骨性关节炎发病机制的研究进展

骨性关节炎(osteoarthritis,OA)是最常见的关节疾病之一。随着中国社会跨入老龄化时代,OA发病率逐年升高,对于其发病机制的研究也受到研究人员不断重视。研究发现,以白细胞介素1β(interle ukin-1β,IL-1β)和肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)为主的炎症细胞因子是组建起OA炎症网络的罪魁祸首。并且发现以基质金属蛋白酶(matrix metalloproteinase,MMPs)和含血小板反应蛋白基序的解聚素样金属蛋白酶(a disintegrin and metalloproteinase with thrombospondin motifs,ADAMTS)为主的蛋白酶过度表达,是造成OA软骨缺如的直接原因。此外,基质细胞衍生因子-1 (stromal cell derived factor-1,SDF-1)和Wnt等信号通路,软骨细胞衰老与衰老相关分泌表型(senescence-associated secretory phenotype,SASP),软骨细胞凋亡与自噬,雌激素等均在OA发病中发挥了重要作用。本文广泛查阅了近几年与OA发病机制有关的研究文献,从分子层次与细胞层次两方面对OA发病机制进行了系统阐述。并且于文末谈论预测了未来OA临床诊疗中的一些潜在方向。     

童年期居住环境卫生对农村居民中老年期慢性病患病的影响研究

目的探讨童年期居住环境卫生对农村居民中老年期慢性病患病的影响, 并检验童年期健康状况在其中的中介效应。方法基于中国健康与养老追踪调查2018年最新调查和2014年生命历程调查共同访问的12 506名农村居民数据, 运用χ2检验、秩和检验、logistic回归分析模型、倾向评分加权法、负二项回归模型和KHB分析法进行分析。结果调整其他混杂因素后, 相比童年期居住环境卫生较好的农村居民, 童年居住环境卫生较差的中老年农村居民患哮喘风险提高23.7%(OR=1.237, 95%CI:1.060～1.445), 患肝脏疾病、肾脏疾病和消化系统疾病的风险增加16.4%(OR=1.164, 95%CI:1.006～1.347)、22.4%(OR=1.224, 95%CI:1.083～1.383)和19.6%(OR=1.196, 95%CI:1.103～1.296), 患血脂异常和心脏病的可能性上升了26.6%(OR=1.266, 95%CI:1.153～1.390)和13.6%(OR=1.136, 95%CI:1.031～1.253)。负二项回归模型分析结果显示, 童年居住环境卫生较差的中老年农村...     

中国公众公共卫生安全素养量表的开发研究

目的开发公共卫生安全素养量表, 为我国公众的公共卫生安全素养测评提供适宜工具。方法通过理论构想、指标池构建、现场验证、题项缩减等步骤编制中国公共卫生安全素养初始量表, 转为"问卷星"电子问卷, 随机抽取4个省份共2 809名居民进行现场测试。利用经典测试理论(CTT)和项目反应理论(IRT)进行题项缩减。使用SPSS 23.0软件进行探索性因子分析(EFA)和单维性检验。使用R 4.1.1软件ltm和mirt包进行题项的心理测量学指标分析, 并绘制项目特征曲线(ICC)和信息函数曲线(IIC和TIF)。结果选用专家一致性系数最优的初始量表3, 共30个题项(B1～B30), 测试对象完成1个题项平均需9.8 s。根据CTT分析, 删除校正题项-总相关系数(CITC)<0.3及题项-维度相关系数(IDCC)<0.4的B2题项;删除CITC<0.3、IDCC<0.4及难度指数<0.2的B23题项;删除CITC<0.3及难度指数<0.2的B30题项。删除后量表总内部一致性信度(Cronbach’’sα)值为0.923。EFA提示删除14个因子载荷较小...     

Patients' and family members' perspectives on the benefits and working mechanisms of family nursing conversations in Dutch home healthcare

The aim of this study is to propose a model of the benefits and working mechanisms of family nursing conversations in home healthcare from the perspective of participating patients and their family members. Family nursing conversations in this study are intended to optimise family functioning, improve collaboration between family and professional caregivers and ultimately prevent or reduce overburden of family caregivers. In a qualitative grounded theory design, data were collected in 2017 using intensive interviewing with participants of family nursing conversations in home healthcare. A total of 26 participants (9 patients and 17 family members) from 11 families participated in a family nursing conversation and the study. Seven nurses who received extensive education in family nursing conversations conducted them as part of their daily practice. Interviews occurred 4–6 weeks after the family nursing conversation. The model that was constructed in close collaboration with the families consists of three parts. The first part outlines working mechanisms of the conversation itself according to participants, i.e. structured and open communication about the care situation and the presence of all of the people who are involved. The second part consists of the benefits that participants experienced during and immediately after the conversation – an increased sense of overview and improved contact among the people involved – and the related working mechanisms. The last part consists of benefits that emerged in the weeks after the conversation – reduced caregiver burden and improved quality of care – and the related working mechanisms. Insight into the benefits and working mechanisms of family nursing conversations may assist healthcare professionals in their application of the intervention and provides directions for outcomes and processes to include in future studies.     

综合护理干预对急性左心衰患者的影响

目的 探究基于自我调节理论的综合性护理干预对急性左心衰患者无创呼吸机治疗依从性的影响。方法 选取来我院就诊的急性左心衰患者83例,随机分成对照组41例和观察组42例。对照组采用常规护理模式,观察组采用基于自我调节理论的综合性护理。比较两组患者干预前后使用无创呼吸机依从性,比较干预后两组患者对无创呼吸机耐受情况、出院3个月后生活质量及干预过程中并发症发生率。结果 两组患者干预后,观察组依从性指数(85.18±4.13)高于对照组(80.45±3.68)(t=5.512,P=0.000);经干预后,观察组无创呼吸机耐受率(92.68%)与对照组(83.33%)无差异(χ2=1.711,P=0.190);两组患者出院3个月后,观察组在生活质量评分中社会功能(83.23±13.45,75.35±12.7,t=2.736,P=0.007)、情绪职能(74.31±13.64,65.34±8.45,t=3.611,P=0.001)、精神健康(76.38±10.24,68.23±11.53,t=3.402,P=0.001)方面分数高于对照组;干预期间,观察组并发症发生率(26.83%)低于对照组(59.52%)(χ2=9.029,P=0.002)。结论 基于自我调节理论的综合性护理干预能提高急性左心衰患者无创呼吸机治疗依从性,适当改善患者对无创呼吸机的耐受性,减轻并发症发生率,改善患者出院后生活质量。     

Pathogenesis of idiopathic IgA nephropathy

Despite a prodigious amount of work on the physiology of IgA production in man, and many studies on the immunopathology of IgA nephropathy, ranging from the immunogenetics to the immune response to chemical characteristics of the IgA, we are hardly any nearer to defining the pathogenesis of this disease. One of the main changes in our understanding has been to recognise that the bone marrow, now known to produce normally one-third of the body's IgA, overproduces this immunoglobulin in IgA nephropathy. This alters the previous notion that IgA nephropathy was due simply to IgA production in the mucosa, although a mucosal component is not excluded. Certain characteristics of the IgA in the diseased kidney and the circulation have been defined: it is of subclass IgA1 and has a higher proportion of light chains and negative charge than in normal subjects. The specificities of the IgA, either in the kidney or in complexes, have not helped to clarify the pathogenesis. They have been found for a wide range of endogenous and exogenous antigens, suggesting that the antibody activity represents polyclonal B cell activation. These findings have not helped to confirm the prevailing theory that IgA nephropathy is an immune complex disease. Other theories put forward are that IgA nephropathy is an autoimmune disease, glomerular components or IgA itself being among the candidate antigens, or that there is primary dysregulation of the IgA immune system. At this stage of development in our understanding of this common nephropathy, it is important to guard against the assumption that idiopathic IgA nephropathy is one disease and is the result of a single pathogenetic mechanism.     

The rheumatic poison: a survey of some published investigations of the immunopathogenesis of Henoch-Schönlein purpura

Laboratory studies of the pathophysiology of Henoch-Schönlein purpura (HSP) have become more numerous in recent years with the recognition of the disease's links with the mucosal immune system in general and IgA nephropathy in particular. There are weak genetic associations with C4 null phenotypes and with HLA B35 and DR4. Studies of plasma proteins in HSP patients show an increased IgA concentration, activation of the alternative pathway of complement and consumption of factor XIII. High molecular weight (polymeric) IgA has been detected in affected individuals, which some investigators have called immune complexes. Many patients synthesise an IgA rheumatoid factor in the acute phase, but other autoantibodies are largely absent. In vitro studies of lymphocytes from HSP patients have demonstrated an increased number of IgA-bearing and secreting B-cells, with altered T-cell regulation of antibody synthesis. While these observations point to immune dysregulation — primarily of IgA production — as a consistent feature of acute HSP, there is as yet insufficient information available to allow a consistent theory of pathogenesis to be formulated.