535 research outputs found

    Mycobiota community and fungal species response to development stage and fire blight disease in apples

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    Fire blight disease, caused by the bacterial pathogen Erwinia amylovora, has been a significant concern for over 50 countries worldwide. The efficacy of chemical pesticides currently available for disease control is limited. To address this issue, research is being conducted to explore environmentally friendly control methods, particularly biological control using beneficial microorganisms. However, there is limited research on the apple microbiota community and minimal research has been conducted on fungal communities that may exhibit reliable performance in apple trees. Therefore, our objective was to analyze the fungal communities present in apples at different developmental stages and in different tissues, aiming to identify potential biological control agents for fire blight disease. Our findings indicate that the fungal communities present in apple buds, flowers and leaves play an important role in inhibiting the invasion of E. amylovora. Specifically, we propose GS11 and Lipomyces starkeyi as potential keystone taxa that respond to fire blight disease. These findings provide insights into the continuity and discontinuity of fungal community structure in different developmental stages of apples and offer predictions for potential biological control agents for fire blight disease

    Effectiveness of regdanvimab on mortality in COVID-19 infected patients on hemodialysis

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    Background Although several therapeutic agents have been evaluated for the treatment of coronavirus disease 2019 (COVID-19), there are lack of effective and proven treatments for end-stage renal disease (ESRD). The present study aims to evaluate the effectiveness of regdanvimab on mortality in COVID-19–infected patients on hemodialysis (HD). Methods We conducted an observational retrospective study in 230 COVID-19–infected patients on HD, of whom 77 (33.5%) were administered regdanvimab alone or in combination with dexamethasone or remdesivir during hospitalization (regdanvimab group) and 153 patients (66.5%) were not (no regdanvimab group). The primary outcome was in-hospital mortality. We compared mortality rates according to the use of regdanvimab and investigated the factors associated with mortality. Results Fifty-nine deaths occurred during hospitalization, 49 in the no regdanvimab group (32.0%) and 10 in the regdanvimab group (13.0%), and the mortality rate was significantly higher in the no regdanvimab group than that in the regdanvimab group (p = 0.001). Multivariate Cox regression analysis showed that malignancy (p = 0.001), SPO2 of <95% at admission (p = 0.003), and administration of antibiotics and regdanvimab (p = 0.007 and p = 0.002, respectively) were significantly associated factors with mortality. Conclusion Regdanvimab administration is beneficial in improving prognosis in hospitalized COVID-19 patients on HD. Considering the vulnerability to infection and high mortality of ESRD patients, regdanvimab may be considered as a therapeutic option in COVID-19 patients on HD

    Soluble Epoxide Hydrolase Activity Determines the Severity of Ischemia-Reperfusion Injury in Kidney

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    Soluble epoxide hydrolase (sEH) in endothelial cells determines the plasma concentrations of epoxyeicosatrienoic acids (EETs), which may act as vasoactive agents to control vascular tone. We hypothesized that the regulation of sEH activity may have a therapeutic value in preventing acute kidney injury by controlling the concentration of EETs. In this study, we therefore induced ischemia-reperfusion injury (IRI) in C57BL/6 mice and controlled sEH activity by intraperitoneal administration of the sEH inhibitor 12-(3-adamantan-1-ylureido)-dodecanoic acid (AUDA). The deterioration of kidney function induced by IRI was partially moderated and prevented by AUDA treatment. In addition, AUDA treatment significantly attenuated tubular necrosis induced by IRI. Ischemic injury induced the down-regulation of sEH, and AUDA administration had no effect on the expression pattern of sEH induced by IRI. In vivo sEH activity was assessed by measuring the substrate epoxyoctadecenoic acid (EpOME) and its metabolite dihydroxyoctadec-12-enoic acid (DHOME). Ischemic injury had no effects on the plasma concentrations of EpOME and DHOME, but inhibition of sEH by AUDA significantly increased plasma EpOME and the EpOME/DHOME ratio. The protective effect of the sEH inhibitor was achieved by suppression of proinflammatory cytokines and up-regulation of regulatory cytokines. AUDA treatment prevented the intrarenal infiltration of inflammatory cells, but promoted endothelial cell migration and neovascularization. The results of this study suggest that treatment with sEH inhibitors can reduce acute kidney injury

    Dielectric functions and electronic band structure of lead zirconate titanate thin films

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    We measure pseudodielectric functions in the visible-deep ultraviolet spectral range of Pb(ZrxTi1−x)O3 (x=0.2,0.56,0.82) (PZT), Pb0.98Nb0.04 (Zr0.2Ti0.8)0.96O3, Pb0.91La0.09 (Zr0.65Ti0.35)0.98O3, and Pb0.85La0.15Ti0.96O3 films grown on platinized silicon substrates using a sol-gel method and on (0001) sapphire using a radio-frequency sputtering method. Using a parametric optical constant model, we estimate the dielectric functions(ϵ) of the perovskite oxide thin films. Taking the second derivative of the fitted layer dielectric functions and using the standard critical-point model, we determine the parameters of the critical points. In the second derivative spectra, the lowest band-gapenergy peak near 4 eVis fitted as a double peak for annealed PZTs due to the perovskite phase. As-grown PZTs have mainly pyrochlore phase and the lowest band-gap peak is fitted as a single peak. We also examine the effect of dopants La and Nb, which substitute at Pb and Zr (Ti) sites, respectively. We found three band gaps Ea(∼3.9eV), Eb (∼4.5eV), and Ec (∼6.5eV) in the order of increasing energy. The Ea and Eb band-gap energies were not sensitive to Zr composition. We discuss the change of critical-point parameters for PZTs in comparison to the band-structure calculations based on local-density approximation. The near constancy of the lowest band-gap energy independent of Zr composition is consistent with the band-structure calculations

    Novel biomarker-based model for the prediction of sorafenib response and overall survival in advanced hepatocellular carcinoma: a prospective cohort study

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    Background Prediction of the outcome of sorafenib therapy using biomarkers is an unmet clinical need in patients with advanced hepatocellular carcinoma (HCC). The aim was to develop and validate a biomarker-based model for predicting sorafenib response and overall survival (OS). Methods This prospective cohort study included 124 consecutive HCC patients (44 with disease control, 80 with progression) with Child-Pugh class A liver function, who received sorafenib. Potential serum biomarkers (namely, hepatocyte growth factor [HGF], fibroblast growth factor [FGF], vascular endothelial growth factor receptor-1, CD117, and angiopoietin-2) were tested. After identifying independent predictors of tumor response, a risk scoring system for predicting OS was developed and 3-fold internal validation was conducted. Results A risk scoring system was developed with six covariates: etiology, platelet count, Barcelona Clinic Liver Cancer stage, protein induced by vitamin K absence-II, HGF, and FGF. When patients were stratified into low-risk (score ≤ 5), intermediate-risk (score 6), and high-risk (score ≥ 7) groups, the model provided good discriminant functions on tumor response (concordance [c]-index, 0.884) and 12-month survival (area under the curve [AUC], 0.825). The median OS was 19.0, 11.2, and 6.1 months in the low-, intermediate-, and high-risk group, respectively (P  0.05 between expected and observed values). Conclusions This new model including serum FGF and HGF showed good performance in predicting the response to sorafenib and survival in patients with advanced HCC.This work was funded by Doosan Yonkang Foundation (Grant No. 30–2016-0240), Liver Research Foundation of Korea as part of Bio Future Strategies Research Project, and Ewha Womans University research grant (2016). The funding bodies had no role in the design of the study, collection, analysis, and interpretation of data and in writing of the manuscript

    A Case of Hemolytic Uremic Syndrome Caused by Escherichia coli O104:H4

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    A 29-year-old woman presented with bloody diarrhea, abdominal pain, hemolytic anemia, thrombocytopenia, and acute renal failure. She was diagnosed with Escherichia coli O104:H4-associated hemolytic-uremic syndrome (HUS) and treated with plasmapheresis and hemodialysis for 3 weeks. She recovered without sequelae. To the best of our knowledge, this is the first report of Escherichia coli O104:H4-associated HUS in Korea. We recommend that Escherichia coli O104:H4, as well as the more common O157:H7, be considered in the diagnosis of bloody diarrhea-associated HUS

    Patients with systemic lupus erythematosus have abnormally elevated Epstein–Barr virus load in blood

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    Various genetic and environmental factors appear to be involved in systemic lupus erythematosus (SLE). Epstein–Barr virus (EBV) is among the environmental factors that are suspected of predisposing to SLE, based on the characteristics of EBV itself and on sequence homologies between autoantigens and EBV antigens. In addition, higher titers of anti-EBV antibodies and increased EBV seroconversion rates have been observed in SLE patients as compared with healthy control individuals. Serologic responses do not directly reflect EBV status within the body. Clarification of the precise status of EBV infection in SLE patients would help to improve our understanding of the role played by EBV in this disease. In the present study we determined EBV types in SLE patients (n = 66) and normal control individual (n = 63) by direct PCR analysis of mouthwash samples. We also compared EBV load in blood between SLE patients (n = 24) and healthy control individuals (n = 29) using semiquantitative PCR assay. The number of infections and EBV type distribution were similar between adult SLE patients and healthy control individuals (98.5% versus 94%). Interestingly, the EBV burden in peripheral blood mononuclear cells (PBMCs) was over 15-fold greater in SLE patients than in healthy control individuals (mean ± standard deviation: 463 ± 570 EBV genome copies/3 μg PBMC DNA versus 30 ± 29 EBV genome copies/3 μg PBMC DNA; P = 0.001), suggesting that EBV infection is abnormally regulated in SLE. The abnormally increased proportion of EBV-infected B cells in the SLE patients may contribute to enhanced autoantibody production in this disease
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