患儿腰背部皮肤辅助治疗小儿肺炎，提示紫外线治疗组与对照组相比，显著缩短患儿发热。咳嗽及肺部湿罗音消失时间（Ｐ＜０．０１）。用化学发光法测定中性粒细胞吞噬功能，治疗组患儿血液内中性粗细胞吞噬功能显著提高（Ｐ＜０．０５）。同时测定治疗组患儿血中ＩＬ－２低于对照组（Ｐ＜０．０５），并对上述结果机理进行了探讨。     

胃癌患者红细胞免疫功能的变化

运用简单形态学方法测定了３０例胃癌患者红细胞免疫功能，结果表明：胃癌患者红细胞Ｃ３ｂ受体花环率及肿瘤红细胞花环率显著低于正常对照（Ｐ＜０．０１）及慢性良性胃病患者（Ｐ＜０．０１），而免疫复合物花环率则高于正常人（Ｐ＜０．０１）及慢性良性胃病患者（Ｐ＜０．０１）；Ⅲ、Ⅳ期胃癌患者肿瘤红细胞复合物花环率明于低于Ⅰ、Ⅱ期患者（Ｐ＜０．０１）；贲门癌肿瘤红细胞花环率显著低于胃窦（体）癌患者（Ｐ＜０．０１）     

Serum levels of interleukin-6 and tumour-necrosis-factor-alpha are not correlated to disease activity in patients with rheumatoid arthritis after treatment with low-dose methotrexate

Abstract. Cytokines are major mediators of inflammatory responses in rheumatoid arthritis. Some of them have been shown to correlate with the disease activity and thus are proposed to be used for monitoring patients. Therefore the effects of a low-dose therapy with methotrexate on serum concentrations of interleukin-6 (IL-6) and tumour-necrosis-factor-alpha (TNF-α) were examined in eight patients with seropositive rheumatoid arthritis. Serum levels of IL-6 and TNF-α were significantly elevated in patients compared to healthy controls. Before the onset of MTX treatment IL-6 concentrations were correlated to the c-reactive protein ( P < 0·05) but the correlation was abolished after treatment. For TNF-α no correlations neither before nor after treatment were observed. Both cytokines remained substantially elevated after MTX treatment despite a clear reduction in disease activity. Thus we suggest that one of the effects of MTX might be the inhibition of some of the actions of IL-6 and TNF-α.     

TIL／rIL－2免疫过继疗法治疗晚期瘤性胸水初探

７例晚期瘤性胸水的肿瘤浸润淋巴细胞（ＴＩＬ）经体外诱导培养３～１２ｄ，扩增１～９倍．其ＣＤ８及ＩＬ－２Ｒ阳性细胞百分率增加２．４３和２．７６倍；ＮＫ活力增加３．２９倍，与培养前后比较有显著差异。ＴＩＬ／ｒＩＬ－２（重组人白细胞介素２）胸腔内回输后，４例胸水及胸水中肿瘤细胞消失，癌胚抗原（ＣＥＡ）回至正常水平，２例胸水减少，１例因多房性胸水停止治疗，ＣＥＡ水平上升。经１～８个月随访患者心、肝、肾功能正常。     

胃癌组织中KAI1、nm23及P53的表达及其临床意义

目的:探讨正常胃黏膜、不典型增生胃黏膜及癌组织中KAI1、nm23及P53蛋白的表达．方法:应用SP法免疫组化检测22例正常胃黏膜,65例不典型增生胃黏膜及74N胃癌组织中的KAI1、nm23及P53蛋白的表达．结果:正常胃黏膜、不典型增生胃黏膜及胃癌组织中,KAI1和nm23阳性率呈降低趋势,组间差异性有统计学意义(x2=20．885, P<0．001;x2=29．133,P<0．05):P53蛋白阳性表达率呈增加趋势,组间差异性有统计学意义(x2=21．954,P<0．001)．Fisher精确概率检验显示:在胃癌组中不同的浸润深度、有无淋巴结转移和脉管侵犯组内KAI1、nm23及 P53组阳性表达率的差异性有统计学意义(x2 =20．885,P<0．001;x2=29．133,P<0．05;x2= 21．954,P<0．001);而在年龄、性别组间的差异性无统计学意义．Spearman等级相关分析显示 KAI1与nm23表达呈正相关(r=0．859,P<0．05); KAI1与P53表达呈负相关(r=-0．859,P<0．05), nm23与P53表达呈负相关(r=-0．874,P<0．05) 结论:抑癌基因KAI1与nm23的缺失以及P53 蛋白的过表达可能是胃癌发生、发展及浸润和转移的重要原因之一．     

肝炎肝硬化患者血清IL-10、IL-18水平的变化及意义

目的探讨血清IL10、IL18在肝炎肝硬化的发病机制中的作用。方法62例肝炎肝硬化患者根据childpugh分级法分为3组:childpughA级组19例、childpughB级组23例和childpughC级组20例。采用ELISA法检测3组患者和20例健康献血员血清IL10、IL18的水平。结果childpughA、B、C级组血清IL18水平均明显高于对照组(P均<0.01),childpughA级组血清IL10水平略高于对照组,但无显著性差异(P>0.05);childpughB、C级组明显低于对照组(P<0.05);有腹水组、无腹水组血清IL18水平均明显高于对照组(P均<0.01),有腹水组血清IL10水平明显低于无腹水组、对照组(P<0.05,P<0.01);血清IL10水平与血清IL8水平呈负相关(r=-0.51,P<0.01);血清白蛋白水平与血清IL10水平呈正相关(r=0.566,P<0.01),与血清IL8水平呈负相关(r=-0.315,P<0.01);血清凝血酶原活动度与血清IL10水平呈正相关(r=0.506,P<0.01),与血清IL18水平呈负相关(r=-0.463,P<0.01);血清总胆红素水平与血清IL8水平呈正相关(r=0.677,P<0.01),与血清IL10水平呈负相关(r=-0.339,P<0.01)。结论IL10、IL18在肝炎肝硬化的发病机制中起一定的作用,其水平与肝损害程度密切相关。