Publications by authors named "S Imaoka"

Left ventricular assist devices (LVADs) are implanted in patients with heart failure to support cardiac circulation. However, no standardized methods have been established for LVAD driveline exit site management for the prevention of infections. Therefore, this study evaluated the efficacy of modified driveline management compared with that of conventional driveline management.

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Substances released outside of the cells during cell necrosis are collectively called danger-associated molecular patterns (DAMPS) or alarmins. A pro-inflammatory cytokine, interleukin-1α (IL-1α) is known as a typical alarmin. IL-1α transmits signals by binding to IL-1 receptor 1 (IL-1R1), type I protein, expressed on the cell membrane of target cells, but detection of IL-1R1 at the protein and mRNA levels is difficult.

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Bleeding complications have emerged as major causes of morbidity and mortality in patients with implantable left ventricular assist devices (LVAD). We hypothesized that the hemodynamics after LVAD implantation may influence the occurrence of bleeding complications after LVAD implantation. We retrospectively evaluated 78 patients who underwent continuous-flow LVAD implantation and hemodynamic ramp test after LVAD implantation between July 2017 and July 2023 at Osaka University.

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Aims: The aim of the present study is to elucidate the mechanism of CYP2E1 induction as a causative factor of Alcoholic Hepatitis (AH) and its relationship with inflammation.

Background: Chronic alcohol consumption induces CYP2E1, which is involved in the development of Alcoholic Hepatitis (AH). However, the mechanisms underlying the induction of CYP2E1 by alcohol remain unclear.

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Soluble epoxide hydrolase (sEH) is a bifunctional enzyme that has epoxide hydrolase activity and phosphatase activity. Our earlier study revealed that lysophosphatidic acids are a substrate of the phosphatase activity of sEH in vitro, but its physiological function remained unknown. Herein, we used the CRISPR/Cas9 system and i-GONAD method to generate mice that are deficient in sEH phosphatase activity.

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