人α肿瘤坏死因子CDNA的体外扩增及分离纯化

通过钙转染法将含有人α肿瘤坏死因子CDNA的质粒PZ_(1p)/TNF转化大肠杆菌E·coliJM109,以Amp~r为标记筛选出阳性菌株.利用此阳性菌株体外培养获得人α肿瘤坏死因子CDNA的大量扩增,然后利用碱解法提取PZ_(1p)/TNF DNA,酶切后经低溶点琼脂糖法分离,回收人的肿瘤坏死因子CDNA.     

阻断糖皮质激素受体对严重烫伤大鼠血浆肿瘤坏死因子含量的影响

目的：为进一步阐明烫伤后糖皮质激素受体（ＧＲ）减少，对血浆肿瘤 坏死因子（ＴＮＦ）含量的影响。方法 以 ＲＵ３８４８６阻断大鼠体内的 ＧＲ，观察其血 浆肿瘤坏死因子（ＴＮＦ）含量的变化。结果 烫伤８小时后，大鼠血浆中ＴＮＦ含量 是对照组的１２．５倍（Ｐ＜０．０１），复合ＧＲ阻断后，将进一步提高。结论 烫伤后 ＧＲ减少，可导致体内ＴＮＦ释放增多，这可能正是ＧＲ减少加重烫伤后肺、肾功能 衰竭的原因之一。     

TNF-α诱导HUVEC的损伤及其意义

通过建立人脐静脉内皮细胞(HUVEC)体外培养,采用电镜、免疫组化等技术观察肿瘤坏死因子-α(TNF-α)对HUVEC的存活率、形态和凋亡相关蛋白的影响,从而探讨TNF-α致血管内皮细胞(VEC)损伤的分子机制以及临床意义.     

脂肪细胞因子及其在2型糖尿病中的作用与机制

脂肪组织不仅是储存脂肪的场所,还是一个功能活跃的内分泌器官,能分泌多种生物活性物质,这些物质统称为脂肪因子.其中有的是近几年发现的,有的则是早已发现但在最近几年才发现其在糖尿病中的作用.本文侧重对将其中的脂联素、内脏脂肪素、瘦素、肿瘤坏死因子α、抵抗素在2型糖尿病的病理生理过程中的一些作用及其机制进行探讨.     

TNF—a诱导HUVEC的损伤及其意义

通过建立人脐静脉内皮细胞（HUVEC）体外培养，采用电镜、免疫组化等技术观察肿瘤坏死因子－a（TNF－a）对HUVEC的存活率、形态和凋亡相关蛋白的影响，从而探讨TNF－a致血管内皮细胞（VEC）损伤的分子机制以及临床意义。     

肿瘤的生物治疗研究新进展(综述)

随着生物高技术的发展和交叉渗透,肿瘤生物治疗进展很快,相继建立并发展了以下各种疗法:一、细胞因子疗法目前有白细胞介素2、干扰素、肿瘤坏死因子、集落刺激因子等四种基因工程型细胞因子通过不同方式用于肿瘤患者的治疗,取得了较好疗效,并具有各自的特点。目前,临床上很注重细胞因子应用策略的改进,如多种细胞因子的协同应用、局部持续性释放以及内源性诱导配以外源性注射的ＥＥＴ疗法等。二、单克隆抗体及其偶联物疗法近年来进展较快的有嵌合抗体、单链抗体等人源化单克隆抗体,及双功能或双特异性抗体的研制和应用,还有抗体与细胞因子的…     

肿瘤坏死因子联合丝裂霉素治疗恶性胸水的临床价值

胸腔积液是晚期肺癌的主要并发症，严重影响了患者的生存质量，其治疗以缓解症状，提高生活质量为主，我院于2004．9-2005．12月对恶性胸腔积液患者采用胸腔内注入肿瘤坏死因子（TNF）＋丝裂霉素（MMC）治疗，现报道如下。     

肿瘤坏死因子受体1是否在体外循环相关的急性肺损伤病例中发挥作用?(英文)

研究目的:通过CAY10500阻断肿瘤坏死因子-α(TNF-α)与肿瘤坏死因子受体1(TNFR1)的结合,评估TNFR1在体外循环诱导的急性肺损伤中的作用。创新要点:使用CAY10500静脉内注射预处理而阻断TNF-α与TNFR1的结合,并降低血浆TNF-α水平,以观察TNFR1对体外循环诱导的急性肺损伤的作用。研究方法:用磷酸盐缓冲液(PBS)或载体或CAY10500静脉内预处理麻醉SD大鼠后,再进行2小时体外循环,诱导其发生急性肺损伤,并观察氧指数、肺部炎症、支气管肺泡灌洗液及其血浆中TNF-α和嗜中性粒细胞的含量。重要结论:使用CAY10500静脉内注射预处理而阻断TNF-α与TNFR1的结合,只能略微减轻肺部炎症,但不能改善肺部功能,表明TNFR1通路在体外循环诱导的急性肺损伤的炎症细胞中作用有限。     

脑出血继发性脑损伤中炎性细胞因子的作用

近年来的研究发现,多种细胞因子如白细胞介素及肿瘤坏死因子介导免疫和炎症反应,参与了继发性脑损伤的病理生理过程。有研究证实,脑出血后脑组织内存在着中性粒细胞和巨噬细胞浸润,小胶质细胞激活和炎性细胞因子参与炎症的反应[1]。动物实验证实,脑出血后存在炎症反应,且较非出     

缺氧在转移前生态位形成中的作用

原发肿瘤通过释放肿瘤分泌因子(Tumor-derived secreted factors,TDSFs)在继发器官募集骨髓来源细胞(bone marrow-derived cells,BMDCs),创建一个适合转移肿瘤转移的转移前生态位(premetastatic niches,PMN),为肿瘤的后期转移做好前期准备。实体肿瘤常因为缺氧而导致不良预后。缺氧是促进PMN形成的重要因素。本文主要介绍了缺氧在PMN形成中的作用机制:缺氧诱导因子(hypoxia-inducible factors,HIFs)依赖的LOX和LOX-like(LOXL)蛋白表达;缺氧肿瘤细胞释放TDSFs;NK细胞杀伤功能降低。     

氟伐他汀对不稳定型心绞痛患者血清白介素-18和肿瘤坏死因子α干预的研究

目的研究氟伐他汀对不稳定型心绞痛患者血清白介素-18（IL-18）和肿瘤坏死因子α（TNFα）的影响。方法选择2006年9月至2007年7月79例不稳定型心绞痛患者,入院后随机分为2组：氟伐他汀干预组42例：常规药物治疗基础上加用氟伐他汀40mg／d;对照组37例：常规药物治疗。分别于药物治疗前、药物治疗后2周采集静脉血,测定血清IL-18和TNFα的浓度。结果药物治疗后,对照组（P〈0．05）及氟伐他汀干预组（P〈0．01）血清IL-18和TNF＆浓度均明显降低;氟伐他汀干预组血清IL-18（P〈0．01）和TNFα（P〈0．01）浓度明显低于同期对照组。结论氟伐他汀可明显降低不稳定型心绞痛患者血清IL-18和TNFα浓度。     

甘草多糖对小鼠细胞免疫的影响

目的：观察甘草的有效成分甘草多糖（GlycyrrhizaPolysaccharide）对细胞免疫的调节作用;方法：给胃灌甘草多糖14d,测定二硝基氟苯诱导的小鼠迟发性超敏反应（DTH）,用放射免疫法检测血中IL-2、TNF—α含量,观察甘草多糖对小鼠细胞免疫功能的影响;结果：与空白组比较,甘草多糖对DTH反应有-定的增强作用,能升高血中IL-2、TNF-α含量;结论：甘草多糖能明显增强小鼠细胞免疫功能。     

姜黄素对胰岛素抵抗大鼠脂肪细胞因子的影响

目的:观察姜黄素对胰岛素抵抗(IR)大鼠糖脂代谢及血清脂肪细胞因子的影响,探讨姜黄素干预IR的作用机制。方法:采用高脂饲料喂养,建立IR大鼠模型。将IR大鼠随机分为3组:模型组、吡咯列酮组和姜黄素组。给药4周后测定空腹血糖、胰岛素、血脂、TN F-α、Leptin等指标。结果:模型组大鼠血清FIN S、TC、TG和LDL水平均较空白组显著升高,而ISI及HDL水平显著下降;血清TN F-α、Leptin及FFA水平也较空白组明显升高;用姜黄素干预后,大鼠ISI较模型组显著升高,血脂得到改善,FINS、TNF-α、Leptin及FFA水平均显著下降。结论:姜黄素可改善IR大鼠糖脂代谢紊乱,增加胰岛素的敏感性,其机制可能与其调节脂肪细胞因子TNF-α、Leptin的分泌有关。     

Phenotypic and functional characteristics of dendritic cells derived from human peripheral blood monocytes

INTRODUCTION Dendritic cells(DCs)are professional anti-gen-presenting cells(APC)that are responsible for the activation of undifferentiated T cells and the generation of primary T-cell responses(Cella et al.,1997).The specific role of DCs is to capture,process and present antigens to T cells.Immunogenic and inflammatory signals are responsible for the migra-tion of DCs from tissues to lymphoid organs where they initiate an immune response.These processes induce the maturation of DCs…     

In vitro study of immunosuppressive effect of apoptotic cells

INTRODUCTION Apoptosis plays an important role in differen- tiation, development and pathophysiological proc- esses such as inflammation, neoplasia and autoim- mune diseases. For a long time, apoptotic cells per se and the clearance of apoptotic cells had been viewed as neutral in immune response. Recently many in- vestigations suggested that apoptotic cells actively regulate the immune response (Voll et al., 1997; Fadok et al., 1998; 2000; Byrne and Reen, 2002). Apoptotic cells release …     

转基因鱼腥藻7120流加培养的研究

流加培养对转TNF—α基因鱼腥藻7120的生长有利.单独流加碳源对转基因鱼腥藻7120生长与外源基因表达影响很小,单独流加氮源和同时流加碳氮源可明显促进生长,生物量达到2.964g/L和3.059g/L,分别增长9.91％和12.71％,而且能轻微促进藻细胞中的TNF表达.     

实验性脂肪肝大鼠的脂肪代谢、细胞因子、瘦素方面的变化

目的:观察脂肪肝大鼠在生化、病理、脂肪代谢、细胞因子、胰岛素及瘦素各方面指标的变化.方法:雄性Wistar大鼠22只,按体重层次随机分为2组,对照组(A)11只,脂肪肝组(B)11只.对照组饲以普通鼠饲料,脂肪肝组饲以高脂饲料.8周后,全部处死,取血及肝组织,测定血中AIT、AST、TG、CHO、INS、FBS、FFA、Ieptin、II-6、TNF.肝组织匀浆测定肝组织TC,TG,SOD、MDA,观察肝脏组织学变化.结果:脂肪肝大鼠存在明显脂肪代谢紊乱,肝功能异常,胰岛素抵抗及瘦素表达增高;细胞因子升高.结论:实验性高脂饮食脂肪肝大鼠存在瘦素抵抗及胰岛素抵抗.     

Associations Between School Readiness and Obesity‐ and Inflammation‐Related Biomarkers in Low‐Income Preschoolers Within the Healthy Kids Study

Previous research suggests obesity is negatively related to cognitive functioning and academic outcomes in addition to physical health. However, not much is known about this association in early childhood or potential physiological underpinnings. Biomarkers related to obesity have been associated with cognition, in particular the adipokine leptin, and pro‐inflammatory cytokines including interleukin‐6 (IL‐6), tumor necrosis factor‐alpha (TNF‐alpha) and C‐reactive protein (CRP). These associations may be further exacerbated for children who experience early life stress. With a sample of low‐income preschoolers, the current study examined associations between obesity‐related biomarkers and aspects of behavioral and cognitive school readiness. Partial correlations controlling for child age show hypothesized negative associations between pro‐inflammatory cytokines and school readiness, while leptin was positively associated with cognitive school readiness and body mass index (BMI) z‐score. Findings suggest connections between obesity, physiology, and school readiness need further examination, but may have implications for early childhood education and health interventions.     

Influence of systemic immune and cytokine responses during the acute phase of zoster on the development of postherpetic neuralgia

Postherpetic neuralgia (PHN) is a severe sequela of herpes zoster (HZ). Until now, only age and pain severity were considered predisposing factors for the development of PHN. We evaluated 49 patients with acute phase HZ, 10 of whom developed PHN (Group A) and 39 of whom did not develop PHN (Group B). Twenty-five healthy volunteers similar in age and gender distribution to the study group were recruited as controls (Group C). Numbers of serum CD3⁺ (pan-T lymphocytes), CD4⁺ (helper/inducer), and CD8⁺ (suppressor/cytotoxic) lymphocytes were decreased significantly in Groups A and B relative to the control group, but there were no statistical differences between Groups A and B. Interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, IL-8, and IL-10 were significantly elevated in Groups A and B relative to Group C. IL-6 was significantly higher in Group A than in Group B, and was significantly positively correlated with pain severity scored on a visual analog scale. Therefore, we suggest that the inflammatory response, especially that of IL-6, in the acute phase of HZ may be associated with hyperalgesia and the development of PHN. Project (No. 2008ZYC07) supported by the Zhejiang Medical Bureau of China     

<Emphasis Type="Italic">Ureaplasma urealyticum</Emphasis>-derived lipid-associated membrane proteins introduce IL-6, IL-8, and TNF-α cytokines into human amniotic epithelial cells via Toll-like receptor 2

Objective

The purpose of this study was to determine the role of Ureaplasma urealyticum-derived lipidassociated membrane proteins (LAMPs) in the host innate immune system, specifically their effect on Toll-like receptors (TLRs).

Methods

LAMPs were derived from U. urealyticum strains, and human amniotic epithelial cells (HAECs) were isolated from healthy full-term placentas. Cytokine concentrations were determined by enzyme-linked immunosorbent assay (ELISA) and TLR2 mRNA by real-time PCR. Expression of TLR2 was confirmed by Western blotting and immunohistochemistry.

Results

LAMPs induced HAECs to produce inflammatory cytokines interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α. Cytokine production was reduced after blocking TLR2 using TLR2 inhibitor (anti-hTLR2-IgA).

Conclusions

LAMPs isolated from U. urealyticum induced TLR2-dependent up-regulation of inflammatory genes and cytokines in HAECs.