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  <Article>
    <Journal>
      <PublisherName>Wiley</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>2050-0904</Issn>
      <Volume>11</Volume>
      <Issue>12</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2023</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Nontuberculous mycobacterial abscess of lacrimal sac and eyelid debridement: Case report</ArticleTitle>
    <FirstPage LZero="delete">e8364</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Toshihiko</FirstName>
        <LastName>Matsuo</LastName>
        <Affiliation>Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takehiro</FirstName>
        <LastName>Tanaka</LastName>
        <Affiliation>Department of Pathology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kiyoshi</FirstName>
        <LastName>Yamada</LastName>
        <Affiliation>Department of Plastic and Reconstructive Surgery, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Motoko</FirstName>
        <LastName>Nose</LastName>
        <Affiliation>Department of Clinical Laboratory, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasushi</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation>Department of Allergy and Respiratory Medicine, Okayama University Hospital</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>A 56-year-old otherwise healthy woman developed abscess from dacryocystitis in the right lower eyelid. The smear of puncture fluid showed acid-fast bacilli and Mycobacterium abscessus was identified after a month. The early start of clarithromycin/ethambutol was switched to clarithromycin/levofloxacin. Debridement specimen after 7-month treatment showed granulomatous tissue with no bacilli.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">debridement</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">eyelid</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">lacrimal sac</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Mycobacterium abscessus</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">nontuberculous mycobacteria</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Public Library of Science</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1932-6203</Issn>
      <Volume>15</Volume>
      <Issue>8</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2020</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Nintedanib can be used safely and effectively for idiopathic pulmonary fibrosis with predicted forced vital capacity &lt;= 50%: A multi-center retrospective analysis</ArticleTitle>
    <FirstPage LZero="delete">e0236935</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Satoru</FirstName>
        <LastName>Senoo</LastName>
        <Affiliation>Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nobuaki</FirstName>
        <LastName>Miyahara</LastName>
        <Affiliation>Department of Medical Technology, Okayama University Graduate School of Health Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akihiko</FirstName>
        <LastName>Taniguchi</LastName>
        <Affiliation>Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naohiro</FirstName>
        <LastName>Oda</LastName>
        <Affiliation>Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Junko</FirstName>
        <LastName>Itano</LastName>
        <Affiliation>Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hisao</FirstName>
        <LastName>Higo</LastName>
        <Affiliation>Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naofumi</FirstName>
        <LastName>Hara</LastName>
        <Affiliation>Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiromi</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation>Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hirohisa</FirstName>
        <LastName>Kano</LastName>
        <Affiliation>Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toshimitsu</FirstName>
        <LastName>Suwaki</LastName>
        <Affiliation>Department of Respiratory Medicine, Okayama City Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasuko</FirstName>
        <LastName>Fuchimoto</LastName>
        <Affiliation>Department of Respiratory Medicine, Japan Organization of Occupational Health and Safety Okayama Rosai Hospita</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazuhiro</FirstName>
        <LastName>Kajimoto</LastName>
        <Affiliation>Department of Respiratory Medicine, Japanese Red Cross Kobe Hospita</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hirohisa</FirstName>
        <LastName>Ichikawa</LastName>
        <Affiliation>Department of Respiratory Medicine, KKR Takamatsu Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenichiro</FirstName>
        <LastName>Kudo</LastName>
        <Affiliation>Department of Respiratory Medicine, National Hospital Organization Okayama Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takuo</FirstName>
        <LastName>Shibayama</LastName>
        <Affiliation>Department of Respiratory Medicine, National Hospital Organization Okayama Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasushi</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation>Department of Respiratory Medicine, National Hospital Organization Minami-Okayama Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shoichi</FirstName>
        <LastName>Kuyama</LastName>
        <Affiliation>Department of Respiratory Medicine, National Hospital Organization Iwakuni Clinical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Arihiko</FirstName>
        <LastName>Kanehiro</LastName>
        <Affiliation>Department of Respiratory Medicine, Japan Organization of Occupational Health and Safety Okayama Rosai Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshinobu</FirstName>
        <LastName>Maeda</LastName>
        <Affiliation>Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Kiura</LastName>
        <Affiliation>Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName>Okayama Respiratory Disease Study Group (ORDSG)</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Background&lt;/br&gt;
Nintedanib is a multi-kinase inhibitor approved for idiopathic pulmonary fibrosis (IPF); however, its efficacy and safety for patients with IPF and restricted pulmonary function remain unclear. Therefore, the objective of this study was to determine the efficacy and safety of nintedanib for patients with IPF and forced vital capacity (FVC) ≤ 50%.&lt;/br&gt; 
Methods&lt;/br&gt;
This was a multi-center retrospective study performed by the Okayama Respiratory Disease Study Group. Patients were allocated into FVC ≤ 50% and FVC &gt; 50% groups based on their predicted FVC. The primary endpoints were FVC changes from baseline after 6 and 12 months.&lt;/br&gt; 
Results&lt;/br&gt;
45 patients were eligible for the study. 18 patients had FVC ≤ 50%, and 27 patients had FVC &gt; 50%. Overall, 31 and 19 patients underwent pulmonary function tests at 6 and 12 months after initiating nintedanib, respectively. FVC changes from baseline at 6 and 12 months after initiating nintedanib were comparable between the two groups. Adverse events were seen in all patients, and the rates of patients who discontinued nintedanib were also comparable (38.9% vs. 37.0%, p = 1.000). Multiple regression analysis showed that age and forced expiratory volume in 1 second (FEV1)/FVC were negatively correlated with changes in FVC at 6 months after initiating nintedanib.&lt;/br&gt;
Conclusions&lt;/br&gt;
Our data suggest that nintedanib can be a useful agent for IPF patients, including those with a low FVC, and that age and FEV1/FVC are predictive markers for changes in FVC following nintedanib treatment.
</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList/>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Elsevier</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>22125345</Issn>
      <Volume>58</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2020</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Deterioration of high-resolution computed tomography findings predicts disease progression after initial decline in forced vital capacity in idiopathic pulmonary fibrosis patients treated with pirfenidone</ArticleTitle>
    <FirstPage LZero="delete">185</FirstPage>
    <LastPage>189</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Hisao</FirstName>
        <LastName>Higo</LastName>
        <Affiliation>Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nobuaki</FirstName>
        <LastName>Miyahara</LastName>
        <Affiliation>Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akihiko</FirstName>
        <LastName>Taniguchi</LastName>
        <Affiliation>Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Satoru</FirstName>
        <LastName>Senoo</LastName>
        <Affiliation>Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Junko</FirstName>
        <LastName>Itano</LastName>
        <Affiliation>Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiromi</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation>Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naohiro</FirstName>
        <LastName>Oda</LastName>
        <Affiliation>Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroe</FirstName>
        <LastName>Kayatani</LastName>
        <Affiliation>National Hospital Organization Okayama Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hirohisa</FirstName>
        <LastName>Ichikawa</LastName>
        <Affiliation>KKR Takamatsu Hospita</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takuo</FirstName>
        <LastName>Shibayama</LastName>
        <Affiliation>National Hospital Organization Okayama Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazuhiro</FirstName>
        <LastName>Kajimoto</LastName>
        <Affiliation>Kobe Red Cross Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasushi</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation>National Hospital Organization Minami-Okayama Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Arihiko</FirstName>
        <LastName>Kanehiro</LastName>
        <Affiliation>Okayama Rosai Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshinobu</FirstName>
        <LastName>Maeda</LastName>
        <Affiliation>Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Kiura</LastName>
        <Affiliation>Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName> OKAYAMA respiratory disease study group (ORDSG)</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Background&lt;/br&gt;
Pirfenidone suppresses the decline of forced vital capacity (FVC) in patients with idiopathic pulmonary fibrosis (IPF). However, IPF progresses in some patients despite treatment. We analyzed patients with meaningful FVC declines during pirfenidone treatment and explored the factors predictive of disease progression after FVC decline.&lt;/br&gt;
Methods&lt;/br&gt;
This study was a retrospective, multicenter, observational study conducted by the Okayama Respiratory Disease Study Group. We defined initial decline in %FVC as 5% or greater per 6-month period during pirfenidone treatment. IPF patients who were treated with pirfenidone and experienced an initial decline from December 2008 to September 2017 were enrolled.&lt;/br&gt;
Results&lt;/br&gt;
We analyzed 21 patients with IPF. After the initial decline, 4 (19.0%) patients showed improvement in disease, 11 (52.4%) showed stable disease, and 6 (28.6%) showed progressive disease. There was no significant correlation between %FVC reduction on initial decline and subsequent %FVC change (p = 0.475). Deterioration of high-resolution computed tomography (HRCT) findings on initial decline was observed significantly more often in the progressive versus improved/stable disease groups (100% vs 20.0%, p = 0.009).&lt;/br&gt;
Conclusions&lt;/br&gt;
We revealed that deterioration of HRCT findings may predict disease progression after the initial decline in %FVC in IPF patients treated with pirfenidone.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Idiopathic pulmonary fibrosis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">High-resolution computed tomography</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Pirfenidone</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Forced vital capacity</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>elsevier</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>00063495</Issn>
      <Volume>117</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2019</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Alteration of Membrane Physicochemical Properties by Two Factors for Membrane Protein Integration</ArticleTitle>
    <FirstPage LZero="delete">99</FirstPage>
    <LastPage>110</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Kaoru</FirstName>
        <LastName>Nomura</LastName>
        <Affiliation>Bioorganic Research Institute, Suntory Foundation for Life Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toshiyuki</FirstName>
        <LastName>Yamaguchi</LastName>
        <Affiliation>Bioorganic Research Institute, Suntory Foundation for Life Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shoko</FirstName>
        <LastName>Mori</LastName>
        <Affiliation>Bioorganic Research Institute, Suntory Foundation for Life Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kohki</FirstName>
        <LastName>Fujikawa</LastName>
        <Affiliation>Bioorganic Research Institute, Suntory Foundation for Life Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ken-ichi</FirstName>
        <LastName>Nishiyama</LastName>
        <Affiliation>Department of Biological Chemistry and Food Sciences, Faculty of Agriculture, Iwate University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toshinori</FirstName>
        <LastName>Shimanouchi</LastName>
        <Affiliation>Graduate School of Environmental Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasushi</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation>Graduate School of Agricultural Science, Kobe University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenichi</FirstName>
        <LastName>Morigaki</LastName>
        <Affiliation>Biosignal Research Center, Kobe University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Keiko</FirstName>
        <LastName>Shimamoto</LastName>
        <Affiliation>Bioorganic Research Institute, Suntory Foundation for Life Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract> After a nascent chain of a membrane protein emerges from the ribosomal tunnel, the protein is integrated into the cell membrane. This process is controlled by a series of proteinaceous molecular devices, such as signal recognition particles and Sec translocons. In addition to these proteins, we discovered two endogenous components regulating membrane protein integration in the inner membrane of Escherichia coli. The integration is blocked by diacylglycerol (DAG), whereas the blocking is relieved by a glycolipid named membrane protein integrase (MPIase). Here, we investigated the influence of these integration-blocking and integration-promoting factors on the physicochemical properties of membrane lipids via solid-state NMR and fluorescence measurements. These factors did not have destructive effects on membrane morphology because the membrane maintained its lamellar structure and did not fuse in the presence of DAG and/or MPIase at their effective concentrations. We next focused on membrane flexibility. DAG did not affect the mobility of the membrane surface, whereas the sugar chain in MPIase was highly mobile and enhanced the flexibility of membrane lipid headgroups. Comparison with a synthetic MPIase analog revealed the effects of the long sugar chain on membrane properties. The acyl chain order inside the membrane was increased by DAG, whereas the increase was cancelled by the addition of MPIase. MPIase also loosened the membrane lipid packing. Focusing on the transbilayer movement, MPIase reduced the rapid flip-flop motion of DAG. On the other hand, MPIase could not compensate for the diminished lateral diffusion by DAG. These results suggest that by manipulating the membrane lipids dynamics, DAG inhibits the protein from contacting the inner membrane, whereas the flexible long sugar chain of MPIase increases the opportunity for interaction between the membrane and the protein, leading to membrane integration of the newly formed protein.</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>124</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2012</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>市中肺炎の診療ガイドライン</ArticleTitle>
    <FirstPage LZero="delete">75</FirstPage>
    <LastPage>77</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Yasushi</FirstName>
        <LastName>Tanimoto</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>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>65</Volume>
      <Issue>6</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2011</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Successful Extracorporeal Life Support for Life-threatening Hypercapnia with Bronchiolitis Obliterans after Allogeneic Hematopoietic Stem Cell Transplantation</ArticleTitle>
    <FirstPage LZero="delete">403</FirstPage>
    <LastPage>406</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Koichi</FirstName>
        <LastName>Waseda</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasushi</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shingo</FirstName>
        <LastName>Ichiba</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nobuaki</FirstName>
        <LastName>Miyahara</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toshi</FirstName>
        <LastName>Murakami</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nobuaki</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Michihisa</FirstName>
        <LastName>Terado</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Osamu</FirstName>
        <LastName>Nagano</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshinobu</FirstName>
        <LastName>Maeda</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Arihiko</FirstName>
        <LastName>Kanehiro</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshihito</FirstName>
        <LastName>Ujike</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mitsune</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Case Report</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/47266</ArticleId>
    </ArticleIdList>
    <Abstract>Bronchiolitis obliterans (BO) is a disease with a poor prognosis, and a key factor that limits long-term survival after allogeneic hematopoietic stem cell transplantation (HSCT). We here report a case of a 31-year woman with acute lymphatic leukemia, which was treated by chemotherapy and HSCT, and consequently developed BO 2 years after HSCT. A non-tuberculous mycobacterial infection occurred and showed gradual exacerbation. She started taking anti-mycobacterial drugs, but lost appetite, felt tired and finally lost consciousness one month after beginning medication. Arterial blood gas revealed marked hypercapnia. Using extracorporeal life support (ECLS), the carbon dioxide concentration was reduced and her consciousness recovered. To our knowledge, this is the first case in which ECLS was successfully used for hypercapnia in a patient with BO.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">extracorporeal life support</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">hypercapnia</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">bronchiolitis obliterans</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">noninvasive positive pressure ventilation</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>123</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2011</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>新型インフルエンザウイルス（A/H1N1）感染後にARDSを来たした1例</ArticleTitle>
    <FirstPage LZero="delete">221</FirstPage>
    <LastPage>225</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Akihiko</FirstName>
        <LastName>Taniguchi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nobuaki</FirstName>
        <LastName>Miyahara</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Atsushi</FirstName>
        <LastName>Nakahara</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Saburo</FirstName>
        <LastName>Takata</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ryo</FirstName>
        <LastName>Sakugawa</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Osamu</FirstName>
        <LastName>Nagano</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasushi</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Arihiko</FirstName>
        <LastName>Kanehiro</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Kiura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshito</FirstName>
        <LastName>Ujike</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mitsune</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
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    </ArticleIdList>
    <Abstract>A 28-year-old man with a history of mental retardation was admitted to our hospital because of dyspnea, cough and high fever. His SpO(2) level at room-environmental conditions was in the eighties, and his chest radiograph showed diffuse infiltrates in both lungs. He was diagnosed as suffering from influenza A by a rapid influenza virus antigen test. The echocardiogram showed no evidence of left cardiac failure; therefore, his symptoms were consistent with acute respiratory distress syndrome (ARDS). Oseltamivir was started, and antibiotics were also given because of the possibility of secondary bacterial infection. Due to respiratory failure and low blood pressure, which suggested septic shock, intensive treatments including mechanical ventilation were performed. Corticosteroid therapy was started for ARDS and sepsis, and these therapies improved his respiratory condition. Polymerase chain reaction of his pharyngeal swab revealed that he had influenza A (H1N1). This is the first case of ARDS following infection by influenza A (H1N1) virus in Japan.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">インフルエンザ Ａ (influenza A)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">H1N1</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">急性呼吸促迫症候群 (acute respiratory distress syndrome)</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>65</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2011</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Churg-Strauss Syndrome with Necrosis of Toe Tips</ArticleTitle>
    <FirstPage LZero="delete">215</FirstPage>
    <LastPage>218</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Koichi</FirstName>
        <LastName>Waseda</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasushi</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenjiro</FirstName>
        <LastName>Hasegawa</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nobuaki</FirstName>
        <LastName>Miyahara</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Daisuke</FirstName>
        <LastName>Nojima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Genyo</FirstName>
        <LastName>Ikeda</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Arihiko</FirstName>
        <LastName>Kanehiro</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Chiharu</FirstName>
        <LastName>Okada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshihiro</FirstName>
        <LastName>Kimata</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mitsune</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Case Report</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/46635</ArticleId>
    </ArticleIdList>
    <Abstract>Churg-Strauss syndrome (CSS) is a granulomatous necrotizing vasculitis of unknown etiology associated with bronchial asthma. Despite affecting small to medium-sized vessels, necrosis of the digits due to vasculitis is extremely rare. We report a case of CSS with necrosis of the toe tips. A 37-year-old woman with asthma, who had been diagnosed with CSS 2 years ago, was admitted to our hospital with an exacerbation of CSS. The patient had a high grade fever and complained of abdominal pain and numbness of the lower extremities. Blood examination revealed marked eosinophilia. The fever pattern, abdominal pain and blood eosinophilia showed improvement by combination treatment with prednisolone and cyclophosphamide. However, the color of her right toe tips changed, and necrosis finally resulted despite antithrombotic therapy. Arteriography showed narrowing of the dorsalis pedis artery and of the more peripheral arteries of her right leg. Stump plasty with negative pressure dressing therapy for the toe tips, but not amputation, was done to preserve the leg function. While numbness of the extremities remained, no recurrence of necrosis was seen. Clinicians need to be aware that rare complications of CSS, including necrosis of the digits, can occur.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">bronchial asthma</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Churg-Strauss syndrome</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">eosinophilia</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">necrosis of toe tips</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">stump plasty</Param>
      </Object>
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    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>123</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2011</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>希少呼吸器疾患の治療・管理</ArticleTitle>
    <FirstPage LZero="delete">49</FirstPage>
    <LastPage>52</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Yasushi</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mitsune</FirstName>
        <LastName>Tanimoto</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>
      <Object Type="keyword">
        <Param Name="value">希少疾病用医薬品</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">特発性間質性肺炎</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">特発性肺線維症</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">ピルフェニドン</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>64</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2010</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Experimental Pulmonary Granuloma Mimicking Sarcoidosis Induced by Propionibacterium acnes in Mice</ArticleTitle>
    <FirstPage LZero="delete">75</FirstPage>
    <LastPage>83</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Kouji</FirstName>
        <LastName>Iio</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomoe Ueno</FirstName>
        <LastName>Iio</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuhei</FirstName>
        <LastName>Okui</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hirohisa</FirstName>
        <LastName>Ichikawa</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasushi</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nobuaki</FirstName>
        <LastName>Miyahara</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Arihiko</FirstName>
        <LastName>Kanehiro</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mitsune</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasunari</FirstName>
        <LastName>Nakata</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mikio</FirstName>
        <LastName>Kataoka</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/32852</ArticleId>
    </ArticleIdList>
    <Abstract>&lt;p&gt;Propionibacterium acnes has been implicated as an etiologic agent of sarcoidosis since the isolation of this bacterium from sarcoid lesions. We experimentally produced a murine pulmonary granuloma model using P. acnes with several features that simulate sarcoidosis. Mice were sensitized with heat-killed P. acnes and complete Freund's adjuvant and were subsequently challenged with heat-killed P. acnes at 2-week intervals. P. acnes-challenged mice developed epitheloid cell granulomas in the lungs. These mice showed a pulmonary immune response characterized by an increased number of T-lymphocytes, especially CD4 cells, and the ratio of CD4/CD8 in bronchoalveolar lavage (BAL) fluid also increased. Furthermore, significant elevations in both angiotensin-converting enzyme (ACE) serum levels and antibody titers against P. acnes were observed. Mice sensitized with P. acnes without complete Freund's adjuvant were capable of forming pulmonary granulomas, which appeared to be caused by indigenous P. acnes. The genome of P. acnes was found in the lungs, BAL cells, hilar lymph nodes, liver, and spleen in non-sensitized mice, which were thought to be germ-free. These results suggest that the immune response against indigenous P. acnes may play an important role in the pathogenesis of granuloma formation in a murine model.&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">Propionibacterium acnes</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">experimental granuloma</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">sarcoidosis</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>60</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2006</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Severe Interstitial Pneumonia Induced by Paclitaxel in a Patient with Adenocarcinoma of the Lung</ArticleTitle>
    <FirstPage LZero="delete">295</FirstPage>
    <LastPage>298</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Noriyuki</FirstName>
        <LastName>Suzaki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akio</FirstName>
        <LastName>Hiraki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nagio</FirstName>
        <LastName>Takigawa</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Ueoka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasushi</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toshiyuki</FirstName>
        <LastName>Kozuki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masahiro</FirstName>
        <LastName>Tabata</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Arihiko</FirstName>
        <LastName>Kanehiro</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Kiura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mitsune</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/30737</ArticleId>
    </ArticleIdList>
    <Abstract>A 71-year-old Japanese man with adenocarcinoma of the lung developed interstitial pneumonia after treatment with paclitaxel. The patient had acute chills and fever on the fourth day after the second exposure to paclitaxel, rapidly got worse despite empiric therapies, and developed prolonged respiratory failure requiring mechanical ventilation. Four months later, he died of respiratory failure due to progression of both interstitial pneumonia and lung cancer. This is the first case developing fatal paclitaxel-induced pulmonary toxicity to date. Interstitial pneumonia should be considered one of the possible life-threatening complications during treatment with paclitaxel.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">paclitaxel</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">adverse effect</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">lung cancer</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">interstitial pneumonia</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>121</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2009</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>感染症法</ArticleTitle>
    <FirstPage LZero="delete">53</FirstPage>
    <LastPage>55</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Yasushi</FirstName>
        <LastName>Tanimoto</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>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>115</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2005</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>重度急性呼吸器症候群SARS</ArticleTitle>
    <FirstPage LZero="delete">63</FirstPage>
    <LastPage>68</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <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>
      <Object Type="keyword">
        <Param Name="value">SARS</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">伝幡経路</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">対策</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">緊急報告</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>116</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2005</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>多剤耐性結核と肺非結核性抗酸菌症</ArticleTitle>
    <FirstPage LZero="delete">287</FirstPage>
    <LastPage>292</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <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>
      <Object Type="keyword">
        <Param Name="value">多剤耐性結核菌</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">DOTS</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">非結核性抗酸菌</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">MAC 症</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">M. kansasii 症</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName/>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn/>
      <Volume/>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1993</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>1. Purification of human blood basophils using negative selection by flow cytometry ; 2. Effects of cytokines on human basophil chemotaxis</ArticleTitle>
    <FirstPage LZero="delete"/>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Yasushi</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>1.Basophils were purified from peripheral blood of normal donors using Percoll discontinuous gradients and negative selection by flow cytometry. The mean purity of basophils obtained was 84.7 +/- 4.1 (s.d.)% (range 77.3-90.0%, n = 13). The overall yield of these procedures was 16.0 +/- 2.6% (range 11.0-19.9%, n = 13), and cell viability of purified basophils exceeded 90%. Properties of highly purified basophils obtained by flow cytometry did not differ from those of partially enriched basophil preparations from Percoll discontinuous gradients in respect of: (i) intracellular histamine content; (ii) percentage of spontaneous histamine release in buffer; and (iii) percentage of histamine release triggered by ionophore A 23187 or anti-IgE. Moreover, purified basophils responded chemotactically to complement C5a in a dose-dependent manner. These findings suggest that our procedure for purification of human basophils does not affect the functions of basophils and may be useful for in vitro studies on the role of basophils in hypersensitivity reactions such as bronchial asthma. ; 
2.Basophil chemotactic activity (BCA) of eight recombinant human (rh) cytokines was examined. Highly purified basophils were obtained by Percoll discontinuous gradients, followed by negative selection using flow cytometry. Then BCA was measured by means of modified Boyden chamber method. Both interleukin (IL)-3 and granulocyte-macrophage colony-stimulating factor (GM-CSF) had much more potent BCA than complement C5a, leukotriene B4 and platelet activating factor, well known as granulocyte chemotactic factors. Chemotaxis rather than chemokinesis was shown in chequerboard analysis of basophil migration induced by IL-3 and GM-CSF. Relatively high concentrations of IL-5 also induced basophil migration, although predominantly chemokinetic. IL-8 had apparent BCA, which was not so high as that of C5a. In contrast, IL-2, IL-4, interferon(IFN)-gamma and granulocyte colony-stimulating factor (G-CSF) had no significant BCA. These findings suggest that IL-3, IL-5, GM-CSF and, perhaps, IL-8 have an effect on basophil migration as well as modulation of basophil mediator release and may provide some insight into the basophil accumulation observed in late-phase allergic responses.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList/>
    <ReferenceList/>
  </Article>
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