10,826 research outputs found

    Measurement of CP asymmetries in D0→hhD^0 \rightarrow hh decays

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    The latest measurements of the individual time-integrated CP asymmetry in the Cabibbo-suppressed decays D0→hhD^0\rightarrow hh decays are presented. The results are based on pppp collision data, corresponding to an integrated luminosity of 3fb−13 fb^{-1}, collected with the LHCb detector at centre-of-mass energies of 7 and 8 TeV. A combination of the asymmetries using both prompt and secondary charm decays is presented ACP(K−K+)=(0.04±0.12(stat)±0.10(syst))A_{CP}(K^-K^+) = (0.04 \pm 0.12(stat) \pm 0.10(syst))%; ACP(π−π+)=(0.07±0.14(stat)±0.11(syst))A_{CP}(\pi^-\pi^+) = (0.07 \pm 0.14(stat) \pm 0.11(syst)). These are the most precise measurements from a single experiment. The result for ACP(K−K+)A_{CP}(K^-K^+) is the most precise determination of a time-integrated CP asymmetry in the charm sector to date, and neither measurement shows evidence of CP asymmetry.Comment: VIII International Workshop On Charm Physics, 5-9 September, 2016, Bologna, Ital

    Precision measurements of rare kaon decays

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    We report the recent results on rare kaon decays from the NA48/2 experiment. The precise measurement of direct photon emission (DE) in the decay K+- -> pi+- pi0 gamma and its interference (INT), with the INT amplitude being observed for the first time, has been finalized. This study is based on the full NA48/2 data set with about 600k reconstructed K+- -> pi+- pi0 gamma decays which is factor of 30 larger than for previous experiments. Samples of about 7200 reconstructed K+- -> pi+- e+ e-, and more than 3000 K+- -> pi+- mu+ mu- events, with very small background contamination, have been collected. The latter is exceeding the total existing statistics by a factor of five. A precise measurement of the branching fractions and the form factors of the rare decays K+- -> pi+- l+ l- has been performed using different theoretical models. The CP violating asymmetry between K+ and K- in this channel is also measured.Comment: Proceedings to the EPS-HEP09 conference, 4 pages, 2 figure

    Direct CPV in two-body and multi-body charm decays at LHCb

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    The Standard Model predicts CP asymmetries in charm decays of O(10−3)O(10^{-3}) and the observation of significantly larger CP violation could indicate non-Standard Model physics effects. During 2011 and 2012, the LHCb experiment collected a sample corresponding to 3/fb yielding the world's largest sample of decays of charmed hadrons. This allowed the CP violation in charm to be studied with unprecedented precision in many two- body and multibody decay modes. The most recent LHCb searches for direct CP violation are presented in these proceedings.Comment: 6 pages, Contribution to proceedings of the 8th International Workshop on the CKM Unitarity Triangle (CKM 2014), Vienna, Austria, September 8-12, 201

    Transcriptional landscape of neuronal and cancer stem cells

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    Tumor mass is composed by heterogeneous cell population including a subset of “cancer stem cells” (CSC). Oncogenic signals foster CSC by transforming tissue stem cells or by reprogramming progenitor/differentiated cells towards stemness. Thus, CSC share features with cancer and stem cells (e.g. self-renewal, hierarchical developmental program leading to differentiated cells, epithelial/mesenchimal transition) and these latter are maintained by the constitutive activation of stemness-promoting signals. CSC could trigger tumor formation, drive to resistance to conventional therapeutics and underlie patients’ relapse. Indeed, stem cell signatures have been associated with poor prognosis in various. This background makes the identification of CSC molecular features mandatory to highlight the survival inner working and to design novel CSC specific therapeutic strategies. Medulloblastoma (MB) is the most common childhood malignant brain tumor and a leading cause of cancerrelated morbidity and mortality. Current multimodal therapies are effective in about 50% of patients but often cause long-term side effects, i.e. developmental, neurological, neuroendocrine and psychosocial deficits (Northcott PA Nature Rev cancer 2012). For many years, MB treated as a single tumor entity despite the divergent tumor histology, patients’ outcome and drug sensitivity, and also by the diversity of the stem cell of origin. Very recently the scenario of human MB has dramatically changed since its heterogeneous biology has been addressed by high-throughput gene expression analysis (oligonucleotide microarrays) or by the powerful genomic next-generation sequencing. These led to the identification of four tumor subgroups (WNT, SHH, Group 3 and Group 4) uncovering the existence of a highly diverse mutational spectra and gene expression. However a quantitative approach has not yet been applied to the transcriptional landscape of Medulloblastoma stem cells (MbSC) through RNA Next Generation Sequencing (RNA-Seq) technology. This is a relevant issue, since RNA-Seq is able to interrogate the genome wide global transcriptome including new transcripts, alternative spliced isoforms and non-coding RNAs. Lower rhombic lip progenitors of the dorsal brainstem are considered the trigger cells in WNT tumors; in SHH subgroup initiation cells are Prominin1+ CD15+ stem cells from the subventricular zone requiring the commitment to Math1+ granule cell progenitors [GCP] of the external granule cell layer [EGL]; while Math1+ or Math1- EGL-GCP or Prominin1+/lineage-negative stem cells sustain the MYC driven Group 3. MbSC derived from SHH tumors and postnatal normal cerebellar stem cells (NcSC) have been reported to share several features. A key signal for both of them is Hedgehog. Furthermore, both NcSC and MbSC display up-regulation of stemness genes (e.g Sox2, Nestin, Nanog, Prom1). Finally, constitutive activation of the Shh pathway by conditional deletion of Ptch1 inhibitory receptor in NcSC, promote medulloblastoma in vivo, producing a mouse model of the human SHH tumor. Acquisition of stemness features may therefore represent the first step of oncogenic conversion. Cooperation with additional oncogenic signals is however needed to enhance MbSC tumorigenicity. In order to understand the MbSCs transcriptional programs, we analyze by RNA-Seq, MbSC derived from Ptch1+/- tumors (Ptch1+/- MbSC). This choice, of a genetically determined model of MB, has allowed us to work with Ptch1+/- MbSC together with appropriate NcSC counterpart, and to analyze biological replicates doing statistical analysis. We identify a number of transcripts, annotated ones, novel isoforms, and long non-coding RNAs, characterizing MbSC and/or NcSC. Some of these genes control stemness or are cancer related and conserved in human medulloblastomas. Interestingly a subset of them, belonging to cell stress response, are of prognostic relevance being significantly related to clinical outcome. Correlation of genes expression characterizing MbSC with survival information from our human medulloblastomas database further demonstrates the significance of these findings. Our data suggest that the modulation of normal and cancer stem cell functions observed in vitro is effective in dissecting the transcriptional programs underlying the in vivo behavior of human medulloblastomas
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