326 research outputs found

    Gauged Flavor Group with Left-Right Symmetry

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    We construct an anomaly-free extension of the left-right symmetric model, where the maximal flavor group is gauged and anomaly cancellation is guaranteed by adding new vectorlike fermion states. We address the question of the lowest allowed flavor symmetry scale consistent with data. Because of the mechanism recently pointed out by Grinstein et al. tree-level flavor changing neutral currents turn out to play a very weak constraining role. The same occurs, in our model, for electroweak precision observables. The main constraint turns out to come from WR-mediated flavor changing neutral current box diagrams, primarily K - Kbar mixing. In the case where discrete parity symmetry is present at the TeV scale, this constraint implies lower bounds on the mass of vectorlike fermions and flavor bosons of 5 and 10 TeV respectively. However, these limits are weakened under the condition that only SU(2)_R x U(1)_{B-L} is restored at the TeV scale, but not parity. For example, assuming the SU(2) gauge couplings in the ratio gR/gL approx 0.7 allows the above limits to go down by half for both vectorlike fermions and flavor bosons. Our model provides a framework for accommodating neutrino masses and, in the parity symmetric case, provides a solution to the strong CP problem. The bound on the lepton flavor gauging scale is somewhat stronger, because of Big Bang Nucleosynthesis constraints. We argue, however, that the applicability of these constraints depends on the mechanism at work for the generation of neutrino masses.Comment: 1+23 pages, 1 table, 5 figures. v3: some more textual fixes (main change: discussion of Lepton Flavor Violating observables rephrased). Matches journal versio

    Low Scale Flavor Gauge Symmetries

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    We study the possibility of gauging the Standard Model flavor group. Anomaly cancellation leads to the addition of fermions whose mass is inversely proportional to the known fermion masses. In this case all flavor violating effects turn out to be controlled roughly by the Standard Model Yukawa, suppressing transitions for the light generations. Due to the inverted hierarchy the scale of new gauge flavor bosons could be as low as the electroweak scale without violating any existing bound but accessible at the Tevatron and the LHC. The mechanism of flavor protection potentially provides an alternative to Minimal Flavor Violation, with flavor violating effects suppressed by hierarchy of scales rather than couplings.Comment: 24 pages + appendices; v2) Refs. added and numerical examples improved. Results unchanged; v3) small typos in appendix B correcte

    The Impact of Flavour Changing Neutral Gauge Bosons on B->X_s gamma

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    The branching ratio of the rare decay B->X_s gamma provides potentially strong constraints on models beyond the Standard Model. Considering a general scenario with new heavy neutral gauge bosons, present in particular in Z' and gauge flavour models, we point out two new contributions to the B->X_s gamma decay. The first one originates from one-loop diagrams mediated by gauge bosons and heavy exotic quarks with electric charge -1/3. The second contribution stems from the QCD mixing of neutral current-current operators generated by heavy neutral gauge bosons and the dipole operators responsible for the B->X_s gamma decay. The latter mixing is calculated here for the first time. We discuss general sum rules which have to be satisfied in any model of this type. We emphasise that the neutral gauge bosons in question could also significantly affect other fermion radiative decays as well as non-leptonic two-body B decays, epsilon'/epsilon, anomalous (g-2)_mu and electric dipole moments.Comment: 31 pages, 5 figures; version published on JHEP; added magic QCD numbers for flavour-violating Z gauge boson contribution to B -> X_s gamm

    Characterisation of feline renal cortical fibroblast cultures and their transcriptional response to transforming growth factor beta 1

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    Chronic kidney disease (CKD) is common in geriatric cats, and the most prevalent pathology is chronic tubulointerstitial inflammation and fibrosis. The cell type predominantly responsible for the production of extra-cellular matrix in renal fibrosis is the myofibroblast, and fibroblast to myofibroblast differentiation is probably a crucial event. The cytokine TGF-β1 is reportedly the most important regulator of myofibroblastic differentiation in other species. The aim of this study was to isolate and characterise renal fibroblasts from cadaverous kidney tissue of cats with and without CKD, and to investigate the transcriptional response to TGF-β1

    Research priorities for the COVID-19 pandemic and beyond: A call to action for psychological science

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    The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) that has caused the coronavirus disease 2019 (COVID-19) pandemic represents the greatest international biopsychosocial emergency the world has faced for a century, and psychological science has an integral role to offer in helping societies recover. The aim of this paper is to set out the shorter- and longer-term priorities for research in psychological science that will (a) frame the breadth and scope of potential contributions from across the discipline; (b) enable researchers to focus their resources on gaps in knowledge; and (c) help funders and policymakers make informed decisions about future research priorities in order to best meet the needs of societies as they emerge from the acute phase of the pandemic. The research priorities were informed by an expert panel convened by the British Psychological Society that reflects the breadth of the discipline; a wider advisory panel with international input; and a survey of 539 psychological scientists conducted early in May 2020. The most pressing need is to research the negative biopsychosocial impacts of the COVID-19 pandemic to facilitate immediate and longer-term recovery, not only in relation to mental health, but also in relation to behaviour change and adherence, work, education, children and families, physical health and the brain, and social cohesion and connectedness. We call on psychological scientists to work collaboratively with other scientists and stakeholders, establish consortia, and develop innovative research methods while maintaining high-quality, open, and rigorous research standards

    Research priorities for the COVID-19 pandemic and beyond: A call to action for psychological science

    Get PDF
    The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) that has caused the coronavirus disease 2019 (COVID-19) pandemic represents the greatest international biopsychosocial emergency the world has faced for a century, and psychological science has an integral role to offer in helping societies recover. The aim of this paper is to set out the shorter- and longer-term priorities for research in psychological science that will (a) frame the breadth and scope of potential contributions from across the discipline; (b) enable researchers to focus their resources on gaps in knowledge; and (c) help funders and policymakers make informed decisions about future research priorities in order to best meet the needs of societies as they emerge from the acute phase of the pandemic. The research priorities were informed by an expert panel convened by the British Psychological Society that reflects the breadth of the discipline; a wider advisory panel with international input; and a survey of 539 psychological scientists conducted early in May 2020. The most pressing need is to research the negative biopsychosocial impacts of the COVID-19 pandemic to facilitate immediate and longer-term recovery, not only in relation to mental health, but also in relation to behaviour change and adherence, work, education, children and families, physical health and the brain, and social cohesion and connectedness. We call on psychological scientists to work collaboratively with other scientists and stakeholders, establish consortia, and develop innovative research methods while maintaining high-quality, open, and rigorous research standards

    A Minimum Column Density of 1 g cm^-2 for Massive Star Formation

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    Massive stars are very rare, but their extreme luminosities make them both the only type of young star we can observe in distant galaxies and the dominant energy sources in the universe today. They form rarely because efficient radiative cooling keeps most star-forming gas clouds close to isothermal as they collapse, and this favors fragmentation into stars <~1 Msun. Heating of a cloud by accreting low-mass stars within it can prevent fragmentation and allow formation of massive stars, but what properties a cloud must have to form massive stars, and thus where massive stars form in a galaxy, has not yet been determined. Here we show that only clouds with column densities >~ 1 g cm^-2 can avoid fragmentation and form massive stars. This threshold, and the environmental variation of the stellar initial mass function (IMF) that it implies, naturally explain the characteristic column densities of massive star clusters and the difference between the radial profiles of Halpha and UV emission in galactic disks. The existence of a threshold also implies that there should be detectable variations in the IMF with environment within the Galaxy and in the characteristic column densities of massive star clusters between galaxies, and that star formation rates in some galactic environments may have been systematically underestimated.Comment: Accepted for publication in Nature; Nature manuscript style; main text: 14 pages, 3 figures; supplementary text: 8 pages, 1 figur

    Elucidating the Role of the Complement Control Protein in Monkeypox Pathogenicity

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    Monkeypox virus (MPXV) causes a smallpox-like disease in humans. Clinical and epidemiological studies provide evidence of pathogenicity differences between two geographically distinct monkeypox virus clades: the West African and Congo Basin. Genomic analysis of strains from both clades identified a ∼10 kbp deletion in the less virulent West African isolates sequenced to date. One absent open reading frame encodes the monkeypox virus homologue of the complement control protein (CCP). This modulatory protein prevents the initiation of both the classical and alternative pathways of complement activation. In monkeypox virus, CCP, also known as MOPICE, is a ∼24 kDa secretory protein with sequence homology to this superfamily of proteins. Here we investigate CCP expression and its role in monkeypox virulence and pathogenesis. CCP was incorporated into the West African strain and removed from the Congo Basin strain by homologous recombination. CCP expression phenotypes were confirmed for both wild type and recombinant monkeypox viruses and CCP activity was confirmed using a C4b binding assay. To characterize the disease, prairie dogs were intranasally infected and disease progression was monitored for 30 days. Removal of CCP from the Congo Basin strain reduced monkeypox disease morbidity and mortality, but did not significantly decrease viral load. The inclusion of CCP in the West African strain produced changes in disease manifestation, but had no apparent effect on disease-associated mortality. This study identifies CCP as an important immuno-modulatory protein in monkeypox pathogenesis but not solely responsible for the increased virulence seen within the Congo Basin clade of monkeypox virus

    Relationship Between Sonic Hedgehog Protein, Brain-Derived Neurotrophic Factor and Oxidative Stress in Autism Spectrum Disorders

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    The etiology of autism spectrum disorders (ASD) is not well known but oxidative stress has been suggested to play a pathological role. We report here that the serum levels of Sonic hedgehog (SHH) protein and brain-derived neurotrophic factor (BDNF) might be linked to oxidative stress in ASD. By using the whole blood or polymorphonuclear leukocytes, we demonstrated that autistic children produced a significantly higher level of oxygen free radicals (OFR). In addition, we found significantly higher levels of serum SHH protein in children with mild as well as severe form of autism. We also found that the serum level of BDNF was significantly reduced in autistic children with mild form of the disorder but not with severe form of the disorder. Our findings are the first to report a correlation between SHH, BDNF and OFR in autistic children, suggesting a pathological role of oxidative stress and SHH in autism spectrum disorders
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