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1. chinaXiv:201711.00133 [pdf]

Solvent Synthesis, Growth Mechanism and Photocatalytic Properties of AgInS2 Nanoplate and Nanoparticle

WANG Yue; SHI Yong-Fang; LI Xiao-Bo; LI Dong-Wei; ZHANG Tao; HE Yu-Cen
Subjects: Chemistry >> Physical Chemistry

Orthorhombic AgInS2 nanoplate and nanoparticle were synthesized using pyridine and 1-dodecanethiol as the solvent. The obtained products were characterized by X-ray diffraction (XRD), field-emission scanning electron microscope (FESEM), field-emission transmission electron microscope (FETEM), and the possible growth mechanism of AgInS2 was also proposed by the exploration of reaction temperature and time. Meanwhile, the bandgap of AgInS2 was calculated by the UV-Vis diffuse reflectance spectrum, and the photocatalytic activity was also investigated. Those experimental results indicate that the reaction temperature, reaction time and solvent have an influence on phase and morphology of AgInS2, and both AgInS2 nanoplate and nanoparticle have some ability on photocatalytic degradation of organic dyes under UV-Vis light irradiation.

submitted time 2017-11-05 From cooperative journals:《结构化学》 Hits1947Downloads1008 Comment 0

2. chinaXiv:201605.01325 [pdf]

Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death

Shi, Jianjin; Shi, Jianjin; Zhao, Yue; Wang, Kun; Shi, Xuyan; Wang, Yue; Huang, Huanwei; Zhuang, Yinghua; Cai, Tao; Wang, Fengchao; Shao, Feng; Shao, Feng; Shao, Feng
Subjects: Biology >> Biophysics

Inflammatory caspases (caspase-1, -4, -5 and -11) are critical for innate defences. Caspase-1 is activated by ligands of various canonical inflammasomes, and caspase-4, -5 and -11 directly recognize bacterial lipopolysaccharide, both of which trigger pyroptosis. Despite the crucial role in immunity and endotoxic shock, the mechanism for pyroptosis induction by inflammatory caspases is unknown. Here we identify gasdermin D (Gsdmd) by genome-wide clustered regularly interspaced palindromic repeat (CRISPR)-Cas9 nuclease screens of caspase-11- and caspase-1-mediated pyroptosis in mouse bone marrow macrophages. GSDMD-deficient cells resisted the induction of pyroptosis by cytosolic lipopolysaccharide and known canonical inflammasome ligands. Interleukin-1 beta release was also diminished in Gsdmd(-/-) cells, despite intact processing by caspase-1. Caspase-1 and caspase-4/5/11 specifically cleaved the linker between the amino-terminal gasdermin-N and carboxy-terminal gasdermin-C domains in GSDMD, which was required and sufficient for pyroptosis. The cleavage released the intramolecular inhibition on the gasdermin-N domain that showed intrinsic pyroptosis-inducing activity. Other gasdermin family members were not cleaved by inflammatory caspases but shared the autoinhibition; gain-of-function mutations in Gsdma3 that cause alopecia and skin defects disrupted the autoinhibition, allowing its gasdermin-N domain to trigger pyroptosis. These findings offer insight into inflammasome-mediated immunity/diseases and also change our understanding of pyroptosis and programmed necrosis.

submitted time 2016-05-11 Hits2422Downloads1741 Comment 0

3. chinaXiv:201605.01297 [pdf]

Asymmetric dimethylarginine exacerbates A beta-induced toxicity and oxidative stress in human cell and Caenorhabditis elegans models of Alzheimer disease

Luo, Yunfeng; Yue, Wenhui; Quan, Xin; Wang, Yue; Lu, Zhongbing; Zhao, Baolu
Subjects: Biology >> Biophysics >> Biochemistry & Molecular Biology

Growing evidence suggests a strong association between cardiovascular risk factors and incidence of Alzheimer disease (AD). Asymmetric dimethylarginine (ADMA), the endogenous nitric oxide synthase inhibitor, has been identified as an independent cardiovascular risk factor and is also increased in plasma of patients with AD. However, whether ADMA is involved in the pathogenesis of AD is unknown. In this study, we found that ADMA content was increased in a transgenic Caenorhabditis elegans beta-amyloid (A beta) overexpression model, strain CL2006, and in human SH-SY5Y cells overexpressing the Swedish mutant form of human A beta precursor protein (APPsw). Moreover, ADMA treatment exacerbated A beta-induced paralysis and oxidative stress in CL2006 worms and further elevated oxidative stress and A beta secretion in APPsw cells. Knockdown of type 1 protein arginine N-methyltransferase to reduce ADMA production failed to show a protective effect against A beta toxicity, but resulted in more paralysis in CL2006 worms as well as increased oxidative stress and A beta secretion in APPsw cells. However, overexpression of dimethylarginine dimethylaminohydrolase 1 (DDAH1) to promote ADMA degradation significantly attenuated oxidative stress and A beta secretion in APPsw cells. Collectively, our data support the hypothesis that elevated ADMA contributes to the pathogenesis of AD. Our findings suggest that strategies to increase DDAH1 activity in neuronal cells may be a novel approach to attenuating AD development. (C) 2014 Elsevier Inc. All rights reserved.

submitted time 2016-05-11 Hits1851Downloads1045 Comment 0

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