γ-干扰素对病毒性心肌炎患者可溶性白细胞介素-2受体和肿瘤坏死因子的影响

目的 :观察 γ-干扰素对病毒性心肌炎 ( VMC)患者血清可溶性白细胞介素 - 2受体 ( s IL-2 R)和肿瘤坏死因子 ( TNF)水平及临床疗效的影响。方法 :将 52例随机分为常规治疗组 (常规组 )和 γ-干扰素治疗组 (干扰素组 )。常规组采用常规治疗 ,干扰素组在常规治疗的基础上加用 γ-干扰素注射液。两组均于治疗前后测定血清 s IL- 2 R和 TNF水平及临床疗效评价。结果 :治疗后两组血清 s IL- 2 R和 TNF水平均有下降 ,但治疗组下降更为明显 ,与治疗前比较差异有非常显著性意义( P <0 .0 0 1 )。结论 :γ-干扰素具有明显降低 VMC患者血清 s IL- 2 R和 TNF水平作用 ,促进病情恢复。     

胃癌患者可溶性白细胞介素-2受体与肿瘤坏死因子-α水平的临床观察

为观察可溶性白细胞介素－２受体（ｓＩＬ－２Ｒ）和肿瘤坏死因子－α（ＴＮＦ－α）对胃癌的诊断及估计预后的价值，应用酶联免疫双抗夹心法对７８例胃癌患者及对照者血清检测上述两种成分，进行临床观察。结果发现：胃癌患者血清ｓＩＬ－２Ｒ和ＴＮＦ－α水平明显高于胃良性疾病和正常人（均Ｐ＜０．０１）；胃癌Ⅲ、Ⅳ期高于Ⅰ、Ⅱ期（均Ｐ＜０．０１）；手术切除后（根治性或姑息性）ｓＩＬ－２Ｒ和ＴＮＦ－α显著下降（均Ｐ＜０．０１）；手术后复发或转移患者血清中ｓＩＬ－２Ｒ和ＴＮＦ－α含量升高（均Ｐ＜０．０１）；如果患者血清ｓＩＬ－２Ｒ含量高于１０００ｋＵ／Ｌ同时伴有ＴＮＦ－α持续高于１２０μｇ／Ｌ，预兆生存期短。提示监测胃癌患者血清ｓＩＬ－２Ｒ和ＴＮＦ－α水平对临床诊断、病情估计和预后有重要意义     

伤寒患者血清可溶性白细胞介素—2受体和肿瘤坏死因子水平变化

伤寒患者血清可溶性白细胞介素２受体和肿瘤坏死因子水平变化沈燕关磊晶熊金凤王成勇本试验动态观察了伤寒患者不同病期中血清可溶性白细胞介素２受体（ｓＩＬ２Ｒ）和肿瘤坏死因子（ＴＮＦ）水平的变化，以探讨二者在伤寒发病机制中所起的作用。现将结果报道如下。...     

风湿热患儿血清肿瘤坏死因子-α和可溶性白细胞介素-2受体水平变化及临床意义

风湿热 (ＡＲＦ)是一组全身性结缔组织病 ,发病与Ａ族Ｂ型溶血性链球菌感染引起的免疫反应有关。本文应用单克隆抗体酶联免疫吸附 (ＥＬＩＳＡ)法检测ＡＲＦ患儿活动期和静止期血清肿瘤坏死因子 α(ＴＮＦ α)、可溶性白细胞介素 2受体 (ｓＩＬ 2Ｒ)水平 ,探讨其在ＡＲＦ发病中的作用及临床意义。1　资料与方法1 1　临床资料根据 1992年Ｊｏｎｅｓ修订标准[1] 收集 1995— 1999年间在我院住院或门诊确诊的风湿热患儿 5 6例 ,其中风湿活动期30例 (活动组 ) ,男性 17例 ,女性 13例 ,年龄 5～ 16岁 ,平均(10± 4)岁 ,风湿性关节炎 (ＲＡ) 12例…     

病毒性心肌炎可溶性白细胞介素2受体、自然杀伤细胞活性及T细胞亚群的检测

应用单克隆与多克隆双抗体夹心法检测３６例病毒性心肌炎（ＶＭＣ）及２４例正常人（ＮＣ）的血清可溶性白细胞介素２受体（ｓＩＬ－２Ｒ），同时测定外周血自然杀伤细胞（ＮＫＣ）活性和Ｔ淋巴细胞亚群。结果显示ＶＭＣ患者ｓＩＬ－２Ｒ明显高于ＮＣ组（Ｐ＜０．００１）．而ＮＫＣ活性明显低于ＮＣ组（Ｐ＜０．０１），Ｔ细胞亚群与ＮＣ组比较，急性ＶＭＣ患者总Ｔ细胞（ＣＤ３），辅助性Ｔ细胞（ＣＤ４）和抑制性Ｔ细胞（ＣＤ８）均减少，ＣＤ４／ＣＤ８比值显著降低（Ｐ＜０．０５．０．０１），以细胞免疫功能低下为明显；而ＶＭＣ后遗症期患者ＣＤ３、ＣＤ４与ＮＣ组无差异（Ｐ＞０．０５），ＣＤ８显著降低（Ｐ＜０．０５），ＣＤ４／ＣＤ８比值显著高于ＮＣ组（Ｐ＜０．０５），以细胞免疫调节失衡为主。上述结果提示细胞免疫功能低下及免疫功能失调为ＶＭＣ发病及影响预后的重要因素。     

胃癌患者血清可溶性白细胞介素—2受体初步研究

应用双抗体夹心ＥＬＩＳＡ法对３０例胃癌患者血清ＳＩＬ－２Ｒ水平进行测定，结果表明，胃癌患者血清ＳＩＬ－２Ｒ水平明显高于正常对照（Ｐ＜０．０１）及慢性良性胃病患者（Ｐ＜０．０５）；Ⅲ－Ⅳ期患者血清ＳＩＬ－２Ｒ水平显著高于Ｉ－ＩＩ期患者（Ｐ＜０．０５）；低度分化者较中度分化者ＳＩＬ－２Ｒ水平明显升高（Ｐ＜０．０１）；贲门癌患者ＳＩＬ－２Ｒ水平较胃窦（体）癌者高，但未达到统计学差别（Ｐ＞０．０５）；胃癌     

病毒性心肌炎患者血清一氧化氮和肿瘤坏死因子含量变化及意义

目的:探讨病毒性心肌炎(VMC)患者血清一氧化氮(NO),肿瘤坏死因子(TNF)含量的变化及其意义。方法:检测70例病毒性心肌炎患者血清一氧化氮和肿瘤坏死因子含量,选择30例健康体检者作对照组。结果:VMC患者血清NO和TNF水平明显高于对照组(P<0.01),且二者含量呈显著正相关(P<0.05)。结论:血清NO和TNF含量增加是VMC病理生理特征之一,且二者在VMC发病中具有协同作用。     

北冬虫夏草多糖对人肿瘤坏死因子α、白细胞介素2及其可溶性受体水平的影响

研究北冬虫夏草多糖对人外周血单个核细胞（ＰＢＭＣ）分泌肿瘤坏死因子α（ＴＮＦ－α），生成可溶性白细胞介素２受体（ｓＩＬ－２Ｒ）及人外周血淋巴细胞（ＰＢＬ）分泌白细胞介素２（ＩＬ－２）的影响。结果表明：北冬虫夏草多糖在１０～５０ｍｇ·Ｌ－１浓度时，刺激单个核细胞分泌ＴＮＦ－α（Ｐ＜０．０５）。在０．１～１０ｍｇ·Ｌ－１浓度时，刺激单个核细胞生成ｓＩＬ－２Ｒ（Ｐ＜０．０５，Ｐ＜０．０１），且在一定浓度范围内ＴＮＦ－α及ｓＩＬ－２Ｒ水平随北冬虫夏草多糖浓度增加而升高；北冬虫夏草多糖对刀豆蛋白Ａ（ＣｏｎＡ）刺激的人外周血淋巴细胞分泌ＩＬ－２水平有明显促进作用（Ｐ＜０．０５）。     

TNF-α和IL-6血清检测在儿童急性病毒性心肌炎诊断中的价值

目的探讨急性病毒性心肌炎患儿血清肿瘤坏死因子-α（TNF-α）及白介素-6（IL-6）水平变化及其临床价值。方法应用放射免疫法（RIA）和酶联免疫法（EIISA）,检测53例急性病毒性心肌炎患儿及20名健康儿童血清中TNF—α及IL-6含量。结果心肌炎组血清TNF—α和IL-6水平分别为（526．7±32．9）mg／L和（3．23±0．53）mg/L,而健康组分别为（383．1±27．5）mg／L和（1．63±0．22）mg／L,二者相比差异有统计学意义（P〈0．05）;临床治愈后,心肌炎组TNF—α及IL-6分别降至（407．3±34．4）mg／L和（1．97±0．29）mg／L,与正常组相比差异无统计学意义（P〉0．05）。结论检测TNF—α及IL-6血清水平及其变化,有助于判断急性病毒性心肌炎患儿病情及心肌损害程度。     

病毒性心肌炎患者血清一氧化氮与肿瘤坏死因子含量的测定及其意义

目的 :探讨一氧化氮 (NO )及肿瘤坏死因子 -α(TNF-α)在病毒性心肌炎 (VMC)患者血清中含量变化及其临床意义。方法 :应用比色法和酶联免疫法测定 6 0例 VMC患者和 40例健康对照者血清 NO和 TNF-α含量。结果 :VMC患者血清 NO和 TNF-α含量均较健康者显著增高 (P <0 .0 1) ,且二者含量变化呈显著正相关 (P<0 .0 5 )。结论 :高浓度的 NO及 TNF-α均与 VMC的病理生理改变有关 ,推测心肌炎患者体内高浓度的 TNF-α可以促进 N O的合成 ,二者协同作用在本病发生中有重要意义     

Study of tumor necrosis factor receptor in the inflammatory bowel disease

Ulcerative colitis(UC) and Crohn’s disease(CD) are part of Inflammatory Bowel Diseases(IBD) and have pathophysiological processes such as bowel necrosis and enteric neurons and enteric glial cells.In addition,the main inflammatory mediator is related to the tumor necrosis factor-alpha(TNF-α).TNF-α is a mediator of the intestinal inflammatory processes,thus being one of the main cytokines involved in the pathogenesis of IBD,however,its levels,when measured,are present in the serum of patients wit...     

吸烟、肿瘤坏死因子及其受体与慢性阻塞性肺疾病

慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)发病率高.发病机制不清.外界环境的刺激导致气道和血管损伤与修复的失平衡可能与COPD的发生相关.其中吸烟致细胞因子、炎症细胞及炎症介质增多,气道和肺实质慢性炎症,导致气道损伤和重构.最终导致气流受限,在肺气肿的形成中起主要作用.肿瘤坏死因子a是重要的炎症因子,通过其主要受体肿瘤坏死因子受体1参与COPD的形成,在COPD的发生、发展中起重要作用.     

不稳定型心绞痛血清中IL-8和TNFa的变化

目的　探讨白细胞介素 -8(IL-8)、肿瘤坏死因子 -a (TNF a)与冠心病不稳定型心绞痛的关系。方法　采用酶联免疫吸附法 (ELISA法 )测定 2 6例冠心病不稳定型心绞痛 ,2 5例稳定型心绞痛及 1 8例正常健康者血清中IL-8、 TNF a的水平。结果　不稳定型心绞痛组、稳定型心绞痛组血清中 IL-8、TNF a水平明显高于正常健康对照组(P<0 .0 0 1 ) ,不稳定型心绞痛组与稳定型心绞痛组比较 ,也存在显著性差异 (P<0 .0 5 )。结论　IL-8、TNF a参与了冠心病不稳定型心绞痛的病理发生过程     

Tumor necrosis family receptor superfamily member 9/tumor necrosis factor receptor-associated factor 1 pathway on hepatitis C viral persistence and natural history

Hepatitis C virus(HCV) infection is an excellent immunological model for understanding the mechanisms developed by non-cytopathic viruses and tumors to evade the adaptative immune response. The antigen-specific cytotoxic T cell response is essential for keeping HCV under control, but during persistent infection, these cells become exhausted or even deleted. The exhaustion process is progressive and depends on the infection duration and level of antigenemia. During high antigenic load and long duration of infection, T cells become extremely exhausted and ultimately disappear due to apoptosis. The development of exhaustion involves the impairment of positive co-stimulation induced by regulatory cytokines, such as transforming growth factor beta 1. This cytokine downregulates tumor necrosis factor receptor(TNFR)-associated factor 1(TRAF1), the signal transducer of the T cell co-stimulatory molecule TNFR superfamily member 9(known as 4-1 BB). This impairment correlates with the low reactivity of T cells and an exhaustion phenotype. Treatment with interleukin-7 in vitro restores TRAF1 expression and rescues T cell effector function. The process of TRAF1 loss and its in vitro recovery is hierarchical, and more affected by severe disease progression. In conclusion, TRAF1 dynamics on T cells define a new pathogenic model that describes some aspects of the natural history of HCV, and sheds light on novel immunotherapy strategies for chronic viral infections and cancer.     

Fractional excretion of tumor necrosis factor receptor 1 and 2 in patients with type 2 diabetes and normal renal function

Aims/IntroductionIncreased concentrations of serum tumor necrosis factor (TNF) receptors (TNFRs; TNFR1 and TNFR2) are positively associated with the urinary albumin‐to‐creatinine ratio (ACR), and negatively associated with the estimated glomerular filtration rate (eGFR) in patients with type 2 diabetes. However, the mechanism underlying this increase and the relationship between TNFRs in serum, and urine and kidney measures (ACR and eGFR) are unclear.Materials and MethodsThis was a cross‐sectional study that included 499 patients with type 2 diabetes and eGFR ≥60 mL/min/1.73 m². The concentrations of TNFRs in serum and urine, and their respective fractional excretion, were measured.ResultsSerum and urinary TNFR levels were positively associated with the ACR, and negatively associated with the eGFR. The fractional excretion of TNFRs did not differ between patients with an eGFR ≥90 and those with an eGFR 60–89 mL/min/1.73 m², and also did not correlate with eGFR. After adjustment for relevant covariates, the serum TNFRs were associated with a lower eGFR (60–89 mL/min/1.73 m²) and an increased ACR (≥30 mg/gCr), but urinary TNFRs were associated with an increased ACR (≥30 mg/gCr) alone, in the multivariate logistic model.ConclusionsThe pattern of fractional excretion TNFRs showed that an increase in serum TNFRs might result from their increased systemic production, including in the kidney, rather than being a simple reflection of GFR decline. Kidney measures appear to be strongly associated with serum TNFRs rather than urinary TNFRs in patients with type 2 diabetes and normal renal function.     

黄芪对病毒性心肌炎小鼠心脏柯萨奇病毒和腺病毒受体表达的影响

目的:研究黄芪对病毒性心肌炎(VMC)小鼠心脏柯萨奇病毒和腺病毒受体(CAR)表达的影响。方法:建立小鼠VMC模型,将120只小鼠随机分为3组:病毒组、治疗组和正常组。在感染病毒后第0、3、7、14天,无菌取出小鼠心脏分别用RT-PCR法半定量检测CAR的表达。结果:病毒组的CAR表达高于正常组,CAR表达高峰在柯萨奇病毒3型(CVB3)感染后第7天;黄芪治疗后的CAR表达明显降低(P<0.01)。结论:感染CVB3后,心脏组织CAR升高,黄芪可降低CAR的表达,从而减轻CVB3对心肌的损害。     

HBV感染时肿瘤坏死因子对肝细胞毒性效应与受体的关系

为了观察ＨＢＶ感染时肿瘤环死因子对肝细胞毒性效应与受体的关系，以进一步阐明慢性乙型肝炎时ＰＣ损伤机制。分别取血清ＨＢＶ感染标志阳性肝癌患者癌周组织及血清ＨＢＶ感染标志阴性肝内胆管结石患者肝组织，作观察组及对照组并行细胞分离培养得ＰＣ及枯否细胞。