検索結果 67 件
| タイトル（別表記） | Adenocarcinoma in the jejunum 20 years after surgery for familial adenomatous polyposis |
|---|---|
| フルテキストURL | 129_111.pdf |
| 著者 | 杉原 雄策| 川野 誠司| 原田 馨太| 高嶋 志保| 竹井 大介| 井口 俊博| 高原 政宏| 平岡 佐規子| 母里 淑子| 岸本 浩行| 永坂 岳司| 岡田 裕之| |
| 抄録 | A 58-year-old Japanese man visited a local clinic for the evaluation of a stomachache. He was diagnosed with intestinal obstruction. His medical history included a proctocolectomy at the age of 38 years, due to familial adenomatous polyposis (FAP). He was referred to our institution, where he underwent a computed tomography examination and endoscopy of the small intestine. The pathological diagnosis was adenocarcinoma. No invasive or metastatic lesions were observed. Therefore, partial resection of the ileum with lymphadenectomy and reconstruction of the ileostomy were performed. Pathological examination revealed that the tumor was type 2, pT3 (SS) , pN1, pPM0, pDM0, pRM0, INFb, ly1, v1, pEX0, PN0. Twenty-nine days after the surgery, the patient was diagnosed with lung metastasis and he underwent lung radiofrequency ablation. We suggest that long-term follow-up is necessary for patients after surgery for FAP, because of the risk of malignant disease developing in other organs. |
| キーワード | 家族性大腸腺腫症 (familial adenomatous polyposis) 小腸癌 (jejunal cancer) 小腸内視鏡検査 (small intestine endoscope) |
| 出版物タイトル | 岡山医学会雑誌 |
| 発行日 | 2017-08-01 |
| 巻 | 129巻 |
| 号 | 2号 |
| 開始ページ | 111 |
| 終了ページ | 114 |
| ISSN | 0030-1558 |
| 関連URL | https://doi.org/10.4044/joma.129.111 |
| 言語 | 日本語 |
| 著作権者 | Copyright (c) 2017 岡山医学会 |
| 論文のバージョン | publisher |
| DOI | 10.4044/joma.129.111 |
| NAID | 130006039373 |
| タイトル（別表記） | Role of COLXV/XVⅢ gene, Multiplexin, as a basement membrane toolkit |
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| フルテキストURL | 127_103.pdf |
| 著者 | 大橋 俊孝| |
| キーワード | 基底膜 ツールキット XV/XVⅢ型コラーゲン プロテオグリカン ミトコンドリア |
| 出版物タイトル | 岡山医学会雑誌 |
| 発行日 | 2015-08-03 |
| 巻 | 127巻 |
| 号 | 2号 |
| 開始ページ | 103 |
| 終了ページ | 109 |
| ISSN | 0030-1558 |
| 関連URL | isVersionOf https://doi.org/10.4044/joma.127.103 |
| 言語 | 日本語 |
| 著作権者 | Copyright (c) 2015 岡山医学会 |
| 論文のバージョン | publisher |
| DOI | 10.4044/joma.127.103 |
| NAID | 130005096251 |
| タイトル（別表記） | Giant rectal gastrointestinal stromal tumor successfully resected by abdominoperineal resection combined with posterior vaginal wall resection |
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| フルテキストURL | 126_217.pdf |
| 著者 | 岩川 和秀| 西江 学| 徳永 尚之| 宮宗 秀明| 岩垣 博巳| |
| 抄録 | We report a case of giant rectal gastrointestinal stromal tumor (GIST) successfully resected by abdominoperineal resection combined with posterior vaginal wall resection. Our patient was a 79-year-old woman had been diagnosed as having von Recklinghausen disease at the age of 30 years. In 2006, a computed tomography (CT) scan revealed a tumor originating from the posterior wall of the rectum. In June 2010, she was admitted to our hospital with the chief complaint of bloody stool. A CT scan revealed a giant tumor that had increased to 9cm in size. Colonoscopy demonstrated a submucosal tumor, which was subsequently diagnosed by biopsy as a GIST. Due to the patient's continuous bleeding and abdominal pain, an emergent abdominoperineal resection was performed at that time. The tumor, which measured 8×9cm, was immunohistochemically positive for c-kit and CD34. Concomitant resection of the posterior wall of the vagina via the perineal approach provided a wide area to expose the tumor for a safe operation. The patient has been well with no sign of recurrence since the operation. This procedure is recommended as a useful approach for giant rectal GISTs or rectal cancer with invasion of the posterior pelvic wall. |
| キーワード | 巨大直腸GIST（giant rectal GIST） 腹会陰式直腸切断術（abdominoperineal resection） |
| 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 | 217 |
| 終了ページ | 221 |
| 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.126.217 |
| NAID | 130004903245 |
| 著者 | 稲田 涼| 永坂 岳司| 竹原 清人| 杉原 正大| 母里 淑子| 楳田 祐三| 久保田 暢人| 森川 達也| 近藤 喜太| 宇野 太| 貞森 裕| 八木 孝仁| 藤原 俊義| |
|---|---|
| 発行日 | 2013-04-01 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 125巻 |
| 号 | 1号 |
| 資料タイプ | 学術雑誌論文 |
| JaLCDOI | 10.18926/AMO/49253 |
|---|---|
| フルテキストURL | 67_1_19.pdf |
| 著者 | Furukawa, Masashi| Soh, Junichi| Yamamoto, Hiromasa| Ichimura, Kouichi| Shien, Kazuhiko| Maki, Yuho| Muraoka, Takayuki| Tanaka, Norimitsu| Ueno, Tsuyoshi| Asano, Hiroaki| Tsukuda, Kazunori| Toyooka, Shinichi| Miyoshi, Shinichiro| |
| 抄録 | Nuclear factor of κ-light polypeptide gene enhancer in B cells inhibitor α (NFKBIA), which is a tumor suppressor gene, was found to be silenced in lung adenocarcinomas. We examined NFKBIA expression, mutations in the EGFR and K-ras genes, and EML4-ALK fusion in 101 resected lung adenocarcinoma samples from never-smokers. NFKBIA expression was evaluated using immunohistochemistry. NFKBIA expression was negative in 16 of the 101 samples (15.8%). EGFR and K-ras mutations and EML4-ALK fusion were detected in 61 (60.5%), 1 (1.0%), and 2 (2.0%) of the 101 samples, respectively, in a completely mutually exclusive manner. Negative NFKBIA expression was observed significantly more frequently among the tumors with none of the three genetic alterations compared to those with such alterations (p＝0.009). In addition, negative NFKBIA expression was significantly more frequent among the EGFR-wild type samples compared to the EGFR-mutant samples (p＝0.013). In conclusion, NFKBIA expression was silenced in adenocarcinomas without EGFR/K-ras mutations or EML4-ALK fusion, suggesting that the silencing of NFKBIA may play an important role in the carcinogenesis of adenocarcinomas independent of EGFR/K-ras mutations or EML4-ALK fusion. |
| キーワード | never-smoker lung cancer adenocarcinoma nuclear factor of κ-light polypeptide gene enhancer in B cells inhibitor α epidermal growth factor receptor |
| Amo Type | Original Article |
| 出版物タイトル | Acta Medica Okayama |
| 発行日 | 2013-02 |
| 巻 | 67巻 |
| 号 | 1号 |
| 出版者 | Okayama University Medical School |
| 開始ページ | 19 |
| 終了ページ | 24 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | 英語 |
| 著作権者 | CopyrightⒸ 2013 by Okayama University Medical School |
| 論文のバージョン | publisher |
| 査読 | 有り |
| PubMed ID | 23439505 |
| Web of Science KeyUT | 000316829900003 |
| 関連URL | http://ousar.lib.okayama-u.ac.jp/metadata/52534 |
| JaLCDOI | 10.18926/AMO/48961 |
|---|---|
| フルテキストURL | 66_5_369.pdf |
| 著者 | Akiyama, Mari| Kobayashi, Katsuhiro| Ohtsuka, Yoko| |
| 抄録 | Dravet syndrome (DS), or severe myoclonic epilepsy in infancy, is one of the most severe types of genetic epilepsy. It is characterized by the initial occurrence of febrile or afebrile seizures that often evolve into status epilepticus in infants with normal development, and by the subsequent appearance of myoclonic and/or atypical absence seizures as well as complex partial seizures. The key feature that characterizes DS is fever sensitivity, although photosensitivity and pattern-sensitivity are also often seen. The prognosis is unfavorable in most cases. Seizures become drug-resistant and persist, with many patients suffering from motor and cognitive impairment. Mutations of SCN1A, which encodes the voltage-gated sodium channel NaV1.1, are the most frequent genetic cause of this syndrome. SCN1A mutations and/or microchromosomal rearrangements involving SCN1A are detected in about 85% of patients. Mutations of PCDH19 have also been reported in female patients with clinical findings compatible with DS. PCDH19 mutations might account for 5% of overall DS cases. Thirty years after its first description, DS is considered as a model of channelopathy. This survey reviews recent developments in the research literature on DS, focusing on the clinical course, as well as its genetic causes. |
| キーワード | Dravet syndrome long-term outcome SCN1A PCDH19 |
| Amo Type | Review |
| 出版物タイトル | Acta Medica Okayama |
| 発行日 | 2012-10 |
| 巻 | 66巻 |
| 号 | 5号 |
| 出版者 | Okayama University Medical School |
| 開始ページ | 369 |
| 終了ページ | 376 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | 英語 |
| 著作権者 | CopyrightⒸ 2012 by Okayama University Medical School |
| 論文のバージョン | publisher |
| 査読 | 有り |
| PubMed ID | 23093055 |
| Web of Science KeyUT | 000310253900001 |
| JaLCDOI | 10.18926/AMO/48262 |
|---|---|
| フルテキストURL | 66_2_119.pdf.pdf |
| 著者 | Oka, Hiroaki| Ouchida, Mamoru| Kondo, Takuya| Morita, Fumio| Shimizu, Kenji| |
| 抄録 | Human lymphoblastoid TK6 and WTK-1 cells are widely used to detect mutagens in vitro. TK6 cells have wild-type TP53 alleles, while WTK-1 cells have one allele of mutated TP53. Both cells were treated with 5-fluorouracil (5-FU), and gene mutation assay and micronucleus assay were performed to clarify the differential response related to the TP53 gene status. The effects of 5-FU on gene expression were assessed by microarray and quantitative RT-PCR analyses. In WTK-1 cells, 5-FU increased the frequency of cells with micronucleus and mutation. In TK6 cells, frequency of cells with micronucleus was increased but the mutation frequency was not. The cytotoxicity induced by 5-FU was more prominent in TK6 cells than in WTK-1 cells. Analysis of gene expression showed that the genes involved in the TP53 pathway were up-regulated in TK6 cells but not in WTK-1 cells. The differential responses to 5-FU between these cell lines appeared to be due to the difference in the TP53 gene status, thus providing a molecular basis for the bioassays using these cell lines in the toxicology field. Our results indicate that the clinical efficacy of 5-FU chemotherapy may depend on the TP53 genotype. |
| キーワード | 5-fluorouracil TP53 Tk mutation assays microarray analysis |
| Amo Type | Original Article |
| 出版物タイトル | Acta Medica Okayama |
| 発行日 | 2012-04 |
| 巻 | 66巻 |
| 号 | 2号 |
| 出版者 | Okayama University Medical School |
| 開始ページ | 119 |
| 終了ページ | 129 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | 英語 |
| 著作権者 | CopyrightⒸ 2012 by Okayama University Medical School |
| 論文のバージョン | publisher |
| 査読 | 有り |
| PubMed ID | 22525470 |
| Web of Science KeyUT | 000303175300005 |
| 著者 | 田中 弘之| |
|---|---|
| 発行日 | 2012-04-01 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 124巻 |
| 号 | 1号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | 秋山 麻里| 小林 勝弘| 吉永 治美| 大塚 頌子| |
|---|---|
| 発行日 | 2011-08-01 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 123巻 |
| 号 | 2号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | Muraguchi, Hajime| Kamada, Takashi| |
|---|---|
| 発行日 | 1998-8 |
| 出版物タイトル | Development |
| 巻 | 125巻 |
| 号 | 16号 |
| 資料タイプ | 学術雑誌論文 |
| JaLCDOI | 10.18926/AMO/30951 |
|---|---|
| フルテキストURL | fulltext.pdf |
| 著者 | Ogata, Masana| Wang, Da-Hong| Ogino, Keiki| |
| 抄録 | The molecular defects in the catalase gene, levels of m-RNA and properties of the residual catalase studied by scientists are reviewed in human (Japanese, Swiss and Hungarian) and non-human (mouse and beagle dog) acatalasemia with reference to the bioinformatics. Japanese acatalasemia-I, the G to A transition at the fifth position of intron 4 of the catalase gene, limited the correct splicing of the mRNA and synthesized trace catalase with normal properties. Hungarian acatalasemia type C showed a splicing mutation. In the Japanese acatalasemia II and the type A and B of Hungarian acatalasemia, the deletion or insertion of nucleotides was observed in the coding regions, and the frame shift altered downstream amino acid sequences and formed truncated proteins. In the Hungarian acatalasemia D, the substitution of a nucleotide in the exon was found. In mouse and beagle dog acatalasemia, the substitution of nucleotides in the coding regions was also observed. Studies of residual catalase in Swiss, mouse and beagle dog acatalasemia showed that aberrant catalase protein degrades more quickly than normal catalase in cells. The experimental research in genetic toxicology concerning the effect of oxidative stressors (nitrogen monoxide, nitrogen dioxide and so on) on Japanese acatalasemic blood and acatalasemic mice is described. The clinical features of Japanese and Hungarian acatalasemic subjects are also described. |
| キーワード | acatalasemia catalase novel mutation bioinformatics genetic toxicology |
| Amo Type | Review |
| 出版物タイトル | Acta Medica Okayama |
| 発行日 | 2008-12 |
| 巻 | 62巻 |
| 号 | 6号 |
| 出版者 | Okayama University Medical School |
| 開始ページ | 345 |
| 終了ページ | 361 |
| 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 |
| Web of Science KeyUT | 000262025000001 |
| 著者 | 有海 康雄| 黒木 美沙緒| 團迫 浩方| 阿部 健一| 池田 正徳| 脇田 隆字| 加藤 宣之| |
|---|---|
| 発行日 | 2010-04-01 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 122巻 |
| 号 | 1号 |
| 資料タイプ | 学術雑誌論文 |
| タイトル（別表記） | A CACNB4 mutation showing altered Ca(v)2.1 function in a patient with Dravet syndrome |
|---|---|
| フルテキストURL | 121_149.pdf |
| 著者 | 大守 伊織| 大内田 守| 御牧 信義| 西木 禎一| 富澤 一仁| 松井 秀樹| |
| キーワード | てんかん Dravet 症候群 CACNB4遺伝子 SCN1A 遺伝子 |
| 出版物タイトル | 岡山医学会雑誌 |
| 発行日 | 2009-12-01 |
| 巻 | 121巻 |
| 号 | 3号 |
| 開始ページ | 149 |
| 終了ページ | 156 |
| ISSN | 0030-1558 |
| 言語 | 日本語 |
| 著作権者 | 岡山医学会 |
| 論文のバージョン | publisher |
| DOI | 10.4044/joma.121.149 |
| NAID | 120002308814 |
| 著者 | 辻 一城| |
|---|---|
| 発行日 | 1991 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 103巻 |
| 号 | 4号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | 黒田 昌宏| 平木 祥夫| 川崎 祥二| |
|---|---|
| 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 | 関籐 典子| |
|---|---|
| 発行日 | 1994 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 106巻 |
| 号 | 3-4号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | 二宮 伸介| |
|---|---|
| 発行日 | 1994-02 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 106巻 |
| 号 | 1-2号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | 小倉 薫| 渡辺 泰宏| 平峯 千春| 中川 利孝| 土岐 彰| 徳田 雅明| |
|---|---|
| 発行日 | 2003-01-31 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 114巻 |
| 号 | 3号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | グンデウズ メーメット| |
|---|---|
| 発行日 | 2003-01-31 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 114巻 |
| 号 | 3号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | 武田 昌也| 大塚 文男| 中村 一文| 稲垣 兼一| 鈴木 二郎| 三浦 大志| 藤尾 栄起| 松原 広己| 伊達 洋至| 大江 透| 槇野 博史| |
|---|---|
| 発行日 | 2006-05-01 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 118巻 |
| 号 | 1号 |
| 資料タイプ | 学術雑誌論文 |