Abstract
Distinct X-ray plateau and flare phases have been observed in the afterglows of gamma-ray bursts (GRBs), and most of them should be related to central engine activities. In this paper, we ...collect 174 GRBs with X-ray plateau phases and 106 GRBs with X-ray flares. There are 51 GRBs that overlap in the two selected samples. We analyze the distributions of the proportions of the plateau energy
E
plateau
and the flare energy
E
flare
relative to the isotropic prompt emission energy
E
γ
,iso
. The results indicate that they well meet the Gaussian distributions and the medians of the logarithmic ratios are ∼−0.96 and −1.39 in the two cases. Moreover, strong positive correlations between
E
plateau
(or
E
flare
) and
E
γ
,iso
with slopes of ∼0.95 (or ∼0.80) are presented. For the overlapping sample, the slope is ∼0.80. We argue that most of X-ray plateaus and flares might have the same physical origin but appear with different features because of the different circumstances and radiation mechanisms. We also test the applicabilities of two models, i.e., black holes surrounded by fractured hyperaccretion disks and millisecond magnetars, on the origins of X-ray plateaus and flares.
Abstract
Long-duration gamma-ray bursts (GRBs) are generally related to the core-collapse of massive stars. In the collapsar scenario, a rotating stellar-mass black hole (BH) surrounded by a ...hyperaccretion disk has been considered as one of the plausible candidates of GRB central engines. In this paper, we work on a sample including 146 long GRBs with significant jet break features in the multiband afterglows. The jet opening angles can then be obtained by the jet break time. By assuming GRB jets powered by the Blandford–Znajek (BZ) mechanism in the BH hyperaccretion system, we analyze the distributions of the long GRB luminosities and durations in the samples, and constrain the accretion rates for the different BH spins. As a result, we find that the BZ mechanism is so powerful that it is possible to interpret the long GRB prompt emissions within reasonable accretion rates.
Abstract
Long gamma-ray bursts (GRBs) are considered to originate from core collapse of massive stars. It is believed that the afterglow property is determined by the density of the material in the ...surrounding interstellar medium (ISM). Therefore, the circumburst density can be used to distinguish between an interstellar wind,
n
(
R
) ∝
R
−
k
, and a constant-density medium (ISM),
n
(
R
)
=
const
. Previous studies with different afterglow samples show that the circumburst medium of GRBs is neither simply supported by an interstellar wind nor completely favored by an ISM. In this work, our new sample consists of 39 GRBs with smoothly onset bump-like features in early X-ray afterglows, in which 20 GRBs have the redshift measurements. By using a smooth broken power-law function to fit the bumps of X-ray light curves, we derive the FWHM as the feature width (
ω
), as well as the rise and decay timescales of the bumps (
T
r
and
T
d
). The correlations between the timescales of X-ray bumps are similar to those found previously in the optical afterglows. Based on the fireball forward shock model of the thin shell case, we obtain the distribution of the electron spectral index
p
and further constrain the medium density distribution index
k
. The new inferred
k
is found to be concentrated at 1.0, with a range from 0.2 to 1.8. This finding is consistent with previous studies. The conclusion of our detailed investigation for X-ray afterglows suggests that the ambient medium of the selected GRBs is not homogeneous, i.e., neither ISM nor the typical interstellar wind.
Macrophage activation participates in the pathogenesis of pulmonary inflammation. As a coenzyme, vitamin B6 (VitB6) is mainly involved in the metabolism of amino acids, nucleic acids, glycogen and ...lipids. We have previously reported that activation of AMP‐activated protein kinase (AMPK) produces anti‐inflammatory effects both in vitro and in vivo. Whether VitB6 via AMPK activation prevents pulmonary inflammation remains unknown. The model of acute pneumonia was induced by injecting mice with lipopolysaccharide (LPS). The inflammation was determined by measuring the levels of interleukin‐1 beta (IL‐1β), IL‐6 and tumour necrosis factor alpha (TNF‐α) using real time PCR, ELISA and immunohistochemistry. Exposure of cultured primary macrophages to VitB6 increased AMP‐activated protein kinase (AMPK) Thr172 phosphorylation in a time/dose‐dependent manner, which was inhibited by compound C. VitB6 downregulated the inflammatory gene expressions including IL‐1β, IL‐6 and TNF‐α in macrophages challenged with LPS. These effects of VitB6 were mirrored by AMPK activator 5‐aminoimidazole‐4‐carboxamide ribonucleoside (AICAR). However, VitB6 was unable to inhibit LPS‐induced macrophage activation if AMPK was in deficient through siRNA‐mediated approaches. Further, the anti‐inflammatory effects produced by VitB6 or AICAR in LPS‐treated macrophages were abolished in DOK3 gene knockout (DOK3−/−) macrophages, but were enhanced in macrophages if DOK3 was overexpressed. In vivo studies indicated that administration of VitB6 remarkably inhibited LPS‐induced both systemic inflammation and acute pneumonia in wild‐type mice, but not in DOK3−/− mice. VitB6 prevents LPS‐induced acute pulmonary inflammation in mice via the inhibition of macrophage activation.
To compare the clinical effects of invisible correction and SGTB in two-stage treatment of mandibular retrusion.
Eighty-five patients with bony mandibular regression who did not pass the peak of ...growth and development were selected. Among them, 40 cases were guided by invisible correction and 45 cases were guided by SGTB functional correction. Lateral head X-rays before and after treatment were measured, and the effect before and after treatment was compared by SPSS 16.0 software package.
After treatment, the SNB angle and NP-FH (face angle) increased and the ANB angle decreased in both groups, all of which had significant changes(P＜0.001). At T1, the changes of SNB angle, ANB angle and NP-FH angle in the invisible group were smaller than those in the SGTB group(P＜0.05). The difference between MP-FH angle and MP-SN angle before and after treatment was greater in the SGTB group than in the invisible group(P＜0.001).
In patients with receding mandible before the peak of growth and development, the mandible was s
Development of nitrate tolerance is a major drawback to nitrate therapy. Prostacyclin (PGI2) is a powerful vasodilator produced from prostaglandin (PGH2) by prostacyclin synthase (PGIS) in ...endothelial cells. This study aimed to determine the role of PGIS S‐nitrosylation in nitrate tolerance induced by nitroglycerin (GTN). In endothelial cells, GTN increased PGIS S‐nitrosylation and disturbed PGH2 metabolism, which were normalized by mutants of PGIS cysteine 231/441 to alanine (C231/441A). Clearance of nitric oxide by carboxy‐PTIO or inhibition of S‐nitrosylation by N‐acetyl‐cysteine decreased GTN‐induced PGIS S‐nitrosylation. Enforced expression of mutated PGIS with C231/441A markedly abolished GTN‐induced PGIS S‐nitrosylation and nitrate cross‐tolerance in Apoe‐/‐ mice. Inhibition of cyclooxygenase 1 by aspirin, supplementation of PGI2 by beraprost, and inhibition of PGIS S‐nitrosylation by N‐acetyl‐cysteine improved GTN‐induced nitrate cross‐tolerance in rats. In patients, increased PGIS S‐nitrosylation was associated with nitrate tolerance. In conclusion, GTN induces nitrate cross‐tolerance through PGIS S‐nitrosylation at cysteine 231/441.
Summary
Staphylococcus epidermidis strains are diverse in their pathogenicity; some are invasive and cause serious nosocomial infections, whereas others are non‐pathogenic commensal organisms. To ...analyse the implications of different virulence factors in Staphylococcus epidermidis infections, the complete genome of Staphylococcus epidermidis strain ATCC 12228, a non‐biofilm forming, non‐infection associated strain used for detection of residual antibiotics in food products, was sequenced. This strain showed low virulence by mouse and rat experimental infections. The genome consists of a single 2499 279 bp chromosome and six plasmids. The chromosomal G + C content is 32.1% and 2419 protein coding sequences (CDS) are predicted, among which 230 are putative novel genes. Compared to the virulence factors in Staphylococcus aureus, aside from δ‐haemolysin and β‐haemolysin, other toxin genes were not found. In contrast, the majority of adhesin genes are intact in ATCC 12228. Most strikingly, the ica operon coding for the enzymes synthesizing interbacterial cellular polysaccharide is missing in ATCC 12228 and rearrangements of adjacent genes are shown. No mec genes, IS256, IS257, were found in ATCC 12228. It is suggested that the absence of the ica operon is a genetic marker in commensal Staphylococcus epidermidis strains which are less likely to become invasive.
Bacterial wilt, caused by
, one of the most destructive phytopathogens, leads to significant annual crop yield losses. Type III effectors (T3Es) mainly contribute to the virulence of
, usually by ...targeting immune-related proteins. Here, we clarified the effect of a novel E3 ubiquitin ligase (NEL) T3E, RipAW, from
on pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and further explored its action mechanism. In the susceptible host
, we monitored the expression of PTI marker genes, flg22-induced ROS burst, and callose deposition in
- and
-transgenic plants. Our results demonstrated that RipAW suppressed host PTI in an NEL-dependent manner. By Split-Luciferase Complementation, Bimolecular Fluorescent Complimentary, and Co-Immunoprecipitation assays, we further showed that RipAW associated with three crucial components of the immune receptor complex, namely FLS2, XLG2, and BIK1. Furthermore, RipAW elevated the ubiquitination levels of FLS2, XLG2, and BIK1, accelerating their degradation via the 26S proteasome pathway. Additionally, co-expression of FLS2, XLG2, or BIK1 with RipAW partially but significantly restored the RipAW-suppressed ROS burst, confirming the involvement of the immune receptor complex in RipAW-regulated PTI. Overall, our results indicate that RipAW impairs host PTI by disrupting the immune receptor complex. Our findings provide new insights into the virulence mechanism of
.
ABSTRACT
X-ray flares in gamma-ray bursts (GRBs) are believed to be generated by the late activities of central engine, and thus provide an useful tool to diagnose the properties of central objects. ...In this paper, we work on a GRB X-ray flare sample whose bulk Lorentz factors are constrained by two different methods and the jet opening angles are determined by the jet breaks in afterglow light curves. Considering a hyperaccreting stellar-mass black hole (BH) as the central engine of GRBs and the Blandford & Znajek process (BZ) as the jet production mechanism, we constrain the parameters of central engine by using the X-ray flare data. We find that the BZ mechanism is so powerful making it possible to interpret both GRB prompt emissions and bright X-ray flares. The wind parameter (p) and accreted mass (Md) fall into reasonable ranges. Our result is also applied to GRB 170817A. The late X-ray flare in GRB 170817A, if it is true, might not be a BH origin.
Diabetes mellitus is one of risk factors of cardiovascular diseases including atherosclerosis. Whether and how diabetes promotes the formation of unstable atherosclerotic plaque is not fully ...understood. Here, we show that streptozotocin-induced type 1 diabetes reduced collagen synthesis, leading to the formation of unstable atherosclerotic plaque induced by collar placement around carotid in apolipoprotein E knockout (
Apoe
−/−
) mice. These detrimental effects of hyperglycemia on plaque stability were reversed by metformin in vivo without altering the levels of blood glucose and lipids. Mechanistically, we found that high glucose reduced the phosphorylated level of AMP-activated protein kinase alpha (AMPKα) and the transcriptional activity of activator protein 2 alpha (AP-2α), increased the expression of miR-124 expression, and downregulated prolyl-4-hydroxylase alpha 1 (P4Hα1) protein expression and collagen biosynthesis in cultured vascular smooth muscle cells. Importantly, these in vitro effects produced by high glucose were abolished by AMPKα pharmacological activation or adenovirus-mediated AMPKα overexpression. Further, adenovirus-mediated AMPKα gain of function remitted the process of diabetes-induced plaque destabilization in
Apoe
−/−
mice injected with streptozotocin. Administration of metformin enhanced pAP-2α level, reduced miR-124 expression, and increased P4Hα1 and collagens in carotid atherosclerotic plaque in diabetic
Apoe
−/−
mice. We conclude that streptozotocin-induced toxic diabetes promotes the formation of unstable atherosclerotic plaques based on the vulnerability index in
Apoe
−/−
mice, which is related to the inactivation of AMPKα/AP-2α/miRNA-124/P4Hα1 axis. Clinically, targeting AMPKα/AP-2α/miRNA-124/P4Hα1 signaling should be considered to increase the plaque stability in patients with atherosclerosis.
Key messages
Hyperglycemia reduced collagen synthesis, leading to the formation of unstable atherosclerotic plaque induced by collar placement around carotid in apolipoprotein E knockout mice.
Hyperglycemia destabilizes atherosclerotic plaque in vivo through an AMPKα/AP-2α/miRNA-124/P4Hα1-dependent collagen synthesis.
Metformin functions as a stabilizer of atherosclerotic plaque to reduce acute coronary accent.
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