MiR-625-5p is a potential therapeutic target in sepsis by regulating CXCL16/CXCR6 axis and endothelial barrier.

Background: MicroRNA plays an important role in the progression of sepsis. We found a significant increase of in miR-625-5p expression in the blood of patients with sepsis, and lipopolysaccharide (LPS)-stimulated EA.hy926 cells.

NETs induce ferroptosis of endothelial cells in LPS-ALI through SDC-1/HS and downstream pathways.

Background: Extracellular neutrophil extracellular traps (NETs) play an important role in acute lung injury (ALI), but their mechanisms are still unclear. The aim of this study is to explore the effects of NETs on endothelial glycocalyx/HGF/cMET pathway and ferroptosis in ALI and elucidate their potential mechanisms.

Methods: Plasma was collected from healthy and sepsis patients to test for differences in neutrophil elastase (NE) expression of NETs components.

PLD2 deletion alleviates disruption of tight junctions in sepsis-induced ALI by regulating PA/STAT3 phosphorylation pathway.

Background: Increased inflammatory exudation caused by endothelium and endothelial junction damage is a typical pathological feature of acute respiratory distress syndrome/acute lung injury (ARDS/ALI). Previous studies have shown that phospholipase D2 (PLD2) can increase the inflammatory response and has a close relationship with the severity of sepsis-induced ALI and the mortality of sepsis, but its mechanism is unknown. This study explored the effect and mechanism of PLD2 deletion on the structure and function of endothelial tight junction (TJ) in lipopolysaccharide (LPS)-induced ALI.

Spatial and Temporal Evolution of Land Use and the Response of Habitat Quality in Wusu, China.

Understanding land use change and its impact on habitat quality (HQ) is conducive to land use management and ecological protection. We used the InVEST model and the GeoDetector model to explore the land use and HQ of Wusu from 1980 to 2020. We found that the spatial distribution of land use in Wusu had the most dramatic change from 2000 to 2010, and accordingly, the habitat quality deteriorated seriously from 2000 to 2010.

[Mechanism of high mobility group protein B1 in lipopolysaccharide-induced acute lung injury/acute respiratory distress syndrome].

Objective: To investigate the role and possible pathogenesis of high mobility group protein B1 (HMGB1) in lipopolysaccharide (LPS)-induced acute lung injury/acute respiratory distress syndrome (ALI/ARDS).

Methods: (1) In vivo, 24 SPFC57BL/6 male mice were randomly divided into normal control group, ALI/ARDS model group, ethyl pyruvate (EP) treatment group and EP control group, with 6 mice in each group. The ALI/ARDS model was established by intraperitoneal injection of 20 mg/kg LPS.

Arabidopsis synaptotagmin 1 mediates lipid transport in a lipid composition-dependent manner.

The endoplasmic reticulum (ER)-plasma membrane (PM) contact sites (EPCSs) are structurally conserved in eukaryotes. The Arabidopsis ER-anchored synaptotagmin 1 (SYT1), enriched in EPCSs, plays a critical role in plant abiotic stress tolerance. It has become clear that SYT1 interacts with PM to mediate ER-PM connectivity.

Calcium-dependent and -independent lipid transfer mediated by tricalbins in yeast.

Membrane contact sites (MCSs) formed between the endoplasmic reticulum (ER) and the plasma membrane (PM) provide a platform for nonvesicular lipid exchange. The ER-anchored tricalbins (Tcb1, Tcb2, and Tcb3) are critical tethering factors at ER-PM MCSs in yeast. Tricalbins possess a synaptotagmin-like mitochondrial-lipid-binding protein (SMP) domain and multiple Ca-binding C2 domains.

Endoplasmic Reticulum-Plasma Membrane Contact Sites: Regulators, Mechanisms, and Physiological Functions.

The endoplasmic reticulum (ER) forms direct membrane contact sites with the plasma membrane (PM) in eukaryotic cells. These ER-PM contact sites play essential roles in lipid homeostasis, ion dynamics, and cell signaling, which are carried out by protein-protein or protein-lipid interactions. Distinct tethering factors dynamically control the architecture of ER-PM junctions in response to intracellular signals or external stimuli.

Radioprotective effects of cimetidine on rats irradiated by long-term, low-dose-rate neutrons and Co γ-rays.

Background: Cimetidine, an antagonist of histamine type II receptors, has shown protective effects against γ-rays or neutrons. However, there have been no reports on the effects of cimetidine against neutrons combined with γ-rays. This study was carried out to evaluate the protective effects of cimetidine on rats exposed to long-term, low-dose-rate neutron and γ-ray combined irradiation (n-γ LDR).