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Abstract To obtain high yield and high concentration glucose from corncob residues (CRs), tetrahydrofuran (THF) + H2O co-solvent pretreatment was employed. The pretreatment parameters were firstly optimized by Box-Behnken Design of response surface method, and the maximum glucose yield (498.2 mg/g CRs) was obtained via enzymatic hydrolysis after pretreated under optimized conditions (53.7% THF concentration, 202.3 °C, 1.05 h). Then, the pretreated CRs under optimized conditions (optimized-CRs) were enzymatically hydrolyzed at high solid loading (15%–20%) and low enzyme input (5–8 FPU/g cellulose). The high concentration glucose production (128.6 mg/mL) was obtained from optimized-CRs after enzymatic hydrolysis at 20% solid loading with 10 FPU/g cellulose for 72 h, and then showed potential for reduction of enzyme input. Finally, the interactions between the 9 substrate-related factors and cellulose conversion were analyzed through correlation analysis, and found that Klason lignin remained in the cellulose-rich fractions and pseudo lignin condensed on the surface of the recovered substrate were the predominant inhibitors for enzymatic hydrolysis.

Abstract The prime purpose of this work is to prepare a novel kind of Pickering interfacial solid catalysts for biodiesel production to meet the requirements of highly efficiency and environmental benign. To achieve this goal, the core–shell P[xSPA-yDABCO]@SiO2@Fe3O4 composite materials with a shell of photo-responsive and base catalytic sites were manufactured by means of layer-by-layer fabrication method. The modified materials, entirely characterized by transmission electron microscopy (TEM), scanning electron microscope (SEM), Fourier transform infrared (FT-IR) spectra, X-ray powder diffraction (XRD) and magnetization versus magnetic (VSM) techniques, demonstrated sufficient catalytic active sites and photo-responsive sites. Among all the so-prepared catalysts, P[3SPA-2DABCO]@SiO2@Fe3O4 performs extremely well and can stabilize soybean oil-in-methanol Pickering emulsion for 24 h, achieving a biodiesel yield up to 98.2% at a catalyst dosage of 5 wt% after the reaction time of 5 h at 60 °C. Furthermore, the double responsive solid catalyst can be readily separated from the mixture of reaction by an external magnet and UV irradiation, and still presented superior catalytic activity after 6 cycles.

The passivation of iron and steel (DIN 1623) was studied by integral and depth selective conversion electron Mossbauer spectroscopy and Auger electron spectroscopy. Thickness and phase composition of the passive layer formed in sulphate solution and in a phosphate buffer were determined in dependence on the anodic potential and the duration of the passivating procedure. The experimental results lead to the conclusion that not the whole oxidic layer is responsible for the passivity but only a very thin intermediate layer formed between the cubic substrate and the rhombic oxide (γ-FeOOH) cover.

AbstractCumulus‐intact and ‐denuded unfertilized oocytes from two mouse strains were exposed to 1.5 m ethanol (EtOH) or two cryoproteclant solutions, 1.5 M propanediol (PROH) or 1.5 M dimethylsulfoxide (DMSO), for 4.5 min at 27°C, and the proportion of activating or degenerating oocytes studied. Exposure to DMSO did not significantly increase activation above that of oocytes not exposed to DMSO. Treatment of oocytes in PROH resulted in the activation of up to 87% of viable oocytes. This was significantly higher (P <01) than in control oocytes and comparable to the rate of activation after treatment with EtOH (59–96% activation). In solutions at 1°C, 47% of control oocytes were activated, which was not significantly different from the rate of activation in EtOH (36%) or PROH (50%) at 1°C. Following treatment with PROH, up to 87% of oocytes degenerated within a period of 6 h in vitro. The age of the oocytes (h post hCG) and the time of cumulus removal with the enzyme hyaluronidase, relative to the time of exposure to the chemicals, influenced the level of degeneration in most groups. Significantly fewer oocytes degenerated when cumulus cells were removed before treatment (0–31%) than when the cumulus was left intact throughout the treatment and 6 h culture period (10–87%). Exposure to PROH at 1°C reduced oocyte degeneration to 5%. We conclude that PROH causes significantly greater losses of oocytes as a result of parthenogenetic activation and degeneration than of exposure to DMSO.

Both long-term and short-term alcohol consumption can cause internal homeostasis imbalance, and they have been proved to be related to the initiation and development of atrial fibrillation (AF). Ferroptosis is an iron-dependent form of non-apoptotic oxidative death which also regulate the cell death homeostasis, but whether it involves in AF induced by alcohol consumption remains unclear. Here, we report a study on the effect of ferroptosis on susceptibility to AF at different alcohol consumption frequencies. We divided the mice into single or frequent excessive alcohol consumption group which given sterile drinking water or alcohol by gavage at different frequencies. Meanwhile, the experimental group was given an intraperitoneal injection of ferroptosis inhibitor (Fer-1) before alcohol drinking. It was found that once exposure to 5 g/kg/d frequent excessive alcohol consumption, compared with the single excessive alcohol consumption group, the mice serum non-heme iron concentration, accumulation of iron and oxidative stress reaction in atrial tissues were increased, while the body weight, heart weight and heart weight to tibia length (HW/TL) ratio were decreased. In addition, the inducibility rate of AF increased, while RR interval, effective refractory periods (ERPs) and 90 % action potential duration (APD90) shortened, as well as QTc interval prolonged. Furthermore, the protein and mRNA expression levels of GPx4, FTL, FTH1, Kv1.5, Kv2.1, Kv4.3, Cav1.2, Serca2α, p-PLB were down-regulated, while PTGS2 was up-regulated. Most of the changes can be partially or completely reversed by Fer-1. These results suggest that frequent excessive alcohol consumption activates ferroptosis and increases the inducibility rate of AF. Nevertheless, inhibition of ferroptosis can balance iron overload disorders and reduce the generation of reactive oxygen species (ROS), eventually decrease the susceptibility to AF. Our results highlight the importance of guidance and warnings for unhealthy alcohol-abuse lifestyle.