Inflammation:an important mechanism for different clinical entities of coronary artery diseases

Although atherosclerosis has been considered to be multi-factorial disease in which genetic, environmental, metabolic factors have been implicated, the gaps remain in our knowledge of the etiopathogenesis of atherosclerosis. There is mounting evidence that inflammation plays an important role in the initiation, development as well as evolution of atherosclerosis, suggesting that atherosclerosis is an inflammation disease.1,2 Although triggers and pathways of inflammation are probably multiple …     

Inflammation in coronary artery diseases

The concept that atherosclerosis is an inflammation has been increasingly recognized, and subsequently resulted in great interest in revealing the inflammatory nature of the atherosclerotic process. More recently, a large body of evidence has supported the idea that inflammatory mechanisms play a pivotal role throughout all phases of atherogenesis, from endothelial dysfunction and the formation of fatty streaks to plaque destabilization and the acute coronary events due to vulnerable plaque rupture. Indeed, although triggers and pathways of inflammation are probably multiple and vary in different clinical entities of atherosclerotic disorders, an imbalance between anti-inflammatory mechanisms and pro-inflammatory factors will result in an atherosclerotic progression. Vascular endothelial dysfunction and lipoprotein retention into the arterial intima have been reported as the earliest events in atherogenesis with which inflammation is linked. Inflammatory has also been extended to the disorders of coronary microvasculature, and associated with special subsets of coronary artery disease such as silent myocardial ischemia, myocardial ischemia-reperfusion, cardiac syndrome X, variant angina, coronary artery ectasia, coronary calcification and in-stent restenosis. Inflammatory biomarkers, originally studied to better understand the pathophysiology of atherosclerosis, have generated increasing interest among researches and clinicians. The identification of inflammatory biomarkers and cellular/molecular pathways in atherosclerotic disease represent important goals in cardiovascular disease research, in particular with respect of the development of therapeutic strategies to prevent or reverse atherosclerotic diseases.

     

Does treatment with statins have the potential of enhancing vascular calcification?

Vascular calcification is commonly found in atherosclerosis and recognized as a marker of atherosclerotic plaque burden. Many evdiences have demonstrated that vascular calcification is an active process and can be seen in all stages of development and intimately associated with atherosclerosis. The correlation between coronary calcifications and subclinical atherosclertotic disease has been well-known for some years. Bone morphogenetic protein-2 （BMP-2） has significant importance in bone development and the development of a wide array of tissues outside of bone. Zhang et al3,4 found mice genetically engineered to be deficient in BMP-2 die between days 7 and 10 of gestation of cardiac defects before bone formation. Many evidences have also confirmed that BMP-2 is a strong basic causative factor in vascular calcification and has been most frequently associated with calcific arteriopathy. Statins are the most powerful cholesterol-lowering drugs available. Although a major beneficial effect of statins in clinical studies is related to a marked reduction in low density lipoprotein （LDL） cholesterol levels, there are good evidences that statins hold multiple vascular protective effects,5 however, the effects of statins therapy in vascular calcification are more complex and less defined. The currently available reports of clinical trials about statins therapy of vascular calcification appeared to be paradoxical.     

Programmed cell death and its role in inflammation

Cell death plays an important role in the regulation of inflammation and may be the result of inflammation. The maintenance of tissue homeostasis necessitates both the recognition and removal of invading microbial pathogens as well as the clearance of dying cells. In the past few decades, emerging knowledge on cell death and inflammation has enriched our molecular understanding of the signaling pathways that mediate various programs of cell death and multiple types of inflammatory responses. This review provides an overview of the major types of cell death related to inflammation. Modification of cell death pathways is likely to be a logical therapeutic target for inflammatory diseases.     

Effect of dexamethasone on the release of transforming growth factor-β1, interleukin-8, interleukin-10 and RANTES release by sputum cells in severe asthma

Bronchial asthma is a reversible obstructive airway disease characterized by persistent airway inflammation and airway remodeling, with eosinophil infiltration of the airway walls as the predominant feature. However, our previous work and other reports have demonstrated that neutrophil predominant inflammation is present in a subgroup of asthmatics, particularly severe asthmatics, and patients with airway neutrophilia are less responsive to glucocorticoid therapy. The mechanisms underlying airway neutrophilia in asthma are still under investigation, but interleukin （IL）-8 as an important neutrophil chemokine may play an important role.     

Anesthetic action of volatile anesthetics by using Paramecium as a model

Although empirically well understood in their clinical administration, volatile anesthetics are not yet well comprehended in their mechanism studies. A major conundrum emerging from these studies is that there is no validated model to assess the presumed candidate sites of the anesthetics. We undertook this study to test the hypothesis that the single-celled Paramecium could be anesthetized and served as a model organism in the study of anesthetics. We assessed the motion of Paramecium cells with Expert Vision system and the chemoresponse of Paramecium cells with T-maze assays in the presence of four different volatile anesthetics, including isoflurane, sevoflurane, enflurane and ether. Each of those volatiles was dissolved in buffers to give drug concentrations equal to 0.8, 1.0, and 1.2 EC50, respectively, in clinical practice. We could see that after application of volatile anesthetics, the swimming of the Paramecium cells was accelerated and then suppressed, or even stopped eventually, and the index of the chemoresponse of the Paramecium cells (denoted as Iche) was decreased. All of the above impacts were found in a concentration-dependent fashion. The biphasic effects of the clinical concentrations of volatile anesthetics on Paramecium simulated the situation of high species in anesthesia, and the inhibition of the chemoresponse also indicated anesthetized. In conclusion, the findings in our studies suggested that the single-celled Paramecium could be anesthetized with clinical concentrations of volatile anesthetics and therefore be utilized as a model organism to study the mechanisms of volatile anesthetics.     

Biliary papillomatosis: analysis of 18 cases

Biliary papillomatosis （BP） is an extremely rare pathological condition, which is characterized by papillary proliferation of the bile duct epithelia. Although initially thought to be a benign entity, this tumor has been shown to have a tendency for malignant transformation. As reported in the literature, malignant degeneration occurs in 20% to 35% of cases. Because patients typically present with abdominal pain, obstructive jaundice and fever, they are usually mistaken as having more serious pathology such as cholangiocarcinoma, cholangitis and so forth. In general, the rate of preoperative diagnosis is very low. At present, the number of published articles about this illness is limited, mainly as single case reports. In addition, the diagnosis, treatment and prognosis of BP have not been well known. We, therefore, discuss age, gender, clinical manifestations, diagnostic approaches, histopathological findings, treatments and prognosis by reviewing the clinical data of eighteen patients with BP treated in our hospital, so as to better understand this rare illness.     

Dyslipidemia promotes the progression of chronic kidney disease?

Dyslipidemia,including hypercholesterolemia,hypertriglyceridemia,and low high-density lipoprotein (HDL) cholesterinemia,is a key risk factor to atherosclerosis.The detrimental effect of elevated low-density lipoprotein (LDL) cholesterol and/or decreased HDL cholesterol on cardiovascular disease risk had been well established from previous studies.1 Recently,emerging evidences suggest that dyslipidemia may also be an important contributor to morbidity and mortality of chronic kidney disease (CKD),which has received more and more attention as the prevalence of CKD increases. In our study published in this issue,2 data were collected among 4779 middle-aged and elderly Chinese population.We found that participants with hypercholesterolemia had greater prevalence of albuminuria and reduced estimated glomerular filtration rate (eGFR).     

The role of inflammatory stress in acute coronary syndrome

Objective To summarize current understanding of the roles of anti-inflammatory and proinflammatory mechanisms in the development of atherosclerosis and acute coronary syndrome and to postulate the novel concept of inflammation stress as the most important factor triggering acute coronary syndrome. Moreover, markers of inflammation stress and ways ,to block involved pathways are elucidated.Data sources A literature search(MEDLINE 1997 to 2002) was performed using the key words “inflammation and cardiovascular disease”. Relevant book chapters were also reviewed.Study selection Well-controlled, prospective landmark studies and review articles on inflammation and acute coronary syndrome were selected.Data extraction Data and conclusions from the selected articles providing solid evidence to elucidate the mechanisms of inflammation and acute coronary syndrome were extracted and interpreted in the light of our own clinical and basic research.Data synthesis Inflammation is closely linked to atherosclerosis and acute coronary syndrome.Chronic and long-lasting inflammation stress, present both systemically or in the vascular walls, can trigger acute coronary syndrome.Conclusions Inflammation stress plays an important role in the process of acute coronary syndrome.Drugs which can modulate the balance of pro- and anti-inflammatory processes and attenuate inflammation stress, such as angiotensin-converting enzyme (ACE) inhibitors/angiotensin Ⅱ receptor blockers, statins, and cytokine antagonists may play active roles in the prevention and treatment of acute coronary syndrome when used in addition to conventional therapies (glycoprotein Ⅱ b/Ⅲ a receptor antagonists, mechanical intervention strategies, etc).     

Effects of allitridin on the expression of transcription factor T-bet mRNA of cytomegalovirus-induced myocarditis in mice

INTRODUCTIONT he cardiovascular disease myocarditis is character ized by inflammation and necrosis of cardiac mus cle. The disease ranges from transient inflammation to afulminant syndrome with manifestations that may includeheart failure, arrhythmias, and sudden death. This dis ease has been associated with various viral etiologies.Although enterovirus infections are recognized as a lead ing cause of myocarditis, at the present studies havedemonstrated that cytomegalovirus…     

动脉粥样硬化的危险因素及保护因素研究进展

在发展中国家,动脉粥样硬化性脑血管病是导致脑梗死发病及致死的主要因素。然而,它是由许多基因及环境因素共同作用产生的复杂病变,是一个由慢性的炎症性进展导致的血管疾病,并最终出现相应部位的临床表现。近年来影响动脉粥样硬化的因素被逐渐运用到临床诊疗中,该文对影响动脉粥样硬化的危险及保护因素的研究进展作一综述。     

骨保护素在急性冠状动脉综合征中的应用价值

骨保护素(OPG)是由成骨细胞分泌的一种无跨膜结构的可溶性糖蛋白,可影响血管钙化和动脉硬化的过程,是动脉粥样硬化进程及心血管病病死率的独立危险因子。OPG与急性冠状动脉综合征(ACS)具有相关性,在急性心肌梗死和不稳定型心绞痛患者的血清中均发现较高水平的OPG表达。虽然这一特点的具体机制尚不明确,但OPG在ACS临床应用中的价值不可忽视。     

同型半胱氨酸致炎作用与动脉粥样硬化

高同型半胱氨酸血症是动脉粥样硬化形成的独立危险因子,但是其致病机制尚未完全阐明。动脉粥样硬化是一种炎症性疾病,从炎症途径出发研究同型半胱氨酸与动脉粥样硬化的关系得到了人们的关注。本文就高同型半胱氨酸致炎效应在动脉粥样硬化中的作用作一综述。     

超敏C反应蛋白与冠状动脉粥样硬化疾病的研究进展

研究表明,超敏C反应蛋白是动脉粥样硬化疾病发生发展的关键因素,各种类型的冠心病可导致其在血清中浓度升高。超敏C反应蛋白在冠状动脉粥样硬化疾病的发病机制中起着很重要的作用。超敏C反应蛋白为冠状动脉粥样硬化疾病的临床诊断、监测、治疗和预后提供了重要价值。     

中风病类、证类与颈动脉粥样硬化的相关性研究

目的探讨中风病辨证类型与颈动脉粥样硬化的关系。方法收集300例中风住院病例,每例均有中医病类、证类诊断,同时有详细的颈动脉彩超检查报告。中风病类分中经络及中脏腑2类,证类分风痰火亢、风火上扰、痰热腑实、风痰瘀阻、痰湿蒙神、气虚血瘀、阴虚风动7型。统计分析中风病类、证类与颈动脉粥样硬化的关系。结果中经络者多为颈动脉粥样硬化无或轻度狭窄,在斑块性质上多为不稳定性斑块;中脏腑者多为中、重度狭窄或闭塞,在斑块性质上多为稳定性斑块。二者比较有统计学差异(P<0.05)。风痰瘀阻、气虚血瘀证患者颈动脉粥样硬化程度较轻(21.8%,21.0%),多为不稳定性斑块(22.4%,24.1%)。痰湿蒙神证患者颈动脉中、重度狭窄或闭塞多见(35.7%)。稳定性斑块在风火上扰证组中多见(27.4%)。结论颈动脉粥样硬化与中风病辨证分型有一定的相关性,具有协助诊断价值。     

代谢性炎症综合征发病机制的研究进展

 代谢性炎症是一种由营养和能量过剩所促发的慢性低度炎症状态。代谢性炎症综合征(metabolic inflammatory syndrome,MIS)则是一组由巨噬细胞所主导的代谢性炎症性疾病,含肥胖、脂肪肝、2型糖尿病、动脉粥样硬化。本文将重点阐述巨噬细胞在MIS发病机制中的作用及相关的抗炎药物。     

易损斑块的研究进展

众所周知,冠状动脉粥样硬化是造成冠状动脉粥样硬化性心脏病的直接原因。随着医学的发展,人们已经认识到冠状动脉粥样斑块中的易损斑块在急性冠状动脉综合征的发病及发展过程中起着至关重要的作用,其相关研究一直是近几年冠心病领域的热点。本文就易损斑块名称的演变、病理学特征、易损机制、血清学标志物及检测与干预的最新进展予以综述。     

INK4基因座中反义非编码RNA调控细胞增殖与凋亡影响动脉粥样硬化的研究进展

动脉粥样硬化是冠心病的重要病理基础,INK4基因座中反义非编码RNA（ANRIL）位于与其相关性最强的遗传易感区段,即9号染色体短臂2区1带（Chr9p21）。ANRIL通过不同的转录剪接方式可产生线性、环状等多种转录本,可调控斑块内相关细胞的增殖和凋亡,与动脉粥样硬化斑块发生发展密切相关。线性ARNIL可通过调节染色质修饰过程调控斑块内血管平滑肌细胞增殖,也可从转录水平调控斑块内巨噬细胞增殖和凋亡;环状ANRIL可调控染色质修饰及干预核糖体RNA加工成熟,进而影响平滑肌细胞的增殖和凋亡。本文对ANRIL的进化特征、转录本的形成及结构、各转录本调节血管细胞增殖和凋亡进而参与动脉粥样硬化的机制进行了系统阐述,以期为深入理解动脉粥样硬化的发病机制,寻找动脉粥样硬化诊治靶点提供依据。