慢阻肺患者CT图像中肺内血管分割及定量分析

目的 肺内血管形态结构的改变是慢性阻塞性肺疾病(慢阻肺)的一种重要病理改变。针对慢阻肺中肺血管疾病的定量评估问题,提出一种基于各向异性连续最大流的肺内血管自动分割方法,并定量分析不同半径的肺内血管体积分布,以研究慢阻肺病程中肺血管重塑规律。方法 使用U-Net分割肺体,获取肺脏区域,减少后续血管增强与分割的运算量;借助基于多尺度Hessian矩阵的血管增强方法,获得血管的似然增强结果和轴向方向;将血管似然结果和轴向信息以数据保真项和各向异性正则项的形式融入到连续最大流分割框架,实现肺血管的自动分割。结果 在公开数据集ArteryVein和仿真数据集VascuSynth上对肺内血管分割方法的有效性进行测试;在从4家医院收集的614例临床影像数据上分析小半径血管体积占比情况,对比慢阻肺组与非慢阻肺组之间肺血管重塑差异。肺血管分割方面,对于增加不同程度的高斯噪声(σ=5,10,15,20,25,30,35)的VascuSynth仿真数据,本文方法获得的Dice值分别为0.87,0.80,0.77,0.75,0.73,0.71,0.69;对于低剂量数据集ArteryVein, Dice值为0....     

肿瘤坏死因子-α和白细胞介素-8与慢性阻塞性肺疾病发病机制的关系

慢性阻塞性肺疾病(Chronic obstructive pulmonary disease,COPD)是呼吸系统常见疾病,近期研究表明,一些细胞因子如肿瘤坏死因子-α(TNF-α)和白细胞介素-8(IL-8)与COPD的发生密切相关。TNF-α和IL-8作为主要的炎性递质参与了介导气道炎症反应,二者相互作用、相互促进、加速局部炎症的发生发展,可导致气道结构的重塑和气流阻塞的形成,最终对COPD的发生、发展产生影响。本文就TNF-α和IL-8与COPD发病机制的关系作一综述。     

Profiling the Proteome of Exhaled Breath Condensate in Healthy Smokers and COPD Patients by LC-MS/MS

Three pools of exhaled breath condensate (EBC) from non-smokers plus healthy smokers (NS + HS, n = 45); chronic obstructive pulmonary disease (COPD) without emphysema (COPD, n = 15) and subjects with pulmonary emphysema associated with α₁-antitrypsin deficiency (AATD, n = 23) were used for an exploratory proteomic study aimed at generating fingerprints of these groups that can be used in future pathophysiological and perhaps even clinical research. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was the platform applied for this hypothesis-free investigation. Analysis of pooled specimens resulted in the production of a “fingerprint” made of 44 proteins for NS/HS; 17 for COPD and 15 for the group of AATD subjects. Several inflammatory cytokines (IL-1α, IL-1β, IL-2; IL-12, α and β subunits, IL-15, interferon α and γ, tumor necrosis factor α); Type I and II cytokeratins; two SP-A isoforms; Calgranulin A and B and α1-antitrypsin were detected and validated through the use of surface enhanced laser-desorption ionization mass spectrometry (SELDI-MS) and/or by Western blot (WB) analysis. These results are the prelude of quantitative studies aimed at identifying which of these proteins hold promise as identifiers of differences that could distinguish healthy subjects from patients.     

Epigenetic Mechanisms in Parenchymal Lung Diseases: Bystanders or Therapeutic Targets?

Epigenetic responses due to environmental changes alter chromatin structure, which in turn modifies the phenotype, gene expression profile, and activity of each cell type that has a role in the pathophysiology of a disease. Pulmonary diseases are one of the major causes of death in the world, including lung cancer, idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD), pulmonary hypertension (PH), lung tuberculosis, pulmonary embolism, and asthma. Several lines of evidence indicate that epigenetic modifications may be one of the main factors to explain the increasing incidence and prevalence of lung diseases including IPF and COPD. Interestingly, isolated fibroblasts and smooth muscle cells from patients with pulmonary diseases such as IPF and PH that were cultured ex vivo maintained the disease phenotype. The cells often show a hyper-proliferative, apoptosis-resistant phenotype with increased expression of extracellular matrix (ECM) and activated focal adhesions suggesting the presence of an epigenetically imprinted phenotype. Moreover, many abnormalities observed in molecular processes in IPF patients are shown to be epigenetically regulated, such as innate immunity, cellular senescence, and apoptotic cell death. DNA methylation, histone modification, and microRNA regulation constitute the most common epigenetic modification mechanisms.     

Involvement of the Innate Immune System in the Pathogenesis of Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is a common, socially significant disease characterized by progressive airflow limitation due to chronic inflammation in the bronchi. Although the causes of COPD are considered to be known, the pathogenesis of the disease continues to be a relevant topic of study. Mechanisms of the innate immune system are involved in various links in the pathogenesis of COPD, leading to persistence of chronic inflammation in the bronchi, their bacterial colonization and disruption of lung structure and function. Bronchial epithelial cells, neutrophils, macrophages and other cells are involved in the development and progression of the disease, demonstrating multiple compromised immune mechanisms.     

四线涡轮式慢阻肺健康监护系统研究

针对传统涡轮式肺活量计存在检测精度不高、可靠性差的问题,该文提出一种新颖的四线涡轮式检测方法,研制了一款高精度、高可靠性的慢阻肺监护系统。在硬件上,根据四线涡轮式检测方法设计了四线式呼气采集电路,提高了光路接收分辨率,并通过合理的元器件布置,减少了发光-光敏二极管相互间串扰,提高了系统的可靠性;在软件上,采用线性回归算法对其脉冲计数与分析得到用力肺活量、峰值流速等早期筛查与诊断指标。该系统利用标准Fluke气流分析仪的进行了数据标定,与传统医用涡轮式肺功能仪测试对比：用力肺活量平均相对误差由1.98%降低至1.47%;峰值流速平均相对误差由2.04%降低至1.02%。实验表明,四线涡轮式慢阻肺监护系统的呼气指标比传统慢阻肺系统检测精度更高,可靠性更好,适用于慢阻肺疾病的早期筛查与精准诊断,结合血氧饱和度、呼气末二氧化碳等指标,能实现对慢阻肺患者的医疗监护,特别对于中度和重度慢阻肺患者能起到预警和控制病情的作用。

     

COPD中西结合支持治疗的疗效观察

目的观察COPD患者中西结合支持治疗的临床疗效。方法将73例COPD住院患者随机分为治疗组36例,对照组37例。治疗组在常规治疗基础上,加用扶正胶囊口服和静脉营养;对照组仅用常规治疗。2周后对比疗效。结果两组%IBW和MAMC治疗前比较,均无显著性差异;两组%IBW和MAMC治疗后比较,均有显著性差异。结论中西结合支持治疗,能改善COPD患者的营养不良状况。     

Anthocyanins from Eugenia brasiliensis edible fruits as potential therapeutics for COPD treatment

Nine anthocyanins (1–9) from the edible fruits of Eugenia brasiliensis were identified by HPLC-PDA and LC–MS, and seven of these are described for the first time in this Brazilian fruit. Two of the major anthocyanins, delphinidin (8) and cyanidin (9), were studied for their inhibitory activity against chemokine interleukin-8 (IL-8) production before and after cigarette smoke extract (CSE) treatment of cells. In non-treated cells the amount of IL-8 was unchanged following treatment with cyanidin and delphinidin in concentrations 0.1–10 μM. Both delphinidin (8) and cyanidin (9) decreased the production of IL-8 in treated cells, at 1 and 10 μM, respectively. Delphinidin (8) demonstrated IL-8 inhibition in the CSE treated cells in a dose-dependent manner.