83 research outputs found

    Hierarchy of B\"acklund Transformation Groups of the Painlev\'e Systems

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    For each Painlev\'e system P_J except the first one, we have a B\"acklund transformation group which is a lift of an affine Weyl group. In this paper, we show that the B\"acklund transformation groups for J=V,IV,III,II are successively obtained from that for J=VI by the well known degeneration or confluence processes.Comment: 11 pages, to be published in J. Math. Soc. Japa

    Relative stable equivalences of Morita type for the principal blocks of finite groups and relative Brauer indecomposability

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    We discuss representations of finite groups having a common central pp-subgroup ZZ, where pp is a prime number. For the principal pp-blocks, we give a method of constructing a relative ZZ-stable equivalence of Morita type, which is a generalization of a stable equivalence of Morita type, and was introduced by Wang and Zhang in a more general setting. Then we generalize Linckelmann's results on stable equivalences of Morita type to relative ZZ-stable equivalences of Morita type. We also introduce the notion of relative Brauer indecomposability, which is a generalization of the notion of Brauer indecomposability. We give an equivalent condition for Scott modules to be relatively Brauer indecomposable, which is an analogue of that given by Ishioka and the first author.Comment: 18 page

    Staged Starnes Operation Preserving Patent Ductus Arteriosus for Neonates with Ebstein’s Anomaly and Pulmonary Atresia

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    We herein reported 2 successful neonates with Ebstein’s anomaly and small pulmonary arteries undergoing Starnes operation preserving the patent ductus arteriosus. Subsequent Blalock-Taussig shunt was carried out 1 or 2 months after the first surgery. One case had already undergone a successful Fontan operation, and the other had a successful bidirectional Glenn shunt so far. This staged Starnes strategy might be a safe and simple choice for neonates with Ebstein’s anomaly and small pulmonary arteries

    Transient IGF-1R inhibition combined with osimertinib eradicates AXL-low expressing EGFR mutated lung cancer

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    Drug tolerance is the basis for acquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) including osimertinib, through mechanisms that still remain unclear. Here, we show that while AXL-low expressing EGFR mutated lung cancer (EGFRmut-LC) cells are more sensitive to osimertinib than AXL-high expressing EGFRmut-LC cells, a small population emerge osimertinib tolerance. The tolerance is mediated by the increased expression and phosphorylation of insulin-like growth factor-1 receptor (IGF-1R), caused by the induction of its transcription factor FOXA1. IGF-1R maintains association with EGFR and adaptor proteins, including Gab1 and IRS1, in the presence of osimertinib and restores the survival signal. In AXL-low-expressing EGFRmut-LC cell-derived xenograft and patient-derived xenograft models, transient IGF-1R inhibition combined with continuous osimertinib treatment could eradicate tumors and prevent regrowth even after the cessation of osimertinib. These results indicate that optimal inhibition of tolerant signals combined with osimertinib may dramatically improve the outcome of EGFRmut-LC
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