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  <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>
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        <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>
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    </ArticleIdList>
    <Abstract>Immune reactions against microorganisms play an important pathogenic role in Adamantiades-Behçet’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>
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        <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>
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    <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>
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      <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>
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      <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>
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      <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>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>113</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2001</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>感染症新法</ArticleTitle>
    <FirstPage LZero="delete">113</FirstPage>
    <LastPage>114</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
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      <ArticleId IdType="doi"/>
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    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList/>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>113</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2001</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>感染症と癌</ArticleTitle>
    <FirstPage LZero="delete">101</FirstPage>
    <LastPage>106</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
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    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">C型肝炎ウィルス</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">EBウィルス</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Helicobacter pylori</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>118</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2007</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>ボツリヌスC型とD型神経毒素を支配するバクテリオファージの遺伝子解析と溶原化の分子機構</ArticleTitle>
    <FirstPage LZero="delete">209</FirstPage>
    <LastPage>213</LastPage>
    <Language>EN</Language>
    <AuthorList>
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        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
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        <FirstName EmptyYN="N"/>
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      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
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      <Author>
        <FirstName EmptyYN="N"/>
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        <Affiliation/>
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        <FirstName EmptyYN="N"/>
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      <Author>
        <FirstName EmptyYN="N"/>
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        <Affiliation/>
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        <FirstName EmptyYN="N"/>
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        <Affiliation/>
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      <Author>
        <FirstName EmptyYN="N"/>
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        <Affiliation/>
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      <Author>
        <FirstName EmptyYN="N"/>
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      <ArticleId IdType="doi"/>
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    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">バクテリオファージ</Param>
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      <Object Type="keyword">
        <Param Name="value">ボツリヌス毒素</Param>
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      <Object Type="keyword">
        <Param Name="value">挿入配列</Param>
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      <Object Type="keyword">
        <Param Name="value">プラスミド</Param>
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      <Object Type="keyword">
        <Param Name="value">プロファージ</Param>
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    <ReferenceList/>
  </Article>
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