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  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>101</Volume>
      <Issue>3-4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>第108回 岡山外科会</ArticleTitle>
    <FirstPage LZero="delete">414</FirstPage>
    <LastPage>422</LastPage>
    <Language>EN</Language>
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        <Affiliation/>
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    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>101</Volume>
      <Issue>3-4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>第107回 岡山外科会</ArticleTitle>
    <FirstPage LZero="delete">403</FirstPage>
    <LastPage>413</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
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    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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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>101</Volume>
      <Issue>3-4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>第106回 岡山外科会</ArticleTitle>
    <FirstPage LZero="delete">395</FirstPage>
    <LastPage>402</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
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      <ArticleId IdType="doi"/>
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    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>101</Volume>
      <Issue>3-4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>代謝性酸・塩基平衡の変化ならびに呼吸性酸・塩基平衡の変化が非脱分極性筋弛緩薬の作用に及ぼす影響に関する研究</ArticleTitle>
    <FirstPage LZero="delete">387</FirstPage>
    <LastPage>394</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Osamu</FirstName>
        <LastName>Nagano</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
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      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>The influences of HCO(3)-induced and CO(2)-induced pH changes on the action of nondepolarizing muscle relaxants (MRs) were investigated using a rat phrenic nervehemidiaphragm preparation. Changes in pH were induced by varying HCO(3) concentration of the modified Krebs' solution (mK') or by varying the CO(2) concentration in the gas aerating the mK'. Changes in [Ca(++)] and [Mg(++)], associated with changes in HCO(3) concentration, were measured and corrected. A change in HCO(3) from 50mM to 13.5mM or a change in CO(2) from 2.5% to 9%, augmented the partial neromuscular blockade produced by d-Tc or vecuronium (p&lt;0.01), while inhibiting that produced by metocurine or pancuronium (p&lt;0.01). A change in HCO(3) from 13.5mM to 50mM or a change in CO(2) from 9% to 2.5%, inhibited the partial neuromuscular blockade produced by d-Tc or vecuronium (p&lt;0.01), while augmenting that produced by metocurine or pancuronium (p&lt;0.01). These findings suggest that the HCO(3)-induced and CO(2)-induced pH changes have a similar influence on the action of MRs. A difference exists between mono- and bisquaternary MRs with regard to their response to pH changes.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">非脱分極性筋弛緩薬</Param>
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        <Param Name="value">代謝性pH変化</Param>
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      <Object Type="keyword">
        <Param Name="value">呼吸性pH変化</Param>
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      <Object Type="keyword">
        <Param Name="value">筋弛緩作用</Param>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>101</Volume>
      <Issue>3-4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>急性腎不全ラットにおける肺内グアニジノ化合物の経日的変化に関する実験的研究</ArticleTitle>
    <FirstPage LZero="delete">379</FirstPage>
    <LastPage>385</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Yoshinori</FirstName>
        <LastName>Kosogabe</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Renal failure causes various metabolic disorders, especially increases of uremic toxins. Of the uremic toxins, guanidino compounds have a main role in uremia. Although lung injury is often complicated by renal failure, the role of guanidino compounds in lung injury is obscure. I have studied the changes in guanidino compounds in the lung of rat with ischemic acute renal failure. Guanidino compounds increased the first day after ischemia, but methylguanidine, which is the most toxic guanidino compound, showed a delayed increase in the lung. These results suggest the de novo synthesis of methylguanidine in the lung. A guanidinogram may by useful to judge changes in guanidino compounds.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">急性腎不全</Param>
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      <Object Type="keyword">
        <Param Name="value">グアニジノ化合物</Param>
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      <Object Type="keyword">
        <Param Name="value">メチルグアニジン</Param>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>101</Volume>
      <Issue>3-4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>ハロセンによる肝腎グアニジノ化合物代謝の変動に関する実験的研究</ArticleTitle>
    <FirstPage LZero="delete">371</FirstPage>
    <LastPage>377</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Michio</FirstName>
        <LastName>Kitaura</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>A metabolic relationship between the liver and kidney exists in combination with the urea cycle. In patients with acute renal or hepatic insufficiency, certain variations among several guanidino compounds are relevant to the condition of the liver or kidney. An experimental model of rats exposed to inhaled halothane was evaluated for metabolic changes in the liver and kidney by measuring guanidino compound levels using high performance liquid chromatography. As a result, no significant difference in serum ornithine carbamoyltransferase (OCT) activities were observed among all groups. In the liver, concentrations of creatine (CR) and guanidinobutyric acid (GBA) were significantly elevated immediately after inhalation of halothane without any accompanying changes in guanidinoacetic acid (GAA) and argnine (ARG). In the kidney, ARG and GAA were significantly decreased without any accompanying changes in CR and GBA. No significant difference in serum GC levels was observed among the groups. The inhalation of halothane appers to change the concentrations of GAA, ARG and CR in the liver and kidney. It also appers that inhalation of halothane caused GBA to appear in the blood, indicating a possible association of halothane with hepatotoxicity.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">ハロセン</Param>
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      <Object Type="keyword">
        <Param Name="value">尿素回路</Param>
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      <Object Type="keyword">
        <Param Name="value">アルギニン</Param>
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      <Object Type="keyword">
        <Param Name="value">肝腎代謝</Param>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>101</Volume>
      <Issue>3-4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>急性肝不全時の窒素代謝に関する基礎的研究―クアニジノ酢酸および腎グリシンアミヂノトランスフェラーゼ活性の変動―</ArticleTitle>
    <FirstPage LZero="delete">363</FirstPage>
    <LastPage>369</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Kabutan</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>It was reported that serum guanidinoacetic acid (GAA) levels are elevated in acute hapatic failure. To explore the mechanism of this GAA level change, the activities of kidney glycine amidinotransferase (GAT) and liver GAA-methyltransferase (GAA-MT) were measured in experimental rat models of acute hepatic failure. GAA is synthesized by the former enzyme and catabolized by the latter enzyme. In the early stage, kidney GAT activity was increased (P&lt;0.1) but the serum GAA level remained normal. In the late stage, liver GAA-MT activity was decreased (P&lt;0.01) and serum GAA level was increased. From this result, it is concluded that GAA synthesis is increased in acute hepatic failure and that serum GAA level is increased when liver is severely damaged.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">急性肝不全</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">グアニジノ酢酸</Param>
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      <Object Type="keyword">
        <Param Name="value">グリシンアミヂノトランスフェラーゼ</Param>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>101</Volume>
      <Issue>3-4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>パーキンソニズムの頭皮上と深部脳波の相関分析</ArticleTitle>
    <FirstPage LZero="delete">327</FirstPage>
    <LastPage>345</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Masahiro</FirstName>
        <LastName>Tanigawa</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Scalp and depth EEG were obtained during thalamotomy in 19 Parkinsonian patients, and a correlation analysis was performed to demonstrate additional information. 1) The decrease in mean frequency of alpha and increase in theta activity constituted a characteristic feature in Parkinsonism. The degree of these findings was closely related to the progression of the disease. 2) Simultaneous recordings in the thalamus and the scalp tended to show approximate spectral values in mild cases, but demonstrated some differences as the disease progressed. 3) Comparison of scalp and thalamic recordings revealed the existence of coincident and independent alpha activities in each area. 4) Cross-correlation analysis of the scalp EEG revealed that there were some progessive changes in phase relationships, including advance of activities from the front and delay of from the occiput with phase shifts over 90°. 5) Travelling waves were also found in the depth EEG, and the direction was from the thalamus to the cortex in some cases, but reversed in others. The phase shifts of alpha activities between the scalp and the thalamus were from 10° to 90°. From these values, the conduction velocity of the spreading alpha were from 2.4m/s to 21.6m/s.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">Parkinsonism</Param>
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      <Object Type="keyword">
        <Param Name="value">Depth EEG</Param>
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      <Object Type="keyword">
        <Param Name="value">Alpha activity Correlation analysis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Travelling wave</Param>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>101</Volume>
      <Issue>3-4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Ehrlich腹水癌細胞の薬剤耐性細胞における温熱によるAdriamycinの効果増強とその修飾</ArticleTitle>
    <FirstPage LZero="delete">315</FirstPage>
    <LastPage>325</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Naoko</FirstName>
        <LastName>Kashitani</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
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    </ArticleIdList>
    <Abstract>Adriamycin (ADR) is a well known anticancer agent which is frequently used alone or combination with other anticancer agents. An ADR-resistant cell line derived from Ehrlich ascites tumor cells (EATC) was established in our laboratory. In this report, differences between wild EATC and ADR resistant EATC were studied. The intracellular ADR uptake increased at a temperature (41.0°C) that had a little effect on the viability of wild EATC. The intracellular ADR uptake of ADR-resistant EATC also increased at elevated temperature (41.0°C). However, ADR resistant EATC had an enhanced acquired capacity that increased the efflux of intracellular ADR. Cepharanthine (CP), 1mcg/ml, inhibited the efflux of intracellular ADR and maintained the retention of ADR at high levels in cells from both cell lines, so the killing effects were enhanced with a combination ADR and CP. From these results, the mechanisms of resistance to ADR may be discussed. The killing effects of ADR depend on intracellular ADR uptake, retention and maintenance. Hyperthermic treatment accelerates the influx of ADR. In addition, CP suppresses the efflux of intracellular ADR, and increased markedly the cytotoxic effect of ADR on ADR resistant EATC. The combination of ADR, CP and hyperthermia may be effective and useful therapy to overcome ADR-resistant cancer cells.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">Ehrlich腹水癌細胞</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Adriamycin</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Hyperthermia</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Multidrug resistance</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Flow cytometry</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>101</Volume>
      <Issue>3-4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Adriamycinの殺細胞効果の加温およびCepharanthineによる修飾</ArticleTitle>
    <FirstPage LZero="delete">303</FirstPage>
    <LastPage>314</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Akifumi</FirstName>
        <LastName>Mizuta</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>The cytotoxic effect of anticancer agents depends markedly on the intracellular uptake of the anticancer drug; its maintenance is increased by accelerating the intracellular uptake of anticancer agent and inchbiting. Using with flow-cytometry, we demonstrated that the intracellular uptake of adriamycin (ADM) is increased by hyperthermia, and that cepharanthine (CEP) and Verapamil inhibit its retention. We investigated the cytotoxic effect of the combination of ADR, CEP and hyperthermia, using a NIH3T3 cell line. The cytotoxic effect of ADR is increased by hyperthermia; its effect is acquired at a lower temperature which has no cytotoxic effect alone. With the conbination of CEP, ADR and hyperthermia, the cytotoxic effect is further increased. The synergism is increased by the elevation of temperature and a long of exposure time of CEP. The increase of the intracellular accumulation anticanceragent is important to overcome multidrugresistance, a phenomenon which has that attracted agreat deal of attention.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">Adriamycin</Param>
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      <Object Type="keyword">
        <Param Name="value">cepharantine</Param>
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      <Object Type="keyword">
        <Param Name="value">加温</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">殺細胞効果</Param>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>101</Volume>
      <Issue>3-4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>頭部MRI像の画質改善について</ArticleTitle>
    <FirstPage LZero="delete">295</FirstPage>
    <LastPage>302</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Noriko</FirstName>
        <LastName>Kanzaki</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>The purpose of this study is to present a method of boundary enhancement algorithms for magnetic resonance images using a V-filter and clinical applications. By iterated V-filtering, the signal-to-noise ratio can be increased with preservation of edge sharpness. This is due to the relationship of the signal-to-noise ratio to the mean-to-variance ratio. These techniques were applied to clinical cases using MRI in the evaluation of the brain tumor. The boundaries of the brain tumor and the edematous region were precisely extracted.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">V-filter</Param>
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      <Object Type="keyword">
        <Param Name="value">MRI</Param>
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      <Object Type="keyword">
        <Param Name="value">Boundary enhancement</Param>
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      <Object Type="keyword">
        <Param Name="value">Edematous region</Param>
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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>101</Volume>
      <Issue>3-4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>ヒト骨・軟部腫瘍組織における癌遺伝子の解析</ArticleTitle>
    <FirstPage LZero="delete">285</FirstPage>
    <LastPage>293</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Sumii</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hajime</FirstName>
        <LastName>Inoue</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shiro</FirstName>
        <LastName>Ito</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Gozo</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideo</FirstName>
        <LastName>Takechi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shogo</FirstName>
        <LastName>Ikeda</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takuzo</FirstName>
        <LastName>Oda</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
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    <Abstract>The amplification and rearrangement of five cellular oncogenes (c-myc, c-K-ras, c-fos, c-raf-1, and N-myc) were studied by Southern hybridization in fourteen human bone and soft tissue tumors obtained at surgery. Amplification of c-myc was detected in the two of four osteosarcomas and one of two malignant fibrous histiocytomas. The c-myc genes in these tissues were amplified 4- to 8-fold in comparision with the placenta DNA. One of these osteosarcomas had 16- to 32-fold amplification of c-raf-1 gene without rearrangement. The clinical course of osteosarcoma and malignant fibrous histiocytoma with the amplified c-myc or c-raf-1 gene showed a rapid malignant progress with lung or bone metastasis. There appears to be a correlation between clinical prognosis and oncogene amplification.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">Oncogene</Param>
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      <Object Type="keyword">
        <Param Name="value">Gene amplification</Param>
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        <Param Name="value">c-myc</Param>
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      <Object Type="keyword">
        <Param Name="value">c-raf-1</Param>
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      <Object Type="keyword">
        <Param Name="value">Osteosarcoma</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">MFH</Param>
      </Object>
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    <ReferenceList/>
  </Article>
</ArticleSet>
