血栓闭塞性脉管炎患者血栓素、前列环素及血液流变学指标的检测分析

目的 :探讨血栓闭塞性脉管炎患者血栓素B2 、前列环素与血液流变学指标的变化及其与发病机制的关系。方法 :用放射免疫法测定TXA2 和PGI2 的代谢产物血栓素B2 (TXB2 )、6 酮 前列腺素F1α( 6 K PGF1α) ,LBY N6A自清洗旋转式粘度计测定血液流变学指标 ,并与对照组对比分析。结果 :血栓闭塞性脉管炎患者TXB2 ( 53.59± 83.2 1ng/L)、6 K PGF1α( 14 .50± 3.4 5ng/L) ,与对照组相比差异显著 ;全血高切粘度、低切粘度、血浆粘度及纤维蛋白原疾病组均高于对照组 ,差异具有统计学意义。结论 :血栓闭塞性脉管炎患者存在TXA2 /PGI2失衡 ,并与血液流变学的改变有密切关系     

EB病毒LMP1在鼻咽癌细胞中通过IκBα的降解活化NF-κB

目的　阐明鼻咽癌细胞中EB病毒编码的潜伏膜蛋白 1(LMP1)活化核转录因子NF κB的机制。方法　利用强力霉素Dox诱导表达LMP1的鼻咽癌细胞株Tet on LMP1 HNE2为实验模型 ,首先应用免疫印迹方法测定Dox诱导后不同时相LMP1的表达动力学以及IκBs蛋白量及功能的改变。进而用间接免疫荧光法检测NF κB的亚细胞定位。最后采用瞬间共转染及报道基因活性分析分析NF κB的活性。结果　在鼻咽癌细胞Tet on LMP1 HNE2中 ,Dox处理 15分钟后LMP1的表达迅速升高并维持与较高水平直至 12 0分钟。LMP1的诱导性表达导致IκBα的磷酸化并降解 ,但IκBα蛋白总量无改变。继IκBα的磷酸化并降解 ,NF κB(P6 5 )自胞浆易位至胞核且活性升高。IκBα的显性负性突变子抑制NF κB(P6 5 )的核易位及报道活性。LMP1的诱导性表达并未引起IκBβ蛋白水平变化。结论　在鼻咽癌细胞Tet on LMP1 HNE2中 ,EB病毒LMP1通过IκBα的磷酸化并降解激活核转录因子NF κB的活性 ,并且 ,LMP1诱导的NF κB活性能被IκBα的显性负性突变子完全抑制。IκBβ在此信号传导途径中无改变。LMP1表达前后IκBα蛋白总量维持恒定可能是由于NF κB的活化迅速启动了IκBα的重头合成这一自身调节环路所致。     

氧化低密度脂蛋白功能性调节人内皮细胞的生长调节致癌基因α

目的　探讨oxLDL对人内皮细胞的CXC亚家族趋化因子GROα的调节作用及生理意义。方法　超高速离心得LDL ,氧化后得oxLDL。逆转录PCR分析人内皮细胞系ECV30 4细胞GROαmRNA。GAPDH被用作PCR中正常改变的对照物。酶联免疫检测仪测定ECV30 4细胞表面连接及分泌到溶液中的GROα蛋白。静态细胞粘附试验测定ECV30 4细胞表面连接的GROα蛋白的生理意义。结果　正常ECV30 4细胞不表达GROαmRNA ;OxLDL显著调节其表达 ,诱导效应首先出现在处理后 1h ,最大在 2h ,在 4h时下降。相比较 ,LDL对其mRNA表达没有影响。正常ECV30 4细胞低水平表达细胞表面的GROα蛋白。OxLDL呈浓度依赖性、时间依赖性地上调其表面的GROα蛋白。相比较 ,LDL对其表面表达的GROα蛋白无调节作用。OxLDL对ECV30 4细胞分泌到细胞溶液中GROα蛋白很少有影响。 4 0 μg/mloxLDL处理ECV30 4细胞 2 4h ,造成显著的人单核细胞系U937细胞粘附到ECV30 4细胞数目的增加。用GROα抗体预处理oxLDL刺激的ECV30 4细胞 ,可显著减低U937细胞粘附到ECV30 4细胞的U937细胞数目 (大约 2 / 3)。结论　oxLDL可能功能性上调内皮细胞GROα的表达。     

尿毒症及血透对血清一氧化氮浓度的影响及其临床意义

为研究尿毒症及血液透析对血清一氧化氮 (NO)浓度的影响及其临床意义 ,应用硝酸盐还原酶法检测了 1 0例尿毒症未透析患者、1 4例维持性血液透析患者透析前后及 1 0例正常对照者血清NO浓度。结果 :尿毒症未透析及血透患者NO水平均较正常对照显著升高 (P <0 .0 5) ,且尿毒症未透析患者血NO浓度与肿瘤坏死因子 α水平呈显著性正相关 (r =0 .858,P <0 .0 0 1 )。血液透析后NO浓度较透析前显著降低 (P <0 .0 5) ,但透析间期又会导致其蓄积。结果提示 :NO的蓄积对尿毒症的临床表现可能有一定影响。     

糖尿病患者血清中IL-4、TNF-a的检测及分析

目的 探讨白介素４（ＩＬ－４）、肿瘤坏死因子（ＴＮＦ－ａ）水平与糖尿病关系。方法 采用ＥＬＩＳＡ法测定５４例糖尿病患者及４０例健康人血清ＩＬ－４、ＴＮＦ－ａ含量。结果 糖尿病患者ＩＬ－４平均含量明显低于健康人（Ｐ〈０．０５）,且与血糖一负相关（ｒ＝－０．３４７,Ｐ〈０．０５）。ＴＮＦ－ａ含量略高于对照组,但无统计学意义。结论 糖尿病患者内存在细胞免疫功功能紊乱,自身免疫功能调节失衡影响糖尿病的发生     

GNAS gene mutations affecting XLαs and bone health: A long neglected relationship

The GNAS locus is an imprinted site. The α-subunit of the stimulatory G protein (Gsα) and extralarge variant (XLαs) are the two important products of the GNAS locus. The abnormal expression of Gsα is associated with pseudohypoparathyroidism (PHP) and related disorders, including Albright hereditary osteodystrophy (AHO), pseudopseudohypoparathyroidism (PPHP), and progressive osseous heteroplasia (POH). XLαs protein can mimic the catalytic intracellular synthesis of cyclic adenosine monophosphate (cAMP) by Gsα in response to parathyroid hormone (PTH) stimulation, which may be involved in the pathogenesis of PPHP and POH in patients with paternal GNAS defects. A paternally inherited nonsense variant in the first exon of XLαs in an adult patient may be associated with fractures and osteopetrosis. The relationship between the XLαs product of the GNAS locus and bone remodeling may have been overlooked. Here, we summarize the phenotypes of genetic mouse models and clinical cases of XLαs variations and suggest that the abnormal paternal expression of XLαs may be associated with the development of POH and affect osteoblast and osteoclast differentiation.     

针刺对糖尿病视网膜病变免疫调节机理的研究

目的：探讨针刺治疗糖尿病视网膜病变的机理,并加以论证,为其临床应用提供理论依据。方法：选择大鼠建立糖尿病视网膜病变动物模型,分别以针刺治疗及胰岛素治疗,并设正常对照组及模型对照组,于３个月及６个月取大鼠血清及视网膜检测ＩＬ－２和ＴＮＦ及电镜检察。结果：各时段ＩＬ－２针刺及胰岛素治疗组明显高于模型对照组：ＴＮＦ明显氏于模型对照组。两与正常对照组无显性差异,针刺后电镜观察视网膜微血管病变得到改善。     

类风湿性关节炎患者血清IL-6、TNF水平变化及其意义探讨

采用细胞生物学方法测定类风湿性关节炎（ Ｒ Ａ）１４ 例血清 Ｉ Ｌ－ ６ 、 Ｔ Ｎ Ｆ 水平,均显著高于正常对照组（ Ｐ＜ ０ ．００１） 。相关分析显示 Ｉ Ｌ－ ６ 与 Ｔ Ｎ Ｆ 水平变化呈正相关（ Ｐ＜ ０ ．０１） , Ｉ Ｌ－ ６ 、 Ｔ Ｎ Ｆ 与血沉亦呈正相关（ Ｐ＜０ ．０５） 。认为, Ｉ Ｌ－ ６ 、 Ｔ Ｎ Ｆ 参与 Ｒ Ａ 的发病,两者在致病中有协同相同;其水平变化与 Ｒ Ａ 的活动性及血沉相关。     

Pentoxifylline reduces plasma tumour necrosis factor-alpha concentration in premature infants with sepsis

Increased plasma tumour necrosis factor (TNF) concentration correlates with mortality in sepsis. We suggested that pentoxifylline (PTXF), which is known to inhibit TNF production, may improve survival and attenuate clinical symptoms of sepsis in neonates. Plasma TNF levels were evaluated in 29 newborn infants with sepsis. Patients were randomly assigned into two groups, receiving PTXF in a dose of 5 mg/kg per hour for 6 h or placebo (saline), on 3 successive days. Both groups were subjected to the same conventional therapy. TNF was evaluated before and after PTXF or placebo administration on the 1 st and 3rd days of therapy. There was a statistically significant decrease in plasma TNF level in the PTXF group when the values before the first and after the last PTXF infusion were compared [mean: 671.5 pg/ml; SD: 438; med: 729.6 vs mean: 41.0 pg/ml; SD: 64.1; med: 11.5;P<0.000004]. In the placebo group, decrease was not significant [mean: 633.0 pg/ml SD: 488.6; med: 618.9 vs 246.9 pg/ml; SD: 243.9; med: 191.0]. A significantly higher plasma TNF level, evaluated after the last PTXF infusion, was found in the placebo group [246,9 pg/ml vs 41.0 pg/ml;P<0.001]. Only one of four infants with signs of shock in the placebo group survived, whereas all of five newborns with symptoms of shock in the PTXF group survived [P<0.04]. An increased incidence of metabolic acidosis [P<0.05], necrotizing enterocolitis [P<0.04] and renal insufficiency [P<0.05] was observed in infants in the placebo group.Conclusion PTXF inhibits production of TNF and may have therapeutic value in the treatment of premature infants with sepsis complicatea by shock.     

IL-1β and TNF-α produced by peripheral blood mononuclear cells before and during interferon therapy in patients with chronic hepatitis C

We investigated the spontaneous and phytohemagglutinin-stimulated production of interleukin-1 (IL-1) and tumor necrosis factor- (TNF-) by peripheral blood mononuclear cells in patients with chronic hepatitis C during treatment with interferon- (IFN-). Spontaneous productions of these were significantly higher in patients with chronic hepatitis C than in healthy subjects. For patients prescribed interferon, stimulated production of TNF- was significantly higher in complete responders than in partial responders, but the differences were small between the other cytokine levels and outcome of IFN treatment. Spontaneous production of these cytokines was higher in patients with genotype III with complete response than in genotype III patients with a partial response, but this was not the case in patients with genotype II. There was a negative correlation between these cytokines and histological activity index. Spontaneous production of cytokines was decreased only in complete responders after the administration of interferon. These data suggest that the elevated production of cytokines in patients with chronic hepatitis C may be due to host response to the virus, and monitoring cytokines along with alanine aminotransferase and hepatitis C virus RNA during treatment may provide more precise information of the effectiveness of therapy.