COPD

Does the Coexistence of Chronic Obstructive Pulmonary Disease and Atrial Fibrillation Affect Nox2 Activity and Urinary Isoprostanes Excretion?

Chronic obstructive pulmonary disease (COPD) and atrial fibrillation (AF) are characterized by increased oxidative stress, but the impact of the coexistence of COPD and AF on systemic oxidative stress is unclear. We performed a cross-sectional study including 157 outpatients to investigate the Nox2-related oxidative stress in patients with AF and COPD. COPD was defined by an FEV1/FVC <0.70. Oxidative stress was measured by sNox2-dp, a marker of Nox2 activation, and urinary isoprostanes.

Cardiometabolic multimorbidity is associated with a worse Covid-19 prognosis than individual cardiometabolic risk factors. A multicentre retrospective study (CoViDiab II)

Background: Cardiometabolic disorders may worsen Covid-19 outcomes. We investigated features and Covid-19 outcomes for patients with or without diabetes, and with or without cardiometabolic multimorbidity. Methods: We collected and compared data retrospectively from patients hospitalized for Covid-19 with and without diabetes, and with and without cardiometabolic multimorbidity (defined as ≥ two of three risk factors of diabetes, hypertension or dyslipidaemia).

Proteomic analysis of hydrogen sulfide effect in inflammation. Preliminary study on the effectiveness of sulfureous mineral water inhalation in COPD

Background: Hydrogen sulphide (H2S) is enzymatically generated in various tissues and exerts many physiological effects that suggest its potential role as a regulatory mediator. H2S is involved in the regulation of vascular tone, erectile function, myocardial contractility, inflammation, neurotransmission and insulin secretion. In particular, this gaseous mediator influences the activation of cellular inflammatory processes.

Assessing static lung hyperinflation by whole-body plethysmography, helium dilution, and impulse oscillometry system (IOS) in patients with COPD

Purpose: Lung hyperinflation is a feature of chronic obstructive pulmonary disease (COPD) and can determine pivotal consequence on symptoms, exercise tolerance and quality of life. Despite the relevance of assessing lung hyperinflation, there is still no single consensus as to what volume should be taken into account. We investigate which spirometric measurement is more reliable in assessing static lung hyperinflation and which is more related with impulse oscillometry system (IOS) measurements in COPD.

Global and regional burden of chronic respiratory disease in 2016 arising from non-infectious airborne occupational exposures: a systematic analysis for the Global Burden of Disease Study 2016

OBJECTIVES: This paper presents detailed analysis of the global and regional burden of chronic respiratory disease arising from occupational airborne exposures, as estimated in the Global Burden of Disease 2016 study. METHODS: The burden of chronic obstructive pulmonary disease (COPD) due to occupational exposure to particulate matter, gases and fumes, and secondhand smoke, and the burden of asthma resulting from occupational exposure to asthmagens, was estimated using the population attributable fraction (PAF), calculated using exposure prevalence and relative risks from the literature.

Integrated transcriptomic correlation network analysis identifies COPD molecular determinants

Chronic obstructive pulmonary disease (COPD) is a complex and heterogeneous syndrome. Network-based analysis implemented by SWIM software can be exploited to identify key molecular switches - called “switch genes” - for the disease. Genes contributing to common biological processes or defining given cell types are usually co-regulated and co-expressed, forming expression network modules.

α1-Antitrypsin Polymerizes in Alveolar Macrophages of Smokers With and Without α1-Antitrypsin Deficiency

Background: The deficiency of α1-antitrypsin (AAT) is secondary to misfolding and polymerization of the abnormal Z-AAT in liver cells and is associated with lung emphysema. Alveolar macrophages (AMs) produce AAT; however, it is not known whether Z-AAT can polymerize in AMs, further decreasing lung AAT and promoting lung inflammation. Our intention was to investigate whether AAT polymerizes in human AMs and to study the possible relation between polymerization and degree of lung inflammation.

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