検索条件

閉じる

検索結果 5711 件

著者 Taguchi, Fumiko| Takeuchi, Kasumi| Katoh, Etsuko| Murata, Katsuyoshi| Suzuki, Tomoko| Marutani, Mizuri| Kawasaki, Takayuki| Eguchi, Minako| Katoh, Shizue| kaku, Hanae| Yasuda, Chihiro| Inagaki, Yoshishige| Toyoda, Kazuhiro| Shiraishi, Tomonori| Ichinose, Yuki|
発行日 2006-6
出版物タイトル Cellular Microbiology
8巻
6号
資料タイプ 学術雑誌論文
著者 Fleischmajer, Raul| Utani, Atsushi| Douglas MacDonald II, E.| Perlish, Jerome S| Pan, Te-Cheng| Chu, Mon-Li| Nomizu, Motoyoshi| Ninomiya, Yoshifumi| Yamada, Yoshihiko|
発行日 1998-7
出版物タイトル Journal of Cell Science
111巻
14号
資料タイプ 学術雑誌論文
著者 Ito, Tatsuo| Ouchida, Mamoru| Morimoto, Yuki| Yoshida, Aki| Jitsumori, Yoshimi| Ozaki, Toshifumi| Sonobe, Hiroshi| Inoue, Hajime| Shimizu, Kenji|
発行日 2005-06-28
出版物タイトル Cancer Letters
224巻
2号
資料タイプ 学術雑誌論文
著者 Kamioka, Hiroshi| Ishihara, Yoshihito| Ris, Hans| Murshid, Sakhr A.| Sugawara, Yasuyo| Yamamoto, Teruko Takano| Lim, Soo-Siang|
発行日 2008-09-21
出版物タイトル Microscopy and Microanalysis
13巻
2号
資料タイプ 学術雑誌論文
著者 Izumi, Yohei| Sonoda, Shoji| Yoshida, Hideya| Danksa, Hugh V| Tsumuki, Hisaaki|
発行日 2006-2
出版物タイトル Journal of Insect Physiology
52巻
2号
資料タイプ 学術雑誌論文
著者 Asaumi, Jun-ichi| Yanagi, Yoshinobu| Konouchi, Hironobu| Hisatomi, Miki| Matsuzaki, Hidenobu| Kishi, Kanji|
発行日 2004-7
出版物タイトル Oral Oncology
40巻
6号
資料タイプ 学術雑誌論文
著者 Maki, Yu| Murakami, Jun| Asaumi, Jun-ichi| Tsujigiwa, Hidetsugu| Nagatsuka, Hitoshi| Kokeguchi, Susumu| Fukui, Kazuhiro| Kawai, Noriko| Yanagi, Yoshinobu| Kuroda, Masahiro| Tanaka, Noriaki| Matsubara, Nagahide| Kishi, Kanji|
発行日 2005-7
出版物タイトル Oral Oncology
41巻
10号
資料タイプ 学術雑誌論文
著者 Murakami, Jun| Asaumi, Jun-ichi| Kawai, Noriko| Tsujigiwa, Hidetsugu| Yanagi, Yoshinobu| Nagatsuka, Hitoshi| Inoue, Tetsuyoshi| Kokeguchi, Susumu| Kawasaki, Shoji| Kuroda, Masahiro| Tanaka, Noriaki| Matsubara, Nagahide| Kishi, Kanji|
発行日 2005-07
出版物タイトル Cancer Chemotherapy and Pharmacology
56巻
1号
資料タイプ 学術雑誌論文
著者 Murakami, Jun| Asaumi, Jun-ichi| Maki, Yuu| Tsujigiwa, Hidetsugu| Kuroda, Masahiro| Nagai, Noriyuki| Yanagi, Yoshinobu| Inoue, Tetsuyoshi| Kawasaki, Shoji| Tanaka, Noriaki| Matsubara, Nagahide| Kishi, Kanji|
発行日 2004-2
出版物タイトル Oral Oncology
40巻
6号
資料タイプ 学術雑誌論文
著者 Demircan, Kadir| Hirohata, Satoshi| Nishida, Keiichiro| Hatipoglu, Omer F.| Oohashi, Toshitaka| Yonezawa, Tomoko| Apte, Suneel S.| Ninomiya, Yoshifumi|
発行日 2005-5
出版物タイトル Arthritis & Rheumatism
52巻
5号
資料タイプ 学術雑誌論文
著者 Kawai, Mariko| Bessho, Kazuhisa| Maruyama, Hiroki| Miyazaki, Jun-ichi| Yamamoto, Toshio|
発行日 2006-08-03
出版物タイトル BMC Musculoskeletal Disorders
7巻
資料タイプ 学術雑誌論文
著者 Fujita, Hirofumi| Shiosaka, Masahiko| Ogino, Tetsuya| Okimura, Yuya| Utsumi, Toshihiko| Sato, Eisuke F.| Akagi, Reiko| Inoue, Masayasu| Utsumi, Kozo| Sasaki, Junzo|
発行日 2008-06-23
出版物タイトル Brain Research
1206巻
資料タイプ 学術雑誌論文
著者 Chian, Ri C.| Chung, Jin T.| Niwa, Koji| Sirard, Marc A.| Downey, Bruce R.| Tan, Seang L.|
発行日 2003-5
出版物タイトル Zygote
11巻
2号
資料タイプ 学術雑誌論文
著者 Kikuchi, Kazuhiro| Ekwall, Hans| Tienthai, Paisan| Kawai, Yasuhiro| Noguchi, Junko| Kaneko, Hiroyuki| Rpdriguez-Martinez, Heriberto|
発行日 2002-07-25
出版物タイトル Zygote
10巻
4号
資料タイプ 学術雑誌論文
著者 Yokoo, Masaki| Tienthai, Paisan| Kimura, Naoko| Niwa, Koji| Sato, Eimei| Rodriguez-Martinez, Heriberto|
発行日 2002-07-25
出版物タイトル Zygote
10巻
4号
資料タイプ 学術雑誌論文
JaLCDOI 10.18926/AMO/32911
フルテキストURL fulltext.pdf
著者 Takemoto, Kei| Ogino, Keiki| Wang, Da-Hong| Takigawa, Tomoko| Kurosawa, Carmen M.| Kambayashi, Yasuhiro| Hibino, Yuri| Hitomi, Yoshiaki| Ichimura, Hiroshi|
抄録

It is well known that eosinophils are involved in tyrosine nitration. In this study, we evaluated tyrosine nitration by rat eosinophils isolated from peritoneal fl uid and constituent eosinophils in the stomach. Rat peritoneal eosinophils activated with 1 μM phorbol myristate acetate (PMA) and 50 μM NO2 ン showed immunostaining for nitrotyrosine only in smaller cells, despite the fact that eosinophils are capable of producing superoxide (O2·ン). Free tyrosine nitrating capacity after incubation with PMA and NO2 ン was 4-fold higher in eosinophils than in neutrophils. Catalase and ク- and コ -tocopherol inhibited free tyrosine nitration by reactive nitrogen species from eosinophils but not that by peroxynitrite. Superoxide dismutase augmented free tyrosine nitration by activated eosinophils and peroxynitrite. The concentration of nitric oxide released from eosinophils was relatively low (0.32 μM/106 cells/h) and did not contribute to the formation of nitrotyrosine. On the other hand, most constituent eosinophils constituent in the rat stomach stimulated by PMA and NO2 ン showed tyrosine nitration capacity. These results suggest that intact cells other than apoptotic-like eosinophils eluted in the intraperitoneal cavity could not generate reactive species responsible for nitration by a peroxidase-dependent mechanism. In contrast, normal eosinophils in the stomach were capable of nitration, suggesting that the characteristics of eosinophils in gastric mucosa are diff erent from those eluted in the peritoneal cavity.

キーワード eosinophil peroxidase reactive nitrogen species nitrotyrosine
Amo Type Article
出版物タイトル Acta Medica Okayama
発行日 2007-02
61巻
1号
出版者 Okayama University Medical School
開始ページ 17
終了ページ 30
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 17332838
Web of Science KeyUT 000244432400003
JaLCDOI 10.18926/AMO/32905
フルテキストURL fulltext.pdf
著者 Wu, Hai-Yan| Tomizawa, Kazuhito| Matsui, Hideki|
抄録 Intracellular calcium is a powerful secondary messenger that affects a number of calcium sensors, including calpain, a Ca2+-dependent cysteine protease, and calcineurin, a Ca2+/calmodulin-dependent protein phosphatase. Maintenance of low basal levels of intracellular calcium allows for the tightly regulated physiological activation of these proteins, which is crucial to a wide variety of cellular processes, such as fertilization, proliferation, development, learning, and memory. Deregulation of calpain and calcineurin has been implicated in the pathogenesis of several disorders, including hypertension, heart disease, diabetes, cerebral ischemia, and Alzheimer's disease. Recent studies have demonstrated an interplay between calpain and calcineurin, in which calpain can directly regulate calcineurin activity through proteolysis in glutamate-stimulated neurons in culture and in vivo. The calpain-mediated proteolytic cleavage of calcineurin increases phosphatase activity, which promotes caspase-mediated neuronal cell death. Thus, the activation of the calpain-calcineurin pathway could contribute to calcium-dependent disorders, especially those associated with Alzheimer's disease and myocardial hypertrophy. Here, we focus briefly on recent advances in revealing the structural and functional properties of these 2 calcium-activated proteins, as well as on the interplay between the 2, in an effort to understand how calpain-calcineurin signaling may relate to the pathogenesis of calcium- dependent disorders.
キーワード calpain calcineurin calcium proteolysis neurodegeneration
Amo Type Review
出版物タイトル Acta Medica Okayama
発行日 2007-06
61巻
3号
出版者 Okayama University Medical School
開始ページ 123
終了ページ 137
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 17593948
Web of Science KeyUT 000247574700001
JaLCDOI 10.18926/AMO/32903
フルテキストURL fulltext.pdf
著者 Wu, Yumei| Tada, Mikiro| Takahata, Kyoya| Tomizawa, Kazuhito| Matsui, Hideki|
抄録 Neuronal apoptosis is involved in neurodegenerative diseases such as Alzheimer's disease and Parkinson.s disease. An efficient means of preventing it remains to be found. Some n-3 polyunsaturated fatty acids (PUFAs) such as docosahexaenoic acid (DHA, 22 : 6n-3) and eicosapentaenoic acid (EPA, 20 : 5n-3) have been reported to be protective against the neuronal apoptosis and neuronal degeneration seen after spinal cord injury (SCI) [1]. However, it is unclear which kinds of PUFAs have the most potent ability to inhibit neuronal apoptosis and whether the simultaneous treatment of PUFAs inhibits the apoptosis. In the present study, we compared the abilities of various n-3- and n-6- PUFAs to inhibit the apoptosis induced after the administration of different apoptotic inducers, etoposide, okadaic acid, and AraC, in mouse neuroblastoma cells (Neuro2a). Preincubation with DHA (22 : 6n-3), eicosapentaenoic acid (EPA, 20 : 5n-3), alpha-linolenic acid (alpha-LNA, 18 : 3n-3), linoleic acid (LA, 18 : 2n-6), arachidonic acid (AA, 20 : 4n-3), and gamma-linolenic acid (gamma-LNA, 18 : 3n-6) significantly inhibited caspase-3 activity and LDH leakage but simultaneous treatment with the PUFAs had no effect on the apoptosis of Neuro2a cells. There were no significant differences of the anti-apoptotic eff ect among the PUFAs. These results suggest that PUFAs may not be effective for inhibiting neuronal cell death after acute and chronic neurodegenerative disorders. However, dietary supplementation with PUFAs may be beneficial as a potential means to delay the onset of the diseases and/or their rate of progression.
キーワード polyunsaturated fatty acid (PUFA) neurodegenerative disease caspase neuronal apoptosis DHA
Amo Type Original Article
出版物タイトル Acta Medica Okayama
発行日 2007-06
61巻
3号
出版者 Okayama University Medical School
開始ページ 147
終了ページ 152
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 17593950
Web of Science KeyUT 000247574700003
JaLCDOI 10.18926/AMO/32893
フルテキストURL fulltext.pdf
著者 Ashizawa, Tatsuto| Hama, Koichiro| Tanaka, Hiroaki| Ando, Masayuki|
抄録 A 64-year-old woman was admitted to our hospital with lower abdominal pain. Routine laboratory values were unremarkable except for the white blood cell count (15,000/micro litter) and the C-reactive protein (CRP) value (22.5 mg/dl). A Computed tomography (CT) scan revealed air collection in the middle of the anterior pararenal space. One day later, CT revealed air collection in the anterior pararenal space spread to the right side and abscess in the sigmoid mesentery. Because an intramesocolic perforation of the sigmoid colon was suspected, an emergency operation was performed. Abscess formation was recognized in the sigmoid mesentery, and sigmoidectomy including the contaminated mesentery and Hartmann.s procedure were performed. The perforation was 3 cm in diameter, and some diverticula were present in the vicinity of the perforated site. The specimen microscopically revealed perforation at the edge of the diverticulum in association with sudden disruption of the proper muscle layer. Based on pathological findings, intramesocolic diverticular perforation of the sigmoid colon was diagnosed. The present case is a very rare condition. However, it was possible to make a diagnosis preoperatively by detecting air collection in the anterior pararenal space on CT scan. If a sigmoid perforation occurs between the leaves of the mesocolon, air extends into the root of the sigmoid mesocolon and within the anterior pararenal space.
キーワード colon diverticulosis intramesocolic perforation computed tomography free air
Amo Type Case Report
出版物タイトル Acta Medica Okayama
発行日 2007-10
61巻
5号
出版者 Okayama University Medical School
開始ページ 299
終了ページ 303
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 17971846
Web of Science KeyUT 000250431700007
JaLCDOI 10.18926/AMO/32892
フルテキストURL fulltext.pdf
著者 Takagi, Koji| Yamada, Teruo| Miki, Yukari| Umegaki, Teruo| Nishimura, Makoto| Sasaki, Junzo|
抄録 To clarify the development of follicular growth and atresia in the immature ovary, rats. ovaries and blood were removed at fixed points during the period from 0 to 35 days after birth (Day 0 to Day 35). The ovaries were immunohistochemically examined, and blood concentrations of serum follicle-stimulating hormone (FSH) and estrogen (E) were measured. We investigated how time-course changes in follicular cell proliferation, estrogen receptor β (ERβ), apoptosis, and FSH and E concentrations are connected with follicular growth and atresia. Apoptosis was found in the ova from Day 0 to Day 3. On Day 15, apoptosis occurred in some granulosa cell nuclei in some follicles, but BrdU uptake and the presence of cyclin D2 and ER β could be observed in other granulosa cells. From Day 17, apoptosis increased in the follicular granulosa cells, and BrdU uptake and the presence of cyclin D2 and ERβ were decreased. Follicular atresia continued, reaching a peak on Day 30. Serum FSH and E concentrations increased until Day 15, then markedly decreased after Day 17. The mechanism of apoptosis in the ova from Day 0 to 3 has not been clarified. However, the onset of follicular atresia was caused by apoptotic degeneration from Days 15 to 17. These results showed that the oocytes were selected by apoptosis at 2 points in the time-course of the maturation of the ovary.
キーワード histology apoptosis proliferation estrogen follicle-stimulating hormone
Amo Type Original Article
出版物タイトル Acta Medica Okayama
発行日 2007-10
61巻
5号
出版者 Okayama University Medical School
開始ページ 283
終了ページ 298
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 17971845
Web of Science KeyUT 000250431700006