Inflammation and cancer

Recent data have expanded the concept that inflammation is a critical component of tumour progression. Many cancers arise from sites of infection, chronic irritation and inflammation. It is now becoming clear that the tumour microenvironment, which is largely orchestrated by inflammatory cells, is an indispensable participant in the neoplastic process, fostering proliferation, survival and migration. In addition, tumour cells have co-opted some of the signalling molecules of the innate immune system, such as selectins, chemokines and their receptors for invasion, migration and metastasis. These insights are fostering new anti-inflammatory therapeutic approaches to cancer development.     

肠道菌群在肥胖及相关的代谢性疾病发生发展中的地位和作用

肥胖及相关的代谢性疾病近年来已经成为威胁全球的公共健康问题。越来越多的证据表明,与人类共生的肠道菌群不仅在消化、免疫和抗病方面有不可替代的作用,而且与非传染性的代谢失调相关,特别是其可以通过调节宿主脂肪吸收存储相关的基因,影响后者的能量平衡。因此,肠道菌群可能是在膳食结构变化与人的遗传体质的相互作用下导致肥胖等代谢性疾病发生的一个重要环节。对该环节的深入研究,可能带来代谢性疾病预防和控制策略的革命性的变化。     

Inflammation in atherosclerosis

Abundant data link hypercholesterolaemia to atherogenesis. However, only recently have we appreciated that inflammatory mechanisms couple dyslipidaemia to atheroma formation. Leukocyte recruitment and expression of pro-inflammatory cytokines characterize early atherogenesis, and malfunction of inflammatory mediators mutes atheroma formation in mice. Moreover, inflammatory pathways promote thrombosis, a late and dreaded complication of atherosclerosis responsible for myocardial infarctions and most strokes. The new appreciation of the role of inflammation in atherosclerosis provides a mechanistic framework for understanding the clinical benefits of lipid-lowering therapies. Identifying the triggers for inflammation and unravelling the details of inflammatory pathways may eventually furnish new therapeutic targets.     

炎症与心房颤动研究进展

心房颤动是一种常见的心律失常，病因目前仍然不清，本文对炎症与房颤的关系研究进展做一概述．     

Inflammation and therapeutic vaccination in CNS diseases

The spectrum of inflammatory diseases of the central nervous system has been steadily expanding from classical autoimmune disorders such as multiple sclerosis to far more diverse diseases. Evidence now suggests that syndromes such as Alzheimer's disease and stroke have important inflammatory and immune components and may be amenable to treatment by anti-inflammatory and immunotherapeutic approaches. The notion of 'vaccinating' individuals against a neurodegenerative disorder such as Alzheimer's disease is a marked departure from classical thinking about mechanism and treatment, and yet therapeutic vaccines for both Alzheimer's disease and multiple sclerosis have been validated in animal models and are in the clinic. Such approaches, however, have the potential to induce unwanted inflammatory responses as well as to provide benefit.     

一氧化氮的生理化学与炎症

目前,关于一氧化氮(NO)在炎症中的作用说法不一,甚至矛盾。有的认为NO具有强烈的抗炎症作用,而有的却认为NO可促进炎症引起的细胞和组织功能障碍。阐明NO的生理化学(physi-ologicalchemistry)将有利于弄清和区别NO各种生物学效应的机制。NO的生理化学包括直接和间接的二种反应。直接反应是NO与一个生物分子或有关靶的直接作用,它在NO呈低速率产生时发生,起着正常生理条件下的调节性和抗炎症效应。间接反应是由NO形成的中间调节物,如NO和氧或超氧起反应衍生的活性氧化氮引起的反应,它在NO产生加快时发生,起促炎症效应。     

炎症与肿瘤的关系研究进展

炎症反应不仅诱导肿瘤的发生,并且促进肿瘤的发展及转移。在炎症尤其是慢性炎症中,炎症细胞会诱导细胞内产生ROS,引起氧化应激反应,致使DNA损伤并抑制损伤后修复,使抑癌基因发生突变,导致肿瘤的发生;肿瘤微环境中存在的大量炎症细胞和炎症因子会诱导多种细胞因子以及趋化因子的表达,促使细胞增殖并诱导血管生成,从而促进肿瘤的发展及转移。此外,以炎症微环境为靶向的药物在肿瘤治疗中起到了一定的作用,也表明炎症与肿瘤的发生、发展密切相关。综述了炎症与肿瘤的发生、发展及转移之间的相互关系,旨在为肿瘤治疗提供新方向。     

小鼠趾叶炎与P物质的相关性研究

采用组织化学和免疫组化的染色方法,检测趾叶炎小鼠趾部组织中炎性细胞、肥大细胞及其脱颗粒数和P物质表达的动态变化.结果表明,炎症组小鼠趾部P物质在真皮网状层及血管和腺体周围随着二磷酸组织胺免疫时间的推移,表达逐渐增强,多呈网状走行,且与肥大细胞串联及相邻排列;炎症组小鼠趾部肥大细胞及其脱颗粒和炎性细胞随二磷酸组织胺免疫时间的延长急剧增多,均极显著高于正常组(P<0.01),在给药后14 h三者达到峰值,而后减少,给药后72 h又出现上升趋势;同时,在真皮出现了许多增生的动脉,管壁增厚,管腔内有血栓形成.由此推断,P物质参与小鼠趾叶炎的发病过程.     

慢性阻塞性肺疾病合并贫血与炎症相关研究

目的研究慢性阻塞性肺疾病(COPD)合并贫血患者与炎症的关系。方法根据贫血标准对273例慢性阻塞性肺疾病急性加重期(AECOPD)患者进行调查,对其中合并贫血的COPD患者(贫血组)40例和非贫血的COPD患者(非贫血组)40例为研究对象。常规行肺功能(FEV1%)检查,测定血清细胞因子白细胞介质IL-6、IL-8与肿瘤坏死因子-α(TNF-α)及流式细胞仪检测CD4+、CD8+T细胞,并计算其相关性。结果贫血组患者的炎症指标IL-6、IL-8、TNF-α水平高于非贫血组(P<0.05),CD4+/CD8+T细胞比例低于非贫血组(P<0.05),差异均有统计学意义。结论 COPD患者合并贫血可能与炎症相关。     

代谢综合症的运动干预

随着社会的发展和人们生活方式的改变,代谢综合症(MS)从1999年命名至今,发病率逐年升高。MS会并发T2DM、心血管疾病、肥胖等疾病,严重影响人们的生活质量甚至危及生命。MS治疗的基本策略是以改善IR为基础的心血管危险因素的综合防治。包括生活方式干预、饮食控制和运动治疗,无效时考虑药物治疗。运动作为MS的重要干预手段,对MS有着显著的影响,本文就MS与运动之间的关系做一综述。     

Abdominal obesity and metabolic syndrome

Metabolic syndrome is associated with abdominal obesity, blood lipid disorders, inflammation, insulin resistance or full-blown diabetes, and increased risk of developing cardiovascular disease. Proposed criteria for identifying patients with metabolic syndrome have contributed greatly to preventive medicine, but the value of metabolic syndrome as a scientific concept remains controversial. The presence of metabolic syndrome alone cannot predict global cardiovascular disease risk. But abdominal obesity - the most prevalent manifestation of metabolic syndrome - is a marker of 'dysfunctional adipose tissue', and is of central importance in clinical diagnosis. Better risk assessment algorithms are needed to quantify diabetes and cardiovascular disease risk on a global scale.     

脂肪组织血管重塑及其与慢性炎症的相互作用

肥胖机体胰岛素抵抗会引起血管并发症已得到认同,但新近关于肥胖机体慢性炎症的研究发现,在出现胰岛素抵抗前脂肪组织脉管系统已发生功能障碍。本研究分析脂肪组织毛细血管发生变化与缺氧的关系和缺氧与慢性炎症的关系,认为肥胖机体脂肪组织毛细血管发生变化,引起脂肪组织缺氧;缺氧诱导慢性炎症,肥胖关联的炎症又引起脂肪组织血管重塑,加剧脂肪组织功能障碍和胰岛素抵抗;提出在肥胖者体内,脂肪组织血管重塑能够调控慢性炎症和全身胰岛素敏感性。     

脑内免疫炎症的发生机制

中枢神经系统神经元退行性变过程中表达主要组织相容性分子、黏附分子和补体受体,并产生多种细胞因子,从而引发脑内的免疫炎症反应。     

一氧化氮对肠炎症的防护效应

阐明一氧化氮 (NO)对肠炎症的防护效应 ,主要内容为 :1 )急性肠炎症时内源性NO的变化 ,2 )炎症过程中NO所起的作用 ,3 )NO合成酶 (NOS)抑制或破坏对急性肠炎症的影响 ,4)NO抗肠炎症的细胞机制。这些内容将为设计胃肠道抗炎药物开辟新的思路。     

Neurogenic hypothesis and psychiatric disorders

Psychiatric illness, such as affective disorders, anxiety disorders and schizophrenia, exerts exceptional personal burden on affected individuals. Although not physically noticeable, these disorders cost enormously on ones’ family and society. Currently pharma-ceutical and psychological treatments are generally accepted as effective for psychiatric disorders, while the exact mechanisms underlying the treatment efficacy, etiology and neurobiology of the disorders remain elusive. In the past decade, neurogenic hy-pothesis emerged as an attempt to explain the nature of psychiatric illness. The origination of the hypothesis is based on several pre-clinical and clinical observations. First, stress, which is a common risk factor of the disorders, was found to suppress neurogenesis; second, treatment for the illnesses like antidepressants and antipsychotics were shown to improve neurogenesis and behavioral deficits simultaneously; and third, the therapeutic effect of antidepressants was abolished in animal models when neuro-genesis was blocked. Increasing efforts were invested to determine whether neurogenesis is a key to the understanding and treatment of psychiatric disorders, although contrasting results are also found and thus the importance of neurogenesis remains a matter of debate. The present chapter will discuss the recent findings about the involvement of neurogenesis in major depression, anxiety disorders and schizophrenia, and whether neurogenesis would be a potential target for development of the treatment in the future.