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Backgroud: This prospective randomized trial evaluated the clinical efficacy of inhaled colistin administered through two distinct nebulizer types, a vibrating mesh nebulizer (VMN) and a jet nebulizer (JN), in the treatment of ventilator-associated pneumonia caused by multidrug-resistant bacteria. In addition, an in vitro model was used to determine the optimal delivery of colistin. Method: Thirty-two patients prescribed intravenous (IV) colistin inhalation were randomized to receive either a VMN (n = 17) or a JN (n = 15), then compared to the control group (IV alone) over a 7-to 10-day period. The primary endpoint was the clinical pulmonary infection score (CPIS), and the secondary endpoints were the Sequential Organ Failure Assessment (SOFA) score, Acute Physiology and Chronic Health Evaluation (APACE) score, and duration of ventilator use. Results: Results from in vitro testing demonstrated that VMN delivered a significantly higher colistin dose than JN (35.68 ± 3.55% vs. 23.56 ± 3.31%; p < 0.001) when positioned at the humidifier inlet. Compared to the IV alone group, the IV with inhalation group yielded significant improvements in CPIS, SOFA score, and APACHE score on day 7; nevertheless, clinical outcomes between the two nebulizers were statistically indistinguishable. Conclusions: In conclusion, although VMN delivers a higher dose in vitro, both nebulizers yielded comparable clinical outcomes. This study was registered at US Clinical Trial Registration (NCT04633317). [ABSTRACT FROM AUTHOR]

The association between influenza infection and thromboembolism (TE) events, including cardiovascular events, cerebrovascular events, pulmonary embolism, and deep vein thrombosis, is supported by compelling evidence. However, there is a disparity in the risk factors that impact the outcomes of severe influenza‐complicated TE in intensive care unit (ICU) patients. The objective of this study was to evaluate the outcomes of severe influenza‐complicated TE in ICU patients and identify any associated risk factors. Methods: A retrospective cohort study was conducted, recruiting consecutive patients with TE events admitted to the ICU between December 2015 through December 2018 at our institution in Taiwan. The study included a group of 108 patients with severe influenza and a control group of 192 patients with severe community‐acquired pneumonia. Associations between complicated TE, length of ICU stay, and 90‐day mortality were evaluated using logistic regression analysis, and risk factors were identified using univariate and multivariate generalized linear regression analyses. Results: TE event prevalence was significantly higher in ICU patients with severe influenza than in ICU patients with severe CAP (21.3% vs. 5.7%, respectively; p < 0.05). Patients with severe influenza who developed TE experienced a significant increase in the ratio of mechanical ventilation use, length of mechanical ventilation use, ICU stay, and 90‐day mortality when compared to patients without TE (all p < 0.05). The comparison of severe CAP patients with and without TE revealed no significant differences (p > 0.05). The development of thromboembolic events in patients with severe influenza or severe noninfluenza CAP is linked to influenza infection and hypertension (p < 0.05). Furthermore, complicated TE and the severity of the APACHE II score are risk factors for 90‐day mortality in ICU patients with severe influenza (p < 0.05). Conclusions: Patients with severe influenza and complicated TE are more likely to have an extended ICU stay and 90‐day mortality than patients with severe CAP. The risk is significantly higher for patients with a higher APACHE II score. The results of this study may aid in defining better strategies for early recognition and prevention of severe influenza‐complicated TE. [ABSTRACT FROM AUTHOR]

The aim of this study is to investigate the seasonal variations and source apportionment on atmospheric fine particulate matter (PM2.5) mass and associated trace element concentrations at a coastal area, in Chiayi County of southwestern Taiwan. Particle measurements were conducted in 2015. Twenty-three trace elements in PM2.5 were analyzed using inductively coupled plasma mass spectrometry (ICP-MS). Multiple approaches of the enrichment factor (EF) analysis and positive matrix fraction (PMF) model were used to identify potential sources of PM2.5-bound trace elements. Daily mean concentration of PM2.5 in cold season (25.41 μg m−3) was higher than that in hot season (13.10 μg m−3). The trace elements contributed 11.02 and 10.74% in total PM2.5 mass concentrations in cold season and hot season, respectively. The results of EF analysis confirmed that Sb, Mo, and Cd were the top three anthropogenic trace elements in the PM2.5; furthermore, carcinogenic elements (Cr, Ni, and As) and other trace elements (Na, K, V, Cu, Zn, Sr, Sn, Ba, and Pb) were attributable to anthropogenic emissions in both cold and hot seasons; however, highly enriched Li and Mn were observed only in cold season. The PMF model identified four main sources: iron and steel industry, soil and road dust, coal combustion, and traffic-related emission. Each of these sources has an annual mean contribution of 8.2, 27.5, 11.2, and 53.1%, respectively, to PM2.5. The relative dominance of each identified source varies with changing seasons. The highest contributions occurred in cold season for iron and steel industry (66.2%), in hot season for traffic-related emission (58.4%), soil and road dust (22.0%), and coal combustion (2.8%). These findings revealed that the PM2.5 mass concentration, PM2.5-bound trace element concentrations, and their contributions were various by seasons. [ABSTRACT FROM AUTHOR]

Mechanical ventilation is usually required for saving lives in critically ill patients; however, it can cause ventilator-induced lung injury (VILI). As VEGF-secreting Ly6Chigh monocytes are involved in VILI pathogenesis, we investigated whether cyclooxygenase-2 (COX-2) activity regulates the recruitment of VEGF-secreting Ly6Chigh monocytes during VILI. The clinically relevant two-hit mouse model of VILI, which involves the intravenous injection of lipopolysaccharide prior to high tidal volume (HTV)-mechanical ventilation, was used in this study. To investigate the role of COX-2 in the recruitment of VEGF-secreting Ly6Chigh monocytes during VILI, celecoxib, which is a clinical COX-2 inhibitor, was administered 1 h prior to HTV-mechanical ventilation. Pulmonary vascular permeability and leakage, inflammatory leukocyte infiltration, and lung oxygenation levels were measured to assess the severity of VILI. HTV-mechanical ventilation significantly increased the recruitment of COX-2-expressing Ly6Chigh, but not Ly6Clow, monocytes. Celecoxib significantly diminished the recruitment of Ly6Chigh monocytes, attenuated the levels of VEGF and total protein in bronchoalveolar lavage fluid, and restored pulmonary oxygenation during VILI. Our findings demonstrate that COX-2 activity is important in the recruitment of VEGF-secreting Ly6Chigh monocytes, which are involved in VILI pathogenesis, and indicate that the suppression of COX-2 activity might be a useful strategy in mitigating VILI. [ABSTRACT FROM AUTHOR]

Background: Exposure to particulate matter (PM) may contribute to lung inflammation and injury. The therapeutic effect of N-acetylcysteine (NAC), a well-known antioxidant, with regards to the prevention and treatment of fine PM (PM2.5)-induced lung injury is poorly understood. This study aimed to determine the effect of PM2.5 on the recruitment of neutrophils and Ly6C high monocytes into lung alveoli and the production of proinflammatory proteins by stimulating the generation of reactive oxygen species (ROS), and to investigate the therapeutic effect of NAC on PM2.5-induced lung injury., Methods: C57BL/6 mice were exposed to a single administration of PM2.5 (200 μg/100 μl/mouse) or phosphate-buffered saline (control) via intratracheal instillation. The mice were injected intratracheally via a microsprayer aerosolizer with NAC (20 or 40 mg/kg) 1 h before PM2.5 instillation and 24 h after PM2.5 instillation. Total protein, VEGF, IL-6, and TNF-α in bronchoalveolar lavage fluid (BALF) were measured. Oxidative stress was evaluated by determining levels of malondialdehyde (MDA) and nitrite in BALF. Flow cytometric analysis was used to identify and quantify neutrophils and Ly6C high and Ly6C low monocyte subsets., Results: Neutrophil count, total protein, and VEGF content in BALF significantly increased after PM2.5 exposure and reached the highest level on day 2. Increased levels of TNF-alpha, IL-6, nitrite, and MDA in BALF were also noted. Flow cytometric analysis showed increased recruitment of neutrophils and Ly6C high , but not Ly6C low monocytes, into lung alveoli. Treatment with NAC via the intratracheal spray significantly attenuated the recruitment of neutrophils and Ly6C high monocytes into lung alveoli in PM2.5-treated mice in a dose-dependent manner. Furthermore, NAC significantly attenuated the production of total protein, VEGF, nitrite, and MDA in the mice with PM2.5-induced lung injury in a dose-dependent manner., Conclusion: PM2.5-induced lung injury caused by the generation of oxidative stress led to the recruitment of neutrophils and Ly6C high monocytes, and production of inflammatory proteins. NAC treatment alleviated PM2.5-induced lung injury by attenuating the ROS-mediated recruitment of neutrophils and Ly6C high monocytes and lung inflammation., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)