検索結果 25 件
フルテキストURL | fulltext.pdf |
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著者 | Murata, Hitoshi| Phoo, May Tha Zin| Ochi, Toshiki| Tomonobu, Nahoko| Yamamoto, Ken-ichi| Kinoshita, Rie| Miyazaki, Ikuko| Nishibori, Masahiro| Asanuma, Masato| Sakaguchi, Masakiyo| |
キーワード | JNK PARK2 Parkinson’sdisease Phosphorylation SARM1 |
発行日 | 2023-09-19 |
出版物タイトル | The Journal of Biochemistry |
巻 | 174巻 |
号 | 6号 |
出版者 | Oxford University Press (OUP) |
開始ページ | 533 |
終了ページ | 548 |
ISSN | 0021-924X |
NCID | AA00694073 |
資料タイプ | 学術雑誌論文 |
言語 | 英語 |
OAI-PMH Set | 岡山大学 |
著作権者 | © The Author(s) 2023. |
論文のバージョン | publisher |
PubMed ID | 37725528 |
DOI | 10.1093/jb/mvad068 |
Web of Science KeyUT | 001079972500001 |
関連URL | isVersionOf https://doi.org/10.1093/jb/mvad068 |
フルテキストURL | fulltext20230629-02.pdf |
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著者 | Murata, Hitoshi| Yasui, Yu| Oiso, Kazuma| Ochi, Toshiki| Tomonobu, Nahoko| Yamamoto, Ken-ichi| Kinoshita, Rie| Sakaguchi, Masakiyo| |
キーワード | NMNAT2 SARM1 NAD+ STAT1/3 IFN-γ |
発行日 | 2023-08 |
出版物タイトル | Cellular Signalling |
巻 | 108巻 |
出版者 | Elsevier BV |
開始ページ | 110717 |
ISSN | 0898-6568 |
NCID | AA10671314 |
資料タイプ | 学術雑誌論文 |
言語 | 英語 |
OAI-PMH Set | 岡山大学 |
著作権者 | © 2023 The Authors. |
論文のバージョン | publisher |
PubMed ID | 37187216 |
DOI | 10.1016/j.cellsig.2023.110717 |
Web of Science KeyUT | 001002867700001 |
関連URL | isVersionOf https://doi.org/10.1016/j.cellsig.2023.110717 |
タイトル(別表記) | Modulation of neuronal function and neuroprotection by astrocytes |
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フルテキストURL | 126_203.pdf |
著者 | 浅沼 幹人| |
キーワード | アストロサイト 抗酸化防御機構 パーキンソン病 メタロチオネイン Nrf2 |
出版物タイトル | 岡山医学会雑誌 |
発行日 | 2014-12-01 |
巻 | 126巻 |
号 | 3号 |
開始ページ | 203 |
終了ページ | 208 |
ISSN | 0030-1558 |
言語 | 日本語 |
著作権者 | Copyright (c) 2014 岡山医学会 |
論文のバージョン | publisher |
DOI | 10.4044/joma.126.203 |
NAID | 130004903243 |
タイトル(別表記) | Uwaga nad podaniem o Piaście |
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フルテキストURL | olj_036_3・4_459_493.pdf |
著者 | 荒木 勝| |
出版物タイトル | 岡山大學法學會雜誌 |
発行日 | 1987-03-10 |
巻 | 36巻 |
号 | 3・4号 |
開始ページ | 459 |
終了ページ | 493 |
ISSN | 0386-3050 |
言語 | 日本語 |
論文のバージョン | publisher |
NAID | 40000325499 |
JaLCDOI | 10.18926/AMO/32747 |
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フルテキストURL | fulltext.pdf |
著者 | Kawashima, Takao| Takeuchi, Kisaburo| Nobuto, Hideo| Seito, Takashi| Ogata, Takuro| |
抄録 | With gastric carcinomas the activities of eight dehydrogenases; succmlC, lactic, malic, α glycerophosphate, glutamic, β-hydroxybutyric, glucose-6-phosphate and isocitric dehydrogenase were statistically estimated. Principal findings may be briefly summarized as follows. These enzymatic activities differed considerably even in the same classification of carcinomas and generally ranged from strong to weak in the following order: lactic, malic, glucose-6-phosphate, isocitric, succinic, α-glycerophosphate, glutamic and β-hydroxybutyric dehydrogenase. The activities of adenocarcinomas were stronger than those in simple ones, and these were not related appreciably to cell differentiation in adenocarcinomas except succinic, glutamic, glucose-6-phosphate and isocitric dehydrogenase. As for succinic dehydrogenase and NAD-linked dehydrogenases except for lactic dehydrogenase, the activities were strongest in intestinal metaplasia and early mucosal carcinomas, the next being in benign adenomatous polyps and weakest in the other carcinomas. As for NADP-linked dehydrogenases and lactic dehydronase, the activities were also strongest in intestinal metaplasia and early carcinomas, the second in the other carcinomas and the third in the benign polyps. Generally, these dehydrogenase activities were strongest in free carcinoma cells in blood and lymph vessels and in actively growing part of several carcinomas and weakest in the central area of tumors, especially almost negative in the central necrotic area. |
Amo Type | Article |
出版物タイトル | Acta Medicinae Okayama |
発行日 | 1966-06 |
巻 | 20巻 |
号 | 3号 |
出版者 | Okayama University Medical School |
開始ページ | 123 |
終了ページ | 136 |
NCID | AA00041342 |
資料タイプ | 学術雑誌論文 |
言語 | 英語 |
論文のバージョン | publisher |
査読 | 有り |
PubMed ID | 4225846 |
NAID | 120002311388 |
JaLCDOI | 10.18926/AMO/32738 |
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フルテキストURL | fulltext.pdf |
著者 | Hondo, Tsutomu| Nishiyama, Akira| Ogasawara, Hisayasu| Takeuchi, Yoshiro| |
抄録 | Recently, by histochemical observations the changed activities of the enzymes of heartr,nuscle in experimentally induced ischemia have been reported by several investigatorsl~4. SHNITKA and NACHLAS4 demonstrated that the ligation of coronal artery of dog heart induced an increase in the activities of succinic dehydrogenase and NAD-diaphorase four to six hours after the ligation. However, extracorporeal circulation induced no distinct changes in the activities of succinic dehydrogenase and cytochrome oxidase as has been revealed quite recently by BJORK and associate5 from their histochemical studies of the specimen from left ventricular myocardium by a method of drill biopsy, but only the myocardial edema and fibrosis ocurred. This report deals with the distribution and activities of oxidative enzymes of human myocardium of fortyone cases of congenital heart disease and four cases of mitral stenosis and two controls, the specimen of which were obtained at the surgical operation. The purpose is to confirm the damaging effect of occlusion of blood flow in surgical operation on muscle fiber. |
Amo Type | Brief Note |
出版物タイトル | Acta Medicinae Okayama |
発行日 | 1966-12 |
巻 | 20巻 |
号 | 6号 |
出版者 | Okayama University Medical School |
開始ページ | 277 |
終了ページ | 282 |
NCID | AA00041342 |
資料タイプ | 学術雑誌論文 |
言語 | 英語 |
論文のバージョン | publisher |
査読 | 有り |
PubMed ID | 4227192 |
NAID | 120002311806 |
JaLCDOI | 10.18926/AMO/32609 |
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フルテキストURL | fulltext.pdf |
著者 | Seki, Shuji| |
抄録 | 1. Addition of nicotinamide (l0-2M) into the culture medium brings about an increase of the NAD content and the inhibition of the growth of L cells in culture. This rise of NAD brought about by nicotinamide lasts for 2 to 3 days, and thereafter gradually subsiding, it returns to normal level. 2. When L cells are cultured for several days in the same medium without addition of nicotinamide, there occurs a slow-down of mitosis with lapse of cultivation time but it has been found that this is in no way connected with the intracellular content of NAD. 3. By the addition of isonicotinic acid hydrazide (l0-2M) into the culture medium, there can be recognized a decrease of NAD content in L cell and the inhibition of cell growth. 4. In the case when 3-acetylpyridine (l0-2M) is added, a decrease of intracellular content of NAD in L cells and a marked inhibition of the cell growth can be observed. In the groups cultured in the media, containing 3-AP at the concentration of l0-3M or l0-4M can be seen neither inhibition nor acceleration of the cell growth. The oxygen uptake of the cells cultured in the medium containing 3-AP (l0-2M) hardly differs from that of the control group cultured in the medium not containing 3-AP. 5. On the basis of these results discussion has been made on the relation ship between mitosis and NAD content in the cell. |
Amo Type | Article |
出版物タイトル | Acta Medicinae Okayama |
発行日 | 1963-06 |
巻 | 17巻 |
号 | 3号 |
出版者 | Okayama University Medical School |
開始ページ | 153 |
終了ページ | 173 |
NCID | AA00041342 |
資料タイプ | 学術雑誌論文 |
言語 | 英語 |
論文のバージョン | publisher |
査読 | 有り |
PubMed ID | 14121942 |
NAID | 120002311399 |
JaLCDOI | 10.18926/AMO/32471 |
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フルテキストURL | fulltext.pdf |
著者 | Seki, Shuji| Oda, Takuzo| Matsuoka, Iwao| Seno, Satimaru| |
抄録 | For the purpose to reveal the mechanism of uptake and degradation of NAD by cells, the authors conducted the observation on the L cells cultured in the medium containing NAD and the following results have been obtained. 1. NAD in the medium is taken up by the cells in its intact form, reaching about twice the value of the control. 2. The spontaneously degraded products of NAD, nicotinamide and adenine dinucleotide ribose, in the same molar concentration as NAD used in the present experiment, have no effect on the NAD content of L cells. 3. The NAD taken up by the cells is degraded into nicotinamide mononucleotide (NMN) and adenine mononucleotide (AMP) by pyrophosphatase including NADpptase and excreted in the medium. Unexpectedly the ingested NAD is not degraded by NADase in the L cell. 4. L cells metabolize the same amount of NAD as that contained originally in the cell for about ten minutes, as calculated from the amount of NMN excreted in the medium. |
Amo Type | Article |
出版物タイトル | Acta Medicinae Okayama |
発行日 | 1964-10 |
巻 | 18巻 |
号 | 5号 |
出版者 | Okayama University Medical School |
開始ページ | 281 |
終了ページ | 295 |
NCID | AA00041342 |
資料タイプ | 学術雑誌論文 |
言語 | 英語 |
論文のバージョン | publisher |
査読 | 有り |
PubMed ID | 14311539 |
NAID | 120002311852 |
JaLCDOI | 10.18926/AMO/30900 |
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フルテキストURL | fulltext.pdf |
著者 | Jinno, Kenji| |
抄録 | The effect of murine sarcoma virus of Moloney strain on central nervous system was examined morphologically in Swiss mice of different age. A single intracranial inoculation of cell-free virus solution resulted in the induction of characteristic intracerebral granulomas in 82.8% of the newborn to 5 day-old group, in 71.4% of the 6 to 10 day-old group, and in 68.0% of the 11 to 20 day-old group. The mean latency periods to tumor recognition were 16.5, 21.1, and 33.5 days, respectively. The granuloma consisted of inflammatory cell infilrations, reactive gliosis, and richly developed blood vessels. The lesions consistently contained numerous characteristic large round cells. In cases of long-survival, the findings included reparative changes, such as extensive gliosis, withdrawal of inflammation, and a decrease in the numbers of large round cells and blood vessels. These lesions were tentatively designated as "large round cell granuloma." The early foci of the granoloma were composed of proliferating glial cells and large round cells at the subependymal regions. Electron microscopically these large round cells had abundant intracytoplasmic fibrils quite similar to gliofibrils. Numerous C-type virus particles were present in the intercellular nad perivascular spaces, and occasionally budded from cell membranes of the large round cells and vascular endothelia. The large round cells were considered to be reactive astrocytes activated by biral infection. It was conclided that MSV-M was not a sarcomogenic but a granulomogenic virus in mice. Control animals showed no pathological changes. |
Amo Type | Article |
出版物タイトル | Acta Medica Okayama |
発行日 | 1975-08 |
巻 | 29巻 |
号 | 4号 |
出版者 | Okayama University Medical School |
開始ページ | 219 |
終了ページ | 317 |
ISSN | 0386-300X |
NCID | AA00508441 |
資料タイプ | 学術雑誌論文 |
言語 | 英語 |
論文のバージョン | publisher |
査読 | 有り |
PubMed ID | 128993 |
NAID | 120002305141 |
著者 | 清藤 敬| |
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発行日 | 1965-06-30 |
出版物タイトル | 岡山医学会雑誌 |
巻 | 77巻 |
号 | 5-6号 |
資料タイプ | 学術雑誌論文 |
著者 | 菊井 茂| |
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発行日 | 1968-08-30 |
出版物タイトル | 岡山医学会雑誌 |
巻 | 80巻 |
号 | 7-8号 |
資料タイプ | 学術雑誌論文 |
著者 | 吉田 宏| |
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発行日 | 1969-06-30 |
出版物タイトル | 岡山医学会雑誌 |
巻 | 81巻 |
号 | 5-6号 |
資料タイプ | 学術雑誌論文 |
著者 | 前島 邦子| 斉藤 大治| 藤田 興| 久松 三生| 原岡 昭一| |
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発行日 | 1975-06-30 |
出版物タイトル | 岡山医学会雑誌 |
巻 | 87巻 |
号 | 5-6号 |
資料タイプ | 学術雑誌論文 |
著者 | 秋山 実男| |
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発行日 | 1979-12-30 |
出版物タイトル | 岡山医学会雑誌 |
巻 | 91巻 |
号 | 11-12号 |
資料タイプ | 学術雑誌論文 |
著者 | 西原 孝雄| |
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発行日 | 1979-06-30 |
出版物タイトル | 岡山医学会雑誌 |
巻 | 91巻 |
号 | 5-6号 |
資料タイプ | 学術雑誌論文 |
著者 | 竹本 茂| |
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発行日 | 1966-09-30 |
出版物タイトル | 岡山医学会雑誌 |
巻 | 78巻 |
号 | 7-9号 |
資料タイプ | 学術雑誌論文 |
著者 | 藤澤 邦康| |
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発行日 | 1990-02 |
出版物タイトル | 岡山医学会雑誌 |
巻 | 102巻 |
号 | 1-2号 |
資料タイプ | 学術雑誌論文 |
著者 | 臼井 正明| |
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発行日 | 1992 |
出版物タイトル | 岡山医学会雑誌 |
巻 | 104巻 |
号 | 3-4号 |
資料タイプ | 学術雑誌論文 |
著者 | 高橋 寿保| |
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発行日 | 1991-08 |
出版物タイトル | 岡山医学会雑誌 |
巻 | 103巻 |
号 | 7-8号 |
資料タイプ | 学術雑誌論文 |
著者 | 中村 一文| 草野 研吾| 垣下 幹夫| 三浦 綾| 久松 研一| 西井 伸洋| 伴場 主一| 渡邊 敦之| 藤尾 栄起| 宮地 克維| 永瀬 聡| 森田 宏| 斎藤 博則| 江森 哲郎| 浅沼 幹人| 宮崎 正博| 中村 陽一| 松原 広己| 伏見 和郎| 豊國 伸哉| 大江 透| |
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発行日 | 2004-05-31 |
出版物タイトル | 岡山医学会雑誌 |
巻 | 116巻 |
号 | 1号 |
資料タイプ | 学術雑誌論文 |