201 research outputs found

    TNF-α, IL-1β, IL-10 and IFN-γ concentrations (pg/ml) in supernatants of whole blood cultures incubated with LPS 10 ng/ml.

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    <p>Data are presented as mean±SD, n = 19. Maximum levels are printed in bold.</p>a<p>ANOVA p<0.001,</p>b<p>p<0.05 compared to the respective cytokine concentration before stimulation.</p

    LiF as an Artificial SEI Layer to Enhance the High-Temperature Cycle Performance of Li<sub>4</sub>Ti<sub>5</sub>O<sub>12</sub>

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    Li<sub>4</sub>Ti<sub>5</sub>O<sub>12</sub> (LTO) is a promising anode material for electric vehicles (EVs) and electrochemical energy storage applications because of its safety, good rate capability, and long cycle life. At elevated temperature, such as 60 °C, it always shows poor cycle performance because of the instability between the electrode material and electrolyte, which may also lead to a serious gassing issue. In this article, a facile hydrothermal method is adopted to coat the LTO powder with a thin LiF layer, in which the LiF acts as an artificial solid electrolyte interface (SEI) layer to prevent the direct contact of LTO and electrolyte, thus improving the high-temperature cycle performance. Electrochemical tests prove that the LiF coating layer has no influence on the kinetics at ambient temperature and greatly enhances the high-temperature cycle stability, and the LTO@LiF composite material keeps 87% of its initial discharge capacity in 300 1C cycles at 60 °C. Moreover, the LiF coating layer exhibits a special self-driven reforming process during the initial cycles, which makes it uniform and more effective at enhancing the stability between electrode/electrolyte interfaces

    Effects of various stimuli on NOP and PNoc mRNA expression in human whole blood.

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    <p>Suppressive effect: <b>↓</b>, ∼25%; <b>↓↓</b>, ∼50%; <b>↓↓↓</b>, ∼75%; →, no significant change compared to base line.</p

    Effects of LPS on NOP and PNoc mRNA expression.

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    <p>Whole blood was cultured without LPS or with increasing concentrations of LPS 0.5–10<sup>4</sup> pg/ml for 6 hrs. LPS suppressed both NOP and PNoc mRNA expression. Data are presented as medians with interquartile ranges. n = 4, Kruskal-Wallis test with subsequent post hoc analysis, *: p<0.05. LPS, lipopolysaccharide; NOP, nociceptin receptor; PNoc, nociceptin precursor.</p

    AUC of NOP and PNoc mRNA expression (median normalized ratio hr with 1st/3rd quartiles) after whole blood was co-cultured with different stimuli for 0, 3, 6 and 24 hrs.

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    a<p>Comparison to blood cultures without any co-incubation; Mann-Whitney U test, p-values were corrected for multiple testing.</p

    UNC-51-like Kinase 1: From an Autophagic Initiator to Multifunctional Drug Target

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    UNC-51-like kinase 1 (ULK1), known as an ortholog of the yeast Atg1, is the serine–threonine kinase and the autophagic initiator in mammals. Accumulating evidence has recently revealed the kinase domain structure of ULK1 and its post-translational modifications, as well as further elucidated its regulatory autophagic pathways and associations with diverse human diseases. Interestingly, a series of small molecules have been recently reported to target ULK1 or ULK1-modulating autophagy, which may provide a clue on exploiting them as novel candidate drugs. Taken together, this review discusses how ULK1 acts as an autophagic initiator for modulation of its intricate mechanisms, as well as how ULK1 becomes a multifunctional target for potential therapeutic applications

    Additional file 1: Table S1. of Canonical correlation analysis (CCA) of anthropometric parameters and physical activities with blood lipids

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    Descriptive statistics for anthropometric parameters, physical activities and blood lipids from Hubei province in 2013, n = 5878. (DOCX 15 kb

    An Integrated Proteomics Reveals Pathological Mechanism of Honeybee (<i>Apis cerena</i>) Sacbrood Disease

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    Viral diseases of honeybees are a major challenge for the global beekeeping industry. Chinese indigenous honeybee (<i>Apis cerana cerana</i>, <i>Acc</i>) is one of the major Asian honeybee species and has a dominant population with more than 3 million colonies. However, <i>Acc</i> is frequently threatened by a viral disease caused by Chinese sacbrood virus (CSBV), which leads to fatal infections and eventually loss of the entire colony. Nevertheless, knowledge on the pathological mechanism of this deadly disease is still unknown. Here, an integrated gel-based and label-free liquid chromatography–mass spectrometry (LC–MS) based proteomic strategy was employed to unravel the molecular event that triggers this disease, by analysis of proteomics and phosphoproteomics alterations between healthy and CSBV infected worker larvae. There were 180 proteins and 19 phosphoproteins which altered their expressions after the viral infection, of which 142 proteins and 12 phosphoproteins were down-regulated in the sick larvae, while only 38 proteins and 7 phosphoproteins were up-regulated. The infected worker larvae were significantly affected by the pathways of carbohydrate and energy metabolism, development, protein metabolism, cytoskeleton, and protein folding, which were important for supporting organ generation and tissue development. Because of abnormal metabolism of these pathways, the sick larvae fail to pupate and eventually death occurs. Our data, for the first time, comprehensively decipher the molecular underpinnings of the viral infection of the <i>Acc</i> and are potentially helpful for sacbrood disease diagnosis and medicinal development for the prevention of this deadly viral disease

    An Integrated Proteomics Reveals Pathological Mechanism of Honeybee (<i>Apis cerena</i>) Sacbrood Disease

    No full text
    Viral diseases of honeybees are a major challenge for the global beekeeping industry. Chinese indigenous honeybee (<i>Apis cerana cerana</i>, <i>Acc</i>) is one of the major Asian honeybee species and has a dominant population with more than 3 million colonies. However, <i>Acc</i> is frequently threatened by a viral disease caused by Chinese sacbrood virus (CSBV), which leads to fatal infections and eventually loss of the entire colony. Nevertheless, knowledge on the pathological mechanism of this deadly disease is still unknown. Here, an integrated gel-based and label-free liquid chromatography–mass spectrometry (LC–MS) based proteomic strategy was employed to unravel the molecular event that triggers this disease, by analysis of proteomics and phosphoproteomics alterations between healthy and CSBV infected worker larvae. There were 180 proteins and 19 phosphoproteins which altered their expressions after the viral infection, of which 142 proteins and 12 phosphoproteins were down-regulated in the sick larvae, while only 38 proteins and 7 phosphoproteins were up-regulated. The infected worker larvae were significantly affected by the pathways of carbohydrate and energy metabolism, development, protein metabolism, cytoskeleton, and protein folding, which were important for supporting organ generation and tissue development. Because of abnormal metabolism of these pathways, the sick larvae fail to pupate and eventually death occurs. Our data, for the first time, comprehensively decipher the molecular underpinnings of the viral infection of the <i>Acc</i> and are potentially helpful for sacbrood disease diagnosis and medicinal development for the prevention of this deadly viral disease
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