血管性痴呆的发病机制研究进展

血管性痴呆发病率逐年上升,发病机制尚不很明确,有效治疗手段缺乏,因此发病机制研究日益受到重视,本文主要从血管性痴呆的中西医发病机制做一综述。     

白癜风发病机制及治疗的研究进展

白癜风主要表现为细胞毒性T细胞破坏表皮黑素细胞造成的皮肤或黏膜白斑[1]。其发病机制尚不明确,研究表明白癜风的发病机制涉及遗传,黑素细胞破坏、氧化应激和自身免疫等多个方面,多个学说交叉及相互作用导致其治疗方法多样而疗效欠佳[2]。白癜风治疗的突破需要我们进一步了解该病发病机制以及基于发病机制制定的治疗策略,本文就白癜风发病机制及治疗进展作一简要综述。     

小儿难治性癫痫病理机制及相关研究

小儿难治性癫痫的发病机制目前仍未完全阐明,研究其病理学特点,探讨可能的发病机制,是迫切需要解决的问题。本文就近几年国内外对小儿难治性癫痫病理与发病机制的研究以及与临床特征的关系进行综述,提示围生期脑损伤,先天性脑损害是小儿难治性癫痫的发病原因。     

多机制多通路参与哮喘新说

目的哮喘发病机制十分复杂,涉及许多方面,对哮喘发病机制的最新研究成果进行综述。方法参阅国外公开发表的相关文献26篇,从炎症及神经体液机制、气道高反应性及气道重塑机制、主要的离子通道等方面阐述了哮喘的发病机制。结果哮喘的发生发展涉及支气管炎症、机体的免疫反应、神经体液信号分子、平滑肌细胞膜及浆膜钙离子通道和钾离子通道等。结论对哮喘发病机制的阐明将为其治疗提供新的思路,同时也为抗哮喘药物的研发奠定基础。     

肠道菌群与高血压相关性的研究进展

高血压的病理机制目前尚不清楚,但近年来不断有研究证实肠道菌群失衡与高血压发病机制相关。故针对高血压发病时肠道菌群变化,肠道菌群在高血压发病机制的作用以及以肠道菌群为干预靶点治疗的措施进行阐述。     

浅析中医药在脑卒中的应用

脑卒中发病机制复杂,本文介绍了中医学的脑卒中发病机制,以及针对各种病因进行辩证施治方法。     

重型肝炎发病机制中细胞因子的作用

重型肝炎病情严重,临床症状复杂,病死率高,严重危害人类健康。其发病机制非常复杂,我们对其还了解甚少。本文从细胞因子在其发病机制中的作用出发,阐述了包括肿瘤坏死因子-α、干扰素-γ、白介素、一氧化氮、肝细胞生长因子、化学趋动因子等在其发病机制中的一些研究进展,为我们更深入了解其发病机制以及在今后的临床诊疗中寻找新的靶点提供一些参考。     

酒精性肝病的治疗进展

酒精性肝病的发病因素单一,因为其发病机制复杂,目前尚不完全清楚。现阶段的治疗只能改善其症状或延缓疾病的进展,需要继续探索发病机制,从而寻找有效的治疗方法。     

炎症性肠病的基础研究与临床应用

炎症性肠病（IBD）包括溃疡性结肠炎（UC）和克罗思病（CD）,是一类病因和发病机制尚不十分清楚的肠道炎症性疾病。现存普遍认为IBD发病机制涉及遗传易感性、环境因素、免疫异常、肠道菌群改变等多个方面,确切病因尚未完全阐明。近年来,随着IBD发病率的逐年上升,人们在探索其发病机制和防治方面展开了大量的基础研究工作,并取得了一定的进展,但日前IBD发病机制仍未明了。     

溃疡性结肠炎的发病机制与治疗进展

目的探讨溃疡性结肠炎的发病机制与治疗进展。方法对当前溃疡性结肠炎的发病机制与治疗的研究成果进行分析。结果溃疡性结肠炎的病因和发病机制可能与免疫因素、遗传因素和环境因素有关。溃疡性结肠炎的治疗药物主要有激素、磺胺类和免疫抑制等。结论溃疡性结肠炎的发病机制现在不明确,是多种因素联合作用的结果,现阶段的治疗仍以药物治疗为主,且生物制剂将会在治疗中起到越来越重要的作用。     

藏药治疗脑缺血疾病的研究进展

脑缺血疾病是危害人类健康的主要疾病之一,其发生机制包括能量代谢障碍、代谢性酸中毒、Ca2+超载、兴奋性氨基酸分泌、自由基生成增多、炎症反应、细胞凋亡及细胞自噬等.藏药性质特殊,且藏药方剂成分复杂、炮制工艺和服用方法独特,使藏药对脑缺血疾病有着巨大的治疗潜力.本文就脑缺血疾病的发病机制及单味藏药和藏药方剂治疗脑缺血疾病的...     

血脂和脂蛋白水平对我国中年人群缺血性心血管疾病事件的预测作用

目的研究分析不同血脂指标对于我国中年人群缺血性心血管疾病事件的预测作用。方法选择住院、门诊、社区及体检人群资料完整的10200人作为研究对象。所有被研究者的平均随访时间为(15.8±2.1)年。观察缺血性心血管疾病事件,其包括冠心病以及缺血性脑卒中。结果在随访期间出现缺血性心血管疾病(ICVD)事件有372例,其中单纯冠心病94例,缺血性脑卒中267例,冠心病合并缺血性脑卒中11例。人群血清总胆固醇水平与ICVD发病呈现出正相关关系,但是HDL-C水平与ICVD发病有负相关关系,但没有统计学意义。结论我国中年人群的血脂水平明显低于西方人群,血清TC、LDL-C以及NHDL-C以及TC/HDL-C水平升高对于ICVD发病具有独立预测的作用,控制血脂在正常的水平下可以有效减少人群中ICVD的发病率,具有比较重要的意义。     

中山市缺血性脑卒中分型的亚型分布：基于中山市人民医院住院病人的初步研究

目的 了解中山市住院缺血性脑卒中患者临床分型的亚型分布,为脑卒中预防、治疗方法的选择、预后评估提供参考依据.方法 按CISS分型对中山市人民医院133例出院的缺血性脑卒中患者进行病因及发病机制分型.结果 中山市人民医院缺血性脑卒中的病因中大动脉粥样硬化性占62.4％,大动脉粥样硬化性是主要病因,与其他病因相比具有统计学差异（P＜0.05）;大动脉粥样硬化脑梗死发病机制中载体动脉阻塞穿支动脉占50.6％,为主要发病机制,与其他发病机制相比,差异具有统计学意义（P＜0.05）.结论 大动脉粥样硬化依然是最主要的病因,其次为穿支动脉疾病,心源性并不少见.以载体动脉阻塞穿支动脉为主要的发病机制.高血压、吸烟、高血脂是最常见的危险因素,需重视加强高血压病管理及注意筛查糖尿病.     

Relationship between deaths from stroke and ischemic heart disease--environmental implications.

We analyzed the ratio of deaths from stroke and ischemic heart disease in Lithuania over a 72-month period (1990-1995) in relation to fluctuations in five physical environmental parameters. Results indicated a highly significant adverse correlation of the stroke/ischemic heart disease death ratio with both solar activity (r = -0.64, p = 0.0001), stronger for women than for men, and the planetary geomagnetic activity index (r = -0.33, p = 0.005). Proton flux > 60 MeV correlated significantly with the death ratio only for the 65-74-year age group (r = -0.36, p = 0.03) (36-month study). The last finding may be a result of different environmental influences on the pathogenesis of ischemic heart disease and cerebral vascular accidents at different ages. We conclude that the monthly ratio of deaths from stroke/ischemic heart disease is related to environmental physical activity.     

Oxidative stress-induced ischemic heart disease: protection by antioxidants

Heart disease is one of the major health problems of advanced as well as developing countries of the world. Extensive research through the last decade has shown beyond doubt that free radicals, particularly, reactive oxygen species play a cardinal role in the pathogenesis of oxidative myocardial damage with consequential cardiac malfunction. This review presents a comprehensive account of the present day knowledge regarding the oxygen free radicals involved in the genesis of ischemic heart disease, the mechanism(s) of oxidative myocardial damage and the endogenous as well as exogenous antioxidant defense systems. Furthermore, the role of ischemic pre-conditioning, some antioxidants and the ability of some cardioprotective drugs in providing protection against the ischemic myocardial damage are also discussed. The text of the article comes to an end with a commentary on the future research perspective in the concerned area, which throws a light on the development of combinatorial therapeutics in the treatment of ischemic myocardial disease.     

右心功能不全在缺血性肝炎发病机制中的作用

目的探讨缺血性肝炎的发病机制,加深对缺血性肝炎的认识。方法回顾性分析26例缺血性肝炎的临床资料,与同期肺源性心脏病和因消化道出血致低血压或休克住院患者临床资料作比较分析。结果 3组患者中缺血性肝炎组和消化道出血组均存有低血压或休克表现,但2组平均动脉压无显著性差异。26例缺血性肝炎中,除有19例患者有下肢水肿、少量腹水或胸水的表现,结合心电图、胸片、彩色多普勒考虑存在右心功能不全;61例因消化道出血致低血压或休克住院患者除消化道出血的临床表现外,无右心功能不全的证据。其中仅有2例肝脏酶学明显升高,而合并诊断缺血性肝炎。结论低血压或休克是引起缺血性肝炎必要条件,但不是唯一条件,右心衰可能对发生缺血性肝炎起一定作用。     

血管性痴呆模型及信号通路研究进展

血管性痴呆是指由缺血性卒中、出血性卒中和造成脑区低灌注的脑血管疾病所致的严重认知功能障碍综合征。血管性痴呆是可以预防的,因为针对致病性脑血管疾病已建立了例如控制血管危险因素、抗血小板治疗和抗凝治疗等预防措施,然而目前尚无针对血管性痴呆的对症治疗方法。了解其基本机制及模型对于血管性痴呆的治疗至关重要。本文简述了血管性痴呆的多种动物模型,并简要介绍了目前针对其发病机制的相关通路研究,为血管性痴呆的治疗和用药提供参考。     

Treatment strategies for chronic stable angina

Introduction: Stable angina pectoris – generally the expression of an imbalance between myocardial oxygen demand and supply – is often the first manifestation of ischemic heart disease. The effective management of this highly prevalent condition is largely dependent on the identification of the prevailing pathogenic mechanism, the implementation of lifestyle changes and the appropriate use of pharmacological agents and revascularization techniques. There is abundant literature on management of chronic stable angina, but publications are generally devoted to focused areas. There is a need for a comprehensive review that addresses both the different types of angina and their pathogenic mechanisms, as well as rational approaches to patient management.

Areas covered: This paper reviews the pathogenesis and pathophysiological mechanisms of myocardial ischemia, along with its consequences and current treatment options. Relevant papers in the English literature were identified via PubMed, using the following keywords relating to chronic stable angina: ischemic heart disease, coronary artery disease and antianginal therapy.

Expert opinion: The treatment of chronic stable angina has improved in recent years as a result of a better understanding of its pathogenic mechanisms, the implementation of lifestyle changes and aggressive management of risk factors, as well as pharmacological advances and better revascularization techniques. Understanding the pathogenesis of the disease is important to identify effective treatment strategies. A careful clinical history, the implementation of appropriate diagnostic tests and a rational use of antianginal drugs and revascularization protocols often ensure the successful control of the patient's symptoms.     

Ischemic heart disease induces upregulation of endothelin receptor mRNA in human coronary arteries

Endothelin has been implicated in the pathogenesis of ischemic heart disease and congestive heart failure. The aims were to quantify endothelin type A (ETA) and type B (ETB) receptor mRNA levels in human coronary arteries from patients with ischemic heart disease, congestive heart failure and controls using real-time polymerase chain reaction (real-time PCR). In addition, the suitability of organ culture as a model mimicking endothelin receptor changes in cardiovascular disease was evaluated by in vitro pharmacology and real-time PCR. Endothelin ETA and ETB receptor mRNA levels were significantly higher in arteries from patients with ischemic heart disease (0.23+/-0.04 and 0.35+/-0.06) as compared to congestive heart failure (0.09+/-0.02 and 0.07+/-0.01) and controls (0.08+/-0.02 and 0.08+/-0.01). After organ culture, the endothelin ETB receptor mRNA levels were elevated, and the sarafotoxin 6c-induced vasoconstriction was more efficacious. Increased endothelin receptor activity may contribute to the increased vascular tone and development of atherosclerotic disease in ischemic heart disease in man.     

Poly(ADP-ribosyl)ation and stroke.

Over the past decade, poly(ADP-ribosyl)ation has emerged as a crucial event in the pathogenesis of ischemic stroke. A large body of evidence unambiguously demonstrates that activity of poly(ADP-ribose) polymerase-1 (PARP-1) significantly increases during brain ischemia, and that inhibition of this enzymatic activity affords substantial neuroprotection from ischemic brain injury. This review strictly focuses on literature on poly(ADP-ribosyl)ation and ischemic stroke, highlighting the pathogenetic role of poly(ADP-ribose) in ischemic neuronal death, and the therapeutic relevance of drugs modulating its metabolism to pharmacological treatment of cerebral ischemia.