CAPN5 attenuates cigarette smoke extract-induced apoptosis and inflammation in BEAS-2B cells.

Introduction: Apoptosis and chronic inflammation are the main phenotypes in chronic obstructive pulmonary disease (COPD) pathogenesis. Cigarette smoke exposure is the leading risk factor for COPD, which causes aberrant airway epithelial structure and function. As a non-classical calpain, the molecular function of calpain5 (CAPN5) in COPD remains unclear.

DNA dioxygenases TET2 deficiency promotes cigarette smoke induced chronic obstructive pulmonary disease by inducing ferroptosis of lung epithelial cell.

Chronic obstructive pulmonary disease (COPD) is a significant global cause of morbidity and mortality currently. Long-term exposure of cigarette smoke (CS) inducing persistent inflammation, small airway remodeling and emphysematous lung are the distinguishing features of COPD. Ferroptosis, occurred in lung epithelial cells has recently been reported to be associated with COPD pathogenesis.

CSE reduces OTUD4 triggering lung epithelial cell apoptosis via PAI-1 degradation.

Ovarian tumor family deubiquitinase 4 (OTUD4), a member of the OTU deubiquitinating enzyme, is implicated to decrease in cancer to regulate cell apoptosis. However, the role of OTUD4 in cigarette smoke induced epithelial cell apoptosis and its mechanism have not been elucidated. In this study, we showed that OTUD4 protein reduced in CSE treated mice and airway epithelial cells.

Follow-Up of Surgical or Nonsurgical Patients with Pulmonary Cryptococcosis: A Real-World Study.

Background: Surgical and medical treatments are applied to pulmonary cryptococcosis (PC) in the real world, while the prognosis of different therapies is uncertain. This study investigated diagnosis, real-world therapy, follow-up outcomes, and prognosis factors, aiming to deepen our understanding of PC.

Methods: Patients pathologically diagnosed with PC were retrospectively reviewed and followed up.

Effect of pirfenidone protecting against cigarette smoke extract induced apoptosis.

Introduction: Apoptosis of lung structural cells is a significant upstream event involved in COPD pathogenesis. This study was designed to explore whether pirfenidone (PFD) was able to attenuate apoptosis induced by cigarette smoke extract (CSE).

Methods: A method of intraperitoneal CSE injection to BALB/C mice was used to establish emphysema mouse model.

Dihydroquercetin suppresses cigarette smoke induced ferroptosis in the pathogenesis of chronic obstructive pulmonary disease by activating Nrf2-mediated pathway.

Background: Dihydroquercetin (DHQ) is a flavonoid with strong anti-inflammatory and antioxidant effects. However, its protective activity against cigarette smoke-induced ferroptosis in the pathogenesis of chronic obstructive pulmonary disease and its underlying mechanisms remain unclear.

Purpose: The present study was conducted to investigate the protective role of DHQ in the pathogenesis of COPD in vivo and in vitro.

Pirfenidone mediates cigarette smoke extract induced inflammation and oxidative stress in vitro and in vivo.

Background: Antioxidant and anti-inflammatory effects are two main pharmacological mechanisms of pirfenidone (PFD) besides the anti-fibrotic effect. This study aims to investigate whether PFD could mediate cigarette smoke extract (CSE) induced inflammation and oxidative stress in vitro and in vivo.

Methods: BALB/C mice and alveolar epithelial (A549) cells treated with CSE were established as disease models in vivo and in vitro.

C-Reactive Protein to Serum Albumin Ratio as a Novel Biomarker to Predict Prognosis in Patients with Chronic Obstructive Pulmonary Disease.

Background: This study aimed to evaluate the C-reactive protein to serum albumin ratio (CAR) to predict prognosis in COPD patients with acute exacerbations (AECOPD).

Methods: A retrospective cohort study of AECOPD patients, admitted to a large tertiary hospital between January 2017 and June 2018, was conducted. Univariate and multivariate logistic regression models were built to assess the relationship between variables and different clinical outcomes in one-year follow up.

Serum uric acid level as a biomarker for chronic obstructive pulmonary disease: a meta-analysis.

Objective: To determine if there is a relationship between the levels of serum uric acid and the different Global Initiative for Chronic Obstructive Lung Disease (GOLD) stages (1-4) classified by the severity of the airflow limitation in patients with stable chronic obstructive pulmonary disease (COPD).

Methods: Electronic databases, including PubMed®, Embase®, Web of Science™ and China National Knowledge Infrastructure (CNKI), were searched from inception to December 2018. Observational studies that reported serum uric acid levels in stable COPD patients were included.

The relationship between inflammation and neurocognitive dysfunction in obstructive sleep apnea syndrome.

Obstructive sleep apnea syndrome (OSAS), a state of sleep disorder, is characterized by repetitive apnea, chronic hypoxia, oxygen desaturation, and hypercapnia. Previous studies have revealed that intermittent hypoxia (IH) conditions in OSAS patients elicited neuron injury (especially in the hippocampus and cortex), leading to cognitive dysfunction, a significant and extraordinary complication of OSAS patients. The repeated courses of airway collapse and obstruction in OSAS patients resulted in apnea and arousal during sleep, leading to IH and excessive daytime sleepiness (EDS) and subsequently contributing to the development of inflammation.

Feasibility of mean platelet volume as a biomarker for chronic obstructive pulmonary disease: A systematic review and meta-analysis.

Objective: To evaluate the feasibility of mean platelet volume (MPV) as a biomarker for chronic obstructive pulmonary disease (COPD).

Methods: A systematic search for studies published up to March 2019 was performed in the PubMed and Web of Science databases. Three independent investigators screened the titles and abstracts of including studies according to eligibility criteria.

Changes of second-time mothers and their infants under the universal two-child policy in Changsha, China.

Background: China announced the implementation of the universal two-child policy in Oct, 2015; every couple was allowed to have two children. However, its influences on maternal well-being and infants' outcomes are still to be discovered.

Objectives: To detect influences of the universal two-child policy.