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
Published Date 2013-04
Publication Title Acta Medica Okayama
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 英語
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 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/30499
FullText URL fulltext.pdf
Author Okada, Hiroyuki| Mizuno, Motowo| Yamamoto, Kazuhide| Tsuji, Takao|
Abstract <p>To characterize primary sclerosing cholangitis (PSC) in Japanese patients and its association with inflammatory bowel disease (IBD), 155 reported cases of PSC, including 6 cases of our own, were reviewed. The prevalence of IBD was less in Japanese PSC patients than in Western patients (23% versus 62-100%). Japanese PSC patients with IBD were younger (mean age, 33.1 versus 51.8 years) and were more often women (51% versus 36%) than those without IBD. Seventy-four percent of PSC patients with IBD had extensive colonic lesions, and 89% of those developed IBD simultaneously, with or prior to PSC. There were 3 cases of neutrophilic cholangitis among the PSC patients with IBD but none in those without IBD. Based on these observations, we speculate that there may be subtypes of PSC which differ pathophysiologically.</p>
Keywords primary sclerosing cholangitis inflammatory bowel disease
Amo Type Article
Published Date 1996-10
Publication Title Acta Medica Okayama
Volume volume50
Issue issue5
Publisher Okayama University Medical School
Start Page 227
End Page 235
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 8914675
Web of Science KeyUT A1996VQ20600001
JaLCDOI 10.18926/AMO/31684
FullText URL fulltext.pdf
Author Ariyoshi, Masanori| MIzuno, Motowo| Morisue, Yoshiko| Shimada, Morizou| Fujita, Shirou| Nasu, Junichirou| Okada, Hiroyuki| Shimomura, Hiroyuki| Yamamoto, Kazuhide| Tsuji, Takao|
Abstract <p>We developed a monoclonal antibody (MoAb) (clone 5E8) against an antigen on the bile canalicular membrane of rat hepatocyte. By immunoblotting, MoAb 5E8 detected a band of 110 kD. In this study, we used the phage display technique to identify the target antigen recognized by MoAb 5E8. We screened a random phage display library expressing 12-mer peptide sequences and identified a peptide sequence, FHFNPYTGHPLT, as an epitope. We compared this peptide sequence with those of dipeptidyl peptidase IV (DPP IV, E.C.3.4.14.5) and Cell-CAM105, which proteins were located by a database search based on the information of tissue localization and approximate molecular weight of the MoAb 5E8 antigen, and sequence similarity with a region in DPP IV (amino acids 225-233) but not with Cell-CAM105 was found. In addition, we immunohistochemically stained various tissues (liver, small intestine, and kidney) of Japanese Fischer 344 rats, known to be deficient for DPP IV, with MoAb 5E8 and showed that the expression of MoAb 5E8 antigen was negligible or weak. In contrast, tissues sampled from the same organs of Sprague-Dawley rats, known to express DPP IV, were positively stained. These findings suggest that the antigen recognized by MoAb 5E8 is DDPIV and its major epitope is located in amino acids at positions 225-233.</p>
Keywords random phage display library dipeptidyl petidase IV monoclonal antibody epitope bile canalicular membrane
Amo Type Article
Published Date 2002-08
Publication Title Acta Medica Okayama
Volume volume56
Issue issue4
Publisher Okayama University Medical School
Start Page 187
End Page 191
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 12199523
Web of Science KeyUT 000177382600003
JaLCDOI 10.18926/AMO/31686
FullText URL fulltext.pdf
Author Ohya, Shogen| Mizuno, Motowo| Kawada, Mikihiro| Nasu, Junichirou| Okada, Hiroyuki| Shimomura, Hiroyuki| Yamamoto, Kazuhide| Fujita, Teizou| Tsuji, Takao|
Abstract <p>We have previously developed an enzyme-linked immunosorbent assay (ELISA) to measure stool decay-accelerating factor (DAF) and found that stool DAF concentrations were significantly elevated in patients with colorectal cancer, suggesting that the measurement of stool DAF may be valuable for the detection of colorectal cancer. In order to refine the assay for the measurement of stool DAF, we investigated 1) effects of centrifugation of stool samples, 2) effects of detergents, and 3) adequate combination of various anti-DAF monoclonal antibodies for the ELISA system using only monoclonal antibodies. We found that high-speed centrifugation could be omitted and that only the removal of large undigested food residues by centrifugation of short duration in a low-speed benchtop microcentrifuge sufficed to adequately prepare the stool samples. Addition of 2 detergents, octyl beta-glucoside and sodium deoxycholate, known to solubilize glycosyl-phosphatidylinositol-anchored proteins such as DAF, did not influence stool DAF values. By using 2 mouse anti-DAF monoclonal antibodies (clone 4F11 and 1C6), we were able to achieve a stable ELISA for the measurement of stool DAF using a uniform source of antibodies. The results should allow us to consistently apply the DAF assay for routine use in the detection of colorectal cancer.</p>
Keywords decay-accelerating factor (DAF) colorectal cancer enzyme-linked immunosorbent assay (ELISA). monoclonal sntibodies
Amo Type Article
Published Date 2002-08
Publication Title Acta Medica Okayama
Volume volume56
Issue issue4
Publisher Okayama University Medical School
Start Page 171
End Page 176
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 12199521
Web of Science KeyUT 000177382600001
JaLCDOI 10.18926/AMO/31695
FullText URL fulltext.pdf
Author Yoshioka, Masao| Mizuno, Motowo| Morisue, Yoshiko| Shimada, Morizou| Hirai, Michio| Nasu, Junichirou| Okada, Hiroyuki| Sakaguchi, Kousaku| Yamamoto, Kazuhide| Tsuji, Takao|
Abstract <p>In autoimmune chronic active hepatitis (AIH) and primary biliary cirrhosis (PBC), various autoantibodies including anti-asialoglycoprotein receptor (ASGPR) antibodies have been found in patients' sera. We have previously developed a mouse monoclonal antibody against rat and human ASGPR. In this study, we developed a capture enzyme-linked immunosorbent assay (ELISA) for detection of anti-ASGPR antibodies using this monoclonal antibody and investigated the occurrence of anti-ASGPR antibodies in the sera of patients with various liver diseases. Serum samples were obtained from 123 patients with various liver diseases, including 21 patients with AIH and 40 patients with PBC. In this capture ELISA, the target antigen in the crude rat liver membrane extracts was captured on the ELISA wells by the ASGPR-specific mouse monoclonal antibody. Thus, the cumbersome process of antigen purification was rendered unnecessary. Using this capture ELISA, we detected the anti-ASGPR antibody in 67% of the patients with AIH, in 100% of the patients with PBC, and in 57% of the patients with acute hepatitis type A. However, the anti-ASGPR antibody was rarely detected in patients with other liver diseases such as primary sclerosing cholangitis and obstructive jaundice. Our findings suggest that this capture ELISA would be useful for the detection of anti-ASGPR antibodies in autoimmune liver diseases.</p>
Keywords autoimmue hepatitis primary biliary cirrhosis asialoglycoprotein receptor autoantibodies
Amo Type Article
Published Date 2002-04
Publication Title Acta Medica Okayama
Volume volume56
Issue issue2
Publisher Okayama University Medical School
Start Page 99
End Page 105
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 12002624
Web of Science KeyUT 000175176900006
JaLCDOI 10.18926/AMO/31715
FullText URL fulltext.pdf
Author Hirai, Michio| Mizuno, Motowo| Morisue, Yoshiko| Yoshioka, Masao| Shimada, Morizou| Nasu, Junichirou| Okada, Hiroyuki| Shimomura, Hiroyuki| Yamamoto, Kazuhide| Tsuji, Takao|
Abstract <p>Anti-idiotype antibodies (Ab2) play an important role in the homeostasis of immune responses and are related to the development and the disease activity of certain autoimmune diseases. The asialoglycoprotein receptor (ASGPR) is considered one of the target antigens in the pathogenesis of autoimmune chronic active hepatitis (AIH). We previously developed a mouse monoclonal antibody (clone 8D7) which recognizes rat and human ASGPR. In this study, to help investigate the anti-ASGPR antibody-anti-idiotype antibody network in patients with AIH, we developed a syngeneic mouse monoclonal Ab2 to the 8D7 anti-ASGPR antibody (Ab1). One clone, designated as 3C8, tested positive for specific reactivity to 8D7-Ab1 and did not bind to other irrelevant immunoglobulins. By competitive inhibition assays, the binding of 8D7-Ab1 to liver membrane extracts, i.e., the crude antigen preparation, was inhibited by 3C8-Ab2 in a dose-dependent manner, and the binding of 8D7-Ab1 to 3C8-Ab2 was inhibited by the liver membrane extracts. In the immunohistochemical analysis, 3C8-Ab2 blocked the specific staining of sinusoidal margins of rat hepatocytes by 8D7-Ab1. These results suggest that 3C8 anti-idiotype antibody recognizes the specific idiotypic determinants within the antigen-binding site of 8D7-Ab1.</p>
Keywords anti-idiotype antibody autoimmune hepatitis asialoglycoprotein receptor monoclonall antibody
Amo Type Article
Published Date 2002-06
Publication Title Acta Medica Okayama
Volume volume56
Issue issue3
Publisher Okayama University Medical School
Start Page 135
End Page 139
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 12108584
Web of Science KeyUT 000176521200003
JaLCDOI 10.18926/AMO/45269
FullText URL 65_2_105.pdf
Author Tsuzuki, Takao| Okada, Hiroyuki| Nasu, Junichiro| Takenaka, Ryuta| Inoue, Masafumi| Kawano, Seiji| Kita, Masahide| Hori, Keisuke| Yamamoto, Kazuhide|
Abstract The objectives of this study were to evaluate the accuracy of endoscopic ultrasonography (EUS) in local and regional staging of early gastric cancer, to analyze the factors influencing the accuracy of EUS, and to reveal the usefulness and problems of EUS in pre-treatment staging of gastric cancer. We examined 105 lesions in 104 patients with histologically confirmed gastric cancer and retrospectively evaluated them with EUS. The diagnostic accuracy, sensitivity, and specificity of EUS were determined by comparing the pre-treatment EUS with the postoperative histopathological findings. The overall diagnostic accuracy of EUS for the depth of cancer invasion was 86%. The overall sensitivity and specificity were 60% and 96%, respectively. The accuracy significantly declined in lesions located in the upper-third of the stomach (70%). Type 0-I lesions tended to be over-staged (12&), and the upper-third lesions tended to be under-staged (23%). The accuracy significantly declined in differentiated adenocarcinoma with massive submucosal invasion (56.5%). EUS is useful for evaluating the depth of gastric cancer invasion which determines the feasibility of endoscopic treatment. However, it is noteworthy that the diagnostic accuracy of the invasion depth diminished for lesions in the upper third of the stomach.
Keywords endoscopic ultrasonography early gastric cancer accuracy sensitivity specificity
Amo Type Original Article
Published Date 2011-04
Publication Title Acta Medica Okayama
Volume volume65
Issue issue2
Publisher Okayama University Medical School
Start Page 105
End Page 112
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2011 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 21519368
Web of Science KeyUT 000289818800006
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 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
Author Uchida, Daisuke| Shiraha, Hidenori| Kato, Hironari| Nagahara, Teruya| Iwamuro, Masaya| Kataoka, Junro| Horiguchi, Shigeru| Watanabe, Masami| Takaki, Akinobu| Nouso, Kazuhiro| Nasu, Yasutomo| Yagi, Takahito| Kumon, Hiromi| Yamamoto, Kazuhide|
Published Date 2014-05
Publication Title Journal of Gastroenterology and Hepatology
Volume volume29
Issue issue5
Content Type Journal Article
Author Yagi, Toru| Kawahara, Yoshiro| Okada, Hiroyuki| Takemoto, Koji| Kato, Jun| Kobayashi, Yoshiyuki| Kawamoto, Hirofumi| Yamamoto, Kazuhide|
Published Date 2008-01-04
Publication Title 岡山医学会雑誌
Volume volume119
Issue issue3
Content Type Journal Article
Author Inoue, Masafumi| Okada, Hiroyuki| Kawahara, Yoshiro| Kawano, Seiji| Yamamoto, Kazuhide|
Published Date 2009-08-03
Publication Title 岡山医学会雑誌
Volume volume121
Issue issue2
Content Type Journal Article
Author Kawano, Seiji| Okada, Hiroyuki| Kawahara, Yoshiro| Inoue, Masafumi| Yamamoto, Kazuhide|
Published Date 2009-08-03
Publication Title 岡山医学会雑誌
Volume volume121
Issue issue2
Content Type Journal Article
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 Higashi, Reiji| Uraoka, Toshio| Kato, Jun| Kuwaki, Kenji| Ishikawa, Shin| Saito, Yutaka| Matsuda, Takahisa| Ikematsu, Hiroaki| Sano, Yasushi| Suzuki, Seiyuu| Murakami, Yoshitaka| Yamamoto, Kazuhide|
Published Date 2010-07
Publication Title Gastrointestinal Endoscopy
Volume volume72
Issue issue1
Content Type Journal Article
JaLCDOI 10.18926/AMO/31685
FullText URL fulltext.pdf
Author Kondo, Junichi| Shimomura, Hiroyuki| Fujioka, Shin-ichi| Iwasaki, Yoshiaki| Takagi, Shinjiro| Ohnishi, Yasuhiro| Tsuji, Hideyuki| Sakaguchi, Kosaku| Yamamoto, Kazuhide| Tsuji, Takao|
Abstract <p>The preS2 region of the hepatitis B virus (HBV) has been reported to have human polymerized albumin receptor (PAR) activity, which correlates with viral replication. Here, we studied the genomic sequence of the preS region from rare patients lacking PAR activity, despite active viral replication. PAR and DNA polymerase activity was identified in 178 HBe antigen-positive HBV carriers, and a significant correlation between 2 markers was shown, except in 2 hepatitis patients lacking PAR activity. Nucleotide sequences of the preS region of HBV from both patients were examined by direct sequencing of PCR products. In one patient, a 45-base deletion was found to overlap half of the putative polymerized human albumin binding site in the preS2 region. In the other patient, a point mutation at the first nucleotide of the start codon of the preS2 region of HBV was found. There was no such genomic change in the 3 control HBV sequences. These results indicate that the preS2 region is necessary for binding of polymerized human albumin, and this is the first report of naturally existing mutant virus with no or low PAR activity.</p>
Keywords hepatitis B virus preS region polymerized albumin receptor genetic mutation genetic deletion
Amo Type Article
Published Date 2002-08
Publication Title Acta Medica Okayama
Volume volume56
Issue issue4
Publisher Okayama University Medical School
Start Page 193
End Page 198
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 12199524
Web of Science KeyUT 000177382600004
JaLCDOI 10.18926/AMO/48568
FullText URL 66_3_279.pdf
Author Nishimura, Mamoru| Nouso, Kazuhiro| Kariyama, Kazuya| Wakuta, Akiko| Kishida, Masayuki| Wada, Nozomu| Higashi, Toshihiro| Yamamoto, Kazuhide|
Abstract The artificial ascites technique is often used during radiofrequency ablation (RFA) for hepatocellular carcinoma (HCC) treatment because it prevents visceral damage and improves visualization by minimizing interference of the lungs and mesentery. This study determined the efficacy and safety of RFA using the artificial ascites technique in HCC patients. We examined 188 HCC patients who were treated by RFA and fulfilled the Milan criteria. Treatment outcomes (complete ablation rate, local recurrence rate, complication rate, liver function including total bilirubin level, alanine aminotransferase level, albumin level, and prothrombin time) were compared among patients divided into 3 groups based on the volume of artificial ascites injected:GroupⅠ (n=86), no artificial ascites injected;GroupⅡ (n=35), <1,000ml artificial ascites injected;and Group Ⅲ (n=67), >1,000ml artificial ascites injected. No significant difference was observed in complete ablation or local recurrence rates among the 3 groups, or in the extent of liver function damage after RFA. Artificial ascites disappeared within 7 days; additional diuretics were needed only in 5 (all from Group Ⅲ) of 102 patients. No serious complications such as intestinal perforation or intraperitoneal bleeding were observed. Thus, we found that artificial ascites injection during RFA is effective and safe, and can be used to prevent major procedural complications.
Keywords radiofrequency ablation hepatocellular carcinoma artificial ascites
Amo Type Original Article
Published Date 2012-06
Publication Title Acta Medica Okayama
Volume volume66
Issue issue3
Publisher Okayama University Medical School
Start Page 279
End Page 284
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2012 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 22729109
Web of Science KeyUT 000305669700012
Author Takeuchi, Yasuto| Ikeda, Fusao| Moritou, Yuki| Hagihara, Hiroaki| Yasunaka, Tetsuya| Kuwaki, Kenji| Miyake, Yasuhiro| Ohnishi, Hideki| Nakamura, Shinichiro| Shiraha, Hidenori| Takaki, Akinobu| Iwasaki, Yoshiaki| Nouso, Kazuhiro| Yamamoto, Kazuhide|
Published Date 2013-03
Publication Title Journal of Gastroenterology
Volume volume48
Issue issue3
Content Type Journal Article
JaLCDOI 10.18926/AMO/53520
FullText URL 69_3_137.pdf
Author Seki, Hiroyuki| Ikeda, Fusao| Nanba, Shintaro| Moritou, Yuki| Takeuchi, Yasuto| Yasunaka, Tetsuya| Onishi, Hideki| Miyake, Yasuhiro| Takaki, Akinobu| Nouso, Kazuhiro| Iwasaki, Yoshiaki| Nakamura, Minoru| Yamamoto, Kazuhide|
Abstract A predictive marker of the rapid progression to hepatic failure is desired for patients with asymptomatic primary biliary cirrhosis (aPBC). We performed a systematic cohort analysis of 101 patients diagnosed as having aPBC and the rapid progression to liver failure in some, by focusing on cholestasis. Cholestasis was assessed by aberrant keratin7 (K-7) expressions in the patientsʼ hepatocytes. Intralobular expressions of K-7 were found in 9 of the 101 patients. The grades of K-7 expression were significantly associated with the levels of alanine aminotransferase, alkaline phosphatase, and total bilirubin at the time of diagnosis, but not with bile duct loss or cholestasis. Stepwise logistic regression analysis revealed that high grades of K-7 expression correlated positively with high levels of total bilirubin. During the follow-up period, 8 patients developed jaundice, and the mean period until the development of jaundice was 5.2 years. The proportional hazards models for the risk of developing jaundice identified a high grade of aberrant K-7 expression in hepatocytes as the only significant risk factor. Aberrant K-7 expression in hepatocytes can be used as an additional marker to predict rapid progression to liver failure in patients with aPBC at the time of diagnosis.
Keywords primary biliary cirrhosis keratin 7 hepatic failure
Amo Type Original Article
Published Date 2015-06
Publication Title Acta Medica Okayama
Volume volume69
Issue issue3
Publisher Okayama University Medical School
Start Page 137
End Page 144
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2015 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 26101189
Web of Science KeyUT 000356903000002