Publications by authors named "M Chapellier"

Neutrinoless double beta decay (0νββ) is a yet unobserved nuclear process that would demonstrate Lepton number violation, a clear evidence of beyond standard model physics. The process two neutrino double beta decay (2νββ) is allowed by the standard model and has been measured in numerous experiments. In this Letter, we report a measurement of 2νββ decay half-life of ^{100}Mo to the ground state of ^{100}Ru of [7.

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We report on the development of scintillating bolometers based on lithium molybdate crystals that contain molybdenum that has depleted into the double-β active isotope 100Mo (Li2100deplMoO4). We used two Li2100deplMoO4 cubic samples, each of which consisted of 45-millimeter sides and had a mass of 0.28 kg; these samples were produced following the purification and crystallization protocols developed for double-β search experiments with 100Mo-enriched Li2MoO4 crystals.

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Article Synopsis
  • CCL22 is an immune-suppressing chemokine produced by macrophages, which promotes the recruitment of regulatory T cells and is linked to hindering anti-cancer immune responses.
  • Researchers discovered that T cells from cancer patients can effectively kill tumor cells that express CCL22 and potentially alter CCL22 levels.
  • The study demonstrated that vaccinating with CCL22-derived peptides encourages the immune system in mice to combat tumors, resulting in decreased tumor growth and improved survival, suggesting a promising new direction for cancer immunotherapy.
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Stem cells have the capacity to ensure the renewal of tissues and organs. They could be used in the future for a wide range of therapeutic purposes and are preserved at liquid nitrogen temperature to prevent any chemical or biological activity up to several decades before their use. We show that the cryogenized cells accumulate damages coming from natural radiations, potentially inducing DNA double-strand breaks (DSBs).

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Expression of the L-arginine catabolizing enzyme arginase 1 (ARG1) is a central immunosuppressive mechanism mediated by tumor-educated myeloid cells. Increased activity of ARG1 promotes the formation of an immunosuppressive microenvironment and leads to a more aggressive phenotype in many cancers. Intrinsic T-cell immunity against ARG1-derived epitopes in the peripheral blood of cancer patients and healthy subjects has previously been demonstrated.

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