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  <Article>
    <Journal>
      <PublisherName>MDPI AG</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>2076-2607</Issn>
      <Volume>14</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2026</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>The Role of Nitrate-Reducing Bacteria Isolated from Helicobacter pylori-Infected Individuals in Gastric Cancer Development</ArticleTitle>
    <FirstPage LZero="delete">760</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Serika</FirstName>
        <LastName>Kuwagi</LastName>
        <Affiliation>Department of Bacteriology, Academic Field of Health Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazuyoshi</FirstName>
        <LastName>Gotoh</LastName>
        <Affiliation>Department of Bacteriology, Academic Field of Health Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Marina</FirstName>
        <LastName>Komatsubara</LastName>
        <Affiliation>Department of Bacteriology, Academic Field of Health Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shuma</FirstName>
        <LastName>Tsuji</LastName>
        <Affiliation>Department of Bacteriology, Academic Field of Health Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shyoutarou</FirstName>
        <LastName>Okanoue</LastName>
        <Affiliation>Department of Gastroenterology and Hepatology, Academic Field of Medicine Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroyuki</FirstName>
        <LastName>Okada</LastName>
        <Affiliation>Himeji Red Cross Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jumpei</FirstName>
        <LastName>Uchiyama</LastName>
        <Affiliation>Department of Bacteriology, Academic Field of Medicine Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akari</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation>Department of Oral Health Care and Rehabilitation, Institute of Biomedical Sciences, Graduate School, Tokushima University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation>Department of Bacteriology, Academic Field of Health Sciences, Okayama University</Affiliation>
      </Author>
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    <Abstract>Helicobacter pylori is a Gram-negative bacterium that inhabits the gastric mucosa, with a global prevalence in humans of approximately 40%. It is likely the cause of 90% of gastric cancer (GC) cases and thus considered the most prominent driver of GC development. However, during gastric mucosal atrophy, other bacteria such as nitrate-reducing bacteria (NRB) also proliferate. In this study, we isolated NRB from patients with gastritis and GC to examine their effects on the epithelial cell cycle and production of various cytokines in monocytic cell lines. Bacterial counts (excluding H. pylori and NRB) increased with the progression of gastric mucosal atrophy and were significantly higher in patients with GC. Gastric epithelial cell lines were stimulated with isolated NRB, and the proportion of cells in each cell cycle was measured. Strains from patients with open-type gastritis progressed more rapidly through cell cycles than those from patients with GC. NRB isolated from gastric cancer had high nitrate-reducing activity. Thus, NRB may contribute to GC progression during H. pylori-induced carcinogenesis. Therefore, evaluating gastric atrophy and microbiota may be important for managing the risk of GC.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">Helicobacter pylori infection</Param>
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        <Param Name="value">gastric cancer</Param>
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      <Object Type="keyword">
        <Param Name="value">nitrate-reducing bacteria</Param>
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      <Object Type="keyword">
        <Param Name="value">gastritis</Param>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>Oxford University Press (OUP)</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1365-2672</Issn>
      <Volume>136</Volume>
      <Issue>10</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2025</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Gut dysbiosis allows foodborne salmonella colonization in edible crickets: a probiotic strategy for enhanced food safety</ArticleTitle>
    <FirstPage LZero="delete">lxaf217</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Shuma</FirstName>
        <LastName>Tsuji</LastName>
        <Affiliation>Department of Medical Laboratory Science, Okayama University Graduate School of Health Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Osamu</FirstName>
        <LastName>Matsushita</LastName>
        <Affiliation>Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jumpei</FirstName>
        <LastName>Uchiyama</LastName>
        <Affiliation>Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation>Department of Medical Laboratory Science, Okayama University Graduate School of Health Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tetsuya</FirstName>
        <LastName>Bando</LastName>
        <Affiliation>Department of Cytology and Histology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideyo</FirstName>
        <LastName>Ohuchi</LastName>
        <Affiliation>Department of Cytology and Histology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazuyoshi</FirstName>
        <LastName>Gotoh</LastName>
        <Affiliation>Department of Medical Laboratory Science, Okayama University Graduate School of Health Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
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    <Abstract>Aims: Edible insects, including crickets, represent a promising protein source, yet concerns over foodborne pathogens limit consumer acceptance. This study investigated whether gut microbiota modulates colonization by Salmonella enterica subsp. enterica serovar Enteritidis (SE) in the two-spotted cricket (Gryllus bimaculatus).&lt;br&gt;
Methods and Results: Under standard conditions, SE was undetectable in crickets despite prolonged exposure; however, antibiotic-induced dysbiosis enabled stable SE colonization. Long-read 16S rRNA sequencing revealed significant microbiota shifts, notably a reduction in Lactococcus garvieae. In vitro assays showed strong inhibitory effects of L. garvieae against SE, and supplementation of dysbiotic crickets with L. garvieae reduced SE colonization by &#8764;1000-fold.&lt;br&gt;
Conclusions: The native cricket gut microbiota, especially L. garvieae, plays a protective role against SE colonization. Enhancing beneficial gut bacteria could mitigate pathogen risks and promote edible insects as a sustainable protein.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">edible crickets</Param>
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        <Param Name="value">Salmonella</Param>
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      <Object Type="keyword">
        <Param Name="value">Lactococcus</Param>
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      <Object Type="keyword">
        <Param Name="value">probiotics</Param>
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      <Object Type="keyword">
        <Param Name="value">microbiome</Param>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>Japanese Society of Internal Medicine</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-2918</Issn>
      <Volume>63</Volume>
      <Issue>21</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2024</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Endoscopic and Histological Gastritis in University Students with Helicobacter pylori Infection</ArticleTitle>
    <FirstPage LZero="delete">2875</FirstPage>
    <LastPage>2884</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Shotaro</FirstName>
        <LastName>Okanoue</LastName>
        <Affiliation>Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroyuki</FirstName>
        <LastName>Sakae</LastName>
        <Affiliation>Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation>Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takehiro</FirstName>
        <LastName>Tanaka</LastName>
        <Affiliation>Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuka</FirstName>
        <LastName>Obayashi</LastName>
        <Affiliation>Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Makoto</FirstName>
        <LastName>Abe</LastName>
        <Affiliation>Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiyasu</FirstName>
        <LastName>Kono</LastName>
        <Affiliation>Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiromitsu</FirstName>
        <LastName>Kanzaki</LastName>
        <Affiliation>Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masaya</FirstName>
        <LastName>Iwamuro</LastName>
        <Affiliation>Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Seiji</FirstName>
        <LastName>Kawano</LastName>
        <Affiliation>Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiro</FirstName>
        <LastName>Kawahara</LastName>
        <Affiliation>Department of Practical Gastrointestinal Endoscopy, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroyuki</FirstName>
        <LastName>Yanai</LastName>
        <Affiliation>Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroyuki</FirstName>
        <LastName>Okada</LastName>
        <Affiliation>Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
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    <Abstract>Objective Although the characteristics of Helicobacter pylori infection have been extensively reported, there is a lack of consensus regarding its characteristics in young adults. The present study examined the endoscopic and histological characteristics of young adults who underwent eradication therapy for H. pylori infection.&lt;br&gt;
Methods We examined the H. pylori infection status of first-year students at Okayama University School of Medicine and Dentistry between 2014 and 2020. A total of 152 (6.8%) students who were positive for H. pylori antibody or pepsinogen tests were enrolled in the study. Among them, 107 students underwent endoscopy, and their biopsy samples were investigated. Seventy-five students were diagnosed with H. pylori infections.&lt;br&gt;
Results Of 75 H. pylori-positive patients, 57 (76.0%) had endoscopic atrophic gastritis, and 42 (56.0%) had histological atrophy. A few patients had severe atrophic gastritis. All 65 patients who underwent an eradication assessment were successfully treated. After successful eradication, 26 patients underwent endoscopic follow-up. The mean follow-up period was 32.9 months. A histological evaluation revealed that gastric antrum atrophy had subsided in 11 of 14 patients, and atrophy in the lesser curvature of the gastric body had subsided in 7 of 8 patients.&lt;br&gt;
Conclusion More than half of young adults with H. pylori infection had atrophic gastritis. We found mild atrophy in young adults, which subsided shortly after eradication treatment. This study provides a foundation for future studies to evaluate the validity of eradication therapy in preventing gastric cancer in patients.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">atrophic gastritis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">gastric cancer</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Helicobacter pylori</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">young adults</Param>
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      <Object Type="keyword">
        <Param Name="value">eradication</Param>
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    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>MDPI</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>2076-2607</Issn>
      <Volume>10</Volume>
      <Issue>12</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2022</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Effects of Helicobacter pylori and Nitrate-Reducing Bacteria Coculture on Cells</ArticleTitle>
    <FirstPage LZero="delete">2495</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Hinako</FirstName>
        <LastName>Ojima</LastName>
        <Affiliation>Department of Bacteriology, Academic Field of Health Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Sakiko</FirstName>
        <LastName>Kuraoka</LastName>
        <Affiliation>Department of Gastroenterology and Hepatology, Academic Field of Medicine Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shyoutarou</FirstName>
        <LastName>Okanoue</LastName>
        <Affiliation>Department of Gastroenterology and Hepatology, Academic Field of Medicine Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroyuki</FirstName>
        <LastName>Okada</LastName>
        <Affiliation>Himeji Red Cross Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazuyoshi</FirstName>
        <LastName>Gotoh</LastName>
        <Affiliation>Department of Bacteriology, Academic Field of Medicine Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Osamu</FirstName>
        <LastName>Matsushita</LastName>
        <Affiliation>Department of Bacteriology, Academic Field of Medicine Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akari</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation>Department of Oral Health Care and Rehabilitation, Institute of Biomedical Sciences, Graduate School, Tokushima University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation>Department of Bacteriology, Academic Field of Health Sciences, Okayama University</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
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    <Abstract>Helicobacter pylori infection is an important risk factor for developing gastric cancer. However, only a few H. pylori-infected people develop gastric cancer. Thus, other risk factors aside from H. pylori infection may be involved in gastric cancer development. This study aimed to investigate whether the nitrate-reducing bacteria isolated from patients with atrophic gastritis caused by H. pylori infection are risk factors for developing atrophic gastritis and gastric neoplasia. Nitrate-reducing bacteria were isolated from patients with atrophic gastritis caused by H. pylori infection. Among the isolated bacteria, Actinomyces oris, Actinomyces odontolyticus, Rothia dentocariosa, and Rothia mucilaginosa were used in the subsequent experiments. Cytokine inducibility was evaluated in monocytic cells, and mitogen-activated protein kinase (MAPK) activity and cell cycle were assessed in the gastric epithelial cells. The cytotoxicities and neutrophil-inducing abilities of the Actinomyces and Rothia species were enhanced when cocultured with H. pylori. Th1/Th2-related cytokines were also expressed, but their expression levels differed depending on the bacterial species. Moreover, H. pylori and Actinomyces activated MAPK (ERK and p38) and affected cell cycle progression. Some nitrate-reducing bacteria cocultured with H. pylori may promote inflammation and atrophy by inducing cytokine production. In addition, the MAPK activation and cell cycle progression caused by these bacteria can contribute to gastric cancer development.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">Helicobacter pylori</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">nitrate-reducing bacteria</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">IL-8</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">TNF-alpha</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">cell cycle</Param>
      </Object>
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    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>MDPI</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>2072-6651</Issn>
      <Volume>13</Volume>
      <Issue>7</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2021</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Serodiagnosis and Bacterial Genome of Helicobacter pylori Infection</ArticleTitle>
    <FirstPage LZero="delete">467</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Aina</FirstName>
        <LastName>Ichihara</LastName>
        <Affiliation>Department of Bacteriology, Academic Field of Health Science Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hinako</FirstName>
        <LastName>Ojima</LastName>
        <Affiliation>Department of Bacteriology, Academic Field of Health Science Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazuyoshi</FirstName>
        <LastName>Gotoh</LastName>
        <Affiliation>Department of Bacteriology, Academic Field of Medicine Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Osamu</FirstName>
        <LastName>Matsushita</LastName>
        <Affiliation>Department of Bacteriology, Academic Field of Medicine Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Susumu</FirstName>
        <LastName>Take</LastName>
        <Affiliation>Department of Gastroenterology and Hepatology, Kurashiki Central Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroyuki</FirstName>
        <LastName>Okada</LastName>
        <Affiliation>Department of Gastroenterology and Hepatology, Academic Field of Medicine Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akari</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation>Department of Oral Health Care and Rehabilitation, Institute of Biomedical Sciences, Tokushima University Graduate School</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation>Department of Bacteriology, Academic Field of Health Science Okayama University</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
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    <Abstract>The infection caused by Helicobacter pylori is associated with several diseases, including gastric cancer. Several methods for the diagnosis of H. pylori infection exist, including endoscopy, the urea breath test, and the fecal antigen test, which is the serum antibody titer test that is often used since it is a simple and highly sensitive test. In this context, this study aims to find the association between different antibody reactivities and the organization of bacterial genomes. Next-generation sequences were performed to determine the genome sequences of four strains of antigens with different reactivity. The search was performed on the common genes, with the homology analysis conducted using a genome ring and dot plot analysis. The two antigens of the highly reactive strains showed a high gene homology, and Western blots for CagA and VacA also showed high expression levels of proteins. In the poorly responsive antigen strains, it was found that the inversion occurred around the vacA gene in the genome. The structure of bacterial genomes might contribute to the poor reactivity exhibited by the antibodies of patients. In the future, an accurate serodiagnosis could be performed by using a strain with few gene mutations of the antigen used for the antibody titer test of H. pylori.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">VacA</Param>
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        <Param Name="value">CagA</Param>
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        <Param Name="value">genome</Param>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>Dove Medical Press Ltd</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1178-6973</Issn>
      <Volume>14</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2021</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Antibacterial Effects of Disulfiram in Helicobacter pylori</ArticleTitle>
    <FirstPage LZero="delete">1757</FirstPage>
    <LastPage>1764</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Tomomi</FirstName>
        <LastName>Kobatake</LastName>
        <Affiliation>Graduate School of Health Science Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Keiki</FirstName>
        <LastName>Ogino</LastName>
        <Affiliation>Department of Environmental Medicine, Koch Medical School</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroyuki</FirstName>
        <LastName>Sakae</LastName>
        <Affiliation>Department of Gastroenterology and Hepatology, Graduate School of Medicine Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazuyoshi</FirstName>
        <LastName>Gotoh</LastName>
        <Affiliation>Department of Bacteriology, Graduate School of Medicine Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akari</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation>Department of Oral Health Care and Rehabilitation, Institute of Biomedical Sciences, Tokushima University Graduate School</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Osamu</FirstName>
        <LastName>Matsushita</LastName>
        <Affiliation>Department of Bacteriology, Graduate School of Medicine Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroyuki</FirstName>
        <LastName>Okada</LastName>
        <Affiliation>Department of Gastroenterology and Hepatology, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation>Graduate School of Health Science Okayama University</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Background: Helicobacter pylori infection poses a risk of the occurrence of gastrointestinal diseases, such as gastric cancer. Its incidence rate is significantly reduced by eradication, and thereby, eradication therapy is generally performed. Disulfiram is an oral prescription drug mainly used for the treatment of alcohol dependence. In recent years, reports have been made on its anticancer and antibacterial effects, and thus, it has recently become an interesting subject. This study aimed to examine the antibacterial activity of disulfiram, investigate the presence or absence of its antibacterial activity on H. pylori, and determine whether it could be a new bactericidal drug against drug-resistant H. pylori.&lt;br&gt;
&lt;br&gt;
Materials and Methods: Drug-sensitive strains of H. pylori and amoxicillin-resistant, clarithromycin-resistant, and metronidazole-resistant strains were used, and a growth inhibition test of H. pylori using disulfiram was performed. Furthermore, the expression of urease, vacuolating cytotoxin A (VacA), and CagA, the virulence proteins of H. pylori, was quantitatively analyzed using the Western blotting method. In addition, for H. pylori used in this study, the 16SrDNA sequence, a ribosomal gene involved in protein production, was analyzed to examine the presence or absence of gene mutation.&lt;br&gt;
&lt;br&gt;
Results: Disulfiram suppressed the growth of 7 out of 12 H. pylori strains at 1 mu g/mL, and no correlation was observed between their susceptibility/resistance to current eradication antimicrobial drugs and disulfiram resistance. Disulfiram reduced the expression levels of urease, VacA, and CagA proteins. H. pylori, which showed resistance to disulfiram, tended to have fewer gene deletions/insertions in the 16S rDNA sequence; however, no specific mutation was detected. Conclusion: Disulfiram has a bactericidal effect on H. pylori at low concentrations, suggesting that it can be used as a supplement for current H. pylori eradication drugs.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">disulfiram</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Helicobacter pylori</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">urease</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">vacuolating toxin</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">CagA</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>67</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2013</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>The Genetic Diversity of Helicobacter pylori Virulence Genes Is  Not Associated with Gastric Atrophy Progression</ArticleTitle>
    <FirstPage LZero="delete">93</FirstPage>
    <LastPage>98</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Masahide</FirstName>
        <LastName>Kita</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroyuki</FirstName>
        <LastName>Okada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Susumu</FirstName>
        <LastName>Take</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ryuta</FirstName>
        <LastName>Takenaka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiro</FirstName>
        <LastName>Kawahara</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Keiji</FirstName>
        <LastName>Oguma</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Osamu</FirstName>
        <LastName>Matsushita</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazuhide</FirstName>
        <LastName>Yamamoto</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/49667</ArticleId>
    </ArticleIdList>
    <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.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Helicobacter pylori</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">virulence genes</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">chronic atrophic gastritis</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>66</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2012</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Clostridium botulinum Type E Toxins Bind to Caco-2 Cells by a Different Mechanism from That of Type A Toxins</ArticleTitle>
    <FirstPage LZero="delete">253</FirstPage>
    <LastPage>261</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Kai</FirstName>
        <LastName>Zhang</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yumiko</FirstName>
        <LastName>Yamamoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomonori</FirstName>
        <LastName>Suzuki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shaobo</FirstName>
        <LastName>Ma</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ni</FirstName>
        <LastName>Nengah Dwi  Fatmawati</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Keiji</FirstName>
        <LastName>Oguma</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/48565</ArticleId>
    </ArticleIdList>
    <Abstract>Cultured Clostridium botulinum strains produce progenitor toxins designated as 12S, 16S, and 19S toxins. The 12S toxin consists of a neurotoxin (NTX, 7S) and a non-toxic non-hemagglutinin (NTNH). The 16S and 19S toxins are formed by conjugation of the 12S toxin with hemagglutinin (HA), and the 19S toxin is a dimer of the 16S toxin. Type A cultures produce all 3 of these progenitor toxins, while type E produces only the 12S toxin. The 7S toxin is cleaved into heavy (H) and light (L) chains by a protease(s) in some strains, and the H chain has 2 domains, the N-terminus (Hn) and C-terminus (Hc). It has been reported that type A toxins bind to the intestinal cells or cultured cells via either HA or Hc. In this study, we investigated the binding of type A and E toxins to Caco-2 cells using Western blot analysis. Both the type E 7S and 12S toxins bound to the cells, with the 7S toxin binding more strongly, whereas, in the type A strain, only the 16S/19S toxins showed obvious binding. Pre-incubation of the type E 7S toxin with IgG against recombinant type E Hc significantly inhibited the 7S toxin binding, indicating that Hc might be a main binding domain of the type E toxin.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Clostridum botulinum</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">neurotoxins</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Caco-2</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">binding</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Hc</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>64</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2010</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Passive Oral Immunization by Egg Yolk Immunoglobulin (IgY) to Vibrio cholerae Effectively Prevents Cholera</ArticleTitle>
    <FirstPage LZero="delete">163</FirstPage>
    <LastPage>170</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Kazuyuki</FirstName>
        <LastName>Hirai</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideyuki</FirstName>
        <LastName>Arimitsu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Umeda</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Lianhua</FirstName>
        <LastName>Shen</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kiyoshi</FirstName>
        <LastName>Ayada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshikatsu</FirstName>
        <LastName>Kodama</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takao</FirstName>
        <LastName>Tsuji</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshikazu</FirstName>
        <LastName>Hirai</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Keiji</FirstName>
        <LastName>Oguma</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/40008</ArticleId>
    </ArticleIdList>
    <Abstract>In an attempt to prepare egg yolk immunoglobulin (IgY) to treat and prevent cholera, hens were immunized by a mixture of heat- or formalin-killed Vibrio cholerae O1 and O139 organisms, or by the recombinant cholera toxin B subunit (CTB). The IgYs were partially purified from egg yolk and orally administered to suckling mice before or after challenge with live O1 or O139 cells. The anti-O1 and O139 IgYs and the mixture of either IgY with anti-CTB IgY significantly protected the occurrence of cholera caused by both O1 and O139 infection. Since large amounts of IgY can be prepared very easily and at low cost, this seems to be a useful procedure for preventing and treating cholera.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Vibrio cholerae</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">O1</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">O139</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">IgY</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Elsevier B.V.</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn/>
      <Volume>43</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2005</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Neutrophil and lymphocyte responses to oral Streptococcus in Adamantiades-Behcet's disease</ArticleTitle>
    <FirstPage LZero="delete">125</FirstPage>
    <LastPage>131</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Tomomi</FirstName>
        <LastName>Kurauchi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toshihiko</FirstName>
        <LastName>Matsuo</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshihito</FirstName>
        <LastName>Fujinami</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Emiko</FirstName>
        <LastName>Isogai</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Isogai</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Ohtsuki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Keiji</FirstName>
        <LastName>Oguma</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Immune reactions against microorganisms play an important pathogenic role in Adamantiades-Beh&#231;et’s disease (ABD). We had previously obtained Streptococcus sanguinis (strain BD113-20) isolated from the oral cavity of patients with ABD. To investigate the pathogenesis of this isolate, we examined neutrophil 5 reactions and level of cytokine production by lymphocytes after stimulation with the strain. The reactions
of neutrophils were examined by chemiluminescence assay using whole blood. The
amounts of interferon gamma (IFN-g) and interleukin (IL)-4, IL-8, IL-10, and IL-12
produced by peripheral blood mononuclear cells (PBMCs) were measured by ELISA. 10 Strain BD113-20 activated neutrophils from patients with ABD and healthy volunteers, and, in addition it increased IFN-g production by lymphocytes. Lymphocyte from the patients with ABD showed a dominant T helper 1 (Th-1) immune response. Results indicated that both bacterial stimulation and host hypersensitivity might be involved in the symptoms and pathogenesis of ABD.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Adamantiades-Behcet's disease</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Streptococcus sanguinis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">neutrophil</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">chemiluminescence</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">IL-8</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">T helper-1</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">IFN-gamma</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">IL-12</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>53</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1999</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Molecular typing of enterohemorrhagic Escherichia coli O157:H7 isolated in Okayama Prefecture using pulsed field gel electrophoresis and random amplification of polymorphic DNA.</ArticleTitle>
    <FirstPage LZero="delete">193</FirstPage>
    <LastPage>200</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Yuka</FirstName>
        <LastName>Funamori</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yukako</FirstName>
        <LastName>Fujinaga</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kaoru</FirstName>
        <LastName>Inoue</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshikazu</FirstName>
        <LastName>Hirai</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Keiji</FirstName>
        <LastName>Oguma</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shohei</FirstName>
        <LastName>Kira</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazuhisa</FirstName>
        <LastName>Taketa</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/31612</ArticleId>
    </ArticleIdList>
    <Abstract>&lt;p&gt;Three outbreaks and many isolated cases of enterohemorrhagic Escherichia coli O157:H7 occurred in 1996 and 1997 in Okayama Prefecture, Japan. In an attempt to investigate the route of these infections, the strains isolated from the 3 outbreaks (total 33 strains) and 15 isolated cases (total 15 strains) were investigated using random amplification of polymorphic DNA (RAPD) and pulsed-field gel electrophoresis (PFGE). In addition, 10 strains from an outbreak in Tojo Cho, Hiroshima Prefecture (June 1996), 2 strains from the particular types of meat in Kochi Prefecture, and 42 strains isolated from bovine feces in a farm in Okayama Prefecture were also investigated in the same manner. PFGE was much more useful than RAPD for molecular typing of the clinical isolates, in that it allowed us to classify them into 10 PFGE groups. We noted that the strains differed according to the time and place of the outbreaks (or isolated cases). This indicates that O157:H7 infections in Okayama Prefecture were caused by different strains (although some cases were aggravated by the same strains as were found in other areas). The isolates from bovine feces were classified into 5 groups by PFGE profiles, but none of them were identical to those of the clinical isolates.&lt;/p&gt;
</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">molecular epidemiology</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">enterohemorrhagic Escherichia coli O157: H7</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">pulsed field gel electrophoresis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">random amplification of polymorphic DNA</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>52</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1998</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Antibody and Cytokine Responses in Helicobacter pylori-Infected Various Mouse Strains</ArticleTitle>
    <FirstPage LZero="delete">41</FirstPage>
    <LastPage>48</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Ashoka</FirstName>
        <LastName>Dey</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Keita</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Keiji</FirstName>
        <LastName>Oguma</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshikazu</FirstName>
        <LastName>Hirai</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tadaatsu</FirstName>
        <LastName>Akagi</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/31337</ArticleId>
    </ArticleIdList>
    <Abstract>&lt;p&gt;Helicobacter pylori (H. pylori) infection in the stomach is etiologically closely associated with chronic active gastritis, peptic ulcer, gastric cancer and gastric mucosa-associated lymphoid tissue lymphoma. In this study, we examined the antibody responses and cytokine profiles of three strains of mice (BALB/c, C3H/He, and C57BL/6) infected with H. pylori. Following this, correlations between host-immune reactions and intensity of inflammation were analyzed. H. pylori (ATCC43504) was intragastrically administered once a week to the mice from 4 weeks of age, and they were sacrificed at the ages of 4 and 7 months. In these mice, we examined the histology of the stomach, antibody titers against H. pylori, and serum levels of cytokines (IL-4, IL-10, TNF-alpha, IL-2 and Interferon-gamma). In BALB/c mice, inflammation of the stomach was minimal. Inflammation was observed in 63.6% of C57BL/6 mice and 33.3% of C3h/He mice. In C57BL/6 and C3H/He mice, all the cytokines tended to increase. In contrast, BALB/c mice were inactive in cytokine production except for IL-2. Two C3H/He mice developed severe inflammation with lymph follicles; one showed a response largely typical of Th-1, and the other showed a response largely typical of Th-2. Although a definite correlation was not shown between Th-1/Th-2 response evaluated by cytokine production and intensity of inflammation, it appears that in H. pylori-induced inflammation both cell-mediated (Th-1) and humoral (Th-2) immunity play a role in pathogenesis.&lt;/p&gt;
</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Helicobacter pylori</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">cytokine</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">humoral immunity</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">cell-mediated immunity</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">gastritis</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>49</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1995</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Lipid profiles of Helicobacter pylori and Helicobacter mustelae grown in serum-supplemented and serum-free media.</ArticleTitle>
    <FirstPage LZero="delete">205</FirstPage>
    <LastPage>211</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Mahmudul</FirstName>
        <LastName>Haque</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshikazu</FirstName>
        <LastName>Hirai</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Keiji</FirstName>
        <LastName>Oguma</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/30380</ArticleId>
    </ArticleIdList>
    <Abstract>&lt;p&gt;Many of Helicobacter species have been found to have novel cholesteryl glucosides (CGs). To study the biosynthetic mechanism of CGs, the lipid profiles of H. pylori and H. mustelae grown in serum-supplemented and cholesterol-restricted serum-free media were investigated. In contrast to the serum-supplemented state, helicobacters had less CGs in the serum-free state; a trace amount of CGs and no CG was detected in H. pylori and H. mustelae, respectively. The proportion of total and individual phospholipid also showed significant alteration. Unknown lipids which did not contain phosphate and sugar were detected in the serum-free state, but not in the serum-supplemented state. The CGs were found to be distributed mainly in the membrane fractions, and one of the unknown lipids was found exclusively in the cytosol fraction. Based on these data, it is apparent that the CGs of helicobacters are synthesized by de novo uptake of cholesterol from the media. The unknown lipids detected in the serum-free state may be storage lipids, appearing in response to depletion of nutrients, especially cholesterol, or other factors in the media.&lt;/p&gt;
</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Helicobacter</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">steryl glycoside</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">cholesteryl glucoside</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部保健学科</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1345-0948</Issn>
      <Volume>14</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2004</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>白癬菌に対する木酢液の発育抑制･殺菌作用</ArticleTitle>
    <FirstPage LZero="delete">129</FirstPage>
    <LastPage>133</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Kumi</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazuko</FirstName>
        <LastName>Sumiyoshi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Noriyo</FirstName>
        <LastName>Kaneko</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Chieko</FirstName>
        <LastName>Kawata</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/15191</ArticleId>
    </ArticleIdList>
    <Abstract>足白癬は糖尿病患者で合併しやすく,高齢者にも多発する｡近年,白癬菌に対する木酢液の抗菌作用が知られており,この最適有効濃度を明らかにするため本研究を企画した｡白癬菌はTrichophyton mentagrophytesとTrichophyton rubrumの2菌種を用い,木酢液は市販品を用いた｡発育抑制テストは終濃度2,3,4,5%の木酢液を含んだ寒天平板希釈法で行った｡殺菌テストは2.5,5,10%溶液を胞子と接触後,寒天平板培地に接種し,菌の発育の有無を観察した｡発育抑制作用は,両菌種とも3%以上で7日培養後の菌糸の発育は見られなかった｡殺菌作用は, T. mentagrophytesでは10%,5%においては6時間接触で,2.5%においては24時間接触で菌糸の発育が見られず, T. rubrumでは,10%以上においては24時間接触で,5%においては48時間接触で菌糸の発育が見られなかった｡足浴等の看護ケアに木酢液を応用するためには,今後より短時間の接触で効果が得られる方法の検討が必要である｡</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">木酢液 (Mokusaku-Eki)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">白癬菌 (Trichophyton)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">発育抑制作用 (Antifungal effect)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">足部白癬 (Trichophytosis)</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>114</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2003</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>ピロリ菌 (Helicobacter pylori)</ArticleTitle>
    <FirstPage LZero="delete">325</FirstPage>
    <LastPage>327</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N"/>
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    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Helicobacter 属</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">胃十二指腸疾患</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName/>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn/>
      <Volume/>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1998</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>IgA Protease Produced by Streptococcus sanguis and Antibody Production against IgA Protease in Patients with Behcet's Disease</ArticleTitle>
    <FirstPage LZero="delete"/>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
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    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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