94 research outputs found

    Detection of Bartonella bovis DNA in blood samples from a veterinarian in Mexico

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    The genus Bartonella encompasses 38 validated species of Gram-negative, facultative intracellular bacteria that colonize the endothelial cells and erythrocytes of a wide spectrum of mammals. To date, 12 Bartonella species have been recorded infecting humans, causing diseases of long historical characterization, such as cat scratch fever and trench fever, and emerging bartonellosis that mainly affect animal health professionals. For this reason, this study aimed to report a documented case of Bartonella bovis infecting a veterinarian from Mexico by the amplification, sequencing and phylogenetic reconstruction of the citrate synthase (gltA) and the RNA polymerase beta-subunit (rpoB) genes, and to report the natural course of this infection. To our knowledge, this work is the first to report the transmission of B. bovis via needlestick transmission to animal health workers in Latin America

    Heterogenous presence of neutrophil extracellular traps in human solid tumours is partially dependent on IL-8

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    Neutrophil extracellular traps (NETs) are webs of extracellular nuclear DNA extruded by dying neutrophils infiltrating tissue. NETs constitute a defence mechanism to entrap and kill fungi and bacteria. Tumours induce the formation of NETs to the advantage of the malignancy via a variety of mechanisms shown in mouse models. Here, we investigated the presence of NETs in a variety of human solid tumours and their association with IL-8 (CXCL8) protein expression and CD8+ T-cell density in the tumour microenvironment. Multiplex immunofluorescence panels were developed to identify NETs in human cancer tissues by co-staining with the granulocyte marker CD15, the neutrophil marker myeloperoxidase and citrullinated histone H3 (H3Cit), as well as IL-8 protein and CD8+ T cells. Three ELISA methods to detect and quantify circulating NETs in serum were optimised and utilised. Whole tumour sections and tissue microarrays from patients with non-small cell lung cancer (NSCLC; n = 14), bladder cancer (n = 14), melanoma (n = 11), breast cancer (n = 31), colorectal cancer (n = 20) and mesothelioma (n = 61) were studied. Also, serum samples collected retrospectively from patients with metastatic melanoma (n = 12) and NSCLC (n = 34) were ELISA assayed to quantify circulating NETs and IL-8. NETs were detected in six different human cancer types with wide individual variation in terms of tissue density and distribution. At least in NSCLC, bladder cancer and metastatic melanoma, NET density positively correlated with IL-8 protein expression and inversely correlated with CD8+ T-cell densities. In a series of serum samples from melanoma and NSCLC patients, a positive correlation between circulating NETs and IL-8 was found. In conclusion, NETs are detectable in formalin-fixed human biopsy samples from solid tumours and in the circulation of cancer patients with a considerable degree of individual variation. NETs show a positive association with IL-8 and a trend towards a negative association with CD8+ tumour-infiltrating lymphocytes

    Confirmation of an He I evaporating atmosphere around the 650-Myr-old sub-Neptune HD235088 b (TOI-1430 b) with CARMENES

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    HD235088 (TOI-1430) is a young star known to host a sub-Neptune-sized planet candidate. We validated the planetary nature of HD235088 b with multiband photometry, refined its planetary parameters, and obtained a new age estimate of the host star, placing it at 600-800 Myr. Previous spectroscopic observations of a single transit detected an excess absorption of He I coincident in time with the planet candidate transit. Here, we confirm the presence of He I in the atmosphere of HD235088 b with one transit observed with CARMENES. We also detected hints of variability in the strength of the helium signal, with an absorption of -0.91±\pm0.11%, which is slightly deeper (2σ\sigma) than the previous measurement. Furthermore, we simulated the He I signal with a spherically symmetric 1D hydrodynamic model, finding that the upper atmosphere of HD235088 b escapes hydrodynamically with a significant mass loss rate of (1.5-5) ×\times1010^{10}g s1^{-1}, in a relatively cold outflow, with TT=3125±\pm375 K, in the photon-limited escape regime. HD235088 b (RpR_{p} = 2.045±\pm0.075 R_{\oplus}) is the smallest planet found to date with a solid atmospheric detection - not just of He I but any other atom or molecule. This positions it a benchmark planet for further analyses of evolving young sub-Neptune atmospheres.Comment: Accepted for publication in A&A. 17 pages, 18 figure

    Abrasive Wear Behavior of Al–4Cu–1.5Mg–WC Composites Synthesized through Powder Metallurgy

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    Different Al–4Cu–1.5Mg/WC composites were synthesized through powder metallurgy to establish the effect of WC particle addition on the abrasive wear behavior of an Al–4Cu–1.5Mg (wt. %) alloy. The wear tests were performed using a pin-on-disc tribometer at room temperature in dry conditions using SiC abrasive sandpaper as a counterbody and tribometer of linear configuration. The results showed that WC additions increase the hardness of the Al–4Cu–1.5Mg alloy due to the strengthening effect of particle dispersion in the aluminum matrix, which generates an improvement in the wear resistance of the composites by preventing direct contact of the sample with the counterbody, in turn delaying the plastic deformation phenomena responsible for the degradation sequence. In addition, the dominant wear mechanism was abrasive wear, and the increased friction coefficient did not bring a rapid wear rate, which was related to the enhanced deformation resistance due to the high hardness

    Comparative Proteomic Analysis of Serum from Patients with Systemic Sclerosis and Sclerodermatous GVHD. Evidence of Defective Function of Factor H

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    BACKGROUND: Systemic sclerosis (SSc) is an autoimmune disease characterized by immunological and vascular abnormalities. Until now, the cause of SSc remains unclear. Sclerodermatous graft-versus-host disease (ScGVHD) is one of the most severe complications following bone marrow transplantation (BMT) for haematological disorders. Since the first cases, the similarity of ScGVHD to SSc has been reported. However, both diseases could have different etiopathogeneses. The objective of this study was to identify new serum biomarkers involved in SSc and ScGVHD. METHODOLOGY: Serum was obtained from patients with SSc and ScGVHD, patients without ScGVHD who received BMT for haematological disorders and healthy controls. Bi-dimensional electrophoresis (2D) was carried out to generate maps of serum proteins from patients and controls. The 2D maps underwent image analysis and differently expressed proteins were identified. Immuno-blot analysis and ELISA assay were used to validate the proteomic data. Hemolytic assay with sheep erythrocytes was performed to evaluate the capacity of Factor H (FH) to control complement activation on the cellular surface. FH binding to endothelial cells (ECs) was also analysed in order to assess possible dysfunctions of this protein. PRINCIPAL FINDINGS: Fourteen differentially expressed proteins were identified. We detected pneumococcal antibody cross-reacting with double stranded DNA in serum of all bone marrow transplanted patients with ScGVHD. We documented higher levels of FH in serum of SSc and ScGVHD patients compared healthy controls and increased sheep erythrocytes lysis after incubation with serum of diffuse SSc patients. In addition, we observed that FH binding to ECs was reduced when we used serum from these patients. CONCLUSIONS: The comparative proteomic analysis of serum from SSc and ScGVHD patients highlighted proteins involved in either promoting or maintaining an inflammatory state. We also found a defective function of Factor H, possibly associated with ECs damage

    Transmission spectroscopy of MASCARA-1b with ESPRESSO: Challenges of overlapping orbital and Doppler tracks

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    Atmospheric studies at high spectral resolution have shown the presence of molecules, neutral and ionised metals, and hydrogen in the transmission spectrum of ultra-hot Jupiters, and have started to probe the dynamics of their atmospheres. We analyse the transmission spectrum of MASCARA-1b, one of the densest ultra-hot Jupiters orbiting a bright (V = 8.3) star. We focus on the CaII H&K, NaI doublet, LiI, Hα, and KI D1 spectral lines and on the cross-correlated FeI, Fe II, CaI, YI, VI, VII, CaH, and TiO lines. For those species that are not present in the stellar spectrum, no detections are reported, but we are able to measure upper limits with an excellent precision (~10 ppm for particular species) thanks to the signal-to-noise ratio (S/N) achieved with Echelle SPectrograph for Rocky Exoplanets and Stable Spectroscopic Observations (ESPRESSO) observations. For those species that are present in the stellar spectrum and whose planet-occulted spectral lines induce spurious features in the planetary transmission spectrum, an accurate modelling of the Rossiter-McLaughlin effect (RM) and centre-to-limb variations (CLV) is necessary to recover possible atmospheric signals. In the case of MASCARA-1b, this is difficult due to the overlap between the radial velocities of the stellar surface regions occulted by MASCARA-1b and the orbital track along which the planet atmospheric signal is expected to be found. To try to disentangle a possible planetary signal, we compare our results with models of the RM and CLV effects, and estimate the uncertainties of our models depending on the different system parameters. Unfortunately, more precise measurements of the spin-orbit angle are necessary to better constrain the planet-occulted track and correct for the transit effects in the transmission spectrum with enough precision to be able to detect or discard possible planetary absorptions. Finally, we discuss the possibility that non-detections are related to the low absorption expected for a high surface gravity planet such as MASCARA-1b. Other techniques such as emission spectroscopy may be more useful for exploring their atmospheric composition. Based on guaranteed time observations (GTOs) collected at the European Southern Observatory (ESO) under ESO programme 1102.C-0744 by the ESPRESSO Consortium

    Abstracts of presentations on plant protection issues at the fifth international Mango Symposium Abstracts of presentations on plant protection issues at the Xth international congress of Virology: September 1-6, 1996 Dan Panorama Hotel, Tel Aviv, Israel August 11-16, 1996 Binyanei haoma, Jerusalem, Israel

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    A Large-Scale Genetic Analysis Reveals a Strong Contribution of the HLA Class II Region to Giant Cell Arteritis Susceptibility

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    We conducted a large-scale genetic analysis on giant cell arteritis (GCA), a polygenic immune-mediated vasculitis. A case-control cohort, comprising 1,651 case subjects with GCA and 15,306 unrelated control subjects from six different countries of European ancestry, was genotyped by the Immunochip array. We also imputed HLA data with a previously validated imputation method to perform a more comprehensive analysis of this genomic region. The strongest association signals were observed in the HLA region, with rs477515 representing the highest peak (p = 4.05 × 10−40, OR = 1.73). A multivariate model including class II amino acids of HLA-DRβ1 and HLA-DQα1 and one class I amino acid of HLA-B explained most of the HLA association with GCA, consistent with previously reported associations of classical HLA alleles like HLA-DRB1∗04. An omnibus test on polymorphic amino acid positions highlighted DRβ1 13 (p = 4.08 × 10−43) and HLA-DQα1 47 (p = 4.02 × 10−46), 56, and 76 (both p = 1.84 × 10−45) as relevant positions for disease susceptibility. Outside the HLA region, the most significant loci included PTPN22 (rs2476601, p = 1.73 × 10−6, OR = 1.38), LRRC32 (rs10160518, p = 4.39 × 10−6, OR = 1.20), and REL (rs115674477, p = 1.10 × 10−5, OR = 1.63). Our study provides evidence of a strong contribution of HLA class I and II molecules to susceptibility to GCA. In the non-HLA region, we confirmed a key role for the functional PTPN22 rs2476601 variant and proposed other putative risk loci for GCA involved in Th1, Th17, and Treg cell function
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