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  <Article>
    <Journal>
      <PublisherName>The Japanese Society of Internal Medicine</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-2918</Issn>
      <Volume>54</Volume>
      <Issue>14</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2015</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Detection of Identical Isolates of Enterococcus faecalis from the Blood and Oral Mucosa in a Patient with Infective Endocarditis</ArticleTitle>
    <FirstPage LZero="delete">1809</FirstPage>
    <LastPage>1814</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Akemi</FirstName>
        <LastName>Okui</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshihiko</FirstName>
        <LastName>Soga</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Susumu</FirstName>
        <LastName>Kokeguchi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Motoko</FirstName>
        <LastName>Nose</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Reiko</FirstName>
        <LastName>Yamanaka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nobuchika</FirstName>
        <LastName>Kusano</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Manabu</FirstName>
        <LastName>Morita</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
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      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>The detection of infective endocarditis (IE) of oral origin has been previously discussed. However, there are few reports confirming this infection using molecular biological techniques. We herein describe the case of a 67-year-old man who developed IE. Blood culture samples and strains obtained from the gingival and buccal mucosa showed 100% identity to Enterococcus faecalis JCM 5803 on sequencing of 16S rRNA gene fragments. A random amplification of polymorphic DNA (RAPD) analysis showed the same pattern for these samples, thus confirming the identity of E. faecalis isolates in the blood and oral mucosa. Our observations provide novel information regarding the level of identity between IE pathogens and oral bacteria.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">causative pathogen</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">identity</Param>
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      <Object Type="keyword">
        <Param Name="value">infective endocarditis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">oral bacteria</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>68</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2014</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Molecular Epidemiology and Clinical Implications of Metallo-β-Lactamase-Producing Pseudomonas aeruginosa Isolated from Urine</ArticleTitle>
    <FirstPage LZero="delete">89</FirstPage>
    <LastPage>99</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Shinichi</FirstName>
        <LastName>Sako</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Reiko</FirstName>
        <LastName>Kariyama</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ritsuko</FirstName>
        <LastName>Mitsuhata</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masumi</FirstName>
        <LastName>Yamamoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koichiro</FirstName>
        <LastName>Wada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ayano</FirstName>
        <LastName>Ishii</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shinya</FirstName>
        <LastName>Uehara</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Susumu</FirstName>
        <LastName>Kokeguchi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nobuchika</FirstName>
        <LastName>Kusano</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiromi</FirstName>
        <LastName>Kumon</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/52405</ArticleId>
    </ArticleIdList>
    <Abstract>We conducted a study on molecular epidemiology and clinical implications of metallo-β-lactamase (MBL)-producing Pseudomonas aeruginosa isolated from urine. Over a 10-year period from 2001 through 2010, a total of 92 MBL-producing P. aeruginosa urine isolates were collected from patients (one isolate per patient) who were admitted to 5 hospitals in Okayama Prefecture, Japan. When cross-infection was suspected in the hospital, pulsed-field gel electrophoresis was performed. In the resulting dendrogram of 79 MBL-producing P. aeruginosa urine isolates, no identical isolates and 7 pairs of isolates with &#8805;80% similarity were found. The biofilm-forming capabilities of 92 MBL-producing P. aeruginosa urine isolates were significantly greater than those of 92 non-MBL-producing urine isolates in a medium of modified artificial urine. The imipenem resistance transferred in 16 of 18 isolates tested, and these frequencies were in the range of 10−3 to 10−9. All of 18 isolates tested belonged to internationally spread sequence type 235 and had 3 gene cassettes of antimicrobial resistance genes in the class 1 integron. The strong biofilm-forming capabilities of MBL-producing P. aeruginosa urine isolates could be seriously implicated in nosocomial infections. To prevent spread of the organism and transferable genes, effective strategies to inhibit biofilm formation in medical settings are needed.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">Pseudomonas aeruginosa</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">metallo-β-lactamase</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">molecular epidemiology</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">biofilm</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">urinary tract infection</Param>
      </Object>
    </ObjectList>
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  </Article>
  <Article>
    <Journal>
      <PublisherName/>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0941-4355</Issn>
      <Volume>18</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2010</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Total bacterial counts on oral mucosa after using a commercial saliva substitute in patients undergoing hematopoietic cell transplantation</ArticleTitle>
    <FirstPage LZero="delete">395</FirstPage>
    <LastPage>398</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Yuko</FirstName>
        <LastName>Sugiura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshihiko</FirstName>
        <LastName>Soga</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kokoro</FirstName>
        <LastName>Yamabe</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Soichiro</FirstName>
        <LastName>Tsutani</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ichiro</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Maeda</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Susumu</FirstName>
        <LastName>Kokeguchi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nobuharu</FirstName>
        <LastName>Fujii</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumihiko</FirstName>
        <LastName>Ishimaru</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mitsune</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fusanori</FirstName>
        <LastName>Nishimura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shogo</FirstName>
        <LastName>Takashiba</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>The commercial saliva substitute OralbalanceA (R) has been reported to alleviate symptoms of postradiotherapy xerostomia in head and neck cancer patients. OralbalanceA (R) may also be effective for xerostomia in patients undergoing hematopoietic cell transplantation (HCT) with high-dose chemotherapy and total-body irradiation. However, HCT patients are in a severely compromised condition, and saliva substitute must not promote infection. We reported previously that OralbalanceA (R) has antimicrobial effects against microbial species detected during HCT in vitro. This study was performed to determine the in vivo effects of OralbalanceA (R) on oral mucosal total bacterial counts in patients undergoing HCT. 

A total of 18 neutropenic patients undergoing HCT were enrolled in this study. Before and after 1 week of OralbalanceA (R) use, bacterial samples were obtained from patients by wiping an area of I center dot 1 cm on the buccal mucosa with sterilized cotton swabs. Total bacterial counts of the obtained samples were examined by quantitative polymerase chain reaction amplification of the bacterial 16S ribosomal RNA gene. As controls, bacterial samples were also obtained from ten healthy subjects, and total bacterial counts were examined. 

No significant increase in bacterial count was observed with use of OralbalanceA (R). None of the patients showed bacterial counts above the range found in healthy controls after using OralbalanceA (R). 

In neutropenic patients undergoing HCT, OralbalanceA (R) did not increase the total counts of oral mucosal bacteria beyond the range found in healthy controls. Oral care using OralbalanceA (R) may alleviate the symptoms induced by hyposalivation without promoting infection.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Hematopoietic cell transplantation</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Xerostomia</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Saliva substitute</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName/>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0941-4355</Issn>
      <Volume>16</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2008</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Antimicrobial effects of the saliva substitute, Oralbalance (R), against microorganisms from oral mucosa in the hematopoietic cell transplantation period</ArticleTitle>
    <FirstPage LZero="delete">421</FirstPage>
    <LastPage>424</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Yuko</FirstName>
        <LastName>Sugiura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshihiko</FirstName>
        <LastName>Soga</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ichiro</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Susumu</FirstName>
        <LastName>Kokeguchi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Sachiko</FirstName>
        <LastName>Nishide</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kotoe</FirstName>
        <LastName>Kono</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kanayo</FirstName>
        <LastName>Takahashi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nobuharu</FirstName>
        <LastName>Fujii</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumihiko</FirstName>
        <LastName>Ishimaru</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mitsune</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kokoro</FirstName>
        <LastName>Yamabe</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Soichiro</FirstName>
        <LastName>Tsutani</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fusanori</FirstName>
        <LastName>Nishimura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shogo</FirstName>
        <LastName>Takashiba</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Goals The commercially available saliva substitute Oralbalance (R) has been reported to alleviate symptoms of post-radiotherapy xerostomia in head and neck cancer patients. Oralbalance (R) may also be effective for xerostomia in patients undergoing hematopoietic cell transplantation (HCT) with high-dose chemotherapy and total-body irradiation. However, HCT patients are severely compromised, and saliva substitute must therefore not promote infection. This study was performed to determine the effects of Oralbalance (R) on microbial species identified during HCT. 

Patients and methods Microbial identification of oral mucosa was performed in 28 patients undergoing HCT. The antimicrobial effects of Oralbalance (R) against bacteria and fungi detected in the HCT period were examined in vitro. Briefly, bacteria and fungi were spread on agar plates, and 0.1g of Oralbalance (R) gel was applied (about phi 1cm). After incubation at 37 degrees C for 24h, the presence of a transparent zone of inhibition around Oralbalance (R) was observed. 

Main results Not only bacterial species constituting normal flora of the oral mucosa but also those not usually constituting normal flora, e.g., coagulase-negative Staphylococcus, were detected. A transparent zone was observed around Oralbalance (R) in all bacterial species examined. No transparent zone was observed for Candida albicans, but growth was inhibited in the area where Oralbalance (R) was applied. 

Conclusions Oralbalance (R) does not facilitate increases in microorganisms in the HCT period. Oral care with Oralbalance (R) does not promote infection in patients undergoing HCT.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Hematopoietic cell transplantation</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Xerostomia</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Saliva substitute</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Antimicrobial activity</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName/>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn/>
      <Volume>41</Volume>
      <Issue>10</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2005</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Role of O-6-methylguanine-DNA methyltransferase and effect of O-6-benzylguanine on the anti-tumor activity of cis-diaminedichloroplatinum(II) in oral cancer cell lines</ArticleTitle>
    <FirstPage LZero="delete">984</FirstPage>
    <LastPage>993</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Yu</FirstName>
        <LastName>Maki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Murakami</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun-ichi</FirstName>
        <LastName>Asaumi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hidetsugu</FirstName>
        <LastName>Tsujigiwa</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hitoshi</FirstName>
        <LastName>Nagatsuka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Susumu</FirstName>
        <LastName>Kokeguchi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazuhiro</FirstName>
        <LastName>Fukui</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Noriko</FirstName>
        <LastName>Kawai</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshinobu</FirstName>
        <LastName>Yanagi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masahiro</FirstName>
        <LastName>Kuroda</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Noriaki</FirstName>
        <LastName>Tanaka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nagahide</FirstName>
        <LastName>Matsubara</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kanji</FirstName>
        <LastName>Kishi</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>&lt;p&gt;The DNA repair enzyme, O-6-methylguanine-DNA methyltransferase (MGMT) modulates the effectiveness of alkylating agents. However, the relationship between MGMT and the sensitivities to other agents has not been explored. In the present study, the association between MGMT expression and the cellular sensitivity to the platinum agent, CDDP was examined in four human oral cancer cell tines. CDDP depleted MGMT protein and mRNA levels in all four cell tines. Two cell lines with low MGMT expression were sensitive to an alkylating agent, N-methyl-N'-nitro-N-nitrosoguanidine and CDDP, whereas two other cell tines with high MGMT expression were resistant to both agents. Furthermore, the addition of the MGMT inhibitor, O-6-benzylguanine (O-6-BG), invariably enhanced CDDP sensitivity. CDDP depleted MGMT expression, and CDDP sensitivity was enhanced by O-6-BG. These results provide valuable information about the relationship between MGMT expression and CDDP sensitivity in oral cancer chemotherapy. (c) 2005 Elsevier Ltd. All rights reserved.
&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">mgmt</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">cddp</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">o-6-bg</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">oral cancer</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Springer</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0344-5704</Issn>
      <Volume>56</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2005</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Effects of histone deacetylase inhibitor FR901228 on expression level of telomerase reverse transcriptase in oral cancer</ArticleTitle>
    <FirstPage LZero="delete">22</FirstPage>
    <LastPage>28</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Murakami</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun-ichi</FirstName>
        <LastName>Asaumi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Noriko</FirstName>
        <LastName>Kawai</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hidetsugu</FirstName>
        <LastName>Tsujigiwa</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshinobu</FirstName>
        <LastName>Yanagi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hitoshi</FirstName>
        <LastName>Nagatsuka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tetsuyoshi</FirstName>
        <LastName>Inoue</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Susumu</FirstName>
        <LastName>Kokeguchi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shoji</FirstName>
        <LastName>Kawasaki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masahiro</FirstName>
        <LastName>Kuroda</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Noriaki</FirstName>
        <LastName>Tanaka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nagahide</FirstName>
        <LastName>Matsubara</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kanji</FirstName>
        <LastName>Kishi</LastName>
        <Affiliation/>
      </Author>
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      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>We speculated whether or not the expression level of telomerase reverse transcriptase (hTERT) would be modulated by agents targeting epigenetics in oral cancer cell lines. Although hTERT is known to be targeted by epigenetic changes, it remains unclear how chemoagents targeting epigenetics work on hTERT transcription. In the present study, the epigenetic effects of histone deacetylase (HDAC) inhibitor FR901228 on hTERT transcription were analysed by RT-PCR in oral cancer cell lines. The mRNA expression of hTERT was upregulated after exposure to FR901228 in hTERT-negative Hep2 cells, even in the hTERT highly expressed SAS and KB cells. Moreover, co-treatment of protein synthesis inhibitor cycloheximide (CHX) resulted in the induction of hTERT transcription by FR901228. This suggests that the induction of hTERT by FR901228 requires de novo protein synthesis to some extent and is more likely a direct than an indirect effect on epigenetic changes such as histone acetylation / deacetylation. We further examined the effect of FR901228 on c-myc protein, which is one of the main hTERT transcription activators. FR901228 repressed c-myc protein only in the absence of CHX, dependent of the enhancement of de novo protein synthesis. Our results indicate that c-myc protein is repressed indirectly by FR901228 but may not contribute FR901228-induced hTERT transcription. The present study showed that the HDAC inhibitor FR901228 induced the hTERT gene by a complex mechanism that involved other transcription factors except for c-myc, in addition to the inhibition of histone deacetylation.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">hTERT</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">FR901228</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">oral cancer</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">HDAC inhibitor</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName/>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn/>
      <Volume/>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1992</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Wolinella recta ATCC 33238 の表層蛋白抗原に関する研究</ArticleTitle>
    <FirstPage LZero="delete"/>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N"/>
        <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>
