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.
<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>
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.
<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.
<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.
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
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
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
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
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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