Detecting abrupt changes in the spectra of high-energy astrophysical sources

Variable-intensity astronomical sources are the result of complex and often extreme physical processes. Abrupt changes in source intensity are typically accompanied by equally sudden spectral shifts, that is, sudden changes in the wavelength distribution of the emission. This article develops a method for modeling photon counts collected from observation of such sources. We embed change points into a marked Poisson process, where photon wavelengths are regarded as marks and both the Poisson intensity parameter and the distribution of the marks are allowed to change. To the best of our knowledge, this is the first effort to embed change points into a marked Poisson process. Between the change points, the spectrum is modeled nonparametrically using a mixture of a smooth radial basis expansion and a number of local deviations from the smooth term representing spectral emission lines. Because the model is over-parameterized, we employ an ℓ1ℓ1 penalty. The tuning parameter in the penalty and the number of change points are determined via the minimum description length principle. Our method is validated via a series of simulation studies and its practical utility is illustrated in the analysis of the ultra-fast rotating yellow giant star known as FK Com

Programme evaluation training for health professionals in francophone Africa: process, competence acquisition and use

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Spatial competition shapes the dynamic mutational landscape of normal esophageal epithelium.

During aging, progenitor cells acquire mutations, which may generate clones that colonize the surrounding tissue. By middle age, normal human tissues, including the esophageal epithelium (EE), become a patchwork of mutant clones. Despite their relevance for understanding aging and cancer, the processes that underpin mutational selection in normal tissues remain poorly understood. Here, we investigated this issue in the esophageal epithelium of mutagen-treated mice. Deep sequencing identified numerous mutant clones with multiple genes under positive selection, including Notch1, Notch2 and Trp53, which are also selected in human esophageal epithelium. Transgenic lineage tracing revealed strong clonal competition that evolved over time. Clone dynamics were consistent with a simple model in which the proliferative advantage conferred by positively selected mutations depends on the nature of the neighboring cells. When clones with similar competitive fitness collide, mutant cell fate reverts towards homeostasis, a constraint that explains how selection operates in normal-appearing epithelium.This work was supported by grants from the Wellcome Trust to the Wellcome SangerInstitute (098051 and 296194) and Cancer Research UK Programme Grants to P.H.J.(C609/A17257 and C609/A27326). G.P. is supported by a Talento program fellowship from Comunidad de Madrid. B.A.H. and M.W.J.H. are supported by the MedicalResearch Council (Grant-in-Aid to the MRC Cancer unit grant no. MC_UU_12022/9 and NIRG to B.A.H. grant no. MR/S000216/1). M.W.J.H. acknowledges support fromthe Harrison Watson Fund at Clare College, Cambridge. B.A.H. acknowledges support from the Royal Society (grant no. UF130039). I.M. is funded by Cancer Research UK (C57387/A21777). S.D. benefited from the award of an ESPOD fellowship, 2018-21, from the Wellcome Sanger Institute and the European Bioinformatics Institute EMBL-EBI