Oxygen vacancies induced by lanthanum-doped indium oxide nanofibers for promoted temperature-dependent triethylamine and formaldehyde sensing.

A novel TEA and HCHO dual-function temperature-dependent sensing material (3La-In2O3) with ultra-high sensitivity was developed via a facile electrospinning process. Though rare earth doped in In2O3-based sensors have been widely reported, the low sensitivity, poor selectivity and high operating temperature remain restrict their application. Herein, the In2O3 nanofibers with different contents of La3+ ions are firstly obtained by a facile electrospinning process. The sensing performance investigation confirms that the 3% La/In molar ratio of La3+ doped in In2O3 nanofibers are more appropriate as the sensing material for TEA and HCHO detection. The 3La-In2O3 exhibits greatest response value of 3721.60-10 ppm TEA and 1469.65-10 ppm HCHO at their best working temperature (100 â„ƒ and 160 â„ƒ), approximately 23.85-fold and 10.85-fold higher than that of pristine In2O3 nanofibers. In addition, the excellent selectivity, repeatability, and long-term stability ensure the further application of the 3La-In2O3-based sensor in actual environment. The promoted sensing performance is mainly ascribed to the more oxygen vacancies, the increasing specific surface area, the smaller grain size of In2O3 nanofibers induced by La3+ doping. The DFT results demonstrate the beneficial effect of La and oxygen vacancies on the improved target gas adsorption energy.

Bifunctionalization of styrene through ring-opening-recombination strategy of phenylpropathiazole salt.

By opening the ring of a benzothiazole salt, we provide a sulfur source for the bifunctional reaction of styrene. The ring-opening-recombination reaction of the benzothiazole salt simultaneously constructs new C-S, C-O, and CO bonds after C-S bond breaking. The reaction proceeds in green solvents, requires no transition metal catalyst, and is compatible with many functional groups.

MicroRNA-16-5p exacerbates sepsis by upregulating aerobic glycolysis via SIRT3-SDHA axis.

Sepsis is a life-threatening condition, and treatment for sepsis in clinic is often not available, partially due to insufficient understanding of the pathogenesis of sepsis. Extensive study to elucidate the pathogenesis is required to improve the clinical management and outcome of sepsis. In this study, we investigated the pathogenesis of sepsis using peripheral blood mononuclear cells (PBMCs) from septic patients and studied the underlying mechanism of miR-16-5p on aerobic glycolysis in lipopolysaccharide (LPS)-treated THP1 and Raw264.7 cells. The levels of RNA and protein were determined by real-time quantitative PCR and immunoblotting assay, respectively. The production of high mobility group box 1 (HMGB1) was measured by enzyme-linked immunosorbent assay. The levels of succinate and lactate were determined using colorimetric kits. The extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) were measured by extracellular flux analyzer. The results showed that the expression of miR-16-5p was elevated, while sirtuin 3 (SIRT3) was decreased in PBMCs from septic patients and LPS-treated cells, along with accumulation of acetylated succinate dehydrogenase complex, subunit A. Concomitantly, an increase in HMGB1, succinate, lactate, as well as ECAR and a decrease in OCR were observed. Knockdown of miR-16-5p upregulated SIRT3 expression, facilitated SDHA deacetylation, and attenuated sepsis-related aerobic glycolysis. Further study identified that SIRT3 is targeted by miR-16-5p, and overexpression of SIRT3 rescued LPS-induced responses via deacetylation of SDHA. Our findings revealed a novel miR-16-5p-regulated SIRT3-SDHA axis in sepsis and provided novel insights for sepsis treatment.