644 research outputs found

    Quark masses with Nf=2 twisted mass lattice QCD

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    We present the results of the recent high precision lattice calculation of the average up/down, strange and charm quark masses performed by ETMC with Nf=2 twisted mass Wilson fermions. The analysis includes data at four values of the lattice spacing and pion masses as low as ~270 MeV, allowing for accurate continuum limit and chiral extrapolation. The strange and charm masses are extracted by using several methods, based on different observables: the kaon and the eta_s meson for the strange quark and the D, D_s and eta_c mesons for the charm. The quark mass renormalization is carried out non-perturbatively using the RI-MOM method. The results for the quark masses in the MSbar scheme read: m_ud(2 GeV)= 3.6(2) MeV, m_s(2 GeV)=95(6) MeV and m_c(m_c)=1.28(4) GeV. We have also obtained the ratios m_s/m_ud=27.3(9) and m_c/m_s=12.0(3). Moreover, we provide the updated result for the bottom quark mass, m_b(m_b)=4.3(2) GeV, obtained using the method presented in 0909.3187 [hep-lat].Comment: 7 pages, 7 figures, talk given at the XXVIII International Symposium on Lattice Field Theory (Lattice 2010), June 14-19 2010, Villasimius, Ital

    f_B and f_Bs with maximally twisted Wilson fermions

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    We present a lattice QCD calculation of the heavy-light decay constants f_B and f_Bs performed with Nf=2 maximally twisted Wilson fermions, at four values of the lattice spacing. The decay constants have been also computed in the static limit and the results are used to interpolate the observables between the charm and the infinite-mass sectors, thus obtaining the value of the decay constants at the physical b quark mass. Our preliminary results are f_B=191(14) MeV, f_Bs=243(14) MeV, f_Bs/f_B=1.27(5). They are in good agreement with those obtained with a novel approach, recently proposed by our Collaboration (ETMC), based on the use of suitable ratios having an exactly known static limit.Comment: Proceedings of the 27th International Symposium on Lattice Field Theory (Lattice 2009), Beijing, China, 2009 July 26-31. 8 pages, 3 figure

    Prone positioning and convalescent plasma therapy in a critically ill pregnant woman with COVID-19

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    Prone positioning is feasible in pregnancy and may have contributed to the positive outcome in this case. Doctors should not be reluctant to move a patient to a prone position just because they are pregnant

    A degrading bouc-wen data-driven model for the cyclic behavior of masonry infilled RC frames

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    Mechanics-based macro-models are often used to simulate the cyclic response of infilled reinforced concrete (RC) frames. However, these approaches are affected by uncertainties regarding damage and failure mechanisms. Therefore, this contribution proposes a new smooth data-driven model for the hysteresis of infilled RC frames. The infill panel is modeled through a damage-based Bouc-Wen element, which accounts for both pinching and deterioration of the mechanical characteristics. The parameters of the model are calibrated from an experimental data set of cyclic responses of RC infilled frames. Analytical correlations between parameters and geometric and mechanical characteristics of the infilled frame are derived. Blind validation tests are carried out in order to demonstrate the effectiveness of the proposed model

    Blastic plasmacytoid dendritic cell neoplasm: Genomics mark epigenetic dysregulation as a primary therapeutic target

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    Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare and aggressive hematologic malignancy for which there is still no effective B therapy. In order to identify genetic alterations useful for a new treatment design, we used whole-exome sequencing to analyze 14 BPDCN patients and the patient-derived CAL-1 cell line. The functional enrichment analysis of mutational data reported the epigenetic regulatory program to be the most significantly undermined (P<0.0001). In particular, twenty-five epigenetic modifiers were found mutated (e.g. ASXL1, TET2, SUZ12, ARID1A, PHF2, CHD8); ASXL1 was the most frequently affected (28.6% of cases). To evaluate the impact of the identified epigenetic mutations at the gene-expression and Histone H3 lysine 27 trimethylation/acetylation levels, we performed additional RNA and pathology tissue-chromatin immunoprecipitation sequencing experiments. The patients displayed enrichment in gene signatures regulated by methylation and modifiable by decitabine administration, shared common H3K27-acetylated regions, and had a set of cell-cycle genes aberrantly up-regulated and marked by promoter acetylation. Collectively, the integration of sequencing data showed the potential of a therapy based on epigenetic agents. Through the adoption of a preclinical BPDCN mouse model, established by CAL-1 cell line xenografting, we demonstrated the efficacy of the combination of the epigenetic drugs 5’-azacytidine and decitabine in controlling disease progression in vivo

    LIGHT/TNFSF14 regulates estrogen deficiency-induced bone loss

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    Bone loss induced by ovariectomy is due to the direct activity on bone cells and mesenchymal cells and to the dysregulated activity of bone marrow cells, including immune cells and stromal cells, but the underlying mechanisms are not completely known. Here, we demonstrate that ovariectomy induces the T-cell co-stimulatory cytokine LIGHT, which stimulates both osteoblastogenesis and osteoclastogenesis by modulating osteoclastogenic cytokine expression, including TNF, osteoprotegerin, and the receptor activator of nuclear factor-κB ligand (RANKL). Predictably, LIGHT-deficient (Tnfsf14−/−) mice are protected from ovariectomy-dependent bone loss, whereas trabecular bone mass increases in mice deficient in both LIGHT and T and B lymphocytes (Rag−/−Tnfsf14−/−) and is associated with an inversion of the TNF and RANKL/OPG ratio. Furthermore, women with postmenopausal osteoporosis display high levels of LIGHT in circulating T cells and monocytes. Taken together, these results indicate that LIGHT mediates bone loss induced by ovariectomy, suggesting that patients with postmenopausal osteoporosis may benefit from LIGHT antagonism. © 2020 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. © 2020 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd

    Mesenchymal stem cells in renal function recovery after acute kidney injury. Use of a differentiating agent in a rat model.

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    Acute kidney injury (AKI) is a major health care condition with limited current treatment options. Within this context, stem cells may provide a clinical approach for AKI. Moreover, a synthetic compound previously developed, hyaluronan monoesters with butyric acid (HB), able to induce metanephric differentiation, formation of capillary-like structures, and secretion of angiogenic cytokines, was tested in vitro. Thereafter, we investigated the effects of human mesenchymal stem cells from fetal membranes (FMhMSCs), both treated and untreated with HB, after induction of ischemic AKI in a rat model. At reperfusion following 45-min clamping of renal pedicles, each rat was randomly assigned to one of four groups: CTR, PBS, MSC, and MSC-HB. Renal function at 1, 3, 5, and 7 days was assessed. Histological samples were analyzed by light and electron microscopy and renal injury was graded. Cytokine analysis on serum samples was performed. FMhMSCs induced an accelerated renal functional recovery, demonstrated by biochemical parameters and confirmed by histology showing that histopathological alterations associated with ischemic injury were less severe in cell-treated kidneys. HB-treated rats showed a minor degree of inflammation, both at cytokine and TEM analyses. Better functional and morphological recovery were not associated to stem cells' regenerative processes, but possibly suggest paracrine effects on microenvironment that induce retrieval of renal damaged tissues. These results suggest that FMhMSCs could be useful in the treatment of AKI and the utilization of synthetic compounds could enhance the recovery induction ability of cells
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