Risk Factors for Development and Mortality of Bloodstream Infections Caused by Carbapenem-Resistant .

Background: Bloodstream infections (BSIs) caused by (AB), especially carbapenem-resistant (CRAB), can lead to a high patient mortality rate.

Methods: This study aimed to analyze the clinical data and prognosis of 191 patients with AB-BSI hospitalized in Southern China from January 2017 to December 2023.

Results: CRAB was diagnosed in 128 (67.

PKM2 regulates cigarette smoke-induced airway inflammation and epithelial-to-mesenchymal transition via modulating PINK1/Parkin-mediated mitophagy.

Cigarette smoke (CS) mediates inflammation and epithelial-mesenchymal transition (EMT) in bronchial epithelial cells, contributing to airway remodeling in chronic obstructive pulmonary disease (COPD). Cross-talk between metabolic pathways and cell signaling has emerged as an important focus of research in the field of inflammation. Here, we established in vitro and in vivo models of CS-induced COPD to elucidate the role of pyruvate kinase M2 (PKM2), a glycolytic enzyme, in CS-induced airway remodeling.

Astrocyte secretes IL-6 to modulate PSD-95 palmitoylation in basolateral amygdala and depression-like behaviors induced by peripheral nerve injury.

Dysfunction of glutamatergic synaptic plasticity in basolateral amygdala (BLA) constitutes a critical pathogenic mechanism underlying the depression-like behaviors induced by chronic pain. Astrocytes serve as an important supporting cell modulating glutamatergic synaptic transmission. Here, we found that peripheral spared nerve injury (SNI) induced astrocyte activation to release IL-6 in BLA.

DKK1 Positively Correlates with Lung Function in COPD Patients and Reduces Airway Inflammation.

Purpose: WNT/β-catenin signal pathway is a potential hope for lung tissue repair. We investigated the levels of Dickkopf-1 (DKK1), an endogenous inhibitor of WNT/β-catenin signal pathway, in chronic obstructive pulmonary disease (COPD) patients and airway inflammation.

Patients And Methods: Collected the demographic and clinical characteristics of 36 healthy controls, 25 stable COPD patients and 10 acute exacerbation of COPD (AECOPD) patients, then performed pulmonary function and detected serum DKK1 levels.

The Association and Influencing Factors between Antipsychotics Exposure and the Risk of VTE and PE: A Systematic Review and Meta-analysis.

Background: Different clinical studies have given inconsistent results on whether the use of antipsychotics increases the risk of thromboembolism. In this paper, we reviewed all relevant literature to provide suggestions for clinical diagnosis and treatment.

Methods: PubMed, Web of Science, EMBASE, MEDLINE, Cochrane and Scopus databases were thoroughly searched up to June 2019.

Diagnostic accuracy of E-cadherin for malignanteffusions: a systematic review and meta-analysis.

Background: The differential diagnosis of malignant effusion remains a clinical challenge. We aim to summarise all relevant literature studies in order to determine the overall clinical value of E-cadherin in the diagnosis of malignant effusion by meta-analysis.

Methods: PubMed, the Cochrane Library Database, Medline (Ovid), Web of Science, CNKI, WANFANG and WEIPU databases are thoroughly searched up to 15 March2018.

The elevated CXCL5 levels in circulation are associated with lung function decline in COPD patients and cigarette smoking-induced mouse model of COPD.

C-X-C motif chemokine 5 is primarily chemotactic for neutrophils and previously shown to increase in the bronchoalveolar lavage fluid of patients with chronic obstructive pulmonary disease. However, whether C-X-C motif chemokine 5 levels correlate with lung function decline in patients or mouse model of chronic obstructive pulmonary disease was not clear. The mouse model was induced by cigarette smoke exposure.

The association of elevated circulating endocan levels with lung function decline in COPD patients.

Background: Endocan is thought to be a novel inflammatory marker that is associated with a variety of inflammatory diseases. However, its role in the pathogenesis of COPD remains unclear. This study aims to explore the potential role of endocan in COPD.

Effects of calcium gluconate on lipopolysaccharide-induced acute lung injury in mice.

Lipopolysaccharide (LPS), which can cause acute airway inflammatory reactions, constitutes one of the most common substances to establish acute lung injury (ALI) models in mice. Studies suggest that calcium gluconate offers the possibility of suppressing the immune response, and this study was intended to explore the effects of calcium gluconate on LPS-induced ALI in mice. Mice inhaled with LPS were intraperitoneally injected with calcium gluconate (12.

Role of Receptor for Advanced Glycation End Products in Regulating Lung Fluid Balance in Lipopolysaccharide-induced Acute Lung Injury and Infection-Related Acute Respiratory Distress Syndrome.

Receptor for advanced glycation end products (RAGE) is implicated in inflammatory responses in acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), but its role in pulmonary edema formation remains unclear, especially in infection-related ARDS mainly caused by pneumonia or sepsis. In this study, we investigated the role of RAGE in alveolar fluid regulation by using RAGE gene knockout (RAGE) mice in a murine ALI model induced by lipopolysaccharide (LPS), and by comparing soluble RAGE (sRAGE) levels in serum and bronchial alveolar lavage fluid between ARDS patients and control subjects. We found that RAGE knockout significantly improved alveolar fluid clearance and reduced pulmonary vascular albumin leakage upon LPS challenge.