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。     

Role and modulation of G protein-coupled receptor signaling in inflammatory processes

Many extracellular stimuli, such as neurotransmitters, hormones, chemokines, proteinases, inflammatory mediators, odorants, and light, are recognized by the superfamily of G protein-coupled receptors (GPCRs). Immune cells express GPCRs for classical chemoattractants, chemokines, neuropeptides, and neurotransmitters. GPCRs transmit information by interacting with heterotrimeric G proteins, resulting in rapid and transient signaling. The signal given by GPCRs is terminated rapidly by the activity of regulators of G protein signaling (RGS). In addition, GPCR responsiveness diminishes after repeated or prolonged exposure to the agonist. This process of homologous desensitization of GPCRs is dependent on receptor phosphorylation by G protein-coupled receptor kinases (GRKs). In this review, we describe the role of RGS and GRKs in the regulation of GPCR signaling in the immune system, with special emphasis on the role of changes in GRKs and RGS expression during (auto) immune processes. Since altered regulation of GPCR signaling can influence disease states, the molecules involved in this process can also represent attractive therapeutic targets.     

GRKs and arrestins: regulators of migration and inflammation

In the immune system, signaling by G protein-coupled receptors (GPCRs) is crucial for the activity of multiple mediators, including chemokines, leukotrienes, and neurotransmitters. GPCR kinases (GRKs) and arrestins control GPCR signaling by mediating desensitization and thus, regulating further signal propagation through G proteins. Recent evidence suggests that the GRK-arrestin desensitization machinery fulfills a vital role in regulating inflammatory processes. First, GRK/arrestin levels in immune cells are dynamically regulated in response to inflammation. Second, in animals with targeted deletion of GRKs or arrestins, the progression of various acute and chronic inflammatory disorders, including autoimmunity and allergy, is profoundly affected. Third, chemokine receptor signaling in vitro is known to be tightly regulated by the GRK/arrestin machinery, and even small changes in GRK/arrestin expression can have a marked effect on cellular responses to chemokines. This review integrates data about the role of GRKs and arrestins in inflammation, with results on the molecular mechanism of action of GRKs/arrestins, and describes the pivotal role of GRKs/arrestins in inflammatory processes, with a special emphasis on regulation of chemokine responsiveness.     

G蛋白偶联受体激酶在细胞迁移和细胞信号转导中的作用

G-protein-coupled receptor kinases (GRKs) are a family of serine/threonine protein kinases. The investigators pay much attention to the roles of GRKs in the signal transduction through G-protein-coupled receptors (GPCRs) with arrestin ever since a long time ago. Due to the physiological and pathological observations with the methods of deletion or overexpression, GRKs are considered as new drug targets. The kinases play a role in the pathogenesis of hypertension and cell migration through GPCRs and Hedgehog signaling pathways. As the development of research techniques, especially bioluminescence resonance energy transfer (BRET) and fluorescence resonance energy transfer (FRET), the special mechanism of GRKs for GPCRs is more evident. In this review, we discuss the recent achievement in the roles of GRKs signaling and the related newest research techniques.     

Accessory proteins for heterotrimeric G-protein: Implication in the cardiovascular system

The G-protein signaling system plays an important role in controlling cellular responses to numerous hormones and neurotransmitters involved in homeostasis of the cardiovascular system. In addition to traditional determinants of G-protein signaling such as the G-protein-coupled receptor (GPCR), heterotrimeric G-proteins and effectors, accumulating data indicate the existence of entities that directly regulate the activation status of G-proteins independent of GPCR. To date, there have been a number of reports on accessory proteins that influence GDP dissociation, affect nucleotide exchange at the Gα subunit, alter subunit interactions within heterotrimeric Gαβγ independent of nucleotide exchange, or form complexes with Gα or Gβγ independent of the typical Gαβγ heterotrimer. Such proteins may provide an additional signal input to the G-protein signaling system in the absence of GPCR or may act as an alternative binding partner of G-protein subunits serving unknown roles of G-proteins in cells. Accumulating information suggests that accessory proteins for G-proteins are actually involved in the regulation of the signaling system to maintain homeostasis and the dynamic responses to physiological and pathological challenges. It is likely that alterations in signal processing may be achieved by the modulation of signal processing within the cell using accessory proteins for G-proteins. The loss of regulation of this system, leading to inappropriate activation or inactivation of G-protein signaling, is strongly implicated in various human diseases. In this review, we update current information and discuss different accessory proteins for heterotrimeric G-proteins in terms of their involvement in the regulation of the cardiovascular system. Such information may contribute to uncovering mechanisms underlying cardiovascular disease as well as the development of novel therapeutic approaches to human disease.     

GRK mythology: G-protein receptor kinases in cardiovascular disease

G-protein receptor kinases (GRKs) are indispensable for terminating signaling of G-protein coupled receptors (GPCR) through receptor desensitization and downregulation. Increased neurohormone levels in heart failure and the adverse consequences of constant neurohormonal stimulation suggest an important protective role for mechanisms that desensitize neurohormone receptor responses. For that reason, GRK2, the first GRK identified in the heart, has been extensively studied in heart failure, cardiac hypertrophy, and myocardial infarction. However, our understanding of the roles of GRKs in general, and the differential effects of cardiac receptor phosphorylation by individual cardiac-expressed GRKs, have evolved considerably in the last few years. Here, recent developments are reviewed, with an emphasis on novel GRK functions and signaling pathways.     

Expression of G protein-coupled receptor kinase 4 is associated with breast cancer tumourigenesis

G-protein-coupled receptor kinases (GRKs) comprise a family of seven mammalian serine/threonine protein kinases that phosphorylate and regulate agonist-bound, activated, G-protein-coupled receptors (GPCRs). GRKs and beta-arrestins are key participants in the canonical pathways leading to phosphorylation-dependent GPCR desensitization, endocytosis, intracellular trafficking and resensitization. Here we show that GRK4 isoforms are expressed in human breast cancer but not in normal epithelia. In addition, GRK4-over-expressing cells activated the mitogen-activated protein kinase (MAPK) mediated by ERK 1/2 and JNK phosphorylation in breast cancer-derived cell lines. Furthermore, suppression of beta-arrestins decreased GRK4-stimulated ERK 1/2 or JNK phosphorylations. These data indicate that high-level expression of GRK4 may activate MAPK signalling pathways mediated by beta-arrestins in breast cancer cells, suggesting that GRK4 may be implicated in breast cancer carcinogenesis.     

G-protein-coupled receptor expression, function, and signaling in macrophages

G-protein-coupled receptors (GPCRs) are widely targeted in drug discovery. As macrophages are key cellular mediators of acute and chronic inflammation, we review here the role of GPCRs in regulating macrophage function, with a focus on contribution to disease pathology and potential therapeutic applications. Within this analysis, we highlight novel GPCRs with a macrophage-restricted expression profile, which provide avenues for further exploration. We also review an emerging literature, which documents novel roles for GPCR signaling components in GPCR-independent signaling in macrophages. In particular, we examine the crosstalk between GPCR and TLR signaling pathways and highlight GPCR signaling molecules which are likely to have uncharacterized functions in this cell lineage.     

Agonistic autoantibodies directed against G-protein-coupled receptors and their relationship to cardiovascular diseases

Agonistic autoantibodies (AABs) against G-protein-coupled receptor (GPCR) are present mainly in diseases of the cardiovascular system or in diseases associated with cardiovascular disturbances. The increasing knowledge about the role of autoantibodies against G-protein-coupled receptor (GPCR-AABs) as pathogenic drivers, the resulting development of strategies aimed at their removal or neutralization, and the evidenced patient benefit associated with such therapies have created the need for a summary of GPCR-AAB-associated diseases. Here, we summarize the present knowledge about GPCR-AABs in cardiovascular diseases. The identity of the GPCR-AABs and their prevalence in each of several specific cardiovascular diseases are documented. The structure of GPCR is also briefly discussed. Using this information, differences between classic agonists and GPCR-AABs in their GPCR binding and activation are presented and the resulting pathogenic consequences are discussed. Furthermore, treatment strategies that are currently under study, most of which are aimed at the removal and in vivo neutralization of GPCR-AABs, are indicated and their patient benefits discussed. In this context, immunoadsorption using peptides/proteins or aptamers as binders are introduced. The use of peptides or aptamers for in vivo neutralization of GPCR-AABs is also described. Particular attention is given to the GPCR-AABs directed against the adrenergic beta1-, beta2-, and α1-receptor as well as the muscarinic receptor M2, angiotensin II-angiotensin receptor type I, endothelin1 receptor type A, angiotensin (1–7) Mas-receptor, and 5-hydroxytryptamine receptor 4. Among the diseases associated with GPCR-AABs, special focus is given to idiopathic dilated cardiomyopathy, Chagas’ cardiomyopathy, malignant and pulmonary hypertension, and kidney diseases. Relationships of GPCR-AABs are indicated to glaucoma, peripartum cardiomyopathy, myocarditis, pericarditis, preeclampsia, Alzheimer’s disease, Sjörgren’s syndrome, and metabolic syndrome after cancer chemotherapy.     

Pepducins: an effective means to inhibit GPCR signaling by neutrophils

G-protein-coupled receptors (GPCRs) have a central role not only in the competent development of an innate myeloid response to foreign pathogens but, if dysregulated, might contribute to phagocyte-mediated organ injury. Here, recent findings from a study in which neutrophil trafficking is inhibited by using a novel family of GPCR signaling inhibitors, known as pepducins, are discussed.