A tsunami depositional model in coastal lowland over sand dune: An example from the 17th century tsunami deposit in the eastern Iburi coast, central Hokkaido, northern Japan Abstract A reconstruction of a paleo-tsunami flow recorded on the eastern Iburi coast of Hokkaido, northern Japan, has been undertaken using sedimentological analysis. Here, distance from the coastline positively correlates with average sediment grain sizes (mean and median grain sizes expressed in phi scale) but inversely correlates with the standard deviation of grain-size and thickness of the tsunami deposit layer. Grain-fabric and grain-size data in this area indicate at least three tsunami inundation events, with grain-fabric data for tsunami deposits at survey site indicating that these deposits were formed by inflows with ENE paleo-flow directions. This evidence has enabled a depositional model of a tsunami flowing over coastal sand dunes to be formulated, with the first tsunami flow eroding surficial sediments and ripping up and carrying peat clasts. The majority of the tsunami-related water did not return to the sea; this return flow was prevented by a seaside beach ridge, leading to the formation of wide water bodies along the coast. In addition, repeated tsunami inflows did not cause intensive erosional effects at the bottom of these water bodies, with these bodies eventually disappearing due to underground seepage or evaporation.
We herein report a case of subcutaneous panniculitis-like T-cell lymphoma (SPTCL) resembling adult-onset Still's disease (AOSD). A 40-year-old woman presented with a fever, erythema, and painful subcutaneous nodules on the trunk. Laboratory data and a bone marrow analysis showed hemophagocytic syndrome. Although AOSD was suspected, based on a histopathological evaluation of the erythema, she was diagnosed with SPTCL. She was refractory to combination chemotherapy but achieved durable remission with cyclosporine monotherapy. Genetic testing revealed a homozygous HAVCR2 c.245A>G variant (rs184868814) that had caused NLRP3 inflammasome activation. SPTCL and AOSD share a pathogenesis in terms of NLRP 3 inflammasome activation, so the clinical phenotype of SPTCL reasonably mimics AOSD.
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