静脉溶栓治疗急性心肌梗死血浆TNF-а动态变化及意义

目的观察急性心肌梗死(AMI)再灌注治疗后血浆肿瘤坏死因子-а(TNF-а)的动态变化并评价其临床意义.方法对48例发病6小时内的AMI患者进行溶栓治疗,用放免法测定患者溶栓前、后0.5、1、2、4、12、48小时及1周血浆TNF-а及肌酸磷酸激酶(CPK)的浓度.结果 48例患者中36例再通,12例未通.溶栓前两组TNF-а浓度都大于正常值3倍.溶栓后 TNF-а于未通组48小时出现峰值(25.8±13.4 ng/ml),再通组无高峰,除峰值外两组无差异.结论 AMI患者血浆TNF-а动态曲线能反映AMI早期炎症情况.AMI炎症高峰在51小时,再灌注后TNF-а高峰不显.溶栓再灌注挽救心肌而减轻的炎症反应程度足以抵消再灌注炎症损伤.     

急性心肌梗死不同时间静脉溶栓的临床研究

目的探讨急性心肌梗死(AMI)静脉溶栓的疗效、安全性和不同时间溶栓对它的影响.方法 55例AMI用尿激酶150万u静脉溶栓,按溶栓距发病时间分为6小时内A组34例及6～12小时B组21例,对比两组再通率、4周死亡率及溶栓副作用.结果 A组再通27例(79.4%),B组再通11例(52.4%),A组再通率高于B组(p<0.05);4周死亡率和出血A组比B组低(p>0.05).结论静脉溶栓是有效、安全且适合我国国情的再灌注疗法.     

急性脑梗塞治疗前后血浆ET和TNF RIA的改变

本文对35例急性脑梗塞患者治疗前后内皮素(ET),肿瘤坏死因子(TNF)浓度的测定,并与30例正常成人进行对照并作初步分析和探讨。 材料和方法 一、对象: 正常对照组选自健康成人30例(男16例,女14例),年龄25～45岁。急性脑梗塞患者35例(男17例女18例),均为住院患者,年龄55～82岁,平均62.岁。均经CT、MRI检查诊断为急性脑梗塞,经用精制蝮蛇抗栓酶、低分子右旋糖酐、维脑路通等治疗,时间15～20天。分别于治疗前和治疗后抽静脉血4.5ml,其中2.5ml注入含10％EDTA-Na_230μl和抑肽酶40μl试管中,混匀4℃,3000rpm离心10min,     

院前静脉溶栓治疗急性心肌梗死50例分析

目的 探索院前静脉溶栓治疗急性心肌梗死的疗效、并发症、安全性。方法 尿激酶快速静滴加抗凝剂治疗急性心肌梗死。结果 尿激酶静脉溶栓的血管再通率为84%，病死率为4％。结论 静脉溶栓治疗急性心肌梗死可显著降低病死率，安全可行。     

过敏性紫癜TNFα变化及意义

利用ＥＬＩＳＡ法检测３５例急性期和２５例恢复期ＨＳＰ患儿血清ＴＮＦα浓度，结果显示，急性期ＨＳＰ病人血清ＴＮＦα浓度明显高于正常对照组（Ｐ〈０．０１），恢复期接近正常（Ｐ〉０．０５）。急性期与恢复期之间也有显著差异（Ｐ〈０．０１），ＣＩＣ阳性与否与ＴＮＦα浓度无相关性，提示ＴＮＦα在ＨＳＰ的发病中可能具有重要意义。     

大鼠肝缺血再灌注后不同时相TNF—α表达和肝损伤的关系

目的探讨肝脏缺血／再灌注过程中TNF-α的表达和肝损伤的关系。方法应用RT-PCR技术，观察缺血时间分别为15min、30min及45min的3组大鼠肝脏于再灌注60min时TNF-α的表达情况。结果三组肝脏缺血前及缺血末组织内仅有少量ITNF-α表达于肝细胞内；但于再灌注60min时，TNF-α表达程度则显著增强，且缺血时间越长的肝脏，其表达强度越大。结论肝脏的缺血能明显诱导再灌注期间肝细胞表达TNF-α，进而引发一系列病理生理改变。     

急性髓细胞白血病血清IL—6,TNF—α水平的变化及意义

急性髓细胞白血病血清ＩＬ－６、ＴＮＦ－α水平的变化及意义马晓星徐军王鲁群杨道理迟翠芳（济南军区总医院免疫科，济南２５００３１）肿瘤坏死因子（ＴＮＦ）和白细胞介素６（ＩＬ－６）具有多种生物学活性。除发挥正常的生理功能外，还参与了某些肿瘤和白血病的发生、...     

重型乙型肝炎患者TNF和IL—1的检测及意义

检测３０例重型乙型病毒性肝炎（重型肝炎）患者血清和外周血单个核细胞培养上清中肿瘤坏死因子水平及ＰＢＭＣ诱生的白细胞介素１活性，结果：重型肝炎患者ＴＮＦ和ＩＬ－１水平均增高，且二者呈正相关。提示ＴＮＦ和ＩＬ－１在重型肝炎的发病机制中起重要作用。     

TNF—α和IL—8在兔创伤性急性肺损伤中的意义

为探讨肿瘤坏死因子α（ＴＮＦ－α）和白细胞介素８（ＩＬ－８）在创伤性急性肺损伤（ＡＬＩ）发生发展中的可能作用，采用兔胸部撞击致创伤性ＡＬＩ模型，利用酶联免疫法观察伤后血浆及支气管肺泡灌洗液（ＢＡＬＦ）中ＴＮＦ－α及ＩＬ－８含量的变化，辅以动脉血氧分压（ＰａＯ２），肺湿／干比值和病理检查，结果显示：伤后兔出现急性呼吸衰竭，严重肺水肿，肺内大量炎性细胞聚集，浸润；血浆，ＢＡＬＦ中ＴＮＦ－α和ＩＬ－８含     

急性心肌梗死患者溶栓治疗后凝血指标的变化及意义

急性心肌梗死（AMI）患者进行静脉溶栓治疗，可使梗死相关血管早期开通，对减少坏死心肌数量、限制梗死范围、改善患者的预后非常有益。同时由于其无创伤性，价格便宜，简便易行，成为目前广为流行的方法。但同时也存在溶栓特异性差、出血并发症、再梗死等问题。其中，出血并发症是临床医生最棘手的问题。因此，选择急时、准确的实验监测时间至关重要。我们动态观察了溶栓治疗后凝血指标的变化规律，报告如下。     

血浆内皮素—1和肿瘤坏死因子与急性心肌梗塞的关系

本文对２０例急性心肌梗塞（ＡＭＩ）患者检测了血浆内皮素－１（ＥＴ－１）和肿瘤坏死因子（ＴＮＦ）的水平，结果表明，ＡＭＩ组的ＥＴ－１、ＴＮＦ均较正常对照明显升高（Ｐ〈０．００１），且二者与肌酸磷酸激酶的ＭＢ同功酶（ＰＣＫ－ＭＢ）均呈正相关（ｒ＝０．０６９８４，Ｐ〈０．００１；ｒ＝０．６０５３，Ｐ〈０．０１）。研究结果说明ＥＴ－１和ＴＮＦ参与了ＡＭＩ的病理损伤过程。     

肿瘤坏死因子和C反应蛋白预测急性心肌梗死泵功能的意义

本文观察８２你急性心肌梗死（ＡＭＩ）患者泵功能与肿瘤坏死因子（ＴＮＦ）和Ｃ反应蛋白（ＣＲＰ）的关系。结果提示，ＴＮＦ的高低与ＡＭＩ泵功能分级无相关性，且在ＡＭＩ发病３６小时内迅速消失；ＣＲＰ与ＡＭＩ泵功能不全呈显著负相关，当ＣＲＰ〉５２５００μｇ／Ｌ时，左室射血分数〈０．３５。     

Bikunin Inhibits Lipopolysaccharide-Induced Tumor Necrosis Factor Alpha Induction in Macrophages

Bikunin, a Kunitz-type protease inhibitor, exhibits anti-inflammatory activity in protection against cancer and inflammation. To investigate the molecular mechanism of this inhibition, we analyzed the effect of bikunin on tumor necrosis factor alpha (TNF-α) production in human peripheral mononuclear cells stimulated by lipopolysaccharide (LPS), an inflammatory inducer. Here, we show the following results. (i) LPS induced TNF-α expression in time- and dose-dependent manners through phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase pathways. (ii) Bikunin inhibits LPS-induced up-regulation of TNF-α protein expression in a dose-dependent manner, reaching 60% inhibition at the highest doses of bikunin tested (5.0 μM). (iii) Inhibition by bikunin of TNF-α induction correlates with the suppressive capacity of ERK1/2, JNK, and p38 signaling pathways, implicating repressions of at least three different signals in the inhibition. (iv) Bikunin blocks the induction of TNF-α target molecules interleukin-1β (IL-1β) and IL-6 proteins. (v) Bikunin is functional in vivo, and this glycoprotein blocks systemic TNF-α release in mice challenged with LPS. (vi) Finally, bikunin can prevent LPS-induced lethality. In conclusion, bikunin significantly inhibits LPS-induced TNF-α production, suggesting a mechanism of anti-inflammation by bikunin through control of cytokine induction during inflammation. Bikunin might be a candidate for the treatment of inflammation, including septic shock.     

Expression of Interleukin-5 and Tumor Necrosis Factor Alpha in Cervical Carcinoma

Interleukin-5 (IL-5) levels were significantly higher in vaginal washing fluids from patients with cervical carcinoma than in those from patients with carcinoma in situ and controls. Tumor necrosis factor alpha levels did not differ among the three groups. Detection of IL-5 in cervical secretions may be a useful marker for evaluating aggressive local immune response in cervical carcinoma.Cellular immune response mediated by cytokines is the main defense against tumors related to cervical carcinogenesis. Previous studies have suggested that decreased T helper 1 (Th1) and increased Th2 responses are associated with cervical carcinogenesis (2, 3, 5, 6, 8). However, Th1 and Th2 cytokines, such as interleukin-1β (IL-1β), IL-10, IL-12, tumor necrosis factor alpha (TNF-α), and transforming growth factor beta, were elevated in cervicovaginal washings from patients with cervical carcinoma (12). Another study reported that the concentrations of TNF-α and IL-10 were increased in cases of cervical intraepithelial neoplasia (1). Although each study was different in terms of increased cytokine profiles, the results reveal that both Th1 and Th2 cytokines are increased in cervical carcinoma, which differs from previous reports of a shift toward a Th2 cytokine pattern during cervical carcinogenesis.To date, most studies have focused on the cytokine profiles of the systemic immune response by analysis of peripheral blood. This study was designed to evaluate the cytokine secretion profiles for the Th2 cytokine IL-5 and the Th1 cytokine TNF-α in cervicovaginal secretions. In addition, we aimed to verify whether the levels of cytokines were related to eosinophil counts and human papillomavirus (HPV) DNA titers.Women with abnormal cervical cytology who had been referred to the Women''s Cancer Clinics of Severance Hospital between May 2006 and November 2006 were included. For all women, a cervical biopsy and HPV sampling were performed. Informed consent was obtained from each patient prior to enrollment. We recruited women who were diagnosed histologically with cervical carcinoma (n = 20) or carcinoma in situ (CIS) of the uterine cervix (n = 6). Women histologically diagnosed with chronic nonspecific inflammation were recruited for the control group (n = 10) ( Table ​Table11).

TABLE 1.

Demographic and clinical characteristics of patients in the control, CIS, and cervical carcinoma groups

Soluble Tumor Necrosis Factor Alpha Receptors in Sera from Leprosy Patients

Serum levels of soluble tumor necrosis factor alpha receptor I (sTNF-RI) were elevated in patients with lepromatous (LL) reactional-state type II leprosy, and sTNF-RII levels were increased in patients with full tuberculoid (TT) or LL type II leprosy. The sTNF-R in sera from patients with type II leprosy, but not other forms of leprosy, inhibited recombinant TNF cytolytic activities in vitro. This suggests that sTNF-R regulatory activities are partially impaired in patients with leprosy.     

Effects of Granulocyte-Macrophage Colony-Stimulating Factor and Tumor Necrosis Factor Alpha on Trypanosoma cruzi Trypomastigotes

We have previously shown that the addition of exogenous granulocyte-macrophage colony-stimulating factor (GM-CSF) to nonactivated mouse peritoneal macrophages (MPM) limits Trypanosoma cruzi infections in vitro (E. Olivares Fontt and B. Vray, Parasite Immunol. 17:135–141, 1995). Lower levels of infection were correlated with a higher level of production of tumor necrosis factor alpha (TNF-α) in the absence of nitric oxide (NO) release. These data suggested that GM-CSF and/or TNF-α might have a direct parasitocidal effect on T. cruzi trypomastigotes, independently of NO release. To address this question, T. cruzi trypomastigotes were treated with recombinant murine GM-CSF (rmGM-CSF), recombinant murine TNF-α (rmTNF-α), or both cytokines in a cell-free system. Treatment with rmGM-CSF but not rmTNF-α caused morphological changes in the parasites, and most became spherical after 7 h of incubation. Both cytokines exerted a cytolytic activity on the trypomastigotes, yet the trypanolytic activity of rmTNF-α was more effective than that of rmGM-CSF. Viable rmGM-CSF- and rmTNF-α-treated parasites were less able to infect MPM than untreated parasites, and this reduction in infectivity was greatest for rmGM-CSF. Treatments with both cytokines resulted in more lysis and almost complete inhibition of infection. The direct parasitocidal activity of rmTNF-α was inhibited by carbohydrates and monoclonal antibodies specific for the lectin-like domain of TNF-α. Collectively, these results suggest that cytokines such as GM-CSF and TNF-α may directly control the level of T. cruzi trypomastigotes at least in vitro and so could determine the outcome of infection in vivo.     

抗重组人肿瘤坏死因子-α(rHTNF-α)单克隆抗体特性及功能的研究

应用杂交瘤技木制备抗重组人肿瘤坏死因子-α单克隆抗体对于r-HTNF-α的纯化和TNF-α分子的抗原性及功能的研究将是一种主要工具。本实验对一组抗rHTNF-α单克隆抗体的特性和功能进行了研究。Western blotting结果表明Z_4、Z_8、Z_(12)、Z_ (20)、Z_(21)、B_3和E_6 抗体特异性地识别分子量为17000道尔顿的TNF-α它们与rIL-1、rIL-2、rIFNγ、rIFNα、和E coli菌裂解液无交叉反应。竞争性ELISA结果证实7种抗体分别识别TNF-α分子上5个不同的抗原决定簇。其中4个抗体可以识别TNF-α活性中心部位。两个抗体还可以识别天然TNF-α分子。     

Carrageenan Primes Leukocytes To Enhance Lipopolysaccharide-Induced Tumor Necrosis Factor Alpha Production

We have previously reported that pretreatment with carrageenan (CAR) enhances lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNF-alpha) production in and lethality for mice. Whole blood cultured in vitro was used to show that CAR pretreatment results in about a 200-fold increase in LPS-induced TNF-alpha production. CAR by itself did not induce TNF-alpha production. However, CAR-treated cultured medium sensitized whole blood to make more LPS-induced TNF than did saline-treated cultured medium in vitro. It was also demonstrated that CAR pretreatment increases TNF-alpha mRNA levels of both blood cells and peritoneal exudate cells, but not of bone marrow cells. Immunoelectron microscopic analysis revealed that polymorphonuclear leukocytes and macrophages are TNF-alpha-producing cells in CAR-treated mice. In CAR-treated mice, TNF-alpha was seen early after LPS injection in leukocytes in hepatic sinusoids and on the surfaces of endothelial cells. TNF-alpha was also detected late after LPS injection in hepatocytes which become edematous. These results suggest that CAR primes leukocytes to produce TNF-alpha in response to LPS and that they play an important role in the pathogenesis of liver injury.     

High Serum Interleukin-10 and Tumor Necrosis Factor Alpha Levels in Chronic Paracoccidioidomycosis

In patients with chronic paracoccidioidomycosis (n = 10), levels of tumor necrosis factor alpha, interleukin-10, and interleukin-2 in serum, measured by enzyme-linked immunosorbent assay (in picograms per milliliter, as mean ± standard error of the mean), were higher than in normal controls (n = 8): 186 ± 40 versus 40 ± 7 (P < 0.05), 203 ± 95 versus 20 ± 8 (P = 0.001), and 96.3 ± 78.57 versus 1.19 ± 1.19 (P = 0.045), respectively. Gamma interferon and interleukin-4 levels were similar in patients and controls.