超声造影评价膳食炎症指数与颈动脉斑块内增强特征的相关性

目的探讨超声造影对膳食炎症指数（DII）与颈动脉斑块内增强特征的相关性。方法选取2015年3月~2019年10月在我院行颈动脉斑块复查的77例患者作为研究对象。采用食物频率问卷表调查患者的日常饮食数据，应用膳食营养软件计算食物的膳食成分/营养素的DII指数。根据患者DII指数分组，即DII指数为正数纳入促炎饮食组（n=35），DII指数为负数纳入抗炎饮食组（n=42）；并根据患者DII指数划分5个等级，即≤-1.05、-1.05~-0.33、-0.33~0.38、0.38~1.22、≥1.22。采用彩色多普勒超声检测患者颈动脉斑块，对其斑块厚度、回声类型、斑块造影剂分布特征进行分析。双变量相关性分析采用Kendall相关系数法检验。结果促炎饮食组35例患者共41枚斑块，抗炎饮食组42例患者共47枚斑块。促炎饮食组的斑块厚度较抗炎饮食组的增厚，差异有统计学意义（P < 0.05）；促炎饮食组超声造影增强多于抗炎饮食组，差异有统计学意义（P < 0.05）。DII指数与颈动脉斑块内膜有无增强呈显著性正相关（Kendall相关系数为0.659，P < 0.001）。结论促炎饮食患者的颈动脉斑块较厚，DII指数越高，颈动脉斑块斑块内增强特征越明显。      

膳食炎症指数与消化道肿瘤发病风险的研究进展

对膳食炎症指数（dietary inflammatory index,DII）的建立、发展、计算方法以及与各种常见消化道肿瘤发生发展的关系进行综述，期望从膳食炎症角度探讨消化道肿瘤的预防措施，为消化道肿瘤高风险人群提供饮食指导，为消化道肿瘤病人的营养教育提供新视角。     

慢性炎症微环境与肿瘤

炎症是机体对致病因素及其损害作用产生的一种免疫防御反应,急性炎症能够消除损伤因子,同时促进受损组织的愈合。然而,致炎因子的持续存在和组织损伤会导致慢性炎症的发生,从而影响人体的健康,推动疾病的发生。肿瘤又被称为"不愈合的伤口",肿瘤微环境一般是炎症相关细胞大量浸润的慢性炎症环境,其中,炎症细胞及炎症相关因子的多样性与肿瘤细胞、基质细胞共同构成了复杂的调控网络。在肿瘤发生、发展的不同阶段,同种细胞类型或同种细胞因子对肿瘤发展却发挥着不同的作用,有时甚至是相反的作用。本文主要就肿瘤慢性炎症微环境的炎症细胞及炎症相关因子如何调控肿瘤的发生、发展作一综述。     

中药抑制炎症标志物干预慢性心力衰竭的研究进展

正慢性心力衰竭是与各种病理生理相关的复杂疾病,多种机制共同参与了疾病的发生发展过程,其中炎性因子在慢性心力衰竭的发展进程中发挥重要作用,现在越来越多的证据支持炎症在慢性心力衰竭进展中的关键作用。慢性心力衰竭有关的炎症标志物较多,如传统炎症标志物C-反应蛋白(CRP),肿瘤坏死因子-α(TNF-α),白细胞介素(IL)6等,已被证实与慢性心力衰竭严重程度密切相关,有助于慢性心力衰竭的危险分层[1]。据近几年文献报道,半乳糖凝集素-3(Galectin-3)、可溶     

炎症体与肿瘤相关血栓形成的研究进展

炎症体是一种蛋白复合物,可以通过模式识别受体识别病原分子和病原体模拟人热休克蛋白两种信号引起自身活化,激活NF-κB通路,诱导产生炎症介质,导致慢性炎性反应并促进血栓形成。文献报道近17%的新发肿瘤可由于慢性炎症所引起,可见肿瘤相关血栓形成与炎症体之间存在复杂的关系。本文就炎症体和肿瘤相关血栓相关性作一综述,其中几种学说印证了两者之间的关系。     

缬沙坦对维持性腹膜透析患者微炎症状态的影响

目前维持性腹膜透析（PD）患者的微炎症状态越来越多的被临床工作者注视。据文献报道：透析人群中处于微炎症状态的患者可达30％～50％。这种慢性炎症与心血管疾病、病死率和营养不良等相关。故及早发现处于微炎症状态的患者并对其进行提早干预治疗是改善此类患者预后的一项极其必要的举措。     

慢性肾功能不全与炎症反应

随着对慢性肾功能不全及其机制的探索,发现炎症反应与慢性肾功能不全之间存在着诸多的联系.甚至有人认为慢性肾功能不全是一个炎症疾病,因为反映炎症活动的炎症标记物已被证明在这个疾病中存在,并且肾取代治疗所应用的一些物质如血液透析中生物不相容性膜等也会导致炎症.炎症反应同时又会加重慢性肾功能不全的发展.我们就慢性肾功能不全引起炎症的原因及炎症加重肾功能不全展开讨论.     

肥胖相关慢性炎症与2型糖尿病

肥胖对健康危害巨大,可诱发一系列代谢性疾病,流行病学调查研究显示,随着超重和肥胖患病率的增加,糖尿病等代谢性疾病的患病率呈现快速增长趋势。相关研究发现,肥胖相关慢性炎症是连接肥胖与胰岛素抵抗及2型糖尿病的枢纽,本文将从肥胖肥胖相关慢性炎症胰岛素抵抗2型糖尿病几个方面对肥胖相关慢性炎症与2型糖尿病的关系进行探讨。     

炎症在糖尿病肾病中的研究进展

糖尿病肾病（DN）是世界范围内最常见的慢性肾脏疾病之一,也是终末期肾病的主要原因。DN的发病是由多种因素共同作用的结果,而导致其病情发展的机制尚不明确。目前越来越多的研究表明,在DN的发生和发展中特定的炎症状态有着举足轻重的地位。该文总结了近年来参与DN发展的相关炎症分子和信号通路以及针对炎症信号通路及其上下游产物作为DN治疗靶点的相关研究。从而让人们更加深入地了解炎症与DN发生发展之间的关系。     

医用生物材料的相关性炎症

目的:概括医用生物材料在宿主体内引起炎症反应的原因和机制.资料来源:以biomaterials,inflammation,mechanism为检索词,检索Pubmed数据库(2004-01/2008-12);以生物材料,炎症,机制为检索词,检索CNKI数据库(2005-01/2008-12).文献检索语种限制为英文和中文.资料选择:纳入产生医用生物材料炎症的原因和机制相关的内容.对医用生物材料的理化特性以及力学方面的研究进行排除.结局评价指标:①材料植入体内后炎症细胞和材料的黏附.②细胞因子的表达.结果:计算机初检得到70篇文献,根据纳入排除标准,对医用生物材料在宿主体内引起炎症反应的原因和机制进行分析.随着组织工程学的发展,各种新型的、具有良好生物相容性、生物活性以及生物降解吸收功能的高分子医学生物材料正不断涌现.生物医学材料是用来修复或替代损伤的组织和器官使其功能恢复的材料,感染仍是医用生物材料植入的严重并发症.生物医学材料导致感染的机制为:血液中的补体黏附生物材料表面,导致整合素介导的白细胞的募集和黏附,黏附的单核,巨噬细胞释放细胞因子和生长因子,导致生物医学材料相关感染的发生.要预防医用生物材料相关性炎症,首先要从材料本身出发,寻找一些对宿主炎症反应小的医用材料.结论:医用生物材料相关性炎症是决定材料植入成功与否的关键因素.生物材料相关炎症的产生是炎症细胞,炎症因子,补体以及酶,氧自由基共同作用的结果.材料表面的微结构、化学和介电等性质都直接影响炎症细胞对材料的反应.     

Dietary Inflammatory Index (DII) is Associated with Movement-Evoked Pain Severity in Adults with Chronic Low Back Pain: Sociodemographic Differences.

Chronic low back pain (CLBP) is one of the leading causes of pain and disability in adults in the United States and disproportionately burdens non-Hispanic Black (NHB) individuals and females. Approximately 90% of CLBP cases are of unknown cause, and it is imperative that potential causes be explored. It has been reported that diet quality can influence pain state via diet-induced inflammation. The present study assessed the relationship between Dietary Inflammatory Index (DII) and movement evoked-pain severity in people with CLBP and investigated whether race/sex moderated the relationship between DII and movement-evoked pain. Results revealed no significant differences in DII scores between males and females, or between NHB and non-Hispanic White (NHW) participants. Participant sex significantly modified the relationship between DII and movement-evoked pain severity (P = .0155), such that movement-evoked pain severity was significantly impacted by DII scores in females, but not males. Participant race did not significantly moderate the DII – movement-evoked pain severity relationship. These results suggest that diet-induced inflammation may impact the CLBP experiences of females to a greater degree than males. Further research is needed to determine whether dietary interventions that reduce inflammation improve CLBP outcomes and whether these interventions may be differentially-beneficial based on sex.PerspectiveThis article highlights the impact of diet-induced inflammation in a community-based sample as a whole, as well as stratified in various sociodemographic groups. This work expands our understanding of the influence of diet on pain experience and suggests that modifications to diet may be efficacious treatments for reducing chronic pain.     

Mechanism of Action of Colchicine in the Treatment of Gout

Purpose

The aims of this article were to systematically review the literature about the mechanism of action of colchicine in the multimodal pathology of acute inflammation associated with gout and to consider the clinical utility of colchicine in other chronic inflammatory diseases.

Methods

The English-language literature on PubMed was searched for articles published between 1990 and October 2013, with a cross-reference to citations across all years. Relevant articles pertaining to the mechanism of action of colchicine and the clinical applications of colchicine in gout and other inflammatory conditions were identified and reviewed.

Findings

The molecular pathology of acute inflammation associated with gouty arthritis involves several concurrent pathways triggered by a variety of interactions between monosodium urate crystals and the surface of cells. Colchicine modulates multiple pro- and antiinflammatory pathways associated with gouty arthritis. Colchicine prevents microtubule assembly and thereby disrupts inflammasome activation, microtubule-based inflammatory cell chemotaxis, generation of leukotrienes and cytokines, and phagocytosis. Many of these cellular processes can be found in other diseases involving chronic inflammation. The multimodal mechanism of action of colchicine suggests potential efficacy of colchicine in other comorbid conditions associated with gout, such as osteoarthritis and cardiovascular disease.

Implications

Colchicine has multiple mechanisms of action that affect inflammatory processes and result in its utility for treating and preventing acute gout flare. Other chronic inflammatory diseases that invoke these molecular pathways may represent new therapeutic applications for colchicine.     

Desquamative Inflammatory Vaginitis: A Closer Look

Desquamative inflammatory vaginitis (DIV) is an uncommon form of vaginitis first described in 1965. Although etiology of this chronic vaginitis is unknown, it is believed to be immune mediated. DIV is a diagnosis of exclusion, characterized by inflammation and a purulent, odorless discharge. The incidence and prevalence are unclear, but perimenopausal, white women seem to be the most affected. DIV has been reported to be present in 0.8% to 4.3% of women with vulvovaginal symptoms. Signs and symptoms are nonspecific. This may be a challenge for the primary care provider treating women’s health issues. Misdiagnosis and incorrect treatment may occur. There is limited information in the literature related to DIV and long-term outcomes. Relatively high relapse rates are common and may require maintenance treatment.     

Positioning ustekinumab in moderate-to-severe ulcerative colitis: new kid on the block

ABSTRACT

Introduction: Ulcerative colitis (UC) is a chronic relapsing disorder of the colonic tract. Dysregulated innate and adaptive immune pathways contribute to intestinal inflammation in IBD, and cytokines, including IL-12 and IL-23, play a key role. The blockade of both IL-12 and IL-23 may have an impact on different pathways of inflammation and could be effective for the treatment of inflammatory bowel diseases.

Ustekinumab is a fully human IgG1κ monoclonal antibody which binds to the shared p40 protein subunit of IL-12 and ?23. It is currently approved for several immune-mediated diseases such as moderate to severe plaque psoriasis, psoriatic arthritis, and Crohn’s disease, and has shown promising results in UC.

Areas covered: A review of the literature was performed to understand several aspects including the role of IL-12 and ?23 in UC, the potential therapeutic role of ustekinumab in inflammatory bowel disease, and the positioning of ustekinumab in the therapeutic algorithm of UC, based on extrapolated data from available randomized clinical trials.

Expert opinion: Ustekinumab is effective and safe in UC, and shows potential advantages compared to other drugs in moderate-to-severe UC.     

Overview of Serum Uric Acid Treatment Targets in Gout: Why Less Than 6 mg/dL?

Gout is a progressive, painful, debilitating form of inflammatory arthritis. It is caused by factors that elevate the concentration of serum uric acid (sUA), leading to hyperuricemia (sUA >6.8 mg/dL). Continued elevated sUA can result in monosodium urate (MSU) crystal deposition in joints and soft tissues, and can cause acute and chronic inflammation. The prevalence of hyperuricemia and gout has increased over the last few decades, likely due to an aging population, changes in lifestyles and diet, and an increase in gout-associated comorbidities. Untreated or improperly treated gout can lead to chronic manifestation of the disease, including persistent inflammation, increased number of flares, development of tophi, and structural joint damage. Data show that even when patients are asymptomatic, ongoing inflammation and subsequent damage occurs locally at the joint and systemically. The aim of long-term treatment of gout is to reduce sUA levels to <6 mg/dL, which is below the saturation point of MSU (6.8 mg/dL), to inhibit formation of new crystals and to promote dissolution of existing crystals. Gout treatment should improve disease outcomes by eliminating gout flares, inducing long-term resolution of tophi, and more effectively managing comorbidities, many of which are associated with hyperuricemia. A number of studies have demonstrated that treating to the target of <6 mg/dL, by using effective therapies to lower sUA, results in reduction in the incidence of gout flares as well as shrinkage and eventual disappearance of tophi. Gout is often poorly managed due to a number of factors including lack of physician and patient adherence to treatment guidelines. Patients need to be educated about their diagnosis and management of the disease, such as the influence of diet and the importance of compliance with long-term treatment. With treatment, regular sUA monitoring, and patient adherence, gout is a curable disease.     

阿莫西林联合果胶铋治疗慢性萎缩性胃炎的临床效果及对血清炎症因子的影响

目的探讨阿莫西林联合果胶铋治疗慢性萎缩性胃炎的临床效果及对血清炎症因子的影响。方法将我院收治的40例慢性萎缩性胃炎患者根据随机数字表法分为对照组与观察组,各20例。对照组采用阿莫西林治疗,观察组采用阿莫西林联合果胶铋治疗。比较两组的治疗效果。结果观察组的治疗总有效率显著高于对照组(P<0.05)。治疗后,两组的肠上皮化生、异型增生、腺体萎缩、慢性炎症、活动性积分、TNF-α、IL-6、CRP水平均降低,且观察组显著低于对照组(P<0.05)。结论阿莫西林联合果胶铋治疗慢性萎缩性胃炎的临床效果显著,可改善患者的临床症状,降低其血清炎症因子水平。     

Anti-inflammatory effects of astaxanthin in the human gingival keratinocyte line NDUSD-1

Oral lichen planus is a chronic inflammatory disease that affects the mucous membrane of the oral cavity and can contribute to the development of other diseases. Inflammation in oral lichen planus is a T-cell-mediated autoimmune disease that acts through cytotoxic CD8⁺ T cells to trigger apoptosis of keratinocytes. However, the specific cause of oral lichen planus remains unknown and no effective medical treatment has yet been established. Astaxanthin is a carotenoid pigment with capacity for anti-inflammatory and anti-oxidant activities. In this study, we evaluated whether astaxanthin could be used to improve the pathology of oral lichen planus by reducing inflammation. In particular, the anti-inflammatory effects of astaxanthin on the chronic inflammation caused by lipopolysaccharide derived from Escherichia coli O55 in human gingival keratinocytes (NDUSD-1) were evaluated. Following astaxanthin treatment, localization of nuclear factor κB/p65 and the level of inflammatory cytokines (interleukin-6, tumor necrosis factor-α) tended to decrease, and cell proliferation significantly increased in vitro. These results suggest that astaxanthin could be useful for improving chronic inflammation such as that associated with oral lichen planus.     

Asthma: 2015 and beyond

Asthma is a multifactorial, chronic inflammatory disease of the airways. The knowledge that asthma is an inflammatory disorder has become a core fundamental in the definition of asthma. Asthma's chief features include a variable degree of air-flow obstruction and bronchial hyper-responsiveness, in addition to the underlying chronic airways inflammation. This underlying chronic airway inflammation substantially contributes to airway hyper-responsiveness, air-flow limitation, respiratory symptoms, and disease chronicity. However, this underlying chronic airway inflammation has implications for the diagnosis, management, and potential prevention of the disease. This review for the respiratory therapy community summarizes these developments as well as providing an update on asthma epidemiology, natural history, cause, and pathogenesis. This paper also provides an overview on appropriate diagnostic and monitoring strategies for asthma, pharmacology, and newer therapies for the future as well as relevant management of acute and ambulatory asthma, and a brief review of educational approaches.     

Immunosuppressive and Anti-inflammatory Properties of Interleukin 10

Interleukin 10 (IL-10) indirectly prevents antigen-specific T-cell activation, which is associated with downregulation of the antigen presentation and accessory cell functions of monocytes, macrophages, Langerhans cells and dendritic cells. In addition, IL-10 inhibits T-cell expansion by directly inhibiting IL-2 production by these cells. These properties of IL-10, together with its capacity to downregulate the production of proinflammatory cytokines and chemokines by activated monocytes, polymorphonuclear leucocytes and eosinophils, indicate that IL-10 is a potent immunosuppressant in vitro. IL-10 has similar activities in vivo. It inhibits lipopolysaccharide or staphylococcal enterotoxin B induced lethal shock in mice. In addition, IL-10 deficient mice develop chronic inflammatory bowel disease, which could be reduced, or prevented by IL-10 treatment. IL-10 also prevented the development of colitis in a SCID mouse model.

Collectively, these data indicate that IL-10 has great potential therapeutical utility in the treatment of diseases, such as chronic inflammation, autoimmune diseases, transplant rejection, graft-versus-host disease and sepsis.     

脑缺血炎症反应与星形胶质细胞的关系

脑缺血后星形胶质细胞作为中枢神经系统第一个受损的细胞，出现肥大、增殖，并合成表达多种炎症介质，启动免疫级联反应。星形胶质细胞产生的炎症介质共同作用于中枢神经系统，损伤和保护脑组织机制并存。了解星形胶质细胞及其表达的炎症介质，对寻找减轻脑缺血后炎症反应损伤的新途径具有重要意义。