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Funding Information: This work was supported Southeast University (SEU) project 3203002003A1 and National Natural Science Foundation of China (NSFC) under the grant 51772080 and 11604088 . Jiangsu Provincial Innovation and Entrepreneurship Talent program Project No. JSSCRC2021491 . Industry-University-Research Cooperation Project of Jiangsu Province in China , Grant No. BY2021057 . Dr. Asghar thanks the Hubei Talent 100 program and Academy of Finland ( 13329016 , 13322738 ) for their financial support. Publisher Copyright: © 2022 The Authors Electrolytes with high-proton conduction and low activation energy are attractive for reducing the high operating temperature of solid-oxide fuel cells to less than <600 °C. In this work, we have fabricated semiconducting electrolyte SrFeTiO3-δ (SFT) material exhibiting high ionic conduction and exceptionally high protonic conduction at low operating temperature but with low electronic conduction to evade the short-circuiting issue. The prepared fuel cell device exhibited high open-circuit voltage (OCV) and a high-power output of 534 mW/cm2, of which 474 mW/cm2 could be for sure be related to the protonic part. The current study suggests that usage of semiconductor SrFeTiO3-δ facilitates a high concentration of oxygen vacancies on the surface of SFT, which mainly benefits proton conduction. Moreover, lower grain boundary resistance leads to obtain higher performance. Also, the Schottky junction phenomena are proposed to inhibit the e-conduction and excel the ions transportation. The high performance and ionic conductivity suggest that SFT could be a promising electrolyte for protonic ceramic fuel cells. Peer reviewed

Abstract Radiation damage in biological systems is initiated by free radicals and progresses with time through a variety of mechanisms. The time-scale and details of these mechanisms are briefly reviewed. Because of the variety of mechanisms of radio-biological damage, any single radio-protective or therapeutic agent can be only partially effective. The potential of and need for simultaneously using several radio-protective and therapeutic agents, including sulfhydryl compounds, superoxide dismutase, antioxidant proteins, and DNA repair enzymes, are examined, based on a priori considerations of the consequences of radiation exposure.

The role of peripherally and centrally acting acetaldehyde in ethanol‐induced conditioned taste aversion (CTA) was investigated using various enzyme manipulations. Cyanamide, an aldehyde dehydrogenase inhibitor (ALDH) elevates blood acetaldehyde levels in the presence of ethanol. Concurrent administration with 4‐methylpyrazole (4MP), an alcohol dehydrogenase inhibitor, prevents peripheral accumulation of acetaldehyde by cyanamide. Under both treatment conditions brain and liver ALDH activity is inhibited. Water‐deprived rats were pretreated 4 hr prior to fluid presentation with intraperitoneal injections of saline (S+S), 4‐methylpyrazole (4MP+S), cyanamide (S+C), or 4‐methylpyrazole + cyanamide (4MP+C). Subsequently, animals were presented with a novel saccharin solution followed immediately by intraperitoneal injection of one of three doses of ethanol (0.4, 0.8, or 1.2 g/kg) or saline vehicle on four occasions. Results suggested that animals pretreated with cyanamide (groups S+C and 4MP+C) drank significantly less saccharin after conditioning with a subthreshold dose of ethanol (0.4 g/kg) in comparison to groups S+S and 4MP+S. Moreover, at the conditioning dose of 1.2 g/kg, cyanamide‐treated animals demonstrated an attenuation of CTA compared to the other two groups. These effects cannot be attributed to elevated blood acetaldehyde levels since pretreatment with 4MP+C prevented peripheral acetaldehyde accumulation. A characteristic common to both cyanamide‐treated groups was the inhibition of brain ALDH. It is therefore suggested that brain ALDH may play a role in the mediation of ethanol‐induced CTAs. It is conceivable that ALDH plays this role by regulating the levels of acetaldehyde in brain.

Background and Purpose— Ischemic stroke induces metabolic disarray. A central regulatory site, pyruvate dehydrogeanse complex (PDHC) sits at the cross-roads of 2 fundamental metabolic pathways: aerobic and anaerobic. In this study, we combined ethanol (EtOH) and normobaric oxygen (NBO) to develop a novel treatment to modulate PDHC and its regulatory proteins, namely pyruvate dehydrogenase phosphatase and pyruvate dehydrogenase kinase, leading to improved metabolism and reduced oxidative damage. Methods— Sprague–Dawley rats were subjected to transient (2, 3, or 4 hours) middle cerebral artery occlusion followed by 3- or 24-hour reperfusion, or permanent (28 hours) middle cerebral artery occlusion without reperfusion. At 2 hours after the onset of ischemia, rats received either an intraperitoneal injection of saline, 1 dose of EtOH (1.5 g/kg) for 2- and 3-hour middle cerebral artery occlusion, 2 doses of EtOH (1.5 g/kg followed by 1.0 g/kg in 2 hours) in 4 hours or permanent middle cerebral artery occlusion, and EtOH+95% NBO (at 2 hours after the onset of ischemia for 6 hours) in permanent stroke. Infarct volumes and neurological deficits were examined. Oxidative metabolism and stress were determined by measuring ADP/ATP ratio and reactive oxygen species levels. Protein levels of PDHC, pyruvate dehydrogenase kinase, and pyruvate dehydrogenase phosphatase were assessed. Results— EtOH induced dose-dependent neuroprotection in transient ischemia. Compared to EtOH or NBO alone, NBO+EtOH produced the best outcomes in permanent ischemia. These therapies improved brain oxidative metabolism by decreasing ADP/ATP ratios and reactive oxygen species levels, in association with significantly raised levels of PDHC and pyruvate dehydrogenase phosphatase, as well as decreased pyruvate dehydrogenase kinase. Conclusions— Both EtOH and EtOH+NBO treatments conferred neuroprotection in severe stroke by affecting brain metabolism. The treatment may modulate the damaging cascade of metabolic events by bringing the PDHC activity back to normal metabolic levels.

PurposeThe purpose of this paper is to study a fractional grey model FAGM(1,1,tα) based on the GM(1,1,tα) model and the fractional accumulated generating operation, and then predict the national health expenditure, the government health expenditure and the out-of-pocket health expenditure of China.Design/methodology/approachThe presented univariate grey model is systematically studied by using the grey modelling technique, the fractional accumulated generating operation and the trapezoid approximation formula of definite integral. The optimal system parametersrandαare evaluated by the particle swarm optimisation algorithm.FindingsThe expressions of the time response function and the restored values of this model are derived. The GM(1,1), NGM(1,1,k,c) and GM(1,1,tα) models are particular cases of the FAGM(1,1,tα) model with deterministicrandα. Compared with other forecasting models, the results of the FAGM(1,1,tα) model have higher precision.Practical implicationsThe superiority of the new model has high potential to be used in the medicine and health fields and others. Results can provide a guideline for government decision making.Originality/valueThe univariate fractional grey model FAGM (1,1,tα) successfully studies the China’s health expenditure.

Abstract Ammonia is a possible candidate as the fuel for solid oxide fuel cells (SOFCs). In this work, an anode-supported SOFC based on yttrium-stabled zircite (YSZ) thin-film electrolyte was fabricated by a simple dry-pressing process. Directly fueled by commercial liquefied ammonia, the single cell was tested at temperatures from 650 to 850 °C. The maximum power densities were 299 and 526 mW cm −2 at 750 and 850 °C, respectively, only slightly lower than that fueled by hydrogen. Analysis of open current voltages (OCVs) of the cell indicated the oxidation of ammonia within a SOFC is a two-stage process. Impedance spectra showed the cell fueled by ammonia had the same electrolyte resistances as that fueled by hydrogen, but a little larger interfacial polarization resistances. Further, the performances of the cell were essentially determined by the interfacial resistances under 750 °C.

Environmental pollution liability insurance is becoming increasingly important for China to achieve its emission reduction targets. Insurance pricing is a crucial factor restricting the market share of environment pollution liability insurance, from the perspective of the Black–Scholes pricing model, which in turn has influenced the solvency of insurance companies in China. Firstly, this study analyzes the problems existing in compulsory liability insurance for environmental pollution in China. It proceeds with analyzing the price of compulsory environmental pollution liability insurance using the Black–Scholes pricing model, and derives a high premium insurance rate of 2.44%. Moreover, it performs a multivariate regression analysis using the asset and liability data, taken from the annual report, to identify three key factors affecting the solvency adequacy ratio, namely, capital debt ratio, reflecting the company asset structure; net interest rate on assets, reflecting the asset scale with actual solvency; and claim ratio, reflecting the business quality. Based on the results of regression analysis and robustness test for the China Insurance Clauses (CIC) company, People’s Insurance Company of China (PICC), and Asia-Pacific Property & Casualty Insurance (API) company, it is shown that the effect of total asset, total debt, capital debt ratio, claim ratio, and net interest rate on assets on the solvency adequacy ratio is significant, with respect to the size of the coefficients. Based on the Black–Scholes pricing model found in the previous cycle of liability insurance, and keeping in view the existing problems of environmental pollution liability insurance expenditure, this paper presents suggestions that are conducive to improving the solvency of insurance companies in China.

Background and Aims: Alcohol-associated liver disease (ALD) accounts for 70% of liver-related deaths in Europe, with no effective approved therapies. Although mitochondrial dysfunction is one of the earliest manifestations of alcohol-induced injury, restoring mitochondrial activity remains a problematic strategy due to oxidative stress. Here, we identify methylation-controlled J protein (MCJ) as a mediator for ALD progression and hypothesize that targeting MCJ may help in recovering mitochondrial fitness without collateral oxidative damage. Approach and Results: C57BL/6 mice [wild-type (Wt)] Mcj knockout and Mcj liver-specific silencing (MCJ-LSS) underwent the NIAAA dietary protocol (Lieber-DeCarli diet containing 5% (vol/vol) ethanol for 10 days, plus a single binge ethanol feeding at day 11). To evaluate the impact of a restored mitochondrial activity in ALD, the liver, gut, and pancreas were characterized, focusing on lipid metabolism, glucose homeostasis, intestinal permeability, and microbiota composition. MCJ, a protein acting as an endogenous negative regulator of mitochondrial respiration, is downregulated in the early stages of ALD and increases with the severity of the disease. Whole-body deficiency of MCJ is detrimental during ALD because it exacerbates the systemic effects of alcohol abuse through altered intestinal permeability, increased endotoxemia, and dysregulation of pancreatic function, which overall worsens liver injury. On the other hand, liver-specific Mcj silencing prevents main ALD hallmarks, that is, mitochondrial dysfunction, steatosis, inflammation, and oxidative stress, as it restores the NAD+/NADH ratio and SIRT1 function, hence preventing de novo lipogenesis and improving lipid oxidation. Conclusions: Improving mitochondrial respiration by liver-specific Mcj silencing might become a novel therapeutic approach for treating ALD.