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。     

内质网应激介导神经变性疾病错折叠蛋白的神经毒性

神经变性疾病(neurodegenerative diseases,NDD)的共同病变基础是细胞内的蛋白处理机制失效而出现错折叠蛋白的集聚并产生神经毒性[1].环境毒素作用、氧化损伤、线粒体功能失常、胞内Ca2 失衡等因素均可能与NDD的发病有关[2].但面对错折叠蛋白,细胞必然通过内质网启动未折叠蛋白反应(unfolded protein response,UPR),这就提示我们内质网应激(endoplasmic reticulum stress,ERstress)可能在NDD发病过程中起关键作用.近期研究表明,内质网应激广泛存在于各种NDD中,并介导错折叠蛋白产生神经毒性及细胞凋亡作用.这里我们主要对内质网应激在发病率最高的3种NDD中所起的作用加以阐述,以期为未来NDD的研究及治疗提供切实可行的思路.     

Metabolic determinants of Alzheimer’s disease: A focus on thermoregulation

Alzheimer’s disease (AD) is a complex age-related neurodegenerative disease, associated with central and peripheral metabolic anomalies, such as impaired glucose utilization and insulin resistance. These observations led to a considerable interest not only in lifestyle-related interventions, but also in repurposing insulin and other anti-diabetic drugs to prevent or treat dementia. Body temperature is the oldest known metabolic readout and mechanisms underlying its maintenance fail in the elderly, when the incidence of AD rises. This raises the possibility that an age-associated thermoregulatory deficit contributes to energy failure underlying AD pathogenesis. Brown adipose tissue (BAT) plays a central role in thermogenesis and maintenance of body temperature. In recent years, the modulation of BAT activity has been increasingly demonstrated to regulate energy expenditure, insulin sensitivity and glucose utilization, which could also provide benefits for AD. Here, we review the evidence linking thermoregulation, BAT and insulin-related metabolic defects with AD, and we propose mechanisms through which correcting thermoregulatory impairments could slow the progression and delay the onset of AD.     

R6/2型亨廷顿病转基因小鼠胰岛β细胞功能损伤

目的：研究R6/2型亨廷顿病(HD) 转基因小鼠胰岛β细胞的功能,揭示HD转基因小鼠继发糖尿病的机制。方法：利用R6/2 型HD转基因小鼠模型,检测正常和HD小鼠空腹血糖以及血清胰岛素水平;并应用HE染色和免疫荧光技术分析正常和HD小鼠胰岛形态学差异。结果：与正常小鼠相比,R6/2 型HD小鼠空腹血糖显著增高,血清胰岛素水平明显降低,胰岛萎缩,β细胞数量减少,细胞功能指数降低,而胰岛素抵抗指数正常。结论：胰岛β细胞功能损伤是引起R6/2 HD转基因小鼠继发糖尿病发生的主要因素。     

Neurodegenerative disorders associated with diabetes mellitus

More than 20 syndromes among the significant and increasing number of degenerative diseases of neuronal tissues are known to be associated with diabetes mellitus, increased insulin resistance and obesity, disturbed insulin sensitivity, and excessive or impaired insulin secretion. This review briefly presents such syndromes, including Alzheimer disease, ataxia-telangiectasia, Down syndrome/trisomy 21, Friedreich ataxia, Huntington disease, several disorders of mitochondria, myotonic dystrophy, Parkinson disease, Prader-Willi syndrome, Werner syndrome, Wolfram syndrome, mitochondrial disorders affecting oxidative phosphorylation, and vitamin B₁ deficiency/inherited thiamine-responsive megaloblastic anemia syndrome as well as their respective relationship to malignancies, cancer, and aging and the nature of their inheritance (including triplet repeat expansions), genetic loci, and corresponding functional biochemistry. Discussed in further detail are disturbances of glucose metabolism including impaired glucose tolerance and both insulin-dependent and non-insulin-dependent diabetes caused by neurodegeneration in humans and mice, sometimes accompanied by degeneration of pancreatic beta-cells. Concordant mouse models obtained by targeted disruption (knock-out), knock-in, or transgenic overexpression of the respective transgene are also described. Preliminary conclusions suggest that many of the diabetogenic neurodegenerative disorders are related to alterations in oxidative phosphorylation (OXPHOS) and mitochondrial nutrient metabolism, which coincide with aberrant protein precipitation in the majority of affected individuals.     

Therapies for Alzheimer’s disease: a metabolic perspective

Alzheimer’s disease (AD) is one of the most common forms of dementia in the elderly. Currently, there are over 50 million cases of dementia worldwide and it is expected that it will reach 136 million by 2050. AD is described as a neurodegenerative disease that gradually compromises memory and learning capacity. Patients often exhibit brain glucose hypometabolism and are more susceptible to develop type 2 diabetes or insulin resistance in comparison with age-matched controls. This suggests that there is a link between both pathologies. Glucose metabolism and the tricarboxylic acid cycle are tightly related to mitochondrial performance and energy production. Impairment of both these pathways can evoke oxidative damage on mitochondria and key proteins linked to several hallmarks of AD. Glycation is also another type of post-translational modification often reported in AD, which might impair the function of proteins that participate in metabolic pathways thought to be involved in this illness. Despite needing further research, therapies based on insulin treatment, usage of anti-diabetes drugs or some form of dietary intervention, have shown to be promising therapeutic approaches for AD in its early stages of progression and will be unveiled in this paper.     

干细胞治疗神经退行性疾病的前景与问题干细胞治疗神经退行性疾病的前景与问题

背景：虽然各种神经退行性疾病的人群发病率居高不下且有上升趋势,但至今仍无有效治疗方法,因此,寻求有效的治疗神经退行性疾病的途径是科学界面临的挑战。 目的：文章分析和综述了对干细胞治疗神经退行性疾病的近年研究进展及热点问题。 方法：文章对干细胞移植治疗神经退行性疾病,如阿尔茨海默病、帕金森病、脑卒中、亨廷顿病、视网膜色素变性疾病、肌萎缩性侧索硬化症、癫痫等疾病的基础与临床研究进展进行概述,探讨干细胞治疗神经退行性疾病的可行性、优势及问题。 结果与结论：干细胞治疗神经退行性疾病大部分研究还是集中在实验动物模型阶段,还没有支持干细胞临床治疗的有效证据,其安全性和有效性还没有确切临床保证和标准,临床治疗效果及不良反应都有待大宗及长期临床试验研究进一步验证。     

Niacin plus simvastatin reduces coronary stenosis progression among patients with metabolic syndrome despite a modest increase in insulin resistance: A subgroup analysis of the HDL-Atherosclerosis treatment study

BackgroundMetabolic syndrome, insulin resistance, and diabetes are associated with an increased risk of cardiovascular disease. Niacin is known to increase insulin resistance and have adverse effects on blood glucose levels, but to have beneficial effects on plasma lipids and lipoproteins. We, therefore, aimed to determine whether intensive lipid therapy with a niacin-containing regimen would have a beneficial effect on cardiovascular disease, despite an expected increase in plasma glucose and insulin resistance in subjects with the metabolic syndrome, insulin resistance, or abnormal fasting plasma glucose levels.MethodsThe effect of 3 years’ treatment with niacin plus simvastatin (N+S) on both angiographic and clinical outcomes was analyzed in the 160 subjects with coronary artery disease and low levels of high-density lipoproteins (HDL) from the HDL-Atherosclerosis Treatment Study. A subgroup analysis was performed on the basis of: (1) the presence or absence of the metabolic syndrome, (2) higher or lower insulin resistance, and (3) the presence or absence of impaired fasting glucose or diabetes (dysglycemia). Individuals classified as having the metabolic syndrome, increased insulin resistance or dysglycemia would be expected to have increased cardiovascular risk.ResultsN+S reduced the change in mean proximal percent stenosis (Δ%S) compared to placebo (PL) in subjects with the metabolic syndrome (Δ%Sprox 0.3 vs 3.0, P = 0.003) and in the more insulin-resistant group of subjects (Δ%Sprox 0.5 vs 2.7, P = 0.001), while subjects with dysglycemia (impaired fasting glucose or diabetes) showed a lesser benefit (Δ%Sprox 1 vs 3.2, P = 0.13). These changes occurred despite increased in-treatment fasting glucose levels (3%), fasting insulin (19%) and decreased insulin sensitivity (−10%). Overall primary clinical events were reduced by 60% with N+S compared to PL (P = 0.02). A similar reduction of the rate of primary events was seen in patients with metabolic syndrome, insulin resistance, and, to a lesser extent, in patients with dysglycemia in the N+S group compared to PL.ConclusionsThese data indicate that, in coronary artery disease patients with low HDL, treating the atherogenic dyslipidemia with a combination of N+S leads to substantial benefits in terms of stenosis progression and clinical events, independently of whether the patient has the metabolic syndrome or is insulin-resistant. During a 3-year period, the beneficial effect of niacin in combination with simvastatin appears to offset the modest adverse effect of niacin on glucose metabolism and insulin resistance in at higher-risk patients, as long as careful attention is paid to glycemic control.     

Should patients with polycystic ovarian syndrome be treated with metformin?: an enthusiastic endorsement

Insulin resistance is a prominent feature of polycystic ovarian syndrome (PCOS), and women with the disorder are at increased risk for the development of other diseases that have been linked to insulin resistance-namely, type 2 diabetes and cardiovascular disease. This association between insulin resistance and PCOS must guide the chronic management of the disorder, and accumulating evidence suggests that administration of insulin-sensitizing drugs to individuals at high risk for type 2 diabetes decreases the rate of conversion to overt disease. In contrast, limited evidence exists to suggest that oral contraceptive pills-the currently standard therapy for PCOS-may actually decrease insulin sensitivity and induce impaired glucose tolerance in women with PCOS. Hence, PCOS should be regarded as a general health issue and the use of insulin-sensitizing drugs such as metformin should be considered for the prevention of type 2 diabetes.     

Chronic peripheral hyperinsulinemia has no substantial influence on tau phosphorylation in vivo

Chronic peripheral hyperinsulinemia is one of the main characteristics of type 2 diabetes accompanied by impaired glucose homeostasis and obesity resulting from increased food intake and decreased physical activity. Patients with type 2 diabetes have a higher risk of cognitive decline and neurodegenerative diseases e.g. Alzheimer's disease (AD). Furthermore, obesity or hyperinsulinemia alone already increase the probability of cognitive decline possibly progressing to AD. Tau hyperphosphorylation is one of the pathological hallmarks of AD and so called tauopathies. Aim of the present study was to analyze the influence of obesity-associated hyperinsulinemia on tau phosphorylation without changes in glucose homeostasis. 15% high fat diet fed over 12-16 weeks induced 2.4-fold increased plasma insulin levels without changing glucose tolerance. However, this diet did not lead to substantial differences in tau phosphorylation in the brain of C57Bl/6 mice. Additionally, chronic hyperinsulinemia did not influence downstream insulin receptor signaling and the expression of the tau kinases (e.g. ERK-1/-2, Akt, GSK-3β, CDK5 or JNK) and tau phosphatases (e.g. PP2A) in the murine central nervous system. Thus, we successfully induced hyperinsulinemia without causing glucose intolerance in our experimental animals but this did not influence central insulin receptor signaling or tau phosphorylation.