Deletion of Atf6α impairs astroglial activation and enhances neuronal death following brain ischemia in mice

13301甲第4164号博士（医学）金沢大学博士論文本文Full 以下に掲載：Journal of Neurochemistry 132(3) pp.342-353 2015. Wiley. 共著者：Akifumi Yoshikawa, Tomoya Kamide, Koji Hashida, Hieu Minhta, Yuki Inahata, Mika Takarada-lemata, Tsuyoshi Hattori, Kazutoshi Mori, Ryosuke Takahashi, Tomohiro Matsuyama, Yutaka Hayashi, Yasuko Kitao, Osamu Hor

Applicability of radiocolloids, blue dyes and fluorescent indocyanine green to sentinel node biopsy in melanoma

Patients with primary cutaneous melanoma underwent sentinel node (SN) mapping and biopsy at 25 facilities in Japan by the combination of radiocolloid with gamma probe and dye. Technetium-99m (99mTc)-tin colloid, 99mTc-phytate, 2% patent blue violet (PBV) and 0.4% indigo carmine were used as tracers. In some hospitals, 0.5% fluorescent indocyanine green, which allows visualization of the SN with an infrared camera, was concomitantly used and examined. A total of 673 patients were enrolled, and 562 cases were eligible. The detection rates of SN were 95.5% (147/154) with the combination of tin colloid and PBV, 98.9% (368/372) with the combination of phytate and PBV, and 97.2% (35/36) with the combination of tin colloid or phytate and indigo carmine. SN was not detected in 12 cases by the combination method, and the primary tumor was in the head and neck in six of those 12 cases. In eight of 526 cases (1.5%), SN was detected by PBV but not by radiocolloid. There were 13 cases (2.5%) in which SN was detected by radiocolloid but not by PBV. In 18 of 36 cases (50%), SN was detected by radiocolloid but not by indigo carmine. Concomitantly used fluorescent indocyanine green detected SN in all of 67 cases. Interference with transcutaneous oximetry by PVB was observed in some cases, although it caused no clinical trouble. Allergic reactions were not reported with any of the tracers. 99mTc-tin colloid, 99mTc-phytate, PBV and indocyanine green are useful tracers for SN mapping.ArticleJOURNAL OF DERMATOLOGY. 39(4):336-338 (2012)journal articl

小胞体ストレス応答制御による神経細胞死の阻止

金沢大学附属病院救急部小胞体ストレス応答の主幹転写因子であるATF6αをノックアウト(KO)したマウスで中大脳動脈閉塞(MCAO)を起こすと、野生型マウスと比べて脳血管関門破綻が顕著であり、亜急性期の梗塞巣増大の要因となっていると考えられた。しかし、慢性期の梗塞巣サイズの比較では差がつかなかった。これまでに当教室では多発性硬化症モデルでの検討で、ATF6αKOマウスではミクログリア活性低下により炎症反応を減弱させていることを報告しているが、MCAOモデルでもATF6αKOマウスでは亜急性期のミクログリア活性低下が確認され、慢性期の梗塞巣増大に抑制的に働いていると示唆された。Deletion of ATF6α gene, a master transcriptional factor in the unfolded protein response worsened the disruption of blood brain barrier and increased the infarction volume of mice after middle cerebral artery occlusion(MCAO) in the subacute phase.However, there was no significant difference in the infarction volume between wild-type and ATF6α knockout mice in the chronic phase. We already reported that ATF6α deficiency suppresses microglial activation and inflammation of mice in multiple sclerosis model. Deterioration of microglial activation was also observed in ATF6αKO mice after MCAO, which probably affect the infarct size in chronic phase.研究課題/領域番号:16K19999, 研究期間(年度):2016-04-01 - 2018-03-3

X線によるブラックホール連星系Swift J1753.-0127の短時間ソフト化の研究

東京理科大学201