16 research outputs found

    ESNOQ, Proteomic Quantification of Endogenous S-Nitrosation

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    S-nitrosation is a post-translational protein modification and is one of the most important mechanisms of NO signaling. Endogenous S-nitrosothiol (SNO) quantification is a challenge for detailed functional studies. Here we developed an ESNOQ (Endogenous SNO Quantification) method which combines the stable isotope labeling by amino acids in cell culture (SILAC) technique with the detergent-free biotin-switch assay and LC-MS/MS. After confirming the accuracy of quantification in this method, we obtained an endogenous S-nitrosation proteome for LPS/IFN-γ induced RAW264.7 cells. 27 S-nitrosated protein targets were confirmed and using our method we were able to obtain quantitative information on the level of S-nitrosation on each modified Cys. With this quantitative information, over 15 more S-nitrosated targets were identified than in previous studies. Based on the quantification results, we found that the S-nitrosation levels of different cysteines varied within one protein, providing direct evidence for differences in the sensitivity of cysteine residues to reactive nitrosative stress and that S-nitrosation is a site-specific modification. Gene ontology clustering shows that S-nitrosation targets in the LPS/IFN-γ induced RAW264.7 cell model were functionally enriched in protein translation and glycolysis, suggesting that S-nitrosation may function by regulating multiple pathways. The ESNOQ method described here thus provides a solution for quantification of multiple endogenous S-nitrosation events, and makes it possible to elucidate the network of relationships between endogenous S-nitrosation targets involved in different cellular processes

    Detection of the damage threshold of fused silica components and morphologies of repaired damage sites based on the beam deflection method

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    This article proposes a method to quickly detect the damage threshold of the fused silica components and the characteristics of the repair point damage. With a device detecting the beam deflection, the laser damage threshold is detected, quickly and effectively. Then, based on the beam deflection though mitigated sites, the beam deflection signals of the damage repair points are measured and the morphologies of mitigated sites are analyzed. This method is helpful in the online assessment of the damage resistance of the downstream optics and provides the guidance of the repair process

    The size prediction of potential inclusions embedded in the sub-surface of fused silica by damage morphology

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    A model for predicting the size ranges of different potential inclusions initiating damage on the surface of fused silica has been presented. This accounts for the heating of nanometric inclusions whose absorptivity is described based on Mie Theory. The depth profile of impurities has been measured by ICP-OES. By the measured temporal pulse profile on the surface of fused silica, the temperature and thermal stress has been calculated. Furthermore, considering the limit conditions of temperature and thermal stress strength for different damage morphologies, the size range of potential inclusions for fused silica is discussed

    Can China achieve a one-third reduction in premature mortality from non-communicable diseases by 2030?

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    Abstract Background The United Nation’s Sustainable Development Goals for 2030 include reducing premature mortality from non-communicable diseases (NCDs) by one third. To assess the feasibility of this goal in China, we projected premature mortality in 2030 of NCDs under different risk factor reduction scenarios. Methods We used China results from the Global Burden of Disease Study 2013 as empirical data for projections. Deaths between 1990 and 2013 for cardiovascular disease (CVD), diabetes, chronic respiratory disease, cancer, and other NCDs were extracted, along with population numbers. We disaggregated deaths into parts attributable and unattributable to high systolic blood pressure (SBP), smoking, high body mass index (BMI), high total cholesterol, physical inactivity, and high fasting glucose. Risk factor exposure and deaths by NCD category were projected to 2030. Eight simulated scenarios were also constructed to explore how premature mortality will be affected if the World Health Organization’s targets for risk factors reduction are achieved by 2030. Results If current trends for each risk factor continued to 2030, the total premature deaths from NCDs would increase from 3.11 million to 3.52 million, but the premature mortality rate would decrease by 13.1%. In the combined scenario in which all risk factor reduction targets are achieved, nearly one million deaths among persons 30 to 70 years old due to NCDs would be avoided, and the one-third reduction goal would be achieved for all NCDs combined. More specifically, the goal would be achieved for CVD and chronic respiratory diseases, but not for cancer and diabetes. Reduction in the prevalence of high SBP, smoking, and high BMI played an important role in achieving the goals. Conclusions Reaching the goal of a one-third reduction in premature mortality from NCDs is possible by 2030 if certain targets for risk factor intervention are reached, but more efforts are required to achieve risk factor reduction

    The kinetics of infection in mice with TgCtwh6 isolates.

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    <p>Kinetics of infection in blood and organs after oral infection with 50 cysts of TgCtwh6 isolate (genotype Chinese 1) in mice. I: the number of DNA copies in blood and tissues of the TgCtwh6 isolate post infection at various intervals by qPCR. Each point represents the mean value of the <i>T. gondii</i> DNA copies for five mice ± SD. II: detection of PCR products of <i>T. gondii</i> 529 bp fragments extracted from brain or ascitic fluid in the recipient mice. Abbreviations: <b>A</b>; blood, <b>B</b>; heart, <b>C</b>; liver, <b>D</b>; brain, and <b>E</b>; lymph node. b, n, and p represent blank, negative and positive control. *<i>P</i><0.05.</p

    The genotypes and geographic regions of <i>T. gondii</i> Chinese isolates.

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    <p>Panel A: a map of China to show the cumulative data of geographic distribution where the Chinese isolates of <i>T. gondii</i> used for genotyping were collected. The provinces and cities where <i>T. gondii</i> isolates were obtained and indicated by red dots and black dots, respectively. Red dots represent the locations (counties) where the isolates were collected in this work. Black dots indicate the locations (counties) where the isolates were collected in the early studies. SX: Shanxi province; SD: Shandong province; HN: Henan province; AH: Anhui province; JS: Jiangsu province; HuB: Hubei province; HuN: Hunan province; GD: Guangdong province; ZJ: Zhejiang province; FJ: Fujian province; YN: Yunnan province; QH: Qinghai province; GS: Gansu province; XJ: Xinjiang province; BJ: Beijing city; SH: Shanghai city. Panel B: a: the cumulative data of genotypes of <i>T. gondii</i> Chinese isolates. b: the genotypes of <i>T. gondii</i> isolates from human patients in mainland China. This is the first report of the genotype ToxoDB#204 from humans.</p

    Phylogenetic network analysis of <i>Toxoplasma gondii</i> isolates from humans and animals in China.

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    <p>From the 23 samples, 5 genotypes were identified. Genotype number (ToxoDB PCR-RFLP #) and the representative strains are listed for each taxonomic branch. The representative strains from each genotype were underlined found in this study. The numbers in parentheses indicate the number of isolates from this study belonging to that genotype. The phylogenetic network analysis with EF1, HP2, UPRT1, UPRT7, GRA6 and GRA7 shows a perfect match with PCR-RFLP allele types at 10 multilocus markers used in the present study.</p
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