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JaLCDOI 10.18926/AMO/49253
FullText URL 67_1_19.pdf
Author 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|
Abstract 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.
Keywords 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
Publication Title Acta Medica Okayama
Published Date 2013-02
Volume volume67
Issue issue1
Publisher Okayama University Medical School
Start Page 19
End Page 24
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2013 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 23439505
Web of Science KeyUT 000316829900003
Related Url http://ousar.lib.okayama-u.ac.jp/metadata/52534
JaLCDOI 10.18926/AMO/49252
FullText URL 67_1_9.pdf
Author Fatmawati, Ni Nengah Dwi| Sakaguchi, Yoshihiko| Suzuki, Tomonori| Oda, Masataka| Shimizu, Kenta| Yamamoto, Yumiko| Sakurai, Jun| Matsushita, Osamu| Oguma, Keiji|
Abstract Clostridium botulinum type C and D strains recently have been found to produce PLC on egg yolk agar plates. To characterize the gene, enzymatic and biological activities of C. botulinum PLCs (Cb-PLCs), the cb-plc genes from 8 strains were sequenced, and 1 representative gene was cloned and expressed as a recombinant protein. The enzymatic and hemolytic activities of the recombinant Cb-PLC were measured and compared with those of the Clostridium perfringens alpha-toxin. Each of the eight cb-plc genes encoded a 399 amino acid residue protein preceded by a 27 residue signal peptide. The protein consists of 2 domains, the N- and C-domains, and the overall amino acid sequence identity between Cb-PLC and alpha-toxin was greater than 50%, suggesting that Cb-PLC is homologous to the alpha-toxin. The key residues in the N-domain were conserved, whereas those in the C-domain which are important in membrane interaction were different than in the alpha-toxin. As expected, Cb-PLC could hydrolyze egg yolk phospholipid, p-nitrophenylphosphorylcholine, and sphingomyelin, and also exhibited hemolytic activity;however, its activities were about 4- to over 200-fold lower than those of alpha-toxin. Although Cb-PLC showed weak enzymatic and biological activities, it is speculated that Cb-PLC might play a role in the pathogenicity of botulism or for bacterial survival.
Keywords botulinum phospholipase C botulinum toxin phospholipase C activity sphingomyelinase activity hemolytic activity
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2013-02
Volume volume67
Issue issue1
Publisher Okayama University Medical School
Start Page 9
End Page 18
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2013 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 23439504
Web of Science KeyUT 000316829900002
Related Url http://ousar.lib.okayama-u.ac.jp/metadata/49731
JaLCDOI 10.18926/AMO/49251
FullText URL 67_1_1.pdf
Author Nishimori, Hisakazu| Maeda, Yoshinobu| Tanimoto, Mitsune|
Abstract Graft-versus-host disease (GVHD) is a major complication after allogeneic hematopoietic stem cell transplantation. Chronic GVHD often presents with clinical manifestations that resemble those observed in autoimmune diseases. Standard treatment is 1-2mg/kg/day of prednisone or an equivalent dose of methylprednisolone, with continued administration of a calcineurin inhibitor for steroid sparing. However, the prognosis of steroid-refractory chronic GVHD remains poor. Classically, chronic GVHD was said to involve predominantly Th2 responses. We are now faced with a more complex picture, involving possible roles for thymic dysfunction, transforming growth factor-β (TGF-β) and platelet-derived growth factor (PDGF), B cells and autoantibodies, and Th1/Th2/Th17 cytokines, as well as regulatory T cells (Tregs), in chronic GVHD. More detailed research on the pathophysiology of chronic GVHD may facilitate the establishment of novel strategies for its prevention and treatment.
Keywords chronic GVHD Th17 Am80 regulatory T cell (Treg) steroid-refractory
Amo Type Review
Publication Title Acta Medica Okayama
Published Date 2013-02
Volume volume67
Issue issue1
Publisher Okayama University Medical School
Start Page 1
End Page 8
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2013 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 23439503
Web of Science KeyUT 000316829900001
Author 近藤 萬太郞|
Published Date 1926-07-10
Publication Title 農学研究
Volume volume9
Content Type Departmental Bulletin Paper
Author 荒川 左千代|
Published Date 1926-07-10
Publication Title 農学研究
Volume volume9
Content Type Departmental Bulletin Paper
Author 岡村 保|
Published Date 1926-07-10
Publication Title 農学研究
Volume volume9
Content Type Departmental Bulletin Paper
Author 西門 義一|
Published Date 1926-07-10
Publication Title 農学研究
Volume volume9
Content Type Departmental Bulletin Paper
Author 板野 新夫|
Published Date 1926-07-10
Publication Title 農学研究
Volume volume9
Content Type Departmental Bulletin Paper
Author 山口 彌輔|
Published Date 1926-07-10
Publication Title 農学研究
Volume volume9
Content Type Departmental Bulletin Paper
Author 西門 義一| 三宅 忠一|
Published Date 1926-03-01
Publication Title 農学研究
Volume volume8
Content Type Departmental Bulletin Paper
Author 笠井 幹夫|
Published Date 1926-03-01
Publication Title 農学研究
Volume volume8
Content Type Departmental Bulletin Paper
Author 春川 忠吉|
Published Date 1926-03-01
Publication Title 農学研究
Volume volume8
Content Type Departmental Bulletin Paper
Author 笠井 幹夫|
Published Date 1926-03-01
Publication Title 農学研究
Volume volume8
Content Type Departmental Bulletin Paper
Author 近藤 萬太郎|
Published Date 1926-03-01
Publication Title 農学研究
Volume volume8
Content Type Departmental Bulletin Paper
Author 西門 義一|
Published Date 1925-03-05
Publication Title 農学研究
Volume volume7
Content Type Departmental Bulletin Paper
Author 春川 忠吉|
Published Date 1925-03-05
Publication Title 農学研究
Volume volume7
Content Type Departmental Bulletin Paper
Author 笠井 幹夫|
Published Date 1925-03-05
Publication Title 農学研究
Volume volume7
Content Type Departmental Bulletin Paper
Author 近藤 萬太郞|
Published Date 1925-03-05
Publication Title 農学研究
Volume volume7
Content Type Departmental Bulletin Paper
Author 宗定 哲二|
Published Date 1924-07-07
Publication Title 農学研究
Volume volume6
Content Type Departmental Bulletin Paper
Author 笠井 幹夫|
Published Date 1924-07-07
Publication Title 農学研究
Volume volume6
Content Type Departmental Bulletin Paper