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  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>66</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2012</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Effect of Taurine on Acinar Cell Apoptosis and Pancreatic Fibrosis in Dibutyltin Dichloride-induced Chronic Pancreatitis</ArticleTitle>
    <FirstPage LZero="delete">329</FirstPage>
    <LastPage>334</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Koki</FirstName>
        <LastName>Matsushita</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akinori</FirstName>
        <LastName>Shirahige</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroaki</FirstName>
        <LastName>Tanioka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kiminari</FirstName>
        <LastName>Sawa</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mitsune</FirstName>
        <LastName>Tanimoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Norio</FirstName>
        <LastName>Koide</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/48687</ArticleId>
    </ArticleIdList>
    <Abstract>The relationship between pancreatic fibrosis and apoptosis of pancreatic acinar cells has not been fully elucidated. We reported that taurine had an anti-fibrotic effect in a dibutyltin dichloride (DBTC)-chronic pancreatitis model. However, the effect of taurine on apoptosis of pancreatic acinar cells is still unclear. Therefore, we examined apoptosis in DBTC-chronic pancreatitis and in the AR42J pancreatic
acinar cell line with/without taurine. Pancreatic fibrosis was induced by a single administration
of DBTC. Rats were fed a taurine-containing diet or a normal diet and were sacrificed at day 5. The AR42J pancreatic acinar cell line was incubated with/without DBTC with taurine chloramines. Apoptosis was determined by using terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) assay. The expression of Bad and Bcl-2 proteins in the AR42J cells lysates was detected by Western blot analysis. The apoptotic index of pancreatic acinar cells in DBTC-administered rats was significantly increased. Taurine treatment inhibited pancreatic fibrosis and apoptosis of acinar cells induced by DBTC. The number of TUNEL-positive cells in the AR42J pancreatic
acinar cell lines was significantly increased by the addition of DBTC. Incubation with taurine chloramines ameliorated these changes. In conclusion, taurine inhibits apoptosis of pancreatic acinar cells and pancreatitis in experimental chronic pancreatitis.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">apoptosis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">chronic pancreatitis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">pancreatic acinar cells</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">taurine</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>66</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2012</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>New Large Bowel Segmentation on Plain Abdominal Radiography in Comparison with the Conventional Method</ArticleTitle>
    <FirstPage LZero="delete">239</FirstPage>
    <LastPage>244</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Kiminari</FirstName>
        <LastName>Sawa</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koki</FirstName>
        <LastName>Matsushita</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akinori</FirstName>
        <LastName>Shirahige</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Norio</FirstName>
        <LastName>Koide</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/48563</ArticleId>
    </ArticleIdList>
    <Abstract>Plain abdominal radiography is a very basic examination and plays an important role in primary care. The objectives of this study were to clarify colon distributions on plain abdominal radiographs. Forty-three healthy volunteers underwent gastric fluoroscopy, and 2 hours later, plain abdominal radiography
in the supine position. A region of interest (ROI) was defined uniformly on each X-ray image to divide the image into 600 zones. The area corresponding to the large bowel within the ROI was divided into 4 segments (ascending colon, transverse colon, descending colon, and sigmoid colon＋rectum). The percentage of barium in each segment relative to the total volume of barium used was calculated to evaluate the percent ROI occupancy. The large bowel covered 76.7% of the entire ROI, with the percent duplication being 55%. The duplicated area corresponded to the transverse colon region. When the method proposed by Arhan et al. was used, the percentage of the colon actually present in each segment relative to that determined theoretically was 99.6% for the right colon segment,
92.2% for the left colon segment, and 92.2% for the sigmoid/rectal segment. However, in cases in which the transverse colon descended partially from the fifth lumbar vertebra, the percentage occupied by the sigmoid colon＋rectum decreased to 57.2%. We applied a new large bowel segmentation
method especially for patients with ptosis, by devising a line joining the lateral side of the right lesser pelvis and the lower ends of both sacroiliac joints.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">large bowel</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">segmentation</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">plain abdominal radiograph</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">classification method</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">primary care</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>58</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2004</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Analysis of HCV genotypes from blood donors shows three new HCV type 6 subgroups exist in Myanmar.</ArticleTitle>
    <FirstPage LZero="delete">135</FirstPage>
    <LastPage>142</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Toshiyuki</FirstName>
        <LastName>Shinji</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yi Yi</FirstName>
        <LastName>Kyaw</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsunori</FirstName>
        <LastName>Gokan</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasuhito</FirstName>
        <LastName>Tanaka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nobuchika</FirstName>
        <LastName>Kusano</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shin-ichi</FirstName>
        <LastName>Fujioka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hidenori</FirstName>
        <LastName>Shiraha</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Aye Aye</FirstName>
        <LastName>Lwin</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasushi</FirstName>
        <LastName>Shiratori</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masashi</FirstName>
        <LastName>Mizokami</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Myo</FirstName>
        <LastName>Khin</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masayuki</FirstName>
        <LastName>Miyahara</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shigeru</FirstName>
        <LastName>Okada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Norio</FirstName>
        <LastName>Koide</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/32110</ArticleId>
    </ArticleIdList>
    <Abstract>The prevalence of hepatitis C virus (HCV) genotypes in Myanmar in comparison with the rest of Southeast Asia is not well known. Serum samples were obtained from 201 HCV antibody-positive volunteer blood donors in and around the Myanmar city of Yangon. Of these, the antibody titers of 101 samples were checked by serial dilution using HCV antibody PA test II and Terasaki microplate as a low-cost method. To compare antibody titers by this method and RNA identification, we also checked HCV-RNA using the Amplicor 2.0 test. Most high-titer groups were positive for HCV-RNA. Of the 201 samples, 110 were successfully polymerase chain reaction (PCR) amplified. Among them, 35 (31.8%) were of genotype 1, 52 (47.3%) were of genotype 3, and 23 (20.9%) were of type 6 variants, and phylogenetic analysis of these type 6 variants revealed that 3 new type 6 subgroups exist in Myanmar. We named the subgroups M6-1, M6-2, and M6-3. M6-1 and M6-2 were relatively close to types 8 and 9, respectively. M6-3, though only found in one sample, was a brand-new subgroup. These subtypes were not seen in Vietnam, where type 6 group variants are widely spread. These findings may be useful for analyzing how and when these subgroups were formed.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">hepatitis C virus(HCV)genotype</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">type 6 variant</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Myanmar</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Southeast Asia</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">phylogenetic analysis</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>52</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1998</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Gastrobiliary Dysmotility in Patients with Chronic Pancreatitis as Assessed by a Single Noninvasive Test</ArticleTitle>
    <FirstPage LZero="delete">55</FirstPage>
    <LastPage>61</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toshinobu</FirstName>
        <LastName>Seno</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoki</FirstName>
        <LastName>Matsumura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideo</FirstName>
        <LastName>Harada</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/31341</ArticleId>
    </ArticleIdList>
    <Abstract>We simultaneously assessed gastric emptying and gallbladder contraction after oral administration of a liquid meal by noninvasive ultrasonography in 17 patients with chronic pancreatitis (CP) and in 17 healthy controls. Gastrointestinal (GI) transit was also assessed by a noninvasive radioopaque marker method. Exocrine pancreatic function was evaluated by analyzing pure pancreatic juice and by analyzing the autonomic nervous system by cardiovascular reflex tests. Patients with CP showed impaired gallbladder contraction at 15 min and hastened gastric emptying. The cause of the former is unclear, whereas the latter was closely related with decreased pancreatic lipase output, but not with autonomic dysfunction. GI transit time did not differ between controls and patients with CP. In conclusion, we succeeded in clearly demonstrating impaired gallbladder contraction and hastened gastric emptying in patients with CP by a single noninvasive test, ultrasonography. We also revealed for the first time that hastened gastric emptying is associated with insufficient pancreatic lipase output.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">chronic pancreatits</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">gastric emptying</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">gallbladder motility</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">colonic transit</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">lipase output</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部附属病院三朝分院</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-7839</Issn>
      <Volume>64</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1993</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>ERCP後CTによる膵嚢胞性疾患の診断</ArticleTitle>
    <FirstPage LZero="delete">65</FirstPage>
    <LastPage>70</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideo</FirstName>
        <LastName>Harada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shuji</FirstName>
        <LastName>Matsumoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tosinobu</FirstName>
        <LastName>Seno</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Juntaro</FirstName>
        <LastName>Tanaka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Keisuke</FirstName>
        <LastName>Sugimoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumihiro</FirstName>
        <LastName>Mitsunobu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiro</FirstName>
        <LastName>Tanizaki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mutsuo</FirstName>
        <LastName>Nakai</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tsuneo</FirstName>
        <LastName>Akiyama</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideaki</FirstName>
        <LastName>Hasuoka</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/15317</ArticleId>
    </ArticleIdList>
    <Abstract>ERCP直後にCTを撮影するERCP後CTはERCPの際に膵内に注入された造影剤をCTで検出するため,ERCPでは得られない情報が得られる利点がある｡われわれはERCP後CTが診断や治療方針の決定に有用であった膵嚢胞の4例を経験した｡膵嚢胞では主膵管との連絡,嚢胞の部位,性状診断にERCP後CTは有用な検査法であり,文献的考察を含めて報告した｡</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">ERCP (Endoscopic retrograde cholangiopancreatography)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">CT (Computed tomography)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">膵嚢胞 (pancreatic cyst)</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部附属病院三朝分院</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-7839</Issn>
      <Volume>65</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1994</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Tropical calcific pancreatitis.........An overview</ArticleTitle>
    <FirstPage LZero="delete">27</FirstPage>
    <LastPage>39</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Riaz</FirstName>
        <LastName>Chowdhury</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Juntaro</FirstName>
        <LastName>Tanaka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shooji</FirstName>
        <LastName>Matsumoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toshinobu</FirstName>
        <LastName>Senou</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideo</FirstName>
        <LastName>Harada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiro</FirstName>
        <LastName>Tanizaki</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/15151</ArticleId>
    </ArticleIdList>
    <Abstract>Tropical calcific pancreatitis is a nonalcoholic type of chronic pancreatitis affecting the childrens and young adults characterized clinically by recurrent abdominal pain in childhood, diabetes in adolescent and death in early childhood. Although the exact etiology is not known, malnutrition and chronic cassava toxicity either singly or
in combination are presumed to be the prime factor in pancreatic injury unopposed by detoxification of free radical. Moreover micronutrients deficiency, oxidant stress and antioxidant deficiency might play substantial role. Diabetes secondary to tropical calcific pancreatitis is a distinctive and frequent problem, being named by W.H.O. study group as 'fibrocalculous pancreatic diabetes (FCPD) and classified as one of the variant of the so-called malnutrition related diabetes mellitus (MRDM).</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Tropical calcific pancreatitis (TCP)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">malnutrition</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">cassava</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">diabetes</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">abdominal pain</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部附属病院三朝分院</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-7839</Issn>
      <Volume>65</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1994</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Sodium picosulfate,PEG腸管洗浄液併用によるTotal colonoscopyの前処置法に関する検討</ArticleTitle>
    <FirstPage LZero="delete">22</FirstPage>
    <LastPage>26</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideo</FirstName>
        <LastName>Harada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Riaz</FirstName>
        <LastName>Chowdhury</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Juntaro</FirstName>
        <LastName>Tanaka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shuji</FirstName>
        <LastName>Matsumoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toshinobu</FirstName>
        <LastName>Seno</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumihiro</FirstName>
        <LastName>Mitsunobu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiro</FirstName>
        <LastName>Tanizaki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tsuneo</FirstName>
        <LastName>Akiyama</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mutsuo</FirstName>
        <LastName>Nakai</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideaki</FirstName>
        <LastName>Hasuoka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tadahiro</FirstName>
        <LastName>Kato</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/15150</ArticleId>
    </ArticleIdList>
    <Abstract>Total colonoscopyの前処置における被検者の負担軽減と良好な腸管洗浄を得る目的で,50例の大腸内視鏡検査において,前日の食事制限せず, sodium picosulfate 20m&#8467;前夜服用,検査当日PEG腸管洗浄液1&#8467;以上服用する前処置法の有用性について検討した。本前処置法によってPEG腸管洗浄液平均1230m&#8467;の服用により,50例中48例で観察可能な腸管洗浄が得られ,PEG腸管洗浄液の服用量の減量が可能であった｡腹痛,嘔気,腹鳴などの症状出現例は認めたが,重篤な副作用は認めなかった｡腸管洗浄度の点で,高齢者の大腸内視鏡検査の前処置として有用である｡以上よりSodium Picosulfate 20m&#8467;をPEG腸管洗浄液と併用することにより,優れた腸管洗浄度を得られると同時にPEG腸管洗浄液服用量の減量か可能であり,total colonoscopyの前処置として有用であることが示された。</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">大腸内視鏡検査 (colonoscopy)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">前処置 (preparation)</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部附属病院三朝分院</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-7839</Issn>
      <Volume>66</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1995</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Experimental model of chronic pancreatitis, a review - Does it really exist?</ArticleTitle>
    <FirstPage LZero="delete">85</FirstPage>
    <LastPage>91</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideo</FirstName>
        <LastName>Harada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Juntaro</FirstName>
        <LastName>Tanaka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shuji</FirstName>
        <LastName>Matsumoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toshinobu</FirstName>
        <LastName>Seno</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mitsuko</FirstName>
        <LastName>Ichimura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tsuneo</FirstName>
        <LastName>Akiyama</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Satoshi</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/15129</ArticleId>
    </ArticleIdList>
    <Abstract>Experimental model of pancreatitis is mandatory for elucidating the pathobiology of the disease and also to see the response of a novel treatment. In addition, the need for an animal model of chronic pancreatitis is further strengthened by the relative inaccessibility and paucity of the human pancreatitis tissue. Whereas various models of acute pancreatitis and also of exocrine pancreatic tumor have been described, chronic pancr-eatitis has not been consistently reproduced in experimental animals. Many researchers attempted to establish an experimental model of chronic pancreatitis either by partially obstructing the drainage of pancreatic secretion in dogs and cats or by feeding alcohol to dogs and rats with and without temporary occlusion of the biliopancreatic duct or by surgically inducing ischaemia in the pancreas of the dogs. But, none of these models is identical with human disease. A consistently reproducible model of human chronic pancr-eatitis probably does not exist. In this expanding era of molecular biology which promises us to enhance greatly our understanding of this disease, a right experimental model of chronic pancreatitis is still in progress.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList/>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部附属病院三朝分院</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-7839</Issn>
      <Volume>66</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1995</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>コラーゲン分解系と疾患</ArticleTitle>
    <FirstPage LZero="delete">78</FirstPage>
    <LastPage>84</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideo</FirstName>
        <LastName>Harada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Haruhiro</FirstName>
        <LastName>Yamashita</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mitsuko</FirstName>
        <LastName>Ichimura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Juntaro</FirstName>
        <LastName>Tanaka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toshinobu</FirstName>
        <LastName>Seno</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shuji</FirstName>
        <LastName>Matsumoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Satoshi</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumihiro</FirstName>
        <LastName>Mitsunobu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiro</FirstName>
        <LastName>Tanizaki</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/15128</ArticleId>
    </ArticleIdList>
    <Abstract>組織のコラーゲン沈着にはコラーゲン合成系と分解系の不均衡によって生ずる｡従来,主としてコラーゲン合成系が注目されていたが,最近の研究の進歩により,コラーゲン分解系が重要な役割を演ずることが明らかになってきた｡コラーゲンの分解系には細胞内と細胞外の二つの経路が存在する｡それぞれcollagenolytic cathepsinおよびmatrix metalloproteinases(
MMP)がコラーゲン分解能を有する重要な酵素である｡その調節因子については細胞外の経路についての解明か進んでいる｡MMPの遺伝子の発現にはサイトカインや成長因子が関与し,IL-1やTNF-αは強力な誘導因子である｡一旦,遺伝子か発現すれば,MMPは合成され,細胞外に不活性型(latent form)で分泌される｡不活性型のMMPが活性化する過程にはplasminogen activator inhibitorやtissue inhibitors of metalloproteinases(TIMP)などの阻害因子が存在し,MMP活性を調節する｡TIMPの遺伝子の発現にもサイトカインや成長因子が関与する｡MMPがTIMPを上回るような病態では組織破壊が,逆にTIMPがMMPを上回るような病態では綿維化が生ずる｡コラーゲン分解能の障害が線維化の維持や不可逆性に関与することが推察される。</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">線維化 (Fibrosis)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">コラーゲン (Collagen)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">TIMP (tissue inhibitor of metalloproteinase)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">MMP (matrix metalloproteinase)</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部附属病院三朝分院</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-7839</Issn>
      <Volume>67</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1996</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>膵液のK-ras遺伝子の突然変異を認めた多発性膵嚢胞の1例</ArticleTitle>
    <FirstPage LZero="delete">121</FirstPage>
    <LastPage>125</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Ryoichi</FirstName>
        <LastName>Yamamoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoki</FirstName>
        <LastName>Matsumura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Juntaro</FirstName>
        <LastName>Tanaka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tadahiro</FirstName>
        <LastName>Kato</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideo</FirstName>
        <LastName>Harada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideaki</FirstName>
        <LastName>Hasuoka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Satoshi</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiro</FirstName>
        <LastName>Tanizaki</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/15109</ArticleId>
    </ArticleIdList>
    <Abstract>膵癌の早期診断を行うために,最近の進歩の著しい遺伝子診断を用いて,膵液中のK-ras遺伝子の点突然変異の検討がなされている｡われわれは膵液の細胞診は陰性であるが,K-ras遺伝子の点突然変異を認め,膵全体に多発する膵嚢胞の1例を経験した｡本例は悪性であるとの確診が得られないことや切除するとなれば膵全摘となることなどのために,経過観察を行っているが,18カ月後の現在,嚢胞の増大など認めていない｡膵癌の遺伝子診断の文献的考察を含め,報告する｡</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">膵嚢胞 (pancreatic cyst)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">膵液 (pancreatic juice)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">K-ras遺伝子 (K-ras oncogene)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">点突然変異 (point mutation)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">細胞診 (cytology)</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部附属病院三朝分院</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-7839</Issn>
      <Volume>67</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1996</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>膵線維化のメカニズム</ArticleTitle>
    <FirstPage LZero="delete">115</FirstPage>
    <LastPage>120</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Riaz</FirstName>
        <LastName>Chowdhury</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mitsuko</FirstName>
        <LastName>Ichimura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoki</FirstName>
        <LastName>Matsumura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Juntaro</FirstName>
        <LastName>Tanaka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ryoichi</FirstName>
        <LastName>Yamamoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideo</FirstName>
        <LastName>Harada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Satoshi</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumihiro</FirstName>
        <LastName>Mitsunobu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasuhiro</FirstName>
        <LastName>Hosaki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiro</FirstName>
        <LastName>Tanizaki</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/15095</ArticleId>
    </ArticleIdList>
    <Abstract>膵の線維化は慢性膵炎に特徴的な病理組織所見の一つであるが,その発生機序については不明な点か多い｡慢性膵炎はいったん発症すれば,進行性かつ非可逆性であるとされるが,その非可逆性に膵の線維化が関与するとされる｡膵の線維化の発生機序を明らかにし,線維化に対する根本的な治療法の確立が望まれるところである｡そこで,本稿では今後の膵の線維化の研究課題を明らかにする目的で,現在までの膵臓線維化の発生機序に関する知見を整理した｡</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">膵臓 (pancreas)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">線維化 (fibrosis)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">サイトカイン (cytokine)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">慢性膵炎 (chronic pancreatitis)</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部附属病院三朝分院</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-7839</Issn>
      <Volume>67</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1996</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>上腹部不定愁訴患者の胃･胆嚢運動に関する研究</ArticleTitle>
    <FirstPage LZero="delete">75</FirstPage>
    <LastPage>78</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ryoichi</FirstName>
        <LastName>Yamamoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoki</FirstName>
        <LastName>Matsumura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Riaz</FirstName>
        <LastName>Chowdhury</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tadahiro</FirstName>
        <LastName>Kato</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Juntaro</FirstName>
        <LastName>Tanaka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideo</FirstName>
        <LastName>Harada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Satoshi</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumihiro</FirstName>
        <LastName>Mitsunobu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Mifune</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiro</FirstName>
        <LastName>Tanizaki</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/15090</ArticleId>
    </ArticleIdList>
    <Abstract>現在,上腹部不定愁訴の原因は特定されていない｡その原因を解明するため,上腹部不定愁訴患者8人と健常対照者10人に対して液体食の胃排出能と,食事負荷による胆嚢収縮能を測定した｡胃排出時間,胆嚢収縮能はいずれも両者に有意な差は認められなかった｡健常対照者では胃排出時間と胆嚢収縮時間に有意な相関関係が認められたが,上腹部不定愁訴群では相関関係は認められなかった｡上腹部不定愁訴の原因として胃･胆嚢協調運動障害の存在が示唆
された。</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">胃運動 (Gastric motility)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">胆嚢運動 (Biliary motility)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">不定愁訴 (indefinite complaint)</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部附属病院三朝分院</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-7839</Issn>
      <Volume>67</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1996</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>大腸前処置法の栄養評価としてのレチノール結合蛋白の有用性の検討</ArticleTitle>
    <FirstPage LZero="delete">71</FirstPage>
    <LastPage>74</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Tadahiro</FirstName>
        <LastName>Kato</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideaki</FirstName>
        <LastName>Hasuoka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoki</FirstName>
        <LastName>Matsumura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ryoichi</FirstName>
        <LastName>Yamamoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Juntaro</FirstName>
        <LastName>Tanaka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideo</FirstName>
        <LastName>Harada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tsuneo</FirstName>
        <LastName>Akiyama</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Satoshi</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumihiro</FirstName>
        <LastName>Mitsunobu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiro</FirstName>
        <LastName>Tanizaki</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/15089</ArticleId>
    </ArticleIdList>
    <Abstract>大腸内視鏡検査の前処置を栄養面から評価する目的で前処置前後にrapid turnover proteinである血中レチノール結合蛋白の変動を検討した｡前日に普通食を用い,当日ニフレックを使用した10例,検査1日前に低残渣食を用いた27例,通常の前処置では良好な腸管洗浄が得られないために検査前2日間低残渣食を用いた27例の3群について,前処置開始前と検査終了後に血中レチノール結合蛋白の変動をみたところ,検査前2日間低残渣食服用群で有意の低下を認めた｡前日普通食群では検査前後で変化を認めず,1日低残渣食服用群では低下傾向を認めたが,有意差は認めなかった｡これまで前処置の成否は腸管洗浄度の面で評価されてきたが,血中レチノール結合蛋白を目標として用いることにより栄養面から評価することができることが考えられた。</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">レチノール結合蛋白 (retinol binding protein)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">大腸内視鏡 (colonoscopy)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">前処置 (preparation)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">栄養評価 (nutritional assessment)</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部附属病院三朝分院</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-7839</Issn>
      <Volume>68</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1997</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>慢性膵炎診療における内視鏡的純粋膵液採取法の意義</ArticleTitle>
    <FirstPage LZero="delete">94</FirstPage>
    <LastPage>98</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoki</FirstName>
        <LastName>Matsumura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tadahiro</FirstName>
        <LastName>Kato</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mitsuko</FirstName>
        <LastName>Ichimura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideo</FirstName>
        <LastName>Harada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiro</FirstName>
        <LastName>Tanizaki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumihiro</FirstName>
        <LastName>Mitsunobu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideaki</FirstName>
        <LastName>Hasuoka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tetsuya</FirstName>
        <LastName>Tsurumi</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/14992</ArticleId>
    </ArticleIdList>
    <Abstract>内視鏡的純粋膵液採取法の慢性膵炎診療における意義を検討した｡本法を用い,セクレパン100単位静注後10分間膵液を採取するintaraductal secretin test(IDST,膵管内セクレチン試験)はこれまで膵外分泌機能検査のgold standardである十二指腸液を採取するセクレチン試験に代用ができ,しかも10分間の採取時間で終了する利点を有する｡本法を施行することにより,蛋白栓が除去され,痔痛の消失に有用である｡また,慢性膵炎と鑑別を要する膵癌を除外診断するために,本法によって採取した膵液の細胞診,腫瘍マーカー,癌遺伝子の検出は有用である｡</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">慢性膵炎 (chronic pancreatitis)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">膵液 (pancreatic juice)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">内視鏡 (endoscopy)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">膵外分泌機能検査 (exocrine pancreatic function test)</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部附属病院三朝分院</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-7839</Issn>
      <Volume>68</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1997</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>大腸の全周性狭窄を呈した好酸球性胃腸炎の1例</ArticleTitle>
    <FirstPage LZero="delete">64</FirstPage>
    <LastPage>70</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoki</FirstName>
        <LastName>Matsumura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tadahiro</FirstName>
        <LastName>Kato</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toshinobu</FirstName>
        <LastName>Seno</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideo</FirstName>
        <LastName>Harada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Mifune</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumihiro</FirstName>
        <LastName>Mitsunobu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiro</FirstName>
        <LastName>Tanizaki</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/14989</ArticleId>
    </ArticleIdList>
    <Abstract>大腸に全周性狭窄をきたした好酸球性胃腸炎の1例を報告した｡症例は54才の女性で,腹痛と下痢を主訴に来院した｡上部消化管検査では異常を認めなかったが,下部消化管造影検査と大腸内視鏡検査で横行結腸の全周性狭窄を認め,生検にて大腸粘膜の好酸球浸潤を認めた｡貝料理の摂取にて腹痛発作が出現したが,原因抗原は同定できなかった｡貝類の摂取を避けることにより,症状は消失し,末梢血液中の好酸球増多は消失した｡本邦ではこれまでに124例
の報告があるが,大腸に全周性の狭窄をきたす症例は稀であり,文献的考察を加え報告する｡</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">好酸球性胃腸炎 (eosinophilic gastroenteropathy)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">大腸 (colon)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">狭窄 (stenosis)</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部附属病院三朝分院</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-7839</Issn>
      <Volume>68</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1997</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Studies on whole gut transit in chronic pancreatitis patients</ArticleTitle>
    <FirstPage LZero="delete">59</FirstPage>
    <LastPage>63</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoki</FirstName>
        <LastName>Matsumura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toshinobu</FirstName>
        <LastName>Seno</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideo</FirstName>
        <LastName>Harada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Mifune</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumihiro</FirstName>
        <LastName>Mitsunobu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiro</FirstName>
        <LastName>Tanizaki</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/14988</ArticleId>
    </ArticleIdList>
    <Abstract>Abnormalities of whole gut transit could contribute to the maldigestion and　digestive symptoms of chronic pancreatitis patients. Whole gut transit was measured
by radiopaque markers method. Fifteen chronic pancreatitis patients (2 females, 13 males; age range 40-78 years) and 17 controls (4 females, 13 males, 32-73 years) were studied. Additionally, we also looked for evidence of autonomic neuropathy in the chronic pancreatitis patients by using cardiovascular tests. In chronic pancreatitis,
whole gut transit was shorter than controls. These abnormalities were not influenced by the degree of autonomic neuropathy. We conclude that whole gut transit is shorter in chronic pancreatitis patients.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">慢性膵炎 (Chronic pancreatitis)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">全消化管通過 (Whole gut transit)</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部附属病院三朝分院</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-7839</Issn>
      <Volume>69</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1998</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Oncogenes and tumor suppressor genes in pancreatic cancer</ArticleTitle>
    <FirstPage LZero="delete">82</FirstPage>
    <LastPage>87</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoki</FirstName>
        <LastName>Matsumura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mitsuko</FirstName>
        <LastName>Ichimura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideo</FirstName>
        <LastName>Harada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideaki</FirstName>
        <LastName>Hasuoka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Motohiro</FirstName>
        <LastName>Yokoyama</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tetsuya</FirstName>
        <LastName>Tsurumi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumihiro</FirstName>
        <LastName>Mitsunobu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiro</FirstName>
        <LastName>Tanizaki</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/14965</ArticleId>
    </ArticleIdList>
    <Abstract>Recent advances in molecular biology have revealed that a number of oncogenes (K-ras, erbB-2, and Met) and tumor suppressor genes (p53, p16, APC, and DCC) contribute to the development of pancreatic cancer. This paper reviewed the present knowledge of oncogenes and tumor suppressor genes relevant to pancreatic cancer. Further studies on molecular alterations in pancreatic cancer may lead to a
better understanding of tumor biology, offering a possibility of development of new diagnostic and therapeutic approaches in the future.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Pancreatic cancer</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">oncogene</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">tumor suppressor gene</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">genetic mutation</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部附属病院三朝分院</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-7839</Issn>
      <Volume>70</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1999</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>膵炎とインターフェロン</ArticleTitle>
    <FirstPage LZero="delete">84</FirstPage>
    <LastPage>87</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoki</FirstName>
        <LastName>Matsumura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideaki</FirstName>
        <LastName>Hasuoka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumihiro</FirstName>
        <LastName>Mitsunobu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiro</FirstName>
        <LastName>Tanizaki</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/14943</ArticleId>
    </ArticleIdList>
    <Abstract>インターフェロンは慢性肝炎や悪性腫瘍の治療など,広く臨床の場に用いられるようになった｡その副作用の一つとして,膵炎があり,その多くは急性膵炎である,慢性膵炎の報告もあり,膵炎はインターフェロンを用いる場合に知っておくべき副作用である｡そこで,膵炎とインターフェロンの関係について現在までに知られている知見について概説する｡</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">インターフェロン (interferon)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">急性膵炎 (acute pancreatitis)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">慢性膵炎 (chronic pancreatitis)</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部附属病院三朝分院</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-7839</Issn>
      <Volume>70</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1999</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Clinical and experimental aspects of free radicals in chronic pancreatitis</ArticleTitle>
    <FirstPage LZero="delete">79</FirstPage>
    <LastPage>83</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoki</FirstName>
        <LastName>Matsumura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumihiro</FirstName>
        <LastName>Mitsunobu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiro</FirstName>
        <LastName>Tanizaki</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/14942</ArticleId>
    </ArticleIdList>
    <Abstract>Free radicals have been suspected to play an important role in the pathogenicity of chronic pancreatitis. We reviewed studies on free radicals in chronic pancreatitis in both c1inical and experimental aspects. Many clinical studies have provided circumstantial evidence for the close relation between free radicals and chronic pancreatitis. However, few experimental studies in animals on relation between free radicals and chronic pancreatitis have been reported, because adequate experimental models for elucidating a pathological role of free radicals in chronic pancreatitis have not been established. The research concerning the role of free radicals in chronic
pancreatitis is expected to improve our understanding the pathological mechanisms of the disease.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">慢性膵炎 (chronic pancreatitis)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">フリーラジカル (free radicals)</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部附属病院三朝分院</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-7839</Issn>
      <Volume>71</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2001</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Matrix metalloproteinases (MMPs) and pancreatic diseases</ArticleTitle>
    <FirstPage LZero="delete">76</FirstPage>
    <LastPage>83</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Motohiro</FirstName>
        <LastName>Yokoyama</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mitsuko</FirstName>
        <LastName>Ichimura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tetsuya</FirstName>
        <LastName>Tsurumi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumihiro</FirstName>
        <LastName>Mitsunobu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiro</FirstName>
        <LastName>Tanizaki</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/14913</ArticleId>
    </ArticleIdList>
    <Abstract>Matrix metalloproteinases (MMPs) is a family of collagenolytic enzymesand are associated with many pathological conditions. Especially, MMPs have a strong relation with tumor progression and invasion. In this review, we focused on association of MMPs and pancreatic diseases, and a potential treatment of MMPs
inhibitors for pancreatic cancer.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">matrix metalloproteinase(MMP)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">tissue inhibitor of metalloproteinase(TIMP)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">pancreatic cancer (膵癌)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">chronic pancreatitis (慢性膵炎)</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部附属病院三朝医療センター</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1348-1258</Issn>
      <Volume>76</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2008</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>IgG4関連疾患</ArticleTitle>
    <FirstPage LZero="delete">60</FirstPage>
    <LastPage>65</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Kazuhisa</FirstName>
        <LastName>Hiramatsu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Motoi</FirstName>
        <LastName>Asano</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koki</FirstName>
        <LastName>Matsushita</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomoko</FirstName>
        <LastName>Miyoshi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Sukio</FirstName>
        <LastName>Nakamura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Norio</FirstName>
        <LastName>Koide</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hitomi</FirstName>
        <LastName>Kataoka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumihiro</FirstName>
        <LastName>Mitsunobu</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/14901</ArticleId>
    </ArticleIdList>
    <Abstract>IgG4関連疾患は21世紀になって提唱された新しい疾患である｡組織学的にはIgG4陽性形質細胞やリンパ球浸潤が涙腺, 唾液腺, 後腹膜, 膵臓, 胆管などで起こり, 臨床的にはMikulicz病, 後腹膜線維症, 自己免疫膵炎, 糖尿病, 原発性硬化性胆管炎類似の胆管病変などを呈する全身性疾患であり, ステロイド治療に対する良好な反応性を認める｡その診断基準は確立されておらず, われわれは, @血清IgG4の高値, A本疾患に特徴的な臓器の障害(唾液腺,涙腺, 膵臓, 後腹膜), B組織学的にIgG4陽性形質細胞とリンパ球の浸潤の確認, の３項目のうち２項目以上認めれば, IgG4関連疾患とするという診断基準を提言する｡</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">IgG4関連疾患 (IgG4-related disease)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">自己免疫膵炎 (autoimmune pancreatitis)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Mikulicz病 (Mikulicz's disease)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">後腹膜線維症 (retroperitoneal fibrosis)</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部附属病院三朝医療センター</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1348-1258</Issn>
      <Volume>74</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2004</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Age and Gender-Related Alterations of Six Serum Pancreatic Enzymes in Healthy Subjects</ArticleTitle>
    <FirstPage LZero="delete">57</FirstPage>
    <LastPage>61</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Toshinobu</FirstName>
        <LastName>Seno</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toshiyuki</FirstName>
        <LastName>Shinji</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Norio</FirstName>
        <LastName>Koide</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/14810</ArticleId>
    </ArticleIdList>
    <Abstract>The serum levels of some pancreatic enzymes have been reported to be affected by age and gender. Currently, serum total amylase, pancreatic isoamylase (P-amylase) , lipase , trypsin (ogen) , pancreatic phospholipase A(2) (PLA(2)) , and
elastase I are utilized in diagnosing pancreatic diseases. We here compared age and gender-related alterations of these six pancreatic enzymes in healthy subjects to delineate different properties among the enzymes. Subjects were 155 males and 172 females between ages 20 and 79 years who were apparently healthy, and were stratified by age and sex. PLA(2) and elastase I were assayed by RIA, trypsin (ogen) by EIA and others by activity. The pancreatic enzymes, except PLA(2), were significantly elevated with age, although they declined in males in the 260 age group. There were significant sex differences in total amylase and P-amylase. Total amylase was significantly higher in females than in males in the 260 age group, P-amylase in the 40-49 age group. Age should be considered in the valuation of serum enzymes except PLA(2), sex difference should be considered in the valuation of amylase (total and P-amylase).</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">pancreatic enzyme</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">amylase</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">phospholipase A(2)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">aging</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">gender</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山大学医学部附属病院三朝医療センター</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1348-1258</Issn>
      <Volume>73</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2003</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Frizzled Activation by Wnt-l Is Required for beta -Catenin -T Cell Factor Dependent Transcription in Esophageal Cancer</ArticleTitle>
    <FirstPage LZero="delete">75</FirstPage>
    <LastPage>80</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Takaaki</FirstName>
        <LastName>Mizushima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Ochi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasuyuki</FirstName>
        <LastName>Emori</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroaki</FirstName>
        <LastName>Tanioka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kiminari</FirstName>
        <LastName>Sawa</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shinichi</FirstName>
        <LastName>Fujioka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toshiyuki</FirstName>
        <LastName>Shinji</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Norio</FirstName>
        <LastName>Koide</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiro</FirstName>
        <LastName>Tanizaki</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/14771</ArticleId>
    </ArticleIdList>
    <Abstract>Although, accumulation of nuclear and cytoplasmic beta-catenin has been observed in ESCCs, mutation of APC and beta-catenin are not found in ESCCs. Therefore, another mechanism for cytoplasmic beta- catenin accumulation might exist in ESCCs. Materials and Methods: Human ESCCs cell lines and the 293 stable transfectants expressing
Wnt-1, Wnt-5A, and Wnt-7A were cultured under standard conditions. The TOPFlash or FOPFlash reporter plasmids were transfected. Results: Transfected mutant beta-catenin as well as an axin fragment harbing the GSK3 beta interaction domain, the latter a potent GSK3 beta inhibitor. both robustly activated pTOPFlash in ESCCs cells. When pTOPFlash/pFOPFlash reporters were transfected in ESCCs cell lines followed by cocultivation with 293 cells that stably express Wnt -1, all cell lines except one demonstrated TCF mediated transcriptional. But, cells were co- cultured, Wnt - 7A or Wnt - 5A did not activate TCF mediated transcription in a cell number dependent fashion. Discussion; We report the activation of TCF promoter gene by extemal Wnt stimuli in ESCCs cells.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">esophageal carcinoma</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Wnt</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">TCF</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">beta-catenin</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName/>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn/>
      <Volume/>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1998</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Gastrobiliary Motility in Patients with Chronic Pancreatitis as Assessed by a Single Noninvasive Test</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>
