应用Ilizarov技术治疗手腕部瘢痕挛缩畸形临床观察

目的 观察Ilizarov技术治疗手腕部瘢痕挛缩畸形的临床效果。 方法 2017年4月~2020年1月,应用Ilizarov技术治疗7例手腕部瘢痕挛缩畸形患者,男3例,女4例;年龄12~52岁,平均24岁;左手部2例,左腕关节1例,右腕关节4例;创面感染致瘢痕增生2例,开水烫伤致瘢痕增生1例,火焰烧伤致瘢痕增生4例。瘢痕形成6月~34年,平均7年。根据Mayo评分法评估手腕部功能,术前患者手腕部功能可5例,差2例。 结果 腕关节畸形均获得矫正,以腕关节中立位为0°测量,腕关节掌屈可达到55~70°,背伸可达0~55°,无明显疼痛及麻木感,手指活动灵活。患者均无针道感染、肢端感觉麻木等并发症。术后随访5月~24月（平均15月）,末次随访时评估手腕部功能,良4例、可3例,较术前显著改善。 结论 应用Ilizarov技术治疗手腕部瘢痕挛缩畸形安全有效,可为烧伤后肢体功能重建提供一种新的疗法。     

蒙娜丽莎之谜

<正>500多年前,意大利人达芬奇创作出历史上最负盛名的肖像画杰作《蒙娜丽莎》。19世纪中叶,"她"正式入驻世界上最著名的艺术博物馆——法国的卢浮宫,刚开始被该馆收藏,"她"的知名度还不是很高,后来到了1911年,该馆的一个油漆     

个体人格类型与气味偏好的关系

目的：探讨气味偏好与个体人格之间的初步关系。为在行为层面上研究人格提供新的路径。方法：以艾森克的现代人格理论模型为框架，采用人格问卷和实验结合的方法进行研究，通过实验法在控制的条件下得到个体的气味偏好数据，通过人格问卷得到同一群体的人格各维度分值。结果：不同人格特征的个体在气味偏好上存在显著差异。结论：气味偏好和人格之间存在一定的联系。     

肾结核病灶中淋巴细胞趋化因子的表达

目的:探讨淋巴细胞趋化因子在正常肾脏和肾结核中的表达以及淋巴细胞趋化因子和浸润CD4 、D8 T细胞在肾脏结核病灶中的分布特点.方法:6例正常肾脏和10例肾结核病变组织,经匀浆后,采用RT-PCR法扩增人淋巴细胞趋化因子(hLptn)的含编码区序列的cDNA;扩增cDNA的克隆至pGM-T Easy T载体,测序;应用免疫组织化学方法检测正常肾脏和肾结核中的hLptn的表达和结核病灶中的CD4、CD8分子的表达.结果:正常肾脏和肾结核组织均表达hLptn mRNA,应用RT-PCR法克隆的cDNA序列与GenBank中U23772的序列一致;hLptn在正常的肾小球、肾小管中和结核病变中残存的肾小球、肾小管中均有表达;结核病变中有散在的CD4和CD8分子阳性细胞,与hLptn的分布无重叠.结论:淋巴细胞趋化因子在肾脏的肾小球和肾小管中呈结构性表达,肾结核肉芽肿中淋巴细胞的募集可能非依赖于hLptn的作用.     

GKT测谎模式研究

犯罪知识测试（Guilty Knowledge Test，简称GKT），是Lykken在1959年引入的一种测谎测试程序。本文就GKT测试的认知原理一定向反应有关理论的发展及其与GKT测试的关系进行了介绍，并以此为起点，对GKT测谎研究的四种范式进行了分析与探讨，最后指出GKT测谎模式还存在的问题、相关的扩展性研究以及发展趋势。     

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敬告作者

本刊编辑部自2011年6月起不再向论著类作者提供纸质单行本,如有需要者可向本刊索取文稿的电子版数据(PDF格式),或登录本刊网站(http://www.cjcep.com)自行下载。     

非实验因素对人体核磁共振代谢组学检测结果的影响

代谢组学被认为是未来诊断疾病和评价患者机能状况的有力手段,但目前的研究结果表明,很多非实验因素,如饮食、运动、环境以及个体差异等均会影响临床实验结果,为保证不同核磁共振(Nuclear magnetic resonance,NMR)实验数据之间的可比性,很有必要在实验设计和数据分析过程中对这些因素进行合理的控制.     

腺病毒介导的肝癌靶向SEA-CD80基因治疗及免疫学机制的初步研究

目的: 观察肝癌靶向性葡萄球菌肠毒素A (SEA)/CD80基因重组腺病毒载体对肝癌的疗效,并对其免疫学机制进行初步研究.方法: 利用AdEasy腺病毒系统分别构建并制备甲胎蛋白(AFP)启动子和增强子Ⅰ调控的SEA和/或CD80基因重组腺病毒载体, 然后采用瘤体内直接注射的方式对小鼠皮下移植性肝癌进行治疗, 采用RT-PCR和Western blot方法检测腺病毒注射部位的SEA和CD80 mRNA和蛋白的表达情况; 采用ELISpot方法和LDH释放实验分别检测脾脏淋巴细胞中肝癌特异性IFN-γ分泌细胞的频数和细胞毒性T细胞(CTLs)对Hepa1-6细胞的特异杀伤活性; 通过观察荷瘤小鼠经治疗后肿瘤体积的变化及生存时间, 评价重组腺病毒对肝癌的治疗作用.结果: 我们构建的腺病毒能够使SEA和/或CD80 mRNA和蛋白靶向地在肝癌组织中表达; 与空载体组和PBS对照组相比, 双基因组和单基因组分泌IFN-γ的T细胞数量均明显增多, CTL对Hepa1-6细胞的特异性杀伤作用均明显增强, 荷瘤小鼠肿瘤体积明显减小, 生存期明显延长; 双基因组的疗效和对免疫系统的激活作用明显高于单基因组; CD80 和SEA的组之间、空载体和PBS组之间无明显差异.结论: 我们制备的肝癌靶向性重组腺病毒对肝癌有良好的治疗作用, 联合基因治疗优于单个基因治疗.     

太行山猕猴距骨的性别判别分析

太行山猕猴主要分布在太行山南坡中条山南端,是我国黄河以北分布最集中、数量最多、面积最大的猕猴自然分布种群。在形态、行为、遗传、食性、骨学方面均具有其特殊性。踝关节的距骨作为最坚固的骨骼之一,在国内有关该部位的研究报道较少。本研究主要对太行山猕猴距骨进行测量统计分析,找出两性间差异较大的变量,建立判别函数,为太行山猕猴的基础研究和生物学研究积累资料。     

Toll样受体调节中性粒细胞免疫作用的研究进展

Toll样受体（TLR）是固有免疫系统中特异的I型跨膜受体及病原模式识别受体。TLR能特异地识别病原体相关分子模式（PAMP）,构成机体抵御病原微生物的第一道防线,因而在固有免疫系统中发挥重要作用,而且TLR还能调节适应性免疫,是连接固有免疫和适应性免疫的桥梁。中性粒细胞（PMN）是机体最重要的炎性细胞,在固有免疫中扮演着十分重要的角色,对炎症的发生、发展及转归起了关键的作用。作为重要受体的TLR能诱导PMN的生存与活化,在急性炎症反应、细胞信号转导和细胞凋亡中起着重要作用。     

Toll样受体与造血

Toll样受体（TLR）是近年来发现的一类天然免疫受体,在天然免疫及获得性免疫过程中均发挥非常重要的作用。对TLR的深入研究表明,TLRs在造血相关细胞（造血干／祖细胞、间充质干细胞、血管内皮细胞等）上均有不同程度的表达,并且发挥一定生物学效应。     

Toll-like receptor 2 modulates the proinflammatory milieu in Staphylococcus aureus-induced brain abscess

Toll-like receptor 2 (TLR2) is a pattern recognition receptor (PRR) that plays an important role in innate immune recognition of conserved structural motifs on a wide array of pathogens, including Staphylococcus aureus. To ascertain the functional significance of TLR2 in the context of central nervous system (CNS) parenchymal infection, we evaluated the pathogenesis of S. aureus-induced experimental brain abscess in TLR2 knockout (KO) and wild-type (WT) mice. The expression of several proinflammatory mediators, including inducible nitric oxide synthase, tumor necrosis factor alpha, and macrophage inflammatory protein-2, was significantly attenuated in brain abscesses of TLR2 KO mice compared to WT mice during the acute phase of infection. Conversely, interleukin-17 (IL-17), a cytokine produced by activated and memory T cells, was significantly elevated in lesions of TLR2 KO mice, suggesting an association between innate and adaptive immunity in brain abscess. Despite these differences, brain abscess severity in TLR2 KO and WT animals was similar, with comparable mortality rates, bacterial titers, and blood-brain barrier permeability, implying a role for alternative PRRs. Expression of the phagocytic PRRs macrophage scavenger receptor type AI/AII and lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) was increased in brain abscesses of both TLR2 KO and WT mice compared to uninfected animals. However, LOX-1 induction in brain abscesses of TLR2 KO mice was significantly attenuated compared to WT animals, revealing that the TLR2-dependent signal(s) influence LOX-1 expression. Collectively, these findings reveal the complex nature of gram-positive bacterial recognition in the CNS which occurs, in part, through engagement of TLR2 and highlight the importance of receptor redundancy for S. aureus detection in the CNS.     

Toll样受体7在抗感染与自身免疫疾病中的作用

Toll样受体7(TLR7)是表达在哺乳动物细胞内涵体膜表面的跨膜信号传导受体,通过识别单链RNA,激活天然免疫系统,同时通过诱导浆细胞样树突状细胞(pDC)分泌Ⅰ型干扰素(IFN-α)来调控获得性免疫反应。TLR7尤其在抗感染与自身免疫方面发挥重要作用。在深入研究TLR7及其信号通路的基础上,以其作为药物干预靶点,对治疗相关感染性疾病、自身免疫性疾病具有重要的科学意义和应用价值。     

Toll样受体4与动脉粥样硬化关系的研究进展

动脉粥样硬化是心脑血管疾病的病理基础。但目前关于动脉粥样硬化的发病机制还不是很清楚。普遍认为免疫应答,包括固有免疫和适应性免疫在动脉粥样硬化的发生发展中起了重要作用。Toll受体4（TLR4）是抗原相关分子模式（PAMP）受体,在识别微生物感染、激发先天性免疫反应中发挥了重要作用。近来发现炎症在动脉粥样硬化发展的各个阶段均发挥了重要作用,虽然目前确切的证据还缺乏,但是越来越多的调查发现,病原体感染引起的分子和细胞的改变表明炎症具有这种作用。     

广谱模式识别分子Toll-like receptor 2的研究进展

TLR-2（Toll-like receptor 2,TLR-2）是哺乳动物TLRs（Toll-like receptors,TLRs）家族的一员,作为细胞表面的天然受体蛋白,主要参与病原微生物产物的识别及炎症信号传导,介导天然抗感染兔疫;最近又发现其参与机体对非感染因子所致炎性组织损伤的识别。通过对TLR-2参与的识别和细胞内信号传导机制的研究,可为深入探讨抵御微生物感染的机制、对自身正常与非正常组织的识别提供新的思路。     

Toll样受体3在病毒感染及细胞凋亡中的生物学功能

Toll样受体3（TLR3）作?《舅碦NA识别受体在机体抗病毒天然免疫中发挥十分重要的作用。TLR3识别配体后通过含TIR结构域的转接蛋白（TRIF）途径活化转录因子NF-κB和干扰素调节因子3（IRF3）,诱导炎症细胞释放炎症因子并介导炎症反应,同时诱导I型干扰素的释放,介导抗病毒天然免疫。在一些病毒感染中TLR3通过诱导组织损伤介导病毒的扩散从而加重疾病的严重程度。部分肿瘤细胞也表达TLR3,活化的TLR3介导细胞凋亡、抑制细胞增殖,提示TLR3可能是肿瘤免疫治疗的新靶点。［关键词］ Toll样受体3;信号转导;病毒;肿瘤;细胞凋亡     

Production of the soluble pattern recognition receptor PTX3 by myeloid, but not plasmacytoid, dendritic cells

PTX3 is a prototypic of long pentraxin consisting of an N-terminal portion coupled to a C-terminal pentraxin domain, the latter related to short pentraxins (C-reactive protein and serum amyloid P component). PTX3 is a soluble pattern recognition receptor, which plays a non-redundant role in resistance against selected pathogens and in female fertility. The present study was designed to analyze the production of PTX3 by human dendritic cells (DC) and to define the role of different innate immunity receptors in its induction. Human monocyte-derived DC produced copious amounts of PTX3in response to microbial ligands engaging different members of the Toll-like receptor (TLR) family (TLR1 through TLR6), whereas engagement of the mannose receptor had no substantial effect. DC werebetter producers of PTX3 than monocytes and macrophages. Freshly isolated peripheral blood myeloid DC produced PTX3 in response to diverse microbial stimuli. In contrast, plasmacytoid DC exposed to influenza virus or to CpG oligodeoxynucleotides engaging TLR9, did not produce PTX3. PTX3-expressing DC were present in inflammatory lymph nodes from HIV-infected patients. These results suggest that DC of myelomonocytic origin are a major source of PTX3, a molecule which facilitates pathogen recognition and subsequent activation of innate and adaptive immunity.     

Enhanced TLR2 responses in multiple sclerosis

The roles of the microbiome and innate immunity in the pathogenesis of multiple sclerosis (MS) remain unclear. We have previously documented abnormally low levels of a microbiome‐derived Toll‐like receptor (TLR)2‐stimulating bacterial lipid in the blood of MS patients and postulated that this is indicative of a deficiency in the innate immune regulating function of the microbiome in MS. We postulated further that the resulting enhanced TLR2 responsiveness plays a critical role in the pathogenesis of MS. As proof‐of‐concept, we reported that decreasing systemic TLR2 responsiveness by administering very low‐dose TLR2 ligands attenuated significantly the mouse model of MS, experimental autoimmune encephalomyelitis. Studies of Toll‐like receptor responses in patients with MS have been conflicting. Importantly, most of these investigations have focused on the response to TLR4 ligation and few have characterized TLR2 responses in MS. In the present study, our goal was to characterize TLR2 responses of MS patients using multiple approaches. Studying a total of 26 MS patients and 32 healthy controls, we now document for the first time that a large fraction of MS patients (50%) demonstrate enhanced responsiveness to TLR2 stimulation. Interestingly, the enhanced TLR2 responders include a significant fraction of those with progressive forms of MS, a subset of patients considered unresponsive to adaptive immune system‐targeting therapies. Our results suggest the presence of a pathologically relevant TLR2 related innate immune abnormality in patients with both relapsing–remitting and progressive MS. These findings may have significant implications for understanding the role of innate immunity in the pathogenesis of MS.