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  <Article>
    <Journal>
      <PublisherName>Springer Science and Business Media LLC</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1757-4749</Issn>
      <Volume>18</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2026</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Sodium butyrate augments the antibacterial activity of tetracycline against clinical isolates of multidrug-resistant Vibrio cholerae</ArticleTitle>
    <FirstPage LZero="delete">9</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Sushmita</FirstName>
        <LastName>Kundu</LastName>
        <Affiliation>Division of Biochemistry, ICMR- National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Sourin</FirstName>
        <LastName>Alu</LastName>
        <Affiliation>Division of Biochemistry, ICMR- National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Abhishek</FirstName>
        <LastName>Singh</LastName>
        <Affiliation>Division of Biochemistry, ICMR- National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Animesh</FirstName>
        <LastName>Gope</LastName>
        <Affiliation>Division of General Medicine, ICMR- National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ranjan Kumar</FirstName>
        <LastName>Nandy</LastName>
        <Affiliation>Division of Bacteriology, ICMR- National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Asish K.</FirstName>
        <LastName>Mukhopadhyay</LastName>
        <Affiliation>Division of Bacteriology, ICMR- National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shin-ichi</FirstName>
        <LastName>Miyoshi</LastName>
        <Affiliation>Division of Pharmaceutical Sciences, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nabendu Sekhar</FirstName>
        <LastName>Chatterjee</LastName>
        <Affiliation>Division of Biochemistry, ICMR- National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Sushmita</FirstName>
        <LastName>Bhattacharya</LastName>
        <Affiliation>Division of Biochemistry, ICMR- National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
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      <ArticleId IdType="doi"/>
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    <Abstract>Background Antibiotic resistance poses a major challenge in treating Vibrio cholerae infections. One promising method to counter resistance is the co-administration of antibiotics with non-antibiotic adjuvants to enhance their efficacy. This study investigated the combined action of sodium butyrate (SB) and tetracycline on tetracycline-resistant V. cholerae strains.&lt;br&gt;
Results The combined activity of SB and antibiotics was assessed on eight V. cholerae clinical isolates using the Fractional Inhibitory Concentration Index (FICI), with SB-Tetracycline showing strong synergy (FICI: 0.09&#8211;0.5). Functional and mechanistic studies, including time-kill kinetics, live/dead staining, SEM-based morphological analysis, and fluorometric assays, demonstrated a synergistic antibacterial effect of SB and Tetracycline. This effect was associated with increased membrane permeability, disruption of membrane integrity, dissipation of the proton motive force, and suppression of efflux activity. These changes collectively led to membrane damage, enhanced intracellular accumulation of Tetracycline, decreased intracellular ATP levels, and ultimately, bacterial cell death. Moreover, GM1-CT ELISA and fluorescence microscopy revealed the synergistic anti-virulence activity of the SB- Tetracycline combination. Finally, the combination of SB and Tetracycline showed enhanced efficacy in animal models compared with monotherapy.&lt;br&gt;
Conclusion: The observed SB-Tetracycline synergy provides a promising therapeutic approach to overcome tetracycline resistance in V. cholerae, offering a potential adjunct strategy for the management of antibiotic-resistant cholera infections.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">V. cholerae</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Sodium butyrate</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Tetracycline</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Synergy</Param>
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      <Object Type="keyword">
        <Param Name="value">Antibiotic adjuvant</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>American Society for Microbiology</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0099-2240</Issn>
      <Volume/>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2025</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Efficient resuscitation of early-stage viable but non-culturable cells of Vibrio cholerae using treatment with proteolytic enzymes</ArticleTitle>
    <FirstPage LZero="delete"/>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Shin-ichi</FirstName>
        <LastName>Miyoshi</LastName>
        <Affiliation>Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mona</FirstName>
        <LastName>Ogasawara</LastName>
        <Affiliation>Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shiho</FirstName>
        <LastName>Niwaki</LastName>
        <Affiliation>Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Rena</FirstName>
        <LastName>Sugihara</LastName>
        <Affiliation>Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Basilua Andre</FirstName>
        <LastName>Muzembo</LastName>
        <Affiliation>Research Institute of Nursing Care for People and Community, University of Hyogo</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Daisuke</FirstName>
        <LastName>Imamura</LastName>
        <Affiliation>Research Center for Intestinal Health Science, Okayama University</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Vibrio cholerae, the etiological agent of cholera, is ubiquitous in environmental brackish waters. Exposure to low water temperatures induces the bacterium to enter a viable but non-culturable (VBNC) state. In this study, a stepwise decrease in water temperature to 4°C was found to delay the transition to the non-culturable state compared to an abrupt temperature drop, suggesting that V. cholerae cells partially adapt to low temperatures. V. cholerae VBNC cells maintained at 4°C gradually lost their ability to revert to a culturable state. However, VBNC cells in the early stage of dormancy were efficiently resuscitated following treatment with proteolytic enzymes, including proteinase K. The abundance of culturable V. cholerae cells in brackish estuarine waters was quantified using the most probable number (MPN)&#8211;quantitative polymerase chain reaction (qPCR) method. Although culturable cells were undetectable in samples treated with bovine serum albumin, they were estimated at 93 and 1,500 MPN/mL in two water samples collected on different days and pre-incubated with proteinase K. Similarly, the abundance of Vibrio species increased markedly following treatment with this enzyme. Additionally, cells of Vibrio species were enumerated by the plating method using CHROMagar Vibrio plates. Consistent with the results of the MPN&#8211;qPCR method, treatment with proteinase K resulted in over a 100-fold increase in colony formation. Collectively, these findings suggest that treatment with proteinase K is effective for resuscitating and quantifying V. cholerae VBNC cells in environmental water samples.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">Vibrio cholerae</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">viable but non-culturable</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">VBNC</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">protease</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">proteolytic enzyme</Param>
      </Object>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>American Society for Microbiology</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0066-4804</Issn>
      <Volume>69</Volume>
      <Issue>12</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2025</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Genomic portrayal of emerging carbapenem-resistant El Tor variant Vibrio cholerae O1</ArticleTitle>
    <FirstPage LZero="delete">e00740-25</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Sreeja</FirstName>
        <LastName>Shaw</LastName>
        <Affiliation>ICMR-National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Agila Kumari</FirstName>
        <LastName>Pragasam</LastName>
        <Affiliation>V. Ramalingaswami Bhawan, Indian Council of Medical Research</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Goutam</FirstName>
        <LastName>Chowdhury</LastName>
        <Affiliation>ICMR-National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Prosenjit</FirstName>
        <LastName>Samanta</LastName>
        <Affiliation>ICMR-National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Deboleena</FirstName>
        <LastName>Roy</LastName>
        <Affiliation>ICMR-National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Debjani</FirstName>
        <LastName>Ghosh</LastName>
        <Affiliation>ICMR-National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Thandavarayan</FirstName>
        <LastName>Ramamurthy</LastName>
        <Affiliation>ICMR-National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jigna</FirstName>
        <LastName>Karia</LastName>
        <Affiliation>Medical College Baroda</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Govind</FirstName>
        <LastName>Ninama</LastName>
        <Affiliation>Medical College Baroda</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shin-ichi</FirstName>
        <LastName>Miyoshi</LastName>
        <Affiliation>Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yukihiro</FirstName>
        <LastName>Akeda</LastName>
        <Affiliation>National Institute of Infectious Diseases</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hemanta</FirstName>
        <LastName>Koley</LastName>
        <Affiliation>ICMR-National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Asish Kumar</FirstName>
        <LastName>Mukhopadhyay</LastName>
        <Affiliation>ICMR-National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>The escalating prevalence of carbapenem-resistant (CR) enteric pathogens elicits significant challenges to public health management and effective antimicrobial therapy. While carbapenem resistance is rare in Vibrio cholerae O1 (VC), the recent emergence of CR strains reveals a concerning shift in their antimicrobial resistance (AMR) landscape. This study aims to characterize the resistance mechanisms in newly identified El Tor CRVC isolated from cholera patients in Gujarat, India during 2019. Fifty VC isolates were screened for major virulence-associated genes along with the determination of their antibiotic resistance profiles using Kirby-Bauer disk diffusion and MIC assays. Whole-genome sequencing (WGS) was employed to investigate the underlying mechanisms of CR. All the isolates exhibited hypervirulent Haitian alleles of major virulence genes and AMR profiles of typical multidrug resistance (MDR). Strikingly, 12% (6/50) of them were resistant to carbapenems and other antibiotics. Molecular analysis revealed that these CR isolates were clonally related and harbored a 142 kbp IncA/C type conjugative mega-plasmid with several AMR encoding genes, including blaNDM-1, that can be easily transferred to other bacterial species and confer donor AMR patterns. The plasmid’s competence for horizontal gene transfer presents a significant risk of dissemination to other enteric pathogens and thereby may complicate the treatment. This finding emphasizes the urgent need for enhanced genomic surveillance and robust antimicrobial stewardship programs aimed at curbing the spread of CRVC strains and mitigating their impact on cholera treatment and containment strategies.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">antimicrobial resistance</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Vibrio cholerae</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">blaNDM-1</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">carbapenem resistance</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">horizontal gene transfer</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">IncA/C plasmid</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Informa UK Limited</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1949-0976</Issn>
      <Volume>17</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2025</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Asiatic acid, a novel ciprofloxacin adjuvant inhibits Shigella flexneri infection</ArticleTitle>
    <FirstPage LZero="delete">2586329</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Priyanka</FirstName>
        <LastName>Maitra</LastName>
        <Affiliation>Division of Biochemistry, ICMR-National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Samhati</FirstName>
        <LastName>Bhukta</LastName>
        <Affiliation>Division of Biochemistry, ICMR-National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Animesh</FirstName>
        <LastName>Gope</LastName>
        <Affiliation>Division of Clinical Medicine, ICMR-National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Pratanu</FirstName>
        <LastName>Kayet</LastName>
        <Affiliation>Division of Bioinformatics, ICMR-National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Surajit</FirstName>
        <LastName>Basak</LastName>
        <Affiliation>Division of Bioinformatics, ICMR-National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shin-Ichi</FirstName>
        <LastName>Miyoshi</LastName>
        <Affiliation>Division of Pharmaceutical Sciences, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kei</FirstName>
        <LastName>Kitahara</LastName>
        <Affiliation>Collaborative Research Center of Okayama University for Infectious Diseases in India, ICMR-National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shanta</FirstName>
        <LastName>Dutta</LastName>
        <Affiliation>Department of Bacteriology, ICMR-National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Sushmita</FirstName>
        <LastName>Bhattacharya</LastName>
        <Affiliation>Division of Biochemistry, ICMR-National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Bacterial infection caused by intracellular pathogens such as Shigella flexneri is a rapidly increasing global health concern that requires urgent and necessary action. The dearth of licensed vaccines against shigellosis and the decline in susceptibility to conventional antibiotics has encouraged the development of new antibiotic principles and drugs. The treatment options are decreasing faster than the discovery rate of new antibacterial agents. Combinatorial approach of antibiotics with non-antibiotic adjuvants is a promising aspect to treat resistant bacterial infections. Asiatic acid, a membrane-disrupting triterpenoid with wide antimicrobial and immunomodulatory properties, can potentiate antibiotics, but the exact mechanisms remain broadly unexplored. Therefore, in this study, we screened the interaction of asiatic acid with several antibiotics. The results showed synergistic interactions of asiatic acid with antibiotics against susceptible and multidrug-resistant S. flexneri clinical isolates. Particularly important was the interaction of asiatic acid with the quinolone antibiotics ciprofloxacin and nalidixic acid. A detailed study showed that combined treatment of asiatic acid with ciprofloxacin inhibited S. flexneri biofilm formation and resistance development. An increase in membrane disruption and depolarization upon co-treatment was evident by surface electron and confocal microscopy. In addition, asiatic acid and ciprofloxacin synergism was identified to inhibit efflux activity and intracellular bacterial viability. However, asiatic acid showed no synergistic toxicity with ciprofloxacin towards mammalian cells. The antibacterial activity was further verified in a S. flexneri infected mice model. Therapeutic benefits were evident with reduced bacterial burden, recovery from intestinal tissue damage and increase in mice survivability. The results showed that this combination can target the bacterial membrane, efflux pump proteins and biofilm formation, thereby preventing resistance development. The combination treatment offers a proof of concept in targeting essential bacterial activities and might be developed into a novel and efficient treatment alternative against S. flexneri.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">Shigella flexneri</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">asiatic acid</Param>
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      <Object Type="keyword">
        <Param Name="value">ciprofloxacin</Param>
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      <Object Type="keyword">
        <Param Name="value">adjuvant</Param>
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      <Object Type="keyword">
        <Param Name="value">membrane damage</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">depolarization</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">nuclear damage</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">efflux inhibitor</Param>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>Springer Science and Business Media LLC</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>2045-2322</Issn>
      <Volume>15</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2025</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Lactose fermenting enteroinvasive Escherichia coli from diarrhoeal cases confers enhanced virulence</ArticleTitle>
    <FirstPage LZero="delete">24040</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Debjani</FirstName>
        <LastName>Ghosh</LastName>
        <Affiliation>Division of Bacteriology, ICMR-National Institute for Research in Bacterial Infections (ICMR-NIRBI)</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Prolay</FirstName>
        <LastName>Halder</LastName>
        <Affiliation>Division of Bacteriology, ICMR-National Institute for Research in Bacterial Infections (ICMR-NIRBI)</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Prosenjit</FirstName>
        <LastName>Samanta</LastName>
        <Affiliation>Division of Bacteriology, ICMR-National Institute for Research in Bacterial Infections (ICMR-NIRBI)</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Goutam</FirstName>
        <LastName>Chowdhury</LastName>
        <Affiliation>Collaborative Research Centre of Okayama University for Infectious Diseases, ICMR-National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Sreeja</FirstName>
        <LastName>Shaw</LastName>
        <Affiliation>Division of Bacteriology, ICMR-National Institute for Research in Bacterial Infections (ICMR-NIRBI)</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Puja</FirstName>
        <LastName>Bose</LastName>
        <Affiliation>Division of Bacteriology, ICMR-National Institute for Research in Bacterial Infections (ICMR-NIRBI)</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Deboleena</FirstName>
        <LastName>Roy</LastName>
        <Affiliation>Division of Bacteriology, ICMR-National Institute for Research in Bacterial Infections (ICMR-NIRBI)</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nivedita</FirstName>
        <LastName>Roy</LastName>
        <Affiliation>Division of Bacteriology, ICMR-National Institute for Research in Bacterial Infections (ICMR-NIRBI)</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kei</FirstName>
        <LastName>Kitahara</LastName>
        <Affiliation>Collaborative Research Centre of Okayama University for Infectious Diseases, ICMR-National Institute for Research in Bacterial Infections</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Thandavarayan</FirstName>
        <LastName>Ramamurthy</LastName>
        <Affiliation>Division of Bacteriology, ICMR-National Institute for Research in Bacterial Infections (ICMR-NIRBI)</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hemanta</FirstName>
        <LastName>Koley</LastName>
        <Affiliation>Division of Bacteriology, ICMR-National Institute for Research in Bacterial Infections (ICMR-NIRBI)</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shin-ichi</FirstName>
        <LastName>Miyoshi</LastName>
        <Affiliation>Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shanta</FirstName>
        <LastName>Dutta</LastName>
        <Affiliation>Division of Bacteriology, ICMR-National Institute for Research in Bacterial Infections (ICMR-NIRBI)</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Asish Kumar</FirstName>
        <LastName>Mukhopadhyay</LastName>
        <Affiliation>Division of Bacteriology, ICMR-National Institute for Research in Bacterial Infections (ICMR-NIRBI)</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Enteroinvasive Escherichia coli (EIEC), known for causing bacillary dysentery akin to Shigella species, comprises both lactose-fermenting (LF) and non-lactose-fermenting (NLF) isolates. While NLF-EIEC is a well-established pathogen associated with acute dysentery and harbours classical Shigella-like virulence factors, the role of LF-EIEC in human disease remains underexplored. In this study, we sought to characterize LF-EIEC clinical isolates and assessed their pathogenic potential in comparison to NLF-EIEC. Among 13,682 diarrhoeal stool specimens, six LF and nine NLF-EIEC were isolated, predominantly belonging to serogroups O28ac, O125, O136, and O152. Unlike other E. coli, all the EIEC isolates were non-motile. Both the types of EIEC had multiple plasmids harbouring several virulence encoding genes (ipaBCD, ial, virF, sig, sepA and ipaH). Resistance to recent generation antibiotics were mostly confined to NLF-EIEC but some of the LF-EIEC were resistant only to ceftriaxone. Higher invasion ability and significant increase in the expression of virulence encoding genes by the LF-EIEC (p&#8201;&lt;&#8201;0.05) were noted during infection to Int407 cell-line. Additionally, LF-EIEC exhibited extensive colonization of the mouse intestine and expressed severe keratoconjunctivitis in guinea pigs. Together, our findings highlight LF-EIEC as an emerging pathogenic variant warranting heightened surveillance and comprehensive investigation to better understand its epidemiological and clinical significance.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">Antibiotic resistance</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Bacterial infections</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Diarrhoea</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Enteroinvasive Escherichia coli</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Keratoconjunctivitis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Pathogenesis</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Elsevier BV</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1046-5928</Issn>
      <Volume>149</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2018</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Functional analysis of N-terminal propeptide in the precursor of Vibrio vulnificus metalloprotease by using cell-free translational system</ArticleTitle>
    <FirstPage LZero="delete">13</FirstPage>
    <LastPage>16</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Tomoka</FirstName>
        <LastName>Kawase</LastName>
        <Affiliation>Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumi</FirstName>
        <LastName>Miura</LastName>
        <Affiliation>Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Anusuya</FirstName>
        <LastName>Debnath</LastName>
        <Affiliation>Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kinuyo</FirstName>
        <LastName>Imakura</LastName>
        <Affiliation>Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shin-ichi</FirstName>
        <LastName>Miyoshi</LastName>
        <Affiliation>Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Vibrio vulnificus is a human pathogen causing fatal septicemia with edematous and hemorrhagic skin damage. Among multiple virulence factors, an extracellular metalloprotease termed as V. vulnificus protease (VVP) is known to play a crucial role in eliciting the skin damage. The mature VVP (413 aa) is composed of two domains, the N-terminal core domain with proteolytic activity and the C-terminal domain mediates efficient attachment to protein substrates. However, VVP is produced as an inactive precursor (609 aa) with a signal peptide (24 aa) and propeptide (172 aa). In order to clarify the function of propeptide, a series of DNA fragments encoding the VVP precursor and its various domains were designed and the proteins were expressed in vitro by using cell-free translational system. The results indicated that the propeptide might function as an intramolecular chaperon to promote the proper folding of both N-terminal and C-terminal domains. The obtained results also suggest that the propeptide, itself was unstable and thus digested easily by the enzymes present in cell lysate used for cell-free system. Additionally, the C-terminal domain in VVP found to inhibit the folding of the N-terminal domain in absence of propeptide.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Vibrio vulnificus</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Protease</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Propeptide</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Domain</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Cell-free translational system</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>American Society for Microbiology</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>2576-098X</Issn>
      <Volume>12</Volume>
      <Issue>12</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2023</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Complete genomic sequence of Vibrio fluvialis strain IDH5335 isolated from a patient with diarrhea in Kolkata, India</ArticleTitle>
    <FirstPage LZero="delete"/>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Goutam</FirstName>
        <LastName>Chowdhury</LastName>
        <Affiliation>Collaborative Research Center of Okayama University for Infectious Diseases in India at ICMR-NICED</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kei</FirstName>
        <LastName>Kitahara</LastName>
        <Affiliation>Collaborative Research Center of Okayama University for Infectious Diseases in India at ICMR-NICED</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Makoto</FirstName>
        <LastName>Taniguchi</LastName>
        <Affiliation>Oral Microbiome Center, Taniguchi Dental Clinic</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazuma</FirstName>
        <LastName>Uesaka</LastName>
        <Affiliation>Graduate School of Bioagricultural Sciences, Nagoya University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Basilua Andre</FirstName>
        <LastName>Muzembo</LastName>
        <Affiliation>Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Debmalya</FirstName>
        <LastName>Mitra</LastName>
        <Affiliation>Collaborative Research Center of Okayama University for Infectious Diseases in India at ICMR-NICED</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ayumu</FirstName>
        <LastName>Ohno</LastName>
        <Affiliation>Collaborative Research Center of Okayama University for Infectious Diseases in India at ICMR-NICED</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Thandavarayan</FirstName>
        <LastName>Ramamurthy</LastName>
        <Affiliation>ICMR-National Institute of Cholera and Enteric Diseases</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shanta</FirstName>
        <LastName>Dutta</LastName>
        <Affiliation>ICMR-National Institute of Cholera and Enteric Diseases</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shin-ichi</FirstName>
        <LastName>Miyoshi</LastName>
        <Affiliation>Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Asish Kumar</FirstName>
        <LastName>Mukhopadhyay</LastName>
        <Affiliation>ICMR-National Institute of Cholera and Enteric Diseases</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>We isolated a Vibrio fluvialis strain (IDH5335) from a stool sample collected from a patient with diarrhea. In this announcement, we report the complete genomic sequence of this organism, which was obtained by combining Illumina and Oxford Nanopore sequencing data.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Vibrio fluvialis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">diarrhea</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">bacteria</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">genome</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Springer Science and Business Media LLC</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0302-8933</Issn>
      <Volume>205</Volume>
      <Issue>10</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2023</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Flavobacterium okayamense sp. nov. isolated from surface seawater</ArticleTitle>
    <FirstPage LZero="delete">346</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Kei</FirstName>
        <LastName>Kitahara</LastName>
        <Affiliation>Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Basilua Andre</FirstName>
        <LastName>Muzembo</LastName>
        <Affiliation>Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Sho</FirstName>
        <LastName>Morohoshi</LastName>
        <Affiliation>TechnoSuruga Laboratory Co., Ltd</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tadao</FirstName>
        <LastName>Kunihiro</LastName>
        <Affiliation>TechnoSuruga Laboratory Co., Ltd</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nozomi</FirstName>
        <LastName>Tazato</LastName>
        <Affiliation>TechnoSuruga Laboratory Co., Ltd</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ayumu</FirstName>
        <LastName>Ohno</LastName>
        <Affiliation>Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazuma</FirstName>
        <LastName>Uesaka</LastName>
        <Affiliation>Graduate School of Bioagricultural Sciences, Nagoya University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Makoto</FirstName>
        <LastName>Taniguchi</LastName>
        <Affiliation>Oral Microbiome Center, Taniguchi Dental Clinic</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shin-ichi</FirstName>
        <LastName>Miyoshi</LastName>
        <Affiliation>Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Strain KK2020170T, a Gram-stain negative, yellow colony-forming bacterium, was isolated from surface seawater sampled in Kojima Bay, Okayama, Japan. Phylogenetic analysis based on the 16S rRNA gene revealed that strain KK2020170T belongs to the genus Flavobacterium, with Flavobacterium haoranii LQY-7T (98.1% similarity) being its closest relative, followed by Flavobacterium sediminis MEBiC07310T (96.9%) and Flavobacterium urocaniciphilum YIT 12746T (96.0%). Whole-genome shotgun sequencing showed that strain KK2020170T, when paralleled with F. haoranii LQY-7 T, had 81.3% average nucleotide identity, and 24.6% in silico DNA&#8211;DNA hybridization values, respectively. The DNA G&#8201;+&#8201;C content of strain KK2020170T was 31.1 mol%. The most abundant fatty acids (&gt;&#8201;10%) of strain KK2020170T were iso-C15:&#8202;0, iso-C17:&#8202;0 3-OH and iso-C15:&#8202;1 G. The dominant respiratory quinone of the strain was menaquinone MK-6. Based on the phylogenetic and phenotypic analysis results, we propose that strain KK2020170T represents a novel species, for which the name Flavobacterium okayamense sp. nov. has been proposed. The type strain is KK2020170T (=&#8201;ATCC TSD-280 T&#8201;=&#8201;NBRC 115344 T).</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Bacteroidota</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Flavobacterium</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">New taxa</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Sea water</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Wiley</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1097-3958</Issn>
      <Volume>25</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2022</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Isolation and identification of soil bacteria resistant to surfactants in washing detergents</ArticleTitle>
    <FirstPage LZero="delete">521</FirstPage>
    <LastPage>525</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Shin-ichi</FirstName>
        <LastName>Miyoshi</LastName>
        <Affiliation>Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naomi</FirstName>
        <LastName>Okubo</LastName>
        <Affiliation>Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Okayama University  Okayama‐City Okayama Japan</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Satoko</FirstName>
        <LastName>Mitsumori</LastName>
        <Affiliation>Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Okayama University  Okayama‐City Okayama Japan</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Linear alkylbenzene sulfonate (LAS) and polyoxyethylene lauryl ether (POLE) are the major surfactants in washing detergents. In the present study, we isolated surfactant-resistant bacteria from soil samples collected from a sports ground and a farm field. The samples were treated with 2.0% LAS or POLE at 25°C for 30&#8201;min and cultivated on agar plates at 25°C for several days, after which manifold bacterial colonies were isolated. Thereafter, we tested the ability of each bacterial isolate to resist the antibacterial activity of the surfactant. Ten LAS-resistant strains were isolated, and all were found to be Gram-negative bacteria such as Enterobacter and Pseudomonas. On the other hand, 18 POLE-resistant strains were isolated, of which 14 were Gram-positive bacteria including Bacillus and Microbacterium. Notably, one POLE-resistant strain was identified as Bacillus cereus, a potential causative agent for foodborne illness. The genera of LAS- and POLE-resistant bacteria did not overlap. Therefore, the combination of LAS and POLE could be more effective to eliminate soil bacteria from clothes and/or daily necessities.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Surfactant</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Washing detergent</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Linear alkylbenzene sulfonate</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Soil bacteria</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Springer</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0959-3993</Issn>
      <Volume>28</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2012</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>An extracellular serine protease produced by Vibrio vulnificus NCIMB 2137, a metalloprotease-gene negative strain isolated from a diseased eel</ArticleTitle>
    <FirstPage LZero="delete">1633</FirstPage>
    <LastPage>1639</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Shin-ichi</FirstName>
        <LastName>Miyoshi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Wang</FirstName>
        <LastName>Jiyou</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Keizo</FirstName>
        <LastName>Katoh</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mitsutoshi</FirstName>
        <LastName>Senoh</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tamaki</FirstName>
        <LastName>Mizuno</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoko</FirstName>
        <LastName>Maehara</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Vibrio vulnificus is a ubiquitous estuarine microorganism but causes fatal systemic infections in immunocompromised humans, cultured eels or shrimps. An extracellular metalloprotease VVP/VvpE has been reported to be a potential virulence factor of the bacterium; however, a few strains isolated from a diseased eel or shrimp were recently found to produce a serine protease termed VvsA, but not VVP/VvpE. In the present study, we found that these strains had lost the 80 kb genomic region including the gene encoding VVP/VvpE. We also purified VvsA from the culture supernatant through ammonium sulfate fractionation, gel filtration and ion-exchange column chromatography, and the enzyme was demonstrated to be a chymotrypsin-like protease, as well as those from some vibrios. The gene vvsA was shown to constitute an operon with a downstream gene vvsB, and several Vibrio species were found to have orthologues of vvsAB. These findings indicate that the genes vvp/vvpE and vvsAB might be mobile genetic elements.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Polymerase chain reaction</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Purification</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Serine protease</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Metalloprotease</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Vibrio vulnificus</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>125</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2013</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>内陸地津山で発症した季節外れのVibrio vulnificus感染症</ArticleTitle>
    <FirstPage LZero="delete">35</FirstPage>
    <LastPage>39</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Hideharu</FirstName>
        <LastName>Hagiya</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Sumiko</FirstName>
        <LastName>Shiota</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shin-ichi</FirstName>
        <LastName>Miyoshi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasutoshi</FirstName>
        <LastName>Kuroe</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroyoshi</FirstName>
        <LastName>Nojima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shinkichi</FirstName>
        <LastName>Otani</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Junichi</FirstName>
        <LastName>Sugiyama</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiromichi</FirstName>
        <LastName>Naito</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Susumu</FirstName>
        <LastName>Kawanishi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shingo</FirstName>
        <LastName>Hagioka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoki</FirstName>
        <LastName>Morimoto</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>　A 68-year-old man with alcohol addiction, who lived in the suburbs of Tsuyama, an inland city located in northeast Okayama prefecture, was transported to the emergency unit of the Tsuyama Central Hospital in a state of cardiopulmonary arrest (CPA). Despite rigorous systemic investigation and treatment, the patient died 2 hours after arrival. After his death, Vibrio vulnificus was isolated from his blood culture.
　Vibrio vulnificus causes fatal infection in humans, usually only in areas located close to the sea where appropriate temperature and suitable salt concentration for its growth are available. Therefore, its occurrence is epidemiologically restricted ; in Japan, the western coastal areas, especially in summers, are reported to be the high-risk regions. This is a rare case because it occurred in a city approximately 50 kilometers from both the Sea of Japan and the Pacific coast of Okayama, and at the end of October in 2011. Economic development and distribution systems have made it possible to transport various food products from coastal areas or abroad to any place in a short time, such that these infections can potentially develop in areas other than expected. We should be aware of the increasing risk of Vibrio vulnificus infection during any season and at any place, especially in patients with abnormal liver function.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Vibrio vulnificus</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Elsevier</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0041-0101</Issn>
      <Volume>57</Volume>
      <Issue>6</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2011</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Inactivation of Vibrio vulnificus hemolysin through mutation of the N- or C-terminus of the lectin-like domain</ArticleTitle>
    <FirstPage LZero="delete">904</FirstPage>
    <LastPage>908</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Shin-ichi</FirstName>
        <LastName>Miyoshi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuki</FirstName>
        <LastName>Abe</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mitsutoshi</FirstName>
        <LastName>Senoh</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tamaki</FirstName>
        <LastName>Mizuno</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoko</FirstName>
        <LastName>Maehara</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Nakao</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Vibrio vulnificus is an etiological agent causing serious systemic infections in the immunocompromised humans or cultured eels. This species commonly produces a hemolytic toxin consisting of the cytolysin domain and the lectin-like domain. For hemolysis, the lectin-like domain specifically binds to cholesterol in the erythrocyte membrane, and to form a hollow oligomer, the toxin is subsequently assembled on the membrane. The cytolysin domain is essential for the process to form the oligomer. Three-dimensional structure model revealed that two domains connected linearly and the C-terminus was located near to the joint of the domains. Insertion of amino acid residues between two domains was found to cause inactivation of the toxin. In the C-terminus, deletion, substitution or addition of an amino acid residue also elicited reduction of the activity. However, the cholesterol-binding ability was not affected by the mutations. These results suggest that mutation of the C- or N-terminus of the lectin-like domain may result in blockage of the toxin assembly.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Vibrio vulnificus</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Hemolysin</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Cell-free translation</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Site-directed mutagenesis</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Elsevier</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0168-1605</Issn>
      <Volume>143</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2010</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Prevalence and antimicrobial resistance of Salmonella in retail foods in northern China</ArticleTitle>
    <FirstPage LZero="delete">230</FirstPage>
    <LastPage>234</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">He</FirstName>
        <LastName>Yan</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Lin</FirstName>
        <LastName>Li</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">M. Jahangir</FirstName>
        <LastName>Alam</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Sumio</FirstName>
        <LastName>Shinoda</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shin-ichi</FirstName>
        <LastName>Miyoshi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Lei</FirstName>
        <LastName>Shi</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>A total of 387 retail meat, seafood and milk powder samples were collected from nine cities in northern China in 2005 and screened for the presence of Salmonella. Salmonella strains isolated were subjected to serotyping and antimicrobial susceptibility testing. Salmonella was isolated from 81 (20.9%, 81/387) samples and classified into 23 serotypes. The isolates were frequently resistant to sulfamethoxazole (86.4%), sulfamethoxazole/trimethoprim (48.1%), nalidixic acid (30.9%), tetracycline (19.8%), carboxybenzylpenicillin (17.3%), amoxicillin (17.3%) and ampicillin (16.0%). The multiple resistance (resistance to &#8805; 3 antibiotics) was found in 29.6% (n = 24) isolates. Additionally, 4 isolates from chicken displayed the ACSSuTNx profile, resistant to ampicillin, chloramphenicol, streptomycin, sulfonamide, tetracycline and nalidixic acid, in particular, strain HBS084 showing the resistance to as many as 20 antibiotics. Salmonella from chicken showed the higher frequency of antimicrobial resistance. Our findings indicate that in northern China food products of animal origin can be a source of exposure for consumers to multiresistant Salmonella strains</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Salmonella</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Prevalence</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Retail meats</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Antimicrobial resistance</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学環境管理センター</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0917-1533</Issn>
      <Volume>22</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2000</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>編集後記</ArticleTitle>
    <FirstPage LZero="delete">81</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Shinichi</FirstName>
        <LastName>Miyoshi</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList/>
    <ReferenceList/>
  </Article>
</ArticleSet>
