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A measurement of CP-violating observables is performed using the decays B $^{±}$→ DK $^{±}$and B $^{±}$→ Dπ $^{±}$ , where the D meson is reconstructed in one of the self-conjugate three-body final states$ {K}_{\\mathrm{S}}^0 $ π $^{+}$ π $^{−}$and$ {K}_{\\mathrm{S}}^0 $ K $^{+}$ K $^{−}$(commonly denoted$ {K}_{\\mathrm{S}}^0 $ h $^{+}$ h $^{−}$ ). The decays are analysed in bins of the D-decay phase space, leading to a measurement that is independent of the modelling of the D-decay amplitude. The observables are inter- preted in terms of the CKM angle γ. Using a data sample corresponding to an integrated luminosity of 9 fb $^{−1}$collected in proton-proton collisions at centre-of mass energies of 7, 8, and 13 TeV with the LHCb experiment, γ is measured to be$ \\left({68.7}_{-5.1}^{+5.2}\\right){}^{\\circ} $ . The hadronic parameters$ {r}_B^{D K},{r}_B^{D\\pi},{\\delta}_B^{D K},\\kern0.5em \\mathrm{and}\\kern0.5em {\\delta}_B^{D\\pi} $ , which are the ratios and strong-phase differences of the suppressed and favoured B $^{±}$decays, are also reported.[graphic not available: see fulltext]

A measurement of Z → τ ⁺ τ ⁻production cross-section is presented using data, corresponding to an integrated luminosity of 2 fb ⁻¹ , from pp collisions at √s̅=8 TeV collected by the LHCb experiment. The τ ⁺ τ ⁻candidates are reconstructed in final states with the first tau lepton decaying leptonically, and the second decaying either leptonically or to one or three charged hadrons. The production cross-section is measured for Z bosons with invariant mass between 60 and 120 GeV/c ² , which decay to tau leptons with transverse momenta greater than 20 GeV/c and pseudorapidities between 2.0 and 4.5. The cross-section is determined to be σ_(pp)_(→ Z→ τ⁺)_(τ⁻)=95.8 ± 2.1 ± 4.6 ± 0.2 ± 1.1 pb, where the first uncertainty is statistical, the second is systematic, the third is due to the LHC beam energy uncertainty, and the fourth to the integrated luminosity uncertainty. This result is compatible with NNLO Standard model predictions. The ratio of the cross-sections for Z → τ ⁺ τ ⁻to Z → μ ⁺ μ ⁻(Z → e ⁺ e ⁻ ), determined to be 1.01 ± 0.05 (1.02 ± 0.06), is consistent with the lepton-universality hypothesis in Z decays.

A test of lepton universality, performed by measuring the ratio of the branching fractions of the B $^{0}$→ K $^{*0}$μ $^{+}$μ $^{−}$and B $^{0}$→ K $^{*0}$e $^{+}$e $^{−}$decays,$ {R}_{K^{*0}} $, is presented. The K $^{*0}$meson is reconstructed in the final state K $^{+}$π $^{−}$ , which is required to have an invariant mass within 100 MeV/c $^{2}$of the known K $^{*}$ (892) $^{0}$mass. The analysis is performed using proton-proton collision data, corresponding to an integrated luminosity of about 3 fb $^{−1}$ , collected by the LHCb experiment at centre-of-mass energies of 7 and 8 TeV. The ratio is measured in two regions of the dilepton invariant mass squared, q $^{2}$ , to be$ {R}_{K^{*0}}=\\left\\{\\begin{array}{l}{0.66_{-}^{+}}_{0.07}^{0.11}\\left(\\mathrm{stat}\\right)\\pm 0.03\\left(\\mathrm{syst}\\right)\\kern1em \\mathrm{f}\\mathrm{o}\\mathrm{r}\\kern1em 0.045<{q}^2<1.1\\kern0.5em {\\mathrm{GeV}}^2/{c}^4,\\hfill \\\ {}{0.69_{-}^{+}}_{0.07}^{0.11}\\left(\\mathrm{stat}\\right)\\pm 0.05\\left(\\mathrm{syst}\\right)\\kern1em \\mathrm{f}\\mathrm{o}\\mathrm{r}\\kern1em 1.1<{q}^2<6.0\\kern0.5em {\\mathrm{GeV}}^2/{c}^4.\\hfill \\end{array}\\right. $

Bose-Einstein correlations of same-sign charged pions, produced in proton-proton 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 decrease.

The resonant structure of the doubly Cabibbo-suppressed decay \\(D^+ \\to K^-K^+K^+\\) is studied for the first time. The measurement is based on a sample of pp-collision data, collected at a centre-of-mass energy of 8 TeV with the LHCb detector and corresponding to an integrated luminosity of 2 fb\\(^-1\\). The amplitude analysis of this decay is performed with the isobar model and a phenomenological model based on an effective chiral Lagrangian. In both models the S-wave component in the \\(K^-K^+\\) system is dominant, with a small contribution of the \\(\\phi(1020)\\) meson and a negligible contribution from tensor resonances. The \\(K^-K^+\\) scattering amplitudes for the considered combinations of spin (0,1) and isospin (0,1) of the two-body system are obtained from the Dalitz plot fit with the phenomenological decay amplitude.

Multiple sclerosis (MS) is a T cell-driven autoimmune disease that attacks the myelin of the central nervous system (CNS) and currently has no cure. MS etiology is linked to both the gut flora and external environmental factors but this connection is not well understood. One immune system regulator responsive to nonpathogenic external stimuli is the aryl hydrocarbon receptor (AHR). The AHR, which binds diverse molecules present in the environment in barrier tissues, is a therapeutic target for MS. However, AHR’s precise function in T lymphocytes, the orchestrators of MS, has not been described. Here, we show that in a mouse model of MS, T cell-specific Ahr knockout leads to recovery driven by a decrease in T cell fitness. At the mechanistic level, we demonstrate that the absence of AHR changes the gut microenvironment composition to generate metabolites that impact T cell viability, such as bile salts and short chain fatty acids. Our study demonstrates a newly emerging role for AHR in mediating the interdependence between T lymphocytes and the microbiota, while simultaneously identifying new potential molecular targets for the treatment of MS and other autoimmune diseases.

Oligodendrocyte progenitor cells (OPCs) account for approximately 5% of the adult brain and have been historically studied for their role in myelination. In the adult brain, OPCs maintain their proliferative capacity and ability to differentiate into oligodendrocytes throughout adulthood, even though relatively few mature oligodendrocytes are produced post-developmental myelination. Recent work has begun to demonstrate that OPCs likely perform multiple functions in both homeostasis and disease and can significantly impact behavioral phenotypes such as food intake and depressive symptoms. However, the exact mechanisms through which OPCs might influence brain function remain unclear. The first step in further exploration of OPC function is to profile the transcriptional repertoire and assess the heterogeneity of adult OPCs. In this work, we demonstrate that adult OPCs are transcriptionally diverse and separate into two distinct populations in the homeostatic brain. These two groups show distinct transcriptional signatures and enrichment of biological processes unique to individual OPC populations. We have validated these OPC populations using multiple methods, including multiplex RNA in situ hybridization and RNA flow cytometry. This study provides an important resource that profiles the transcriptome of adult OPCs and will provide a toolbox for further investigation into novel OPC functions.

The understanding of mechanisms linking psychological stress to disease risk depend on reliable stress biomarkers. Circulating cell-free DNA (cfDNA) has emerged as a potential biomarker of cellular stress, aging, inflammatory processes, and cell death. Recent studies indicated that psychosocial stress and physical exercise might also influence its release. We compared the effects of acute psychosocial and physical exercise stress on cfDNA release by exposing 20 young, healthy men to both an acute psychosocial laboratory stressor and an acute physical exercise stressor. Venous blood and saliva samples were collected before and after stress exposure. Cell-free DNA was extracted from plasma and quantified by qPCR. Furthermore, cfDNA fragment length was analyzed and cfDNA methylation patterns were assayed across time. In addition, release of stress hormones and subjective stress responses were measured. Results showed a twofold increase of cfDNA after TSST and fivefold increase after exhaustive treadmill exercise, with an overabundance of shorter cfDNA fragments after physical exhaustion. Interestingly, cell-free mitochondrial DNA showed similar increase after both stress paradigms. Furthermore, cfDNA methylation signatures—used here as a marker for diverse cellular origin—were significantly different post stress tests. While DNA methylation decreased immediately after psychosocial stress, it increased after physical stress, suggesting different cellular sources of active DNA release. In summary, our results suggest stimulus and cell-specific regulation of cfDNA release. Whereas the functional role of stress-associated cfDNA release remains elusive, it might serve as a valuable biomarker in molecular stress research as a part of the psychophysiological stress response.