Sn-doped induced stable 1T-WSe_(2)nanosheets entrenched on N-doped carbon with extraordinary half/full sodium/potassium storage performance

At present,there have been some reports on the application of metal phase selenide(1T-MSe_(2))in the field of energy storage.In this manuscript,a stable Sn-doped metal phase tungsten selenide(1T-WSe_(2)-Sn)was elaborately fabricated in situ by a simple calcination technique.N-doping was introduced by employing chitosan as precursor and nanoreactor,the Sn-doping induces 1T phase of WSe_(2)and enlarges the layer space to promote the electron/ion transport and structural stability.The optimized 1T-WSe_(2)-Sn electrode delivers prominent cycling lifespan(285 mAh·g^(-1)at 1.0 A·g^(-1)after 900 cycles)along with decent rate capability when applied as an anode of sodium ion batteries(SIBs).The specific capacity was determined to be of 460 mAh·g^(-1)at 0.1 A·g^(-1)after 100cycles.It also displays superior capacity of 183 mAh·g^(-1)at0.5 A·g^(-1)for 200 cycles when paired with Na_(3)V_(2)(PO_(4))_(3)cathode.Applied as the anode for potassium ion batteries(PIBs),it exhibits a satisfactory specific capacity of 345mAh·g^(-1)at 0.1 A·g^(-1)after 50 cycles.

Improved Performance in Differentiating Benign from Malignant Sinonasal Tumors Using Diffusion-weighted Combined with Dynamic Contrast-enhanced Magnetic Resonance Imaging

Background：Differentiating benign from malignant sinonsal lesions is essential for treatment planning as well as determining the patient＇s prognosis,but the differentiation is often difficult in clinical practice.The study aimed to determine whether the combination of diffusion-weighted （DW） and dynamic contrast-enhanced magnetic resonance imaging （DCE-MRI） can improve the performance in differentiating benign from malignant sinonasal tumors.Methods：This retrospective study included 197 consecutive patients with sinonasal tumors （116 malignant tumors and 81 benign tumors）.All patients underwent both DW and DCE-MRI in a 3-T magnetic resonance scanner.Two different settings ofb values （0,700 and 0,1000 s/mm^2） and two different strategies of region of interest （ROI） including whole slice （WS） and partial slice （PS） were used to calculate apparent diffusion coefficients （ADCs）.A DW parameter with WS ADCsb0.1000 and two DCE-MRI parameters （time intensity curve [TIC] and time to peak enhancement [Tpeak]） were finally combined to use in differentiating the benign from the malignant tumors in this study.Results：The mean ADCs of malignant sinonasal tumors （WS ADCsb0,1000=1.084 × 10^-3 mm^2/s） were significantly lower than those of benign tumors （WS ADCsb0,1000=1.617 × 10^-3 mm^2/s,P 〈 0.001）.The accuracy using WS ADCsb0,1000 alone was 83.7% in differentiating the benign from the malignant tumors （85.3% sensitivity,81.2% specificity,86.4% positive predictive value [PPV],and 79.5% negative predictive value [NPV]）.The accuracy using DCE with Tpeak and TIC alone was 72.1% （69.1% sensitivity,74.1% specificity,77.5% PPV,and 65.1% NPV）.Using DW-MRI parameter was superior than using DCE parameters in differentiation between benign and malignant sinonasal tumors （P 〈 0.001）.The accuracy was 87.3% （90.5% sensitivity,82.7% specificity,88.2% PPV,and 85.9% NPV） using DW-MRI combined with DCE-MRI,which was superior than that using DCE-MRI alone or using DW-MRI alone （both P 〈 0.001） in differentiating the benign from the malignant tumors.Conclusions：Diffusion-weighted combined with DCE-MRI can improve imaging performance in differentiating benign from malignant sinonasal tumors,which has the potential to improve diagnostic accuracy and to provide added value in the management for these tumors.

Sulfur Dioxide Inhibits Extracellular Signal-regulated Kinase Signaling to Attenuate Vascular Smooth Muscle Cell Proliferation in Angiotensin II-induced Hypertensive Mice

Background： Clarifying the mechanisms underlying vascular smooth muscle cell （VSMC） proliferation is important for the prevention and treatment of vascular remodeling and the reverse of hyperplastic lesions. Previous research has shown that the gaseous signaling molecule sulfur dioxide （SO2） inhibits VSMC proliferation, but the mechanism for the inhibition of the angiotensin Ⅱ （Angll）-induced VSMC proliferation by SO, has not been fully elucidated. This study was designed to investigate if SO2 inhibited VSMC proliferation in mice with hypertension induced by Angll. Methods： Thirty-six male C57 mice were randomly divided into control, Angll, and Angll ＋ SO2 groups. Mice in Angll group and Angl I ＋ SO2 group received a capsule-type Angll pump implanted under the skin of the back at a slow-release dose of 1000 ng-kg^-1min In addition, mice in Angll ＋ SO2 received intraperitoneal injections of SO., donor. Arterial blood pressure of tail artery was determined. The thickness of the aorta was measured by elastic fiber staining, and proliferating cell nuclear antigen （PCNA） and phosphorylated-extracellular signal-regulated kinase （P-ERK） were detected in aortic tissues. The concentration of SO~ in serum and aortic tissue homogenate supernatant was measured using high-performance liquid chromatography with fluorescence determination. In the in vio＇o study, VSMC of A7R5 cell lines was divided into six groups： control, Angll, Angll ＋ SO2 PD98059 （an inhibitor of ERK phosphorylation）, Angll ＋ PD98059, and Angll ＋ SO, ＋ PD98059. Expression of PCNA, ERK, and P-ERK was determined by Western blotting. Results： In animal experiment, compared with the control group, Angll markedly increased blood pressure （P 〈 0.01 ） and thickened the aortic wall in mice （P 〈 0.05） with an increase in the expression of PCNA （P 〈 0.05）. SO2 however, reduced the systemic hypertension and the wall thickness induced by AnglI （P 〈 0.05）. It inhibited the increased expression of PCNA and P-ERK induced by AnglI （P 〈 0.05）. In cell experiment, PD98059, an ERK phosphorylation inhibitor, blocked the inhibitory effect of SO, on VSMC proliferation （P 〈 0.05）. Conclusions： ERK signaling is involved in the mechanisms by which SO, inhibits VSMC proliferation in Angll-induced hypertensive mice via ERK signaling.

Hydrogen Sulfide Regulating Myocardial Structure and Function by Targeting Cardiomyocyte Autophagy

Objective： Hydrogen sulfide （H2S）, a gaseous signal molecule, plays a crucial role in many pathophysiologic processes in the cardiovascular system. Autophagy has been shown to participate in the occurrence of many cardiac diseases. Increasing evidences indicated that H,S regulates myocardial structure and function in association with the altered autophagy and plays a ＂switcher＂ role in the autophagy of myocardial diseases. The airn of this review was to summarize these insights and provide the experimental evidence that H2S targets cardiomyocyte autophagy to regulate cardiovascular function. Data Sources： This review was based on data in articles published in the PubMed databases up to October 30, 2017, with the following keywords： ＂hydrogen sulfide,＂ ＂autophagy,＂ and ＂cardiovascular diseases.＂ Study Selection： Original articles and critical reviews on H,S and autophagy were selected for this review. Results： When autophagy plays an adaptive role in the pathogenesis of diseases, H2S restores autophagy; otherwise, when autophagy plays a detrimental role, H2S downregulates autophagy to exert a cardioprotective function. For example, H2S has beneficial effects by regulating autophagy in myocardial ischemia/reperfusion and plays a protective role by inhibiting autophagy during the operation of cardioplegia and cardiopuhnonary bypass. H2S postpones cardiac aging associated with the upregulation of autophagy but improves the left ventricular function of smoking rats by lowering autophagy. Conclusions： H2S exerts cardiovascular protection by regulating autophagy. Cardiovascular autophagy would likely become a potential target of H2S therapy for cardiovascular diseases.