Relationship of influenza virus to inflammatory factors and immune function in elderly patients with COPD: A retrospective analysis.

Objective: The aim of this retrospective study was to investigate the relevance of influenza A virus (IAV) in acutely exacerbating airway inflammatory response and disrupting immune function in elderly COPD patients.

Methods: The group conducted a pre-test: using multiplex combined real-time PCR detection kits Multiple real⁃time PCR was used to detect twenty-four pathogens, 385 patients clinically diagnosed with COPD were tested for viral nucleic acid in throat swabs. At the same time, peripheral blood leukapheresis was collected from both groups of patients, and their IL-6, IL-8, IL-1β, and TNF-α levels were detected, along with the levels of T-cell differentiation markers CD4 and CD8, to assess the influence of influenza virus on the immune function of elderly COPD patients and its relevance to the acute exacerbation of airway inflammatory response in elderly COPD patients.

Amorphous silica nanoparticles cause abnormal cytokinesis and multinucleation through dysfunction of the centralspindlin complex and microfilaments.

Background: With the large-scale production and application of amorphous silica nanoparticles (aSiNPs), its adverse health effects are more worthy of our attention. Our previous research has demonstrated for the first time that aSiNPs induced cytokinesis failure, which resulted in abnormally high incidences of multinucleation in vitro, but the underlying mechanisms remain unclear. Therefore, the purpose of this study was firstly to explore whether aSiNPs induced multinucleation in vivo, and secondly to investigate the underlying mechanism of how aSiNPs caused abnormal cytokinesis and multinucleation.

Four different frailty models predict health outcomes in older patients with stable chronic obstructive pulmonary disease.

Background: Frail patients with chronic obstructive pulmonary disease (COPD) face a higher risk of adverse outcomes, but there is no clear consensus on which frailty measures are most suitable for COPD patients. Herein we evaluated the ability of frailty measurements in predicting 1-year acute exacerbation, hospitalization, and mortality in older patients with COPD.

Methods: A total of 302 patients [median age: 86 years (IQR: 80-90), 22.

Impact of Frailty on the Risk of Exacerbations and All-Cause Mortality in Elderly Patients with Stable Chronic Obstructive Pulmonary Disease.

Rationale: For the high prevalence of frail in patients with chronic obstructive pulmonary disease (COPD), further study should explore an in-depth understanding of the relationship between frailty and prognosis of COPD.

Objective: To determine the correlation between frailty and risk of acute exacerbation, hospitalizations, and mortality in older patients with stable COPD.

Participants And Methods: Consecutive older adults (≥65) diagnosed with stable COPD from January 2018 to July 2019, with an average follow-up of 546 days (N = 309).

Characterization of fluorescent NBD‑cholesterol efflux in THP‑1‑derived macrophages.

Macrophage cholesterol efflux is important in maintaining cellular lipid homeostasis and preventing the formation of lipid‑laden foam cells. Although radioactive [3H]‑cholesterol is widely used as a tracer in cholesterol efflux assays, the lengthy and labor‑intensive assay procedure, and the radioactivity disposal procedure limit the use of this assay for high‑throughput screening. In the present study, a novel procedure using fluorescent N‑(7‑nitrobenz‑2‑oxa‑1,3‑diazol‑4‑yl)amino)‑23,24‑bisnor‑5‑xholen‑3β‑ol (NBD)‑cholesterol was developed as a substitute for [3H]‑cholesterol for the measurement of cholesterol efflux in THP‑1‑derived macrophages.

The implication of cigarette smoking and cessation on macrophage cholesterol efflux in coronary artery disease patients.

We investigated ATP-binding cassette transporters A1/G1 expression and function in mediating cholesterol efflux by examining the macrophages of cigarette-smoking patients with coronary artery disease (CAD) before and after smoking abstinence. Peripheral blood monocyte cells were collected from nonsmokers (n = 17), non-CAD (NCAD) smokers (n = 35), and CAD smokers (n = 32) before and after 3 months of smoking cessation. We found that the ABCA1 expression level was lower in macrophages from NCAD and CAD smokers than from nonsmokers at baseline.

Ghrelin inhibit cell apoptosis in pancreatic beta cell line HIT-T15 via mitogen-activated protein kinase/phosphoinositide 3-kinase pathways.

Ghrelin stimulates growth hormone (GH) release and induces positive energy balances. Previous studies have reported that ghrelin inhibits apoptosis in several cell types but the precise underlying protective mechanisms in pancreatic beta cells are poorly understood. Therefore, we investigated which pathway was related with its anti-apoptotic effect in pancreatic beta cells.

Mechanical strain-induced c-fos expression in pulmonary epithelial cell line A549.

Pulmonary epithelial cells are exposed to mechanical strain during physiological breathing and mechanical ventilation. It was not clear which style was more related with cell mechanotransduction. c-fos is known to be a component of a transcription factor, activator protein-1, which is induced by oxidative stress.