An oxygen vacancy-rich BiO2-x/COF heterojunction for photocatalytic degradation of diclofenac.

A BiO2-x/COF composite was successfully synthesized by simple mechanical ball milling. Compared to pure BiO2-x and COFs, the BiO2-x/COF composite (1 : 9) showed superior photocatalytic capability. Under visible light irradiation for 90 min, the photocatalytic degradation rate of DCF reached 97%. In addition, the characterization results showed that the formation of heterojunctions and the increase in oxygen vacancy concentration were the reasons for the enhancement of the photocatalytic activity. It is confirmed by free radical capture experiments that ˙O2- and h+ are the main reactive substances in the photocatalytic process. The photocatalytic degradation mechanism of the composite and the photocatalytic degradation pathway of diclofenac were deduced.

WO3/MIL-125 (Ti) composite material for enhancing the reduction of Cr(vi) under visible light.

In wastewater containing heavy metals, Cr(vi) is a potentially toxic metal, mainly derived from production and processing processes such as textile printing, dyeing, ore mining, battery applications, metal cleaning and electroplating. WO3 is widely used in photocatalytic degradation and reduction, and its utilization rate of visible light is high. However, the rapid recombination of photogenerated electron-hole pairs of WO3 limits its use. In this work, the composite material (WxMy) of WO3 and MIL-125 (Ti) was prepared by the ball milling method, and the catalyst was used to photocatalytically reduce Cr(vi). After using W90M10 as a photocatalyst for 50 min, the reduction rate of Cr(vi) can reach 99.2%, and the reduction rate is 2.3 times that of WO3. After 5 cycles of use, the reduction rate can still reach 91.3%. It is mainly due to the formation of a II-type heterojunction between WO3 and MIL-125 (Ti), which promotes the separation of photogenerated electron-hole pairs, thus improving the efficiency of photocatalytic reduction of Cr(vi).

Effects of anode materials on nitrate reduction and microbial community in a three-dimensional electrode biofilm reactor with sulfate.

Graphite rod corrosion and peeling are serious problems in three-dimensional electrode biofilm reactors (3D-BERs). In this study, titanium rods, titanium suboxide-coated titanium rods and graphite rods were used as anodes to investigate the effect of anodic materials on the electrochemical and bioelectrochemical reduction of nitrate and sulfate. The results showed that the reactor with the titanium suboxide-coated titanium rod anode (3D-ER-T) exhibited a stable NO3--N removal efficiency (46%-95%) with a current range of 160-320 mA in the electrochemical reduction process. In the bioelectrochemical reduction, the removal efficiencies of NO3--N and SO42- and nitrogen selectivity in the 3D-BER with titanium suboxide-coated titanium rod anode (3D-BER-T) were higher than those in the 3D-BER with titanium suboxide-coated graphite rod anode (3D-BER-G). The removal efficiencies of NO3--N and SO42- and nitrogen selectivity were 92%, 43% and 86%, respectively, in 3D-BER-T under 320 mA and HRT 12 h. Anode materials affected the microbial community. Hydrogenophaga and Dethiobacter were the dominant bacteria in 3D-BER-T, while OPB41 and Sulfurospirillum were dominant in 3D-BER-G. Nitrate and sulfate were effectively removed in 3D-BER-T by the synergistic work of electrochemical reduction, bioelectrochemical reduction and indirect electrochemical reduction. The resupply/reserve mode of the electron donor promoted the load of shock resistance of 3D-BER-T via the sulfur cycle. Titanium suboxide coating could significantly enhance the anti-corrosion ability of matrix anodes.

Dual-Motor Synchronization Control Design Based on Adaptive Neural Networks Considering Full-State Constraints and Partial Asymmetric Dead-Zone.

This paper proposes a command filtering backstepping (CFB) scheme with full-state constraints by leading into time-varying barrier Lyapunov functions (T-BLFs) for a dual-motor servo system with partial asymmetric dead-zone. Firstly, for the convenience of the controller design, the conventional partial asymmetric dead-zone model was replaced with a new smooth differentiable model owing to its non-smoothness. Secondly, neural networks (NNs) were utilized to approximate the nonlinearity that exists in the dead-zone model, improving the control performance. In addition, CFB was utilized to deal with the inherent computational explosion problem of the traditional backstepping method, and an error compensation mechanism was introduced to further reduce the filtering errors. Then, by applying the T-BLF to the CFB process, the states of the system never violated the prescribed constraints, and all signals in the dual-motor servo system were bounded. The tracking error and synchronization error could converge to a small desired neighborhood of the origin. In the end, the effectiveness of the proposed control scheme was verified through simulations.

Mitochondrial K+ channels are involved in ischemic postconditioning in rat hearts.

The mitochondrial calcium-activated potassium channel (mitoK(Ca)) and the mitochondrial ATP-sensitive potassium channel (mitoK(ATP)) are both involved in cardiac preconditioning. Here, we examined whether these two channels are also involved in ischemic or pharmacological postconditioning. Using Langendorff perfusion, rat hearts were made hypoxic for 45 min and then reoxygenated for 30 min. Ischemic postconditioning (IPT) was achieved through application of 3 cycles of 10 s of reperfusion and 10 s of ischemia before reoxygenation, with and without paxilline (Pax; a mitoK(Ca) blocker) or 5-hydroxydecanoate (5-HD; a mitoK(ATP) blocker). Pharmacological postconditioning was carried out for 5 min at the onset of reoxygenation using NS1619 (a mitoK(Ca) opener) or diazoxide (Dia; a mitoK(ATP) opener). Pax and 5-HD abolished IPT-induced cardioprotection from reoxygenation injury, whereas administration of NS1619 or Dia significantly improved cardiac contractile activity and reduced aspartate aminotransferase (an index of myocyte injury) release following reoxygenation. In addition, isolated rat myocytes were loaded with tetramethylrhodamine methyl ester (TMRE; fluorescent mitochondrial membrane potential indicator) and 2',7'-dichlorofluorescein [DCFH; fluorescent reactive oxygen species (ROS) indicator] or Fluo-4-acetoxymethyl ester (Fluo-4-AM; fluorescent calcium indicator). When TMRE-loaded myocytes were laser illuminated, the DCFH and Fluo-4 fluorescence increased, and TMRE fluorescence decreased. These effects were significantly inhibited by NS1619 and Dia. We therefore conclude that IPT may protect the heart through activation of mitoK(ATP) and mitoK(Ca) channels, and that opening of these channels at the onset of reoxygenation protects the heart from reoxygenation injury, most likely by reducing excess generation of ROS and the resultant Ca(2+) overload.

Sevoflurane and nitrous oxide exert cardioprotective effects against hypoxia-reoxygenation injury in the isolated rat heart.

It is unclear whether nitrous oxide (N(2)O) has a protective effect on cardiac function in vitro. In addition, little is known about the cardioprotective effect of anesthesia administered during hypoxia or ischemia. We therefore studied the cardioprotective effects of N(2)O and sevoflurane administered before or during hypoxia in isolated rat hearts. Rat hearts were excised and perfused using the Langendorff technique. For hypoxia-reoxygenation, hearts were made hypoxic (95% N(2), 5% CO(2)) for 45 min and then reoxygenated (95% O(2), 5% CO(2)) for 40 min (control: CT group). Preconditioning was achieved through three cycles of application of 4% sevoflurane (sevo-pre group) or 50% N(2)O (N(2)O-pre group) for 5 min with 5-min washouts in between. Hypoxic conditions were achieved by administering the 4% sevoflurane (sevo-hypo group) or 50% N(2)O (N(2)O-hypo group) during the 45-min hypoxic period. L-type calcium channel currents (I(Ca,L)) were recorded on rabbit myocytes. (1) Both 4% sevoflurane and 50% N(2)O significantly reduced left ventricular developed pressure (LVDP). Sevoflurane also increased left ventricular end-diastolic pressure, though N(2)O did not. (2) The recoveries of LVDP and pressure-rate product (PRP) after hypoxia-reoxygenation were better in the sevo-pre group than in the CT or N(2)O-pre group. (3) Application of either sevoflurane or N(2)O during hypoxia improved recovery of LVDP and PRP, and GOT release was significantly lower than in the CT group. (4) Sevoflurane and N(2)O reduced I(Ca,L) to similar extents. Although sevoflurane administered before or during hypoxia exerts a cardioprotective effect, while N(2)O shows a cardioprotective effect only when administered during hypoxia.