Author Tatsukawa, Masashi| Takaki, Akinobu| Shiraha, Hidenori| Koike, Kazuko| Iwasaki, Yoshiaki| Kobashi, Haruhiko| Fujioka, Shin-Ichi| Sakaguchi, Kohsaku| Yamamoto, Kazuhide|
Published Date 2011-10-21
Publication Title BMC Cancer
Volume volume11
Content Type Journal Article
JaLCDOI 10.18926/AMO/52139
FullText URL 68_1_17.pdf
Author Moritou, Yuki| Ikeda, Fusao| Iwasaki, Yoshiaki| Baba, Nobuyuki| Takaguchi, Kouichi| Senoh, Tomonori| Nagano, Takuya| Takeuchi, Yasuto| Yasunaka, Tetsuya| Ohnishi, Hideki| Miyake, Yasuhiro| Takaki, Akinobu| Nouso, Kazuhiro| Yamamoto, Kazuhide|
Abstract The impact of hepatic steatosis on interferon therapy for patients with chronic hepatitis C (CHC) has been associated with single-nucleotide polymorphisms (SNP) of IL28B, patatin-like phospholipase domain-containing protein 3 (PNPLA3), and low-density lipoprotein (LDL) receptor. Whether this holds true for Japanese patients, however, remains unresolved. The present study prospectively enrolled 226 Japanese patients with CHC, and investigated the impact of hepatic steatosis and its related SNPs, including rs8099917 of IL28B, rs738409 of PNPLA3, and rs14158 of LDL receptor, on outcomes of peg-interferon and ribavirin therapy. In multivariate logistic regression analysis, significant factors affecting the severity of hepatic steatosis were high body mass index and the minor alleles of IL28B SNP (p=0.020 and 0.039, respectively). The risk alleles of PNPLA3 SNP also showed weak association (p=0.059). Severe steatosis and the minor alleles of IL28B SNP were significantly associated with null or partial virological response in patients with HCV genotype 1, as were female gender, and low LDL cholesterol (p=0.049, and <0.001, respectively). The SNP genotype of PNPLA3 and LDL receptor did not have a significant impact on therapeutic outcomes. With respect to the SNP sites examined, the SNP of PNPLA3 has a weak association with severe hepatic steatosis, but not with the outcome of interferon therapy.
Keywords hepatic steatosis genetic polymorphism interferon HCV
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2014-02
Volume volume68
Issue issue1
Publisher Okayama University Medical School
Start Page 17
End Page 22
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2014 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 24553484
Web of Science KeyUT 000331592800003
Author Kinugasa, Hideaki| Nouso, Kazuhiro| Takeuchi, Yasuto| Yasunaka, Tetsuya| Onishi, Hideki| Nakamura, Shin-ichiro| Shiraha, Hidenori| Kuwaki, Kenji| Hagihara, Hiroaki| Ikeda, Fusao| Miyake, Yasuhiro| Takaki, Akinobu| Yamamoto, Kazuhide|
Published Date 2012-04
Publication Title Journal of Gastroenterology
Volume volume47
Issue issue4
Content Type Journal Article
Author Onji, Masahiro| Kanno, Atsuo| Saitoh, Shin-Ichiroh| Fukui, Ryutaro| Motoi, Yuji| Shibata, Takuma| Matsumoto, Fumi| Lamichhane, Aayam| Sato, Shintaro| Kiyono, Hiroshi| Yamamoto, Kazuhide| Miyake, Kensuke|
Published Date 2013-06
Publication Title Nature Communications
Volume volume4
Content Type Journal Article
Author Kubota, Junichi| Ikeda, Fusao| Terada, Ryo| Kobashi, Haruhiko| Fujioka, Shin-ichi| Okamoto, Ryoichi| Baba, Shinsuke| Morimoto, Youichi| Ando, Masaharu| Makino, Yasuhiro| Taniguchi, Hideaki| Yasunaka, Tetsuya| Miyake, Yasuhiro| Iwasaki, Yoshiaki| Yamamoto, Kazuhide|
Published Date 2009-09
Publication Title Journal of Gastroenterology
Volume volume44
Issue issue9
Content Type Journal Article
Author Saito, Shunsuke| Kato, Jun| Hiraoka, Sakiko| Horii, Joichiro| Suzuki, Hideyuki| Higashi, Reiji| Kaji, Eisuke| Kondo, Yoshitaka| Yamamoto, Kazuhide|
Published Date 2011-09
Publication Title Inflammatory Bowel Diseases
Volume volume17
Issue issue9
Content Type Journal Article
Author Matsubara, Minoru| Shiraha, Hidenori| Kataoka, Jyunro| Iwamuro, Masaya| Horiguchi, Shigeru| Nishina, Shin-ichi| Takaoka, Nobuyuki| Uemura, Masayuki| Takaki, Akinobu| Nakamura, Shinichiro| Kobayashi, Yoshiyuki| Nouso, Kazuhiro| Yamamoto, Kazuhide|
Published Date 2012-10
Publication Title Journal of Gastroenterology and Hepatology
Volume volume27
Issue issue10
Content Type Journal Article
Author Fujii, Masakuni| Kawamoto, Hirofumi| Tsutsumi, Koichiro| Kato, Hironari| Hirao, Ken| Kurihara, Naoko| Mizuno, Osamu| Ishida, Etsuji| Ogawa, Tsuneyoshi| Fukatsu, Hirotoshi| Yamamoto, Kazuhide|
Published Date 2013-05
Publication Title Hepato-Gastroenterology
Volume volume60
Issue issue123
Content Type Journal Article
Author Nakarai, Asuka| Kato, Jun| Hiraoka, Sakiko| Kuriyama, Motoaki| Inokuchi, Toshihiro| Takei, Daisuke| Moritou, Yuki| Akita, Mitsuhiro| Takahashi, Sakuma| Harada, Keita| Okada, Hiroyuki| Yamamoto, Kazuhide|
Published Date 2013-12-02
Publication Title 岡山医学会雑誌
Volume volume125
Issue issue3
Content Type Journal Article
Author Kawai, Daisuke| Takaki, Akinobu| Yamamoto, Kazuhide|
Published Date 2013-12-02
Publication Title 岡山医学会雑誌
Volume volume125
Issue issue3
Content Type Journal Article
JaLCDOI 10.18926/AMO/51864
FullText URL 67_5_285.pdf
Author Akita, Mitsuhiro| Hiraoka, Sakiko| Kaji, Eisuke| Takemoto, Koji| Nagahara, Yasuhiro| Yamamoto, Hiroshi| Yamamoto, Kazuhide| Kato, Jun|
Abstract Whether presence or history of extracolonic primary malignancy is a risk for colorectal neoplasia is not fully known. In this study, 26,452 first-time colonoscopy cases were examined using a colonoscopy database. Among the analyzed subjects, 3,026 (11%) subjects had history or concomitance of extracolonic primary malignancy, while the remaining 23,426 subjects did not. Colorectal neoplasia was observed in 39% of all the subjects. A crude comparison showed that the prevalence of any type of colorectal neoplasia was higher in subjects with extracolonic malignancy than in those without (42% vs. 39%, p=0.0012). However, after adjusting for confounding factors, the odds ratios (ORs) of subjects with extracolonic malignancy for having colorectal neoplasia, advanced neoplasia, and cancer were all less than 1.0, and all significantly different from those of subjects without extracolonic malignancy. Analysis according to the type of extracolonic malignancy revealed that gastric cancer cases had a significantly lower risk for colorectal advanced neoplasia (OR:0.81;95% CI:0.67-0.99). Among major malignancies, only esophageal squamous cell cancer cases had increased risk for colorectal neoplasia (OR:1.66;95% CI:1.20-2.29). Patients with presence or history of extracolonic malignancy did not carry a higher risk of occurrence of colorectal neoplasia.
Keywords colorectal cancer colonoscopy risk factor database
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2013-10
Volume volume67
Issue issue5
Publisher Okayama University Medical School
Start Page 285
End Page 292
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 24145728
Web of Science KeyUT 000325836100002
Author Nishimura, Mamoru| Takaki, Akinobu| Tamaki, Naofumi| Maruyama, Takayuki| Onishi, Hideki| Kobayashi, Sayo| Nouso, Kazuhiro| Yasunaka, Tetsuya| Koike, Kazuko| Hagihara, Hiroaki| Kuwaki, Kenji| Nakamura, Shinichiro| Ikeda, Fusao| Iwasaki, Yoshiaki| Tomofuji, Takaaki| Morita, Manabu| Yamamoto, Kazuhide|
Published Date 2013-01-30
Publication Title Hepatology Research
Volume volume43
Issue issue10
Content Type Journal Article
Author Tsutsumi, Koichiro| Kawamoto, Hirofumi| Hirao, Ken| Sakakihara, Ichiro| Yamamoto, Naoki| Noma, Yasuhiro| Fujii, Masakuni| Kato, Hironari| Ogawa, Tsuneyoshi| Ishida, Etsuji| Kuwaki, Kenji| Nouso, Kazuhiro| Okada, Hiroyuki| Yamamoto, Kazuhide|
Published Date 2012-09
Publication Title Pancreatology
Volume volume12
Issue issue5
Content Type Journal Article
Author Asagi, Akinori| Ohta, Koji| Nasu, Junichirou| Tanada, Minoru| Nadano, Seijin| Nishimura, Rieko| Teramoto, Norihiro| Yamamoto, Kazuhide| Inoue, Takeshi| Iguchi, Haruo|
Published Date 2013-01
Publication Title Pancreas
Volume volume42
Issue issue1
Content Type Journal Article
Author Tanaka, Shigetomi| Shiraha, Hidenori| Nakanishi, Yutaka| Nishina, Shin-Ichi| Matsubara, Minoru| Horiguchi, Shigeru| Takaoka, Nobuyuki| Iwamuro, Masaya| Kataoka, Junro| Kuwaki, Kenji| Hagihara, Hiroaki| Toshimori, Junichi| Ohnishi, Hideki| Takaki, Akinobu| Nakamura, Shinichiro| Nouso, Kazuhiro| Yagi, Takahito| Yamamoto, Kazuhide|
Published Date 2012-12-01
Publication Title International Journal of Cancer
Volume volume131
Issue issue11
Content Type Journal Article
JaLCDOI 10.18926/AMO/49667
FullText URL 67_2_93.pdf
Author Kita, Masahide| Yokota, Kenji| Okada, Hiroyuki| Take, Susumu| Takenaka, Ryuta| Kawahara, Yoshiro| Oguma, Keiji| Matsushita, Osamu| Yamamoto, Kazuhide|
Abstract Atrophy of the gastric mucosa is a precursor of intestinal-type gastric cancer, and Helicobacter pylori infection causes atrophic gastritis. The aim of this study was to determine whether the genetic diversity of H. pylori virulence genes is associated with the development and progression of gastric atrophy in humans. We isolated and cultured H. pylori strains from patients with gastric ulcer and duodenal ulcer accompanied by atrophic gastritis in background mucosa. H. pylori strains were stored at -80℃ prior to the experiments being carried out. We analyzed iceA, babA, vacA, cagA, and cagE genes by PCR. The cagA gene was analyzed through sequencing of the C-terminal region containing the EPIYA motif, which is related to tyrosine phosphorylation. Severe atrophy was observed in patients with gastric ulcer. The major phenotype of the vacA gene was s1c/m1 (93オ). The cagA gene was detected in all strains. The cagE gene was not detected in 2 and 5 strains from the mild cases and severe cases, respectively. The major cagA EPIYA motif, which is amino acids repeat in the C terminus, was the A-B-D type (44 of 58 strains). The virulence genes were not statistically associated with the severity of atrophy in the background gastric mucosa in humans. Not only identification of bacterial virulence factors but also studies of the host response will be necessary to investigate the progression of gastric atrophy and subsequent cancer development in humans.
Keywords Helicobacter pylori virulence genes chronic atrophic gastritis
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2013-04
Volume volume67
Issue issue2
Publisher Okayama University Medical School
Start Page 93
End Page 98
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 23603925
Web of Science KeyUT 000317801700003
Related Url http://ousar.lib.okayama-u.ac.jp/metadata/52508
Author Hirakawa, Tomoko| Kato, Jun| Okumura, Yoshihiro| Hori, Keisuke| Takahashi, Sakuma| Suzuki, Hideyuki| Akita, Mitsuhiro| Higashi, Reiji| Saito, Shunsuke| Kaji, Eisuke| Uraoka, Toshio| Hiraoka, Sakiko| Yamamoto, Kazuhide|
Published Date 2012-02
Publication Title Journal of Gastroenterology
Volume volume47
Issue issue2
Content Type Journal Article
JaLCDOI 10.18926/AMO/49042
FullText URL 66_6_461.pdf
Author Koike, Kazuko| Takaki, Akinobu| Kato, Nobuyuki| Ouchida, Mamoru| Kanzaki, Hirotaka| Yasunaka, Tetsuya| Shiraha, Hidenori| Miyake, Yasuhiro| Yamamoto, Kazuhide|
Abstract Hepatitis C virus (HCV) infection induces several changes in hepatocytes, such as oxidative stress, steatosis, and hepatocarcinogenesis. Although considerable progress has been made during recent years, the mechanisms underlying these functions remain unclear. We employed proteomic techniques in HCV replicon-harboring cells to determine the effects of HCV replication on host-cell protein expression. We examined two-dimensional electrophoresis (2-DE) and mass spectrometry to compare and identify differentially expressed proteins between HCV subgenomic replicon-harboring cells and their “cured” cells. One of the identified proteins was confirmed using enzyme-linked immunosorbent assay (ELISA) and Western blot analysis. Full-length HCV genome RNA replicating and cured cells were also assessed using ELISA. Replicon-harboring cells showed higher expression of retinal dehydrogenase 1 (RALDH-1), which converts retinol to retinoic acid, and the cured cells showed higher expression of retinol-binding protein (RBP), which transports retinol from the liver to target tissues. The alteration in RBP expression was also confirmed by ELISA and Western blot analysis. We conclude that protein expression profiling demonstrated that HCV replicon eradication affected retinol-related protein expression.
Keywords hepatitis C virus retinol-binding protein
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2012-12
Volume volume66
Issue issue6
Publisher Okayama University Medical School
Start Page 461
End Page 468
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2012 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 23254580
Web of Science KeyUT 000312966100005
Author Nakanishi, Yutaka| Shiraha, Hidenori| Nishina, Shin-ichi| Tanaka, Shigetomi| Matsubara, Minoru| Horiguchi, Shigeru| Iwamuro, Masaya| Takaoka, Nobuyuki| Uemura, Masayuki| Kuwaki, Kenji| Hagihara, Hiroaki| Toshimori, Junichi| Ohnishi, Hideki| Takaki, Akinobu| Nakamura, Shinichiro| Kobayashi, Yoshiyuki| Nouso, Kazuhiro| Yagi, Takahito| Yamamoto, Kazuhide|
Published Date 2011-01-04
Publication Title BMC Cancer
Volume volume11
Content Type Journal Article
Author Matsuo, Noriyuki| Shiraha, Hidenori| Fujikawa, Tatsuya| Takaoka, Nobuyuki| Ueda, Naoki| Tanaka, Shigetomi| Nishina, Shinichi| Nakanishi, Yutaka| Uemura, Masayuki| Takaki, Akinobu| Nakamura, Shinichiro| Kobayashi, Yoshiyuki| Nouso, Kazuhiro| Yagi, Takahito| Yamamoto, Kazuhide|
Published Date 2009-07-18
Publication Title BMC Cancer
Volume volume9
Content Type Journal Article