学生による企画展の報告「写真で見る前身校PartⅡ～キンダイ医学の源流を辿る～」

In this article, we look back on the studentʼs exhibition “Kanazawa Universityʼs Former Schools seen in the photos, Part II : Tracing the origins of modern medicine,” at Kanazawa University (9/11/2020-20/01/2021) and it will be evaluated by the students who actuary participated in this exhibition program. Kawai and Matsunaga introduce this article, presenting the background of the special exhibition by the students at Kanazawa University as a part of the class “Museum Training” and the overview of the class schedule. Furuta discusses Chapter 2, 4, 5, 6, while Ooki discusses Chapter 3. In Chapter 2, Furuta explains the idea of this exhibition, and provides selection and research of the materials in Chapter 3, focuses on the display of the exhibition in Chapter 4, describes on the exhibition devices in Chapter 5, discuses related events in Chapter 6. Finally, Matsunaga, who is another instructor of the class and a curator of Kanazawa University Museum, considers this significance of the special exhibition conducted by the students in the University Museum

Autophagy requires endoplasmic reticulum targeting of the PI3-kinase complex via Atg14L

Generation of PI3P in the normally PI3P-deficient ER membrane makes the organelle a platform for autophagosome formation

Cysteinyl-tRNA synthetase governs cysteine polysulfidation and mitochondrial bioenergetics

Cysteine hydropersulfide (CysSSH) occurs in abundant quantities in various organisms, yet little is known about its biosynthesis and physiological functions. Extensive persulfide formation is apparent in cysteine-containing proteins in Escherichia coli and mammalian cells and is believed to result from post-translational processes involving hydrogen sulfide-related chemistry. Here we demonstrate effective CysSSH synthesis from the substrate l-cysteine, a reaction catalyzed by prokaryotic and mammalian cysteinyl-tRNA synthetases (CARSs). Targeted disruption of the genes encoding mitochondrial CARSs in mice and human cells shows that CARSs have a crucial role in endogenous CysSSH production and suggests that these enzymes serve as the principal cysteine persulfide synthases in vivo. CARSs also catalyze co-translational cysteine polysulfidation and are involved in the regulation of mitochondrial biogenesis and bioenergetics. Investigating CARS-dependent persulfide production may thus clarify aberrant redox signaling in physiological and pathophysiological conditions, and suggest therapeutic targets based on oxidative stress and mitochondrial dysfunction

Differences between acoustic trauma and other types of acute noise-induced hearing loss in terms of treatment and hearing prognosis

Objectives: To evaluate the differences between acoustic trauma (AT) and other types of acute noise-induced hearing loss (ANIHL), we performed a literature search and case reviews.Methods: The literature search based on online databases was completed in September 2016. Articles on ANIHL and steroid treatment for human subjects were reviewed. The source sounds and treatment sequelae of our accumulated cases were also reviewed. Hearing loss caused by gun-shots and explosions was categorized into the AT group, while hearing loss caused by concerts and other noises was categorized into the ANIHL group.Results: Systemic steroid treatment did not appear to be effective, at least in the AT group, based on both the literature and our case reviews. However, effective recovery after treatment including steroids was observed in the ANIHL group. The difference in hearing recovery between the AT and ANIHL groups was statistically significant (p = .030), although differences in age, days from the onset to treatment and pretreatment hearing levels were not significant.Conclusions: Hearing recovery from AT is very poor, whereas, ANIHL is recoverable to some extent. Therefore, it is essential to differentiate between these two groups for accurate prediction of the hearing prognosis and evaluation of treatment effects

Sulfide Catabolism Ameliorates Hypoxic Brain Injury

The mammalian brain is highly vulnerable to oxygen deprivation, yet the mechanism underlying the brain’s sensitivity to hypoxia is incompletely understood. Hypoxia induces accumulation of hydrogen sulfide, a gas that inhibits mitochondrial respiration. Here, we show that, in mice, rats, and naturally hypoxia-tolerant ground squirrels, the sensitivity of the brain to hypoxia is inversely related to the levels of sulfide:quinone oxidoreductase (SQOR) and the capacity to catabolize sulfide. Silencing SQOR increased the sensitivity of the brain to hypoxia, whereas neuron-specific SQOR expression prevented hypoxia-induced sulfide accumulation, bioenergetic failure, and ischemic brain injury. Excluding SQOR from mitochondria increased sensitivity to hypoxia not only in the brain but also in heart and liver. Pharmacological scavenging of sulfide maintained mitochondrial respiration in hypoxic neurons and made mice resistant to hypoxia. These results illuminate the critical role of sulfide catabolism in energy homeostasis during hypoxia and identify a therapeutic target for ischemic brain injury

G タンパクシツ アドレナリン ジュヨウタイ レニン - アンジオテンシンケイ ニ オケル イデンシ タケイ ト ジリツ シンケイ キノウ ト ノ カンレン カイセキ

京都大学0048新制・課程博士博士(人間・環境学)甲第13148号人博第355号新制||人||88(附属図書館)18||D||156(吉田南総合図書館)UT51-2007-H421京都大学大学院人間・環境学研究科共生人間学(主査)教授 津田 謹輔, 教授 森谷 敏夫, 助教授 林 達也学位規則第4条第1項該当Doctor of Human and Environmental StudiesKyoto UniversityDA