1,019 research outputs found

    Characterization of the nodulation plasmid encoded chemoreceptor gene mcpG from Rhizobium leguminosarum

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    BACKGROUND: In general, chemotaxis in Rhizobium has not been well characterized. Methyl accepting chemotaxis proteins are sensory proteins important in chemotaxis of numerous bacteria, but their involvement in Rhizobium chemotaxis is unclear and merits further investigation. RESULTS: A putative methyl accepting chemotaxis protein gene (mcpG) of Rhizobium leguminosarum VF39SM was isolated and characterized. The gene was found to reside on the nodulation plasmid, pRleVF39d. The predicted mcpG ORF displayed motifs common to known methyl-accepting chemotaxis proteins, such as two transmembrane domains and high homology to the conserved methylation and signaling domains of well-characterized MCPs. Phenotypic analysis of mcpG mutants using swarm plates did not identify ligands for this putative receptor. Additionally, gene knockouts of mcpG did not affect a mutant strain's ability to compete for nodulation with the wild type. Notably, mcpG was found to be plasmid-encoded in all strains of R. leguminosarum and R. etli examined, though it was found on the nodulation plasmid only in a minority of strains. CONCLUSIONS: Based on sequence homology R. leguminosarum mcpG gene codes for a methyl accepting chemotaxis protein. The gene is plasmid localized in numerous Rhizobium spp. Although localized to the sym plasmid of VF39SM mcpG does not appear to participate in early nodulation events. A ligand for McpG remains to be found. Apparent McpG orthologs appear in a diverse range of proteobacteria. Identification and characterization of mcpG adds to the family of mcp genes already identified in this organism

    IVIg and LPS Co-stimulation Induces IL-10 Production by Human Monocytes, Which Is Compromised by an FcÎłRIIA Disease-Associated Gene Variant

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    Intravenous Immunoglobulin (IVIg) is used to treat autoimmune or inflammatory diseases, but its mechanism of action is not completely understood. We asked whether IVIg can induce interleukin-10 (IL-10) and reduce pro-inflammatory cytokine production in human monocytes, and whether this response is reduced in monocytes from people with an FcÎł receptor IIA (FcÎłRIIA) gene variant, which is associated with increased risk of inflammatory diseases and poor response to antibody-based biological therapy. IVIg increased IL-10 production and reduced pro-inflammatory cytokine production in response to bacterial lipopolysaccharide (LPS), which required FcÎłRI and FcÎłRIIB and activation of MAPKs, extracellular signal-regulated kinase 1/2 (ERK1/2), and p38. IL-10 production was lower and pro-inflammatory cytokine production was higher in monocytes from people with the FcÎłRIIA risk variant and the risk variant prevented IL-10 production in response to (IVIg+LPS). Finally, we show that IVIg did not induce MAPK activation in monocytes from people with the risk variant. Our results demonstrate that IVIg can skew human monocytes to an anti-inflammatory, IL-10-producing activation state, which is compromised in monocytes from people with the FcÎłRIIA risk variant. This research has profound implications for the use of IVIg because 25% of the population is homozygous for the FcÎłRIIA risk variant and its efficacy may be reduced in those individuals. In addition, this research may be useful to develop new therapeutic strategies to replace IVIg by cross-linking FcÎłRIs and FcÎłRIIBs to promote anti-inflammatory macrophage activation, independent of the FcÎłRIIA genotype

    Swift/XRT follow-up observation on IGR J17177-3656 at soft X-rays

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    Following the discovery of IGR J17177-3656 (Frankowski et al. 2011, ATel #3223) on 2011-03-15, we requested a Swift ToO, which was executed on 2011-03-16 from 18:39:24 to 20:41:01 UT with a total exposure of ~3.9 ks. 2266 photons have been extracted from the source region between 0.2 and 10 keV, corresponding to a net count rate of ~0.59 cts/s. Using the online Swift tool we find an enhanced position of RA = 259.428 (17h17m43s), Dec = -36.934 deg (-36:56:03s) (J2000), with a 90% confidence level error of 2.1 arcsec, consistent with the position measurements made by IBIS/ISGRI and JEM-X (ATel #3223)

    The 28 November 2020 Landslide, Tsunami, and Outburst Flood – A Hazard Cascade Associated With Rapid Deglaciation at Elliot Creek, British Columbia, Canada

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    We describe and model the evolution of a recent landslide, tsunami, outburst flood, and sediment plume in the southern Coast Mountains, British Columbia, Canada. On November 28, 2020, about 18 million m3 of rock descended 1,000 m from a steep valley wall and traveled across the toe of a glacier before entering a 0.6 km2 glacier lake and producing >100-m high run-up. Water overtopped the lake outlet and scoured a 10-km long channel before depositing debris on a 2-km2 fan below the lake outlet. Floodwater, organic debris, and fine sediment entered a fjord where it produced a 60+km long sediment plume and altered turbidity, water temperature, and water chemistry for weeks. The outburst flood destroyed forest and salmon spawning habitat. Physically based models of the landslide, tsunami, and flood provide real-time simulations of the event and can improve understanding of similar hazard cascades and the risk they pose

    Gluten Induces Subtle Histological Changes in Duodenal Mu-cosa of Patients with Non-Coeliac Gluten Sensitivity: A Multi-center Study

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    Histological changes induced by gluten in the duodenal mucosa of patients with non-coeliac gluten sensitivity (NCGS) are poorly defined. Objectives: To evaluate the structural and inflammatory features of NCGS compared to controls and coeliac disease (CeD) with milder enteropathy (Marsh I-II). Methods: Well-oriented biopsies of 262 control cases with normal gastroscopy and histologic findings, 261 CeD, and 175 NCGS biopsies from 9 contributing countries were examined. Villus height (VH, in ÎŒm), crypt depth (CrD, in ÎŒm), villus-to-crypt ratios (VCR), IELs (intraepithelial lymphocytes/100 enterocytes), and other relevant histological, serologic, and demographic parameters were quantified. Results: The median VH in NCGS was significantly shorter (600, IQR: 400−705) than controls (900, IQR: 667−1112) (p < 0.001). NCGS patients with Marsh I-II had similar VH and VCR to CeD [465 ”m (IQR: 390−620) vs. 427 ”m (IQR: 348−569, p = 0·176)]. The VCR in NCGS with Marsh 0 was lower than controls (p < 0.001). The median IEL in NCGS with Marsh 0 was higher than controls (23.0 vs. 13.7, p < 0.001). To distinguish Marsh 0 NCGS from controls, an IEL cut-off of 14 showed 79% sensitivity and 55% specificity. IEL densities in Marsh I-II NCGS and CeD groups were similar. Conclusion: NCGS duodenal mucosa exhibits distinctive changes consistent with an intestinal response to luminal antigens, even at the Marsh 0 stage of villus architecture

    Measurement of the Bs0→J/ψηB_{s}^{0} \rightarrow J/\psi \eta lifetime

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    Using a data set corresponding to an integrated luminosity of 3fb−13 fb^{-1}, collected by the LHCb experiment in pppp collisions at centre-of-mass energies of 7 and 8 TeV, the effective lifetime in the Bs0→J/ψηB^0_s \rightarrow J/\psi \eta decay mode, τeff\tau_{\textrm{eff}}, is measured to be τeff=1.479±0.034 (stat)±0.011 (syst)\tau_{\textrm{eff}} = 1.479 \pm 0.034~\textrm{(stat)} \pm 0.011 ~\textrm{(syst)} ps. Assuming CPCP conservation, τeff\tau_{\textrm{eff}} corresponds to the lifetime of the light Bs0B_s^0 mass eigenstate. This is the first measurement of the effective lifetime in this decay mode.Comment: All figures and tables, along with any supplementary material and additional information, are available at https://lhcbproject.web.cern.ch/lhcbproject/Publications/LHCbProjectPublic/LHCb-PAPER-2016-017.htm

    Measurement of the mass and lifetime of the Ωb−\Omega_b^- baryon

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    A proton-proton collision data sample, corresponding to an integrated luminosity of 3 fb−1^{-1} collected by LHCb at s=7\sqrt{s}=7 and 8 TeV, is used to reconstruct 63±963\pm9 Ωb−→Ωc0π−\Omega_b^-\to\Omega_c^0\pi^-, Ωc0→pK−K−π+\Omega_c^0\to pK^-K^-\pi^+ decays. Using the Ξb−→Ξc0π−\Xi_b^-\to\Xi_c^0\pi^-, Ξc0→pK−K−π+\Xi_c^0\to pK^-K^-\pi^+ decay mode for calibration, the lifetime ratio and absolute lifetime of the Ωb−\Omega_b^- baryon are measured to be \begin{align*} \frac{\tau_{\Omega_b^-}}{\tau_{\Xi_b^-}} &= 1.11\pm0.16\pm0.03, \\ \tau_{\Omega_b^-} &= 1.78\pm0.26\pm0.05\pm0.06~{\rm ps}, \end{align*} where the uncertainties are statistical, systematic and from the calibration mode (for τΩb−\tau_{\Omega_b^-} only). A measurement is also made of the mass difference, mΩb−−mΞb−m_{\Omega_b^-}-m_{\Xi_b^-}, and the corresponding Ωb−\Omega_b^- mass, which yields \begin{align*} m_{\Omega_b^-}-m_{\Xi_b^-} &= 247.4\pm3.2\pm0.5~{\rm MeV}/c^2, \\ m_{\Omega_b^-} &= 6045.1\pm3.2\pm 0.5\pm0.6~{\rm MeV}/c^2. \end{align*} These results are consistent with previous measurements.Comment: 11 pages, 5 figures, All figures and tables, along with any supplementary material and additional information, are available at https://lhcbproject.web.cern.ch/lhcbproject/Publications/LHCbProjectPublic/LHCb-PAPER-2016-008.htm

    Bose-Einstein correlations of same-sign charged pions in the forward region in pp collisions at √s=7 TeV

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    Bose-Einstein correlations of same-sign charged pions, produced in protonproton collisions at a 7 TeV centre-of-mass energy, are studied using a data sample collected by the LHCb experiment. The signature for Bose-Einstein correlations is observed in the form of an enhancement of pairs of like-sign charged pions with small four-momentum difference squared. The charged-particle multiplicity dependence of the Bose-Einstein correlation parameters describing the correlation strength and the size of the emitting source is investigated, determining both the correlation radius and the chaoticity parameter. The measured correlation radius is found to increase as a function of increasing charged-particle multiplicity, while the chaoticity parameter is seen to decreas
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