组蛋白去乙酰化酶2在烟雾致COPD大鼠肺组织中表达下降

慢性阻塞性肺疾病(chronic obstructive pneumonia disease,COPD)是一种有多种炎性因子、炎性介子参与的气道慢性炎性反应疾病,其炎性反应过程复杂使病情反复迁延[1]。组蛋白乙酰化酶(histone acetylase,HAT)和组蛋白去乙酰化酶(histone deacetylase,HDAC)在各种炎性反应基因的表达中起重要作用。因此,COPD气道炎性反应可能与之变化所致的炎性反应基因表达增加有关。本实验使用烟熏制备     

C反应蛋白与冠脉病变程度的相关性以及PCI术后的变化

近年来的研究发现，血清C反应蛋白（C-reactive protein．CRP）是一种机体炎性反应的敏感标志物，机体有炎症存在时。CRP水平会升高。炎症反应与动脉粥样硬化密切相关．而动脉粥样硬化是冠心病的病理基础。本文通过测定冠心病患者CRP水平以了解其与冠状动脉病变程度的关系以及经皮冠状动脉介入治疗（PCI）术后的变化。     

IL-37及其与疾病相关性的研究进展

白细胞介素-37(IL-37)是一种新型炎性抑制因子,目前发现IL-37通过抑制促炎性细胞因子、趋化因子等的产生及对基因转录的调节,参与免疫和炎性反应,在多种炎性反应及免疫相关性疾病中起重要作用,为这些疾病提供新的治疗思路和新靶点。     

血清hs-CRP的水平变化及其临床意义

超敏C反应蛋白（hs-CRP）是肝脏合成的一种急性时相反应蛋白,对急性炎性反应、组织损伤、细菌性感染[1]和恶性肿瘤等的诊断、治疗及预后的观察有临床价值。为探讨血清hs-CRP水平在冠心病（CHD）、糖尿病肾病（DN）和急性脑梗死（ACI）的发生、转归过程的临床应用,本文对693例患者和100名健康者血清hs-CRP水平进行对比分析,     

动脉粥样硬化中炎性反应与内质网应激的相互作用

炎性反应和内质网应激均是动脉粥样硬化发生和发展过程中的重要事件。炎性反应可通过多条途径诱发内质网应激,而内质网应激在疾病的不同阶段可抑制或者促进炎性反应。     

NLRP3炎性小体研究进展

炎性小体是一种多蛋白复合体,它能够识别多种病原微生物及应激相关内源性信号分子,在固有免疫中发挥重要作用。炎性小体可通过活化半胱氨酸天冬氨酸酶-1(caspase-1)诱导促炎因子IL-1β和IL-18的成熟、释放,引起炎性反应,参与多种疾病如家族性周期性自身炎性反应、缺血再灌注损伤和动脉粥样硬化等的发生发展过程。     

动脉粥样硬化中炎性反应与内质网应激的相互作用简

 炎性反应和内质网应激均是动脉粥样硬化发生和发展过程中的重要事件。炎性反应可通过多条途径诱发内质网应激，而内质网应激在疾病的不同阶段可抑制或者促进炎性反应。     

自噬与炎性反应之间分子联系的研究进展

自噬是机体重要的代谢过程,参与细胞的多种应激反应如炎性反应。自噬与炎性反应之间具有密切的分子联系。一方面,多种炎性反应介质可调控自噬发生及自噬基因的转录;另一方面,自噬通过多种方式可抑制机体过激的炎性反应。因此,机体的多种炎性反应疾病包括克罗恩病(CD)可能与自噬缺陷相关。     

日开发出新的抗炎性反应物质

新华社东京电（记者钱铮）日本研究人员新开发出一种效果不亚于类固醇的抗炎性反应物质。这种肽能够抑制在炎性反应中起核心作用的物质的活性，不良反应小，可望用来治疗过敏和皮炎。[第一段]     

SIRT1在糖尿病肾病进展中的作用

SIRT1是一种高度保守的NAD~+依赖的Ⅲ类组蛋白去乙酰化酶,广泛存在于胚胎以及人类组织中,通过染色质的修饰促进染色质沉默,通过去乙酰化非组蛋白调节糖和脂代谢、应激反应、凋亡、炎性反应和自噬等。糖尿病肾病的发生发展与炎性反应、氧化应激、缺血缺氧和衰老密切相关,SIRT1可能是该病进展中的上游调控因子。     

C-reactive protein (CRP) in the cardiovascular system

CRP (C-reactive protein) is an acute-phase reactant, the levels of which increase dramatically in response to severe bacterial infection, physical trauma, and other inflammatory conditions. CRP is found in human atherosclerotic lesions. Atherosclerosis is clearly multifactorial in origin, and chronic inflammation is an important component in its pathogenesis. Focus on inflammation is critical in research on atherosclerosis. Elevated levels of CRP have been associated with increased risk of future coronary artery disease (CAD) events. I have summarized the recent literature on CRP studies in CAD. Both coronary heart disease and dilated cardiomyopathy(DCM) result in congestive heart failure due to myocardial damage. The inflammatory state produced by myocarditis of viral or other origin may induce advanced myocardial damage, resulting in heart failure with a poor prognosis. Routine CRP measurement proved to be valuable for identifying high-risk patients with DCM and lymphocytic myocarditis. I suggest that measurement of circulating CRP would be useful for the diagnosis of and for selecting therapeutic strategies for cardiovascular disorders.     

Animal models of coronary heart disease

Cardiovascular disease, predominantly coronary heart disease and stroke, leads to high morbidity and mortality not only in developed worlds but also in underdeveloped regions. The dominant pathologic foundation for cardiovascular disease is atherosclerosis and, as to coronary heart disease, coronary atherosclerosis and resulting lumen stenosis, even total occlusions. In translational research, several animals, such as mice, rabbits and pigs, have been used as disease models of human atherosclerosis and related cardiovascular disorders. However, coronary lesions are either naturally rare or hard to be fast induced in these models, hence, coronary heart disease induction mostly relies on surgical or pharmaceutical interventions with no or limited primary coronary lesions, thus unrepresentative of human coronary heart disease progression and pathology. In this review, we describe the progress of animal models of coronary heart disease following either spontaneous or diet accelerated coronary lesions.     

Comparison of coronary atherosclerosis in middle-aged Norwegian and Japanese men. An autopsy study

We compared the extent of lesions in the coronary arteries of autopsied middle-aged men from Oslo, Norway, with lesions in autopsied men of similar ages in Tokyo, Japan. Certain risk factors for coronary heart disease as serum cholesterol, triglycerides, and blood pressure were also available from these men in the two locations. Our comparisons reveal large differences in the extent of atherosclerosis between Oslo and Tokyo, which are reflected in the levels of the risk factors, particularly serum cholesterol levels. Our findings suggest that preventive strategies could retard the development of atherosclerosis and coronary heart disease without the economic and nutritional problems that affect technically underdeveloped societies where atherosclerosis and coronary heart disease are not prevalent.     

Inflammation markers in acute coronary syndrome

Inflammation is a component of atherosclerotic plaque, but it is also a possible pathogenetic factor of acute coronary event responsible for coronary instability. Inflammatory markers are considered as new risk factors for atherosclerosis. Among others (C-reactive protein (CRP) is the best known marker of inflammatory response which is most frequently found in patients with acute myocardial infarction preceded by a period of instability. High values of inflammatory markers indicate poor prognosis after acute myocardial infarction. Therapy may lower the inflammatory component and the risk of coronary disease. Specific response of inflammatory marker during diagnostic and percutaneous coronary interventions indicates more severe coronary disease.     

Inflammation in variant angina: Is there any evidence?

Variant angina, defined as spontaneous angina pectoris associated with transient ST-segment elevation, has proved to be caused usually by episodic coronary spasm since Prinzmetal and his associates described a form of angina quite different from classic Heberden angina pectoris in 1959. Currently, coronary artery spasm is defined as reversible coronary stenosis, which limits coronary blood flow under resting conditions, and it plays an important role in ischemic heart disease, particularly in variant angina. Data available in respect of coronary vasospasm showed that it is closely related to atherosclerotic coronary artery disease, since intravascular ultrasound studies reveal atherosclerotic plaques in almost any spastic segment. Risk factors for coronary artery disease and coronary vasospasm, however, differ profoundly. Cigarette smoking is the only established risk factor. Although several candidates and predisposing factors, such as serotonin, histamine, thromboxane, and endothelin, have been described, the mediators and the pathogenesis of the disease remain unknown. There are abundant studies that inflammation plays an important role in the initiation, development as well as evolution of atherosclerosis, suggesting that atherosclerosis is an inflammation disease. The evidence regarding the role of inflammatory pathways in different clinical entities of coronary artery disease has significantly been accumulated. And also, primary studies have showed that inflammation may be a contributor for variant angina or vasospastic coronary disease is at least partially driven by inflammation. Although much more research is obviously needed, primary evidence provide us with some direction for that research.     

2nd conference on heart, rheumatism and autoimmunity, Pescara, Italy, May 19-20, 2005

Systemic autoimmune diseases, which comprise a family of conditions which share common pathogenetic mechanisms, are frequently associated to cardiac involvement and to a high prevalence of ischemic coronary events often occurring at a younger age than in normal population. A large increase in mortality is related to premature atherosclerosis with coronary artery disease and stroke in patients with connective tissue diseases. Coronary heart disease is responsible for 40-50% of the death of patients with rheumatoid arthritis. Moreover, a growing body of evidence supports the view that autoimmune mechanisms are involved in the pathogenesis of cardiovascular disease. Inflammatory heart disease is a rising concern worldwide. Similar mechanisms link autoimmune diseases, including the association of increased disease with proinflammatory cytokines and the importance of regulatory mechanisms in the control of chronic inflammation. The role of the immune system in modulating atherosclerosis has recently been well documented. Studies have revealed that cellular and humoral immunity plays crucial roles in atherogenic plaque formation. This includes macrophages, CD4+ T cells and dendritic cells as well as autoantigens such as oxidized low-density lipoprotein (oxLDL), heat shock proteins and beta2-glycoprotein I. The inflammatory component is not localized to the "culprit" plaque, but it is diffused to the entire coronary vascular bed, and involves also the myocardium. The aim of the conference (2nd conference on heart, rheumatism and autoimmunity) was to focus the attention of the participants on some pathogenetic, clinical and therapeutic aspects at the boundary between cardiology and rheumatology and to encourage the debate among clinicians and basic researchers with different backgrounds and experiences.     

吸烟对女性冠心病患者冠状动脉粥样硬化的影响

心血管疾病是女性的头号死因,在美国,每分钟就有1名女性死于心血管疾病,其中绝大多数为冠心病。流行病学调查显示,在中国女性的死因排序中,心脏疾病已超过脑卒中和肿瘤,成为头号死因。多数女性甚至内科医生都认为,女性不易患冠心病,这是一个亟需纠正的误区。女性冠心病患者无论是吸烟患者或是被动吸烟患者,均会增加患者发生心血管风险事件概率,而戒烟是冠心病患者容易进行控制的危险因素,有效戒烟可以降低患者心血管风险,延长患者生命周期,保证患者生活质量。本文主要综述烟草对女性冠心病患者冠状动脉粥样硬化发生发展的影响。     

Inflammatory aneurysm of the aorta, aortitis, and coronary arteritis

Inflammatory aneurysm of the aorta is not merely a variant of atherosclerosis, but more probably it is a manifestation of a peculiar systemic disease related to idiopathic retroperitoneal and mediastinal fibrosis. Rarely, aortitis and coronary arteritis may coexist with the inflammatory aneurysm; one of each of such unusual cases are described. Because inflammatory aneurysms of the aorta tend to occur in elderly persons, aortitis and coronary arteritis, when present, cannot be distinguished from the concomitant age-related atherosclerosis without a careful histologic examination.     

Atherosclerotic lesions. Natural history, risk factors, and topography.

This article describes the development of human atherosclerosis as a framework on which to integrate and incorporate the research on thrombosis and hemostasis of participants in the 1992 College of American Pathologists Conference XXII on Hemostasis and Atherosclerotic Disease. Included are the early classic studies of the morphological features of atherosclerosis, atherosclerosis in different populations, the distribution of atherosclerotic lesions among arterial segments, the topography of atherosclerotic lesions within arterial segments, and the relationship of risk factors for coronary heart disease to the arterial lesions of atherosclerosis. Special attention is given to the development of atherosclerosis in young people, including findings from the Pathobiological Determinants of Atherosclerosis in Youth study. The data in this review provide confirmation of the development of atherosclerosis at an early age and relate atherosclerotic lesions to certain coronary heart disease risk factors. Any role of thrombosis or hemostasis in atherosclerosis must be integrated into this framework.     

同型半胱氨酸、脂蛋白(a)和超敏CRP的变化与冠状动脉粥样硬化的关系

探讨血清同型半胱氨酸(Hcy)、脂蛋白(a)[LP(a)]、超敏C反应蛋白(hs-CRP)的变化与冠状动脉粥样硬化及其程度的关系.应用冠状动脉造影判定144例患者冠状动脉粥样硬化及其程度,同时抽取患者血液测定血清中Hcy、LP(a)及hs-CRP的水平.结果表明冠状动脉粥样硬化的患者血清Hcy、LP(a)及hs-CRP的水平比冠状动脉正常的患者明显增高,二者有显著性差异(P＜0.01);且血清Hcy、LP(a)及hs-CRP的水平随病变支数增加而增高.Hcy、LP(a)、hs-CRP作为独立的动脉粥样硬化危险因素对冠心病的诊断及程度的判定有积极的临床意义.