Self-Supported Nanoporous Gold with Gradient Tin Oxide for Sustainable and Efficient Hydrogen Evolution in Neutral Media

Hydrogen evolution reaction(HER)in neutral medium suffers from slow kinetics as compared to that in alkaline or acidic conditions,owing to larger Ohmic loss and low proton concentration.Here we report that a self-supported nanoporous Au-SnO_(x)(NP Au-SnO_(x))catalyst with gradient tin oxide surface could significantly enhance HER activity in neutral buffer solution(0.2 M PBS).The NP Au-SnO_(x)catalyst exhibits a low onset overpotential of 38 mV and a small Tafel slope of 79 mV dec^(−1).The current density of 10 mA cm^(−2)is manifested at an overpotential as low as 148 mV,representing the comparable performance of Pt/C catalyst.This high catalytic activity can retain at least 10 hours without any detectable decay.The superior HER activity is proposed to originate from the gradient SnO_(x)structure and metal/oxide interfaces in nanoporous ligaments.Furthermore,the X-ray photoelectron spectroscopy reveals that the gradient oxide in the ligament is remarkably stable during long-term reaction.

钠电池失效研究进展

钠电池因原料钠储量丰富、成本低廉、电极材料来源多样等优点,持续受到人们的关注.但是,在没有外部因素的影响下,钠电池正常运行时会发生一定概率的失效,以电化学性能变化与电池零部件发生破坏的失效模式表现出来,产生电池热失控、短路、起火等失效后果.本文依据失效模式与影响分析(FMEA)技术的理论失效链模型,分别对不同种类钠电池的正极、负极、电解质、隔膜、集流体和外壳等构件进行失效原因分析,基于钠电池构件概述了钠电池失效研究的进展,并提出了钠电池失效分析流程,最后对钠电池失效分析体系的构建进行了展望,旨在为钠电池的失效研究、安全使用与设计制造提供参考.

Nanoporous Au-Sn with solute strain for simultaneously enhanced selectivity and durability during electrochemical CO2 reduction

Electrochemical carbon dioxide reduction meditated by metallic catalysts suffers from restricted selectivity and competition from hydrogen evolution, which sensitively depends on ambiguous contributions of alloying and strain state in bimetallic catalysts. Herein, nanoporous Au-Sn(NPAS) containing trace tin solute in Au lattices is delicately designed to convince real strain effect, while eliminating other undesirable factors, such as alloying, crystal facets and surface composition. Compared with nanoporous gold(NPG), the NPAS with a solute strain of ~2.2% enables more efficient CO2-to-CO conversion, with an efficiency as high as 92% at-0.85 V versus reversible hydrogen electrode(vs. RHE), and the high activity can retain for more than 8 h. The combination of HRTEM and surface valence band photoemission spectra reveals that the tensile strain on the surface of 3 D nanoporous structure promotes the catalytic activity by shifting up the d-band center and strengthening the adsorption of key intermediate *COOH. A small amount of Sn solute in the nanoporous alloy can prevent ligament coarsening effectively and improve the electrochemical stability.

Sudden cardiac death of Duchenne muscular dystrophy with NT-proBNP in pericardial fluid as a useful biomarker for diagnosis of the cause of death: a case report

Duchenne muscular dystrophy(DMD)is one of the most common and severest muscular dystrophies.Although it can be a cause of death when associated with cardiac muscle and/or respiratory muscles,no cases of sudden deaths in the setting of undiagnosed DMD with cardiac involvement have been reported in the literatures.Previous studies showed that N-terminal-proBNP(NT-proBNP)was a robust laboratory biomarker to diagnose and monitor cardiac failure in clinical situations,suggesting that it may be used as an auxiliary indicator for diagnosis on left ventricular dysfunction in sudden cardiac deaths in forensic settings.Here,we reported a case of 29-year-old man who died suddenly.Autopsy revealed that muscles of the body were almost replaced by fatty and fibrotic tissues.The heart was enlarged with disarray and degeneration of cardiomyocytes in cardiac muscle.Total absence of dystrophin was detected by immunohistochemical staining,which confirmed DMD.Postmortem biochemical test of pericardial fluid revealed a high level of NT-proBNP,indicating dysfunction of the left ventricle before death.The cause of death was certified as an early dilated cardiomyopathy(DCM)/dysfunction of the left ventricle secondary to DMD,suggesting that sudden cardiac death with cardiac dysfunction could be identified by immunohistochemical method in combination with pericardial fluid NT-proBNP determination after systemic autopsy.

Quantitative Analysis of Kruppel‑Like Factor 5‑Related Messenger RNA Transcripts in Ischemic Myocardium for Discrimination of Death Causes

Background:Accumulated studies have demonstrated that Kruppel‑like factor 5(KLF5),a transcription factor,plays an important role in regulating cell proliferation and tissue remodeling through the expression of its downstream genes.KLF5‑related factors are expected to be involved in the healing process after myocardial injury or myocardial ischemic changes,especially for the forensic diagnosis of myocardial ischemic physiopathology.Aim and Objectives:This study aimed to explore the discrimination ability and applicability of KLF5-related factors in SCD caused by MI compared with other causes of death to provide further insights into the forensic diagnosis of myocardial ischemic pathology.Materials and Methods:The relative quantification of F‑Box and WD Repeat Domain Containing 7(FBW7),KLF5,factor‑binding protein(FGFBP)1,and FGFBP2 messenger RNAs(mRNAs)in myocardial tissue samples was performed using real‑time fluorescence quantitative reverse transcription polymerase chain reaction.KLF5 and FGFBP1/2 protein levels were examined using immunohistochemistry(IHC).The forensic autopsy cases(27 in total,autopsy within 72 h postmortem)included seven cases of acute myocardial infarction and 10 cases of acute myocardial ischemia.There were 10 cases in the control group,including four cases of traffic injury one case of injury by fall from height,one case of electric death,and four cases of blunt force injury.Results:Characteristic results were found in myocardial samples from three groups of deaths:KLF5 and FGFBP1 mRNA levels were significantly elevated in the infarction and ischemia groups,while FBW7 mRNA levels were significantly decreased.FBW7 is an important ubiquitin ligase that can mediate the degradation of KLF5 protein.In addition,FBW7 and FGFBP2 mRNA levels were decreased in the infarction group compared with the ischemia group.The IHC results were consistent with the observed mRNA expression patterns.Conclusions:Quantitative detection of FBW7,KLF5,FGFBP1,and FGFBP2 mRNA transcripts in myocardial tissues supports the pathophysiological study of myocardial ischemic diseases and provides molecular pathological evidence for forensic discrimination of death causes.

Primary Screening for Proteins Differentially Expressed in the Myocardium of a Rat Model of Acute Methamphetamine Intoxication

The mechanism of myocardial injury induced by the cardiovascular toxicity of methamphetamine(MA)has been shown to depend onalterations in myocardial proteins caused by MA.Primary screening of the expression of myocardial proteins in a rat model of MA intoxicationwas achieved by combining two‑dimensional electrophoresis and mass spectrometry analyses,which revealed a total of 100 differentiallyexpressed proteins.Of these,13 displayed significantly altered expression.Moreover,Western blotting and real‑time reverse transcriptionquantitative polymerase chain reaction analyses of several relative proteins demonstrated that acute MA intoxication lowers protein expressionand mRNA transcription of aldehyde dehydrogenase‑2 and NADH dehydrogenase(ubiquinone)1 alpha subcomplex subunit 10.In contrast,MA intoxication elevated the protein expression and mRNA transcription of heat shock protein family B(small)member 1.By combiningbehavioral assessments of experimental rat models with the histological and pathological changes evident in cardiomyocytes,a mechanismaccounting for MA myocardial toxicity was suggested.MA alters the regulation of gene transcription and the subsequent expression of certainproteins that participate in myocardial respiration and in responding to oxidative stress,resulting in myocardial dysfunction and structuralchanges that affect the functioning of the cardiovascular system.