共查询到17条相似文献,搜索用时 468 毫秒
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表观遗传修饰异常见于人类的多种疾病(如肿瘤、老年性疾病、发育源性疾病等),影响着这些疾病的发生发展。已有的研究表明,异常表观遗传改变可以作为疾病状态和疾病预测的生物标志物。表观遗传修饰改变的可逆性和可控性也为疾病早期的预防和治疗提供了新策略。本文对DNA甲基化修饰、组蛋白共价修饰、非编码RNA等三种表观遗传方式在肿瘤、老年性疾病和发育源性疾病的研究,以及三者作为表遗传生物标志物在疾病早期诊断和治疗的应用展开介绍,以期为肿瘤、老年性和发育源性相关疾病的诊断与治疗提供借鉴和 参考。 相似文献
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近20年来,随着我国经济的快速发展和膳食结构的不断西化,肥胖、2型糖尿病和心脑血管疾病等一些与营养、代谢和生活方式密切相关的慢性代谢性疾病在我国的发病率急剧上升,成为我国居民健康的主要威胁和主要致死性、致残性疾病。世界卫生组织2005年一份控制慢性疾病的报告预计,如果不采取有效措施,在未来10年中仅心脏病、中风和糖尿病就将给中国带来至少5500亿美元的经济损失。此外,我国人口老龄化发展迅速,已成为世界上目前唯一的老年人口超过1亿的国家。由于老龄化本身与各种慢性疾病关系密切,发现危害老年人健康的主要危险因素,对预防疾病和促进老年人的健康至关重要。 相似文献
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医学研究中的转谷氨酰胺酶 总被引:3,自引:0,他引:3
在哺乳动物中,存在各种转谷氨酰胺酶,它们通过催化的酰基转移反应,使蛋白质发生修饰。它们参与了多种生理过程,同时和多种疾病相关,其中主要为炎症性疾病,神经退行性病变和肿瘤性疾病等三大类疾病。随着对其参与疾病的机理逐渐明了,转谷氨酰胺酶开始用于疾病的诊断和治疗 。 相似文献
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P2X受体是一类离子型配体门控通道,分为7个不同的亚型(P2X1~7)。嘌呤能离子通道型受体7(purinergic ligand-gated ion channel 7 receptor, P2X7R)是ATP门控的,非选择性的阳离子通道,属于嘌呤受体P2X家族。P2X7受体广泛表达于神经系统、肌肉组织和免疫系统。在胞外ATP作用下,P2X7受体偶联多种胞内信号通路,参与细胞增殖、凋亡及炎症因子的释放等多种生理功能。研究发现,P2X7受体与诸多疾病有着密切联系,包括自身免疫性疾病(如关节炎和炎症性肠病)、神经退行性疾病、慢性疼痛、情绪障碍和癌症等。P2X7受体异常表达会导致这些疾病的发生,增加疾病的易感性与病变程度。现就P2X7受体的生物学特征、P2X7受体与疾病的关系及其特异性阻断剂和激动剂进行综述。 相似文献
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弥漫性结缔组织病在多系统损害中的临床表现 总被引:1,自引:0,他引:1
风湿性疾病范畴很广,按WHO分类共达10大类,近120种疾病。风湿性疾病特别是风湿病中的弥漫性结缔组织疾病(CTD)往往可引起多个系统受累。有时还以某一系统的表现为首发症状,在治疗中容易造成误诊或延误诊断。因此,我们应当重视风湿性疾病多系统损伤的临床特点。 相似文献
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免疫毒素药物在治疗疾病方面取得了一些成功,能治疗一些与免疫相关的动物和人类的疾病,如血癌、自身免疫性疾病、GvHD病、HIV感染的细胞疾病以及一些实体瘤等,同时,在临床上也取得了一些进展,获得了一些数据,本文作一简要介绍。 相似文献
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Mitochondrial Dysfunction in Neurodegeneration 总被引:4,自引:0,他引:4
Numerous toxins are known to interfere with mitochondrial respiratory chain function. Use has been made of these in the development of pesticides and herbicides, and accidental use in man has led to the development of animal models for human disease. The propensity for mitochondrial toxins to induce neuronal cell death may well reflect not only their metabolic pathways but also the sensitivity of neurons to inhibition of oxidative phosphorylation. Thus, the accidental exposure of humans to l-methyl-4-phenyl-l,2,3,6-tetrahydropyridine and to 3-nitropropionic acid has led to primate models of Parkinson's disease and Huntington's disease, respectively. These models were made all the more remarkable when identical biochemical deficiencies were identified in relevant areas of humans suffering from the respective idiopathic diseases. The place of complex I deficiency in Parkinson's disease remains undetermined, but there is recent evidence to suggest that, in some cases at least, it may play a primary role. The complex II/III deficiency in Huntington's disease is likely to be secondary and induced by other pathogenetic factors. The potential to intervene in the cascade of reactions involving mitochondrial dysfunction and cell death offers prospects for the development of new treatment strategies either for neuroprotection in prophylaxis or rescue. 相似文献
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Fulvio Celsi Paola Pizzo Sara Leo Carmen Fotino Paolo Pinton Rosario Rizzuto 《BBA》2009,1787(5):335-344
Mitochondrial Ca2+ accumulation is a tightly controlled process, in turn regulating functions as diverse as aerobic metabolism and induction of cell death. The link between Ca2+ (dys)regulation, mitochondria and cellular derangement is particularly evident in neurodegenerative disorders, in which genetic models and environmental factors allowed to identify common traits in the pathogenic routes. We will here summarize: i) the current view of mechanisms and functions of mitochondrial Ca2+ homeostasis, ii) the basic principles of organelle Ca2+ transport, iii) the role of Ca2+ in neuronal cell death, and iv) the new information on the pathogenesis of Alzheimer's, Huntington's and Parkinson's diseases, highlighting the role of Ca2+ and mitochondria. 相似文献
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Autophagy is now emerging as a spotlight in trafficking events that activate innate and adaptive immunity. It facilitates innate pathogen detection and antigen presentation, as well as pathogen clearance and lymphocyte homeostasis. In this review, we first summarize new insights into its functions in immunity, which underlie its associations with autoimmunity. As some lines of evidence are emerging to support its role in autoimmune and autoinflammatory diseases, we further discuss whether and how it affects autoimmune diseases including systemic lupus erythematosus, rheumatoid arthritis, diabetes mellitus and multiple sclerosis, as well as autoinflammatory diseases, such as Crohn disease and vitiligo. 相似文献
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《Autophagy》2013,9(9):1286-1299
Autophagy is now emerging as a spotlight in trafficking events that activate innate and adaptive immunity. It facilitates innate pathogen detection and antigen presentation, as well as pathogen clearance and lymphocyte homeostasis. In this review, we first summarize new insights into its functions in immunity, which underlie its associations with autoimmunity. As some lines of evidence are emerging to support its role in autoimmune and autoinflammatory diseases, we further discuss whether and how it affects autoimmune diseases including systemic lupus erythematosus, rheumatoid arthritis, diabetes mellitus and multiple sclerosis, as well as autoinflammatory diseases, such as Crohn disease and vitiligo. 相似文献
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José Naranjo Ottorino Cosivi 《Philosophical transactions of the Royal Society of London. Series B, Biological sciences》2013,368(1623)
Foot-and-mouth disease (FMD) is a highly transmissible and economically devastating disease of cloven-hoofed livestock. Although vaccines are available and have been instrumental in eliminating the disease from most of the South American animal population, viral circulation still persists in some countries and areas, posing a threat to the advances of the last 60 years by the official veterinary services with considerable support of the livestock sectors. The importance of the disease for the social and economic development of the American continent led to the establishment in 1951 of the Pan American Centre for Foot-and-Mouth Disease (PANAFTOSA), which has been providing technical cooperation to countries for the elimination of the disease. The first FMD national elimination programmes were established in South America around the 1960s and 1970s. To advance the regional elimination efforts in the 1980s, countries agreed on a Plan of Action 1988–2009 of the Hemispheric Program for the Eradication of Foot-and-Mouth Disease. The Plan of Action 1988–2009 did not reach the goal of elimination from the continent; and a new Plan of Action 2011–2020 was developed in 2010 based on the experience acquired by the countries and PANAFTOSA during the past 60 years. This plan is now being implemented; several challenges are still to be overcome to ensure the elimination of FMD from the Americas by 2020, however, the goal is achievable. 相似文献
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New functions have been identified for glyceraldehyde-3-phosphate dehydrogenase (GAPDH) including its role in neurodegenerative disease and in apoptosis. GAPDH binds specifically to proteins implicated in the pathogenesis of a variety of neurodegenerative disorders including the beta-amyloid precursor protein and the huntingtin protein. However, the pathophysiological significance of such interactions is unknown. In accordance with published data, our initial results indicated there was no measurable difference in GAPDH glycolytic activity in crude whole-cell sonicates of Alzheimer's and Huntington's disease fibroblasts. However, subcellular-specific GAPDH-protein interactions resulting in diminution of GAPDH glycolytic activity may be disrupted or masked in whole-cell preparations. For that reason, we examined GAPDH glycolytic activity as well as GAPDH-protein distribution as a function of its subcellular localization in 12 separate cell strains. We now report evidence of an impairment of GAPDH glycolytic function in Alzheimer's and Huntington's disease subcellular fractions despite unchanged gene expression. In the postnuclear fraction, GAPDH was 27% less glycolytically active in Alzheimer's cells as compared with age-matched controls. In the nuclear fraction, deficits of 27% and 33% in GAPDH function were observed in Alzheimer's and Huntington's disease, respectively. This evidence supports a functional role for GAPDH in neurodegenerative diseases. The possibility is considered that GAPDH:neuronal protein interaction may affect its functional diversity including energy production and as well as its role in apoptosis. 相似文献