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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>9-10</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>第20回 岡山リウマチ研究会抄録</ArticleTitle>
    <FirstPage LZero="delete">973</FirstPage>
    <LastPage>976</LastPage>
    <Language>EN</Language>
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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>9-10</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>第88回 岡山医学会総会演題抄録</ArticleTitle>
    <FirstPage LZero="delete">963</FirstPage>
    <LastPage>972</LastPage>
    <Language>EN</Language>
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        <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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  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>101</Volume>
      <Issue>9-10</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>一過性虚血時の冠血管トーヌス調節機構に関する研究―反応性充血に対するアデニレートサイクラーゼの関与―</ArticleTitle>
    <FirstPage LZero="delete">953</FirstPage>
    <LastPage>962</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Kazuyoshi</FirstName>
        <LastName>Hina</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
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    <Abstract>Many lines of evidence suggest that adenosine partly regulates coronary vascular tone in response to myocardial ischemia after a brief coronary occlusion. However, the basic mechanisms of blood flow regulation of myocardial reactive hyperemia still remain unknown. This experiment was performed using the selective effect of forskolin to enhance the effects of agonists which exert receptor-mediated stimulation of adenylate cyclase. We exploited the potentiating effect of forskolin to test the hypothesis that activation of adenylate cyclase contributes to myocardial reactive hyperemia, especially by release of adenosine at the time of brief coronary occlusions. In ten open-chest dogs, intracoronary forskolin infusions, which produced plasma concentrations between 0.22 and 0.34 μM, slightly increased coronary blood flow and had no effect on hemodynamics or myocardial metabolism. Under these conditions, although peak reactive hyperemic flow rates were not affected, forskolin infusions reversibly increased repayments of flow debt significantly by 28, 25 and 27% following coronary occlusions of 15, 20 and 30 second, respectively (p&lt;0.05). In other seven dogs, after observations of the effects of forskolin (0.16-0.26μM), 10μM of 8-phenyltheophylline, a potent adenosine antagonist, was intracoronarily infused simultaneously with forskolin. Forskolin potentiated debt repayments by about 23-27% following 15, 20 and 30 second occlusions. However, with simultaneous 8-phenyltheophylline, the effects of forskolin were eliminated significantly (p&lt;0.05). The present results demonstrate that adenylate cyclase contributes to myocardial reactive hyperemia and adenosine has a significant role as metabolic regulator of reactive hyperemia through activation of adenylate cyclase.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">アデニレートサイクラーゼ</Param>
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        <Param Name="value">アデノシン</Param>
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        <Param Name="value">反応性充血</Param>
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        <Param Name="value">forskolin</Param>
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        <Param Name="value">Raレセプター</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>9-10</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>膠原病患者末梢血単核細胞からのトランスフェリンの放出異常</ArticleTitle>
    <FirstPage LZero="delete">941</FirstPage>
    <LastPage>952</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Makoto</FirstName>
        <LastName>Hatano</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
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    <Abstract>The concentration of human transferrin (TF) in culture supernatants and intracellular TF contents of normal human peripheral blood mononuclear cells (MNC) after incubation with or without mitogens (PHA, ConA, PWM) for different periods of time were measured by enzyme-linked immunosorbent assay. TF concentrations in culture supernatant tended to gradually increase from the beginning of MNC culture to a peak at day 3 to 5. In contrast, intracellular concentrations of TF were decreased after MNC culture in parallel with the increase of TF concentration in the supernatants. The presence of mitogens mostly diminished TF concentrations in culture supernatant at the time when DNA synthesis maximally occurred. Transferrin release from MNC cultured at 4°C was minimal. A higher iron ion concentration of the culture medium suppressed the TF release from MNC. These results suggested that TF was actually released from MNC when cells were resting but in active metabolism at low iron concentration. In addition, the kinetics of TF release by MNC from systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) patients were different from that of healthy controls. Low spontaneous TF release from SLE MNC through the culture and higher TF release from RA MNC in PHA stimulation after culture for 5 days were observed. These abnormalities found in SLE and RA might be one of causes of the low responsiveness of MNC in these patients to various mitogens.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">human peripheral blood mononuclear cells</Param>
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      <Object Type="keyword">
        <Param Name="value">lymphocyte proliferation</Param>
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      <Object Type="keyword">
        <Param Name="value">transferrin release</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">transferrin receptor</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">IL-2 receptor</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>9-10</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>左室肥大例における心室性期外収縮―Holter心電図と運動負荷(201)T1心筋シンチグラムおよびUCGとの対比検討―</ArticleTitle>
    <FirstPage LZero="delete">931</FirstPage>
    <LastPage>940</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Naoki</FirstName>
        <LastName>Kobiki</LastName>
        <Affiliation/>
      </Author>
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    <Abstract>In order to investigate the relationship of different morbid states of the hypertrophied myocardium to the appearance of ventricular premature contraction (VPC), we compared the VPC findings from Holter ECG with those of UCG and stress thallium-201 myocardial SPECT scintigraphy (stress scinti) in 31 patients with hypertrophic cardiomyopathy (HCM) and 20 with essential hypertension (HT). The HCM patients consisted of 21 with asymmetric hypertrophy (ASH), 3 with symmetric hypertrophy (SH), and 7 with apical hypertrophy (APH). We recognized positive findings on the stress scinti such as fixed perfusion defect (FD) or reversible perfusion defect (RD) in 11 patients (ASH 10, APH 1) out of 31 patients with HCM (35%). Positive findings were observed in only one patient out of 20 with HT (5%). We recognized a high grade VPC (grade 4a and 4b of Lown's criteria) in 8 of 11 scinti positive patients with HCM (ASH 7, APH 1) (73%), while high grade VPC appeared in 5 (all of them are ASH) out of 20 scinti negative patients with HCM (25%). Therefore, these findings suggest that high grade VPCs in HCM occur in relation to a myocardial perfusion defect.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">心室性期外収縮</Param>
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      <Object Type="keyword">
        <Param Name="value">肥大型心筋症</Param>
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      <Object Type="keyword">
        <Param Name="value">Holter心電図運動負荷(201)Tl心筋シンチグラム</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>9-10</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>脳虚血に関する実験的研究―脳虚血および血行再開時におけるprostaglandin-thromboxane系代謝産物の関与について―</ArticleTitle>
    <FirstPage LZero="delete">911</FirstPage>
    <LastPage>930</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Akihiko</FirstName>
        <LastName>Yamanaka</LastName>
        <Affiliation/>
      </Author>
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    <Abstract>The left middle cerebral artery and the common trunk of the anterior cerebral artery were simultaneously occluded via a transorbital approach in 35 dogs. Local cerebral blood flow (1-CBF) and platelet aggregability were measured during 2 hours of arterial occlusion followed by 2 hours of recirculation. The animals were divided into four groups according to drug administration. Eight dogs were control animals. Nine dogs received OKY-1581, a selective thromboxane A(2) synthetase inhibitor 75mg/kg intravenously 1 hour before cerebral ischemia. In another 9 dogs, OKY-1581 was infused intravenously at a rate of 100μg/kg/min during the ischemia and recirculation periods. The remaining 9 dogs received indomethacin, a selective cyclooxygenase inhibitor 4mg/kg intravenously 1 hour before occlusion of the vessels. Both OKY-1581 75mg/kg and indomethacin 4mg/kg resulted in a slight reduction in mean 1-CBF before ischemia. In control animals, mean 1-CBF decreased by 70% following clipping of the arteries. By releasing the clips, mean 1-CBF was restored to near the pre-occlusion level, followed by another decrease (postischemic hypoperfusion). In animals which received OKY-1581 100μg/kg/min, hyperemia was apparent in the immediate post-recirculation period, followed by aggravation of hypoperfusion. In animals which received indomethacin 4mg/kg, neither hyperemia nor hypoperfusion was demonstrated through recirculation period. Changes in platelet aggregability induced by ADP was not observed by cerebral ischemia and restoration of circulation. The platelet aggregability was reduced only by surgical procedures and by administration of indomethacin. These results suggest that the postischemic recirculation is strongly influenced by arachidonic acid degradation products, such as thromboxane A(2) and other cyclooxygenase products. It seems that the inhibition of cyclooxygenase is more beneficial than that of thromboxane A(2) synthetase, in the protection of hypoperfusion after recirculation of cerebral blood flow.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">脳虚血</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">local cerebral blood flow</Param>
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      <Object Type="keyword">
        <Param Name="value">血小板凝集能</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">OKY-1581</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">indomethacin</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>9-10</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>老人発症慢性関節リウマチの臨床的およびX線学的研究</ArticleTitle>
    <FirstPage LZero="delete">901</FirstPage>
    <LastPage>910</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Nakashima</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>A clinical and radiological study was performed in forty patients (male 10, female 30) with onset of definite or classical RA over 60 years. There were no statistically significant differences in the sex ratio, positive rate of latex fixation test (85%), distribution of affected joints, efficacy of treatments and prognosis between the elderly-onset and ordinary rheumatoid patients described previously. However, complications such as renal dysfunction and pulmonary fibrosis were higher. More careful use of long-term drug therapy may be essential for these elderly patients. The degree of radiographic changes, evaluated by Larsen's grade, showed no correlation with the sex, latex fixation test or Lansbury's index. However, the patients who had an increased erythrocyte sedimentation rate (over 30 mm/hour), a higher amount of plasma IgM and a longer duration of illness (over 5 years) showed significantly higher Larsen's grades. Single photon absorptiometry (Norland Model 278) both of the distal one third and one sixth of the radius, showed that the former correlated more highly with Larsen's grade than the latter.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">老人発症</Param>
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      <Object Type="keyword">
        <Param Name="value">慢性関節リウマチ</Param>
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      <Object Type="keyword">
        <Param Name="value">臨床所見</Param>
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      <Object Type="keyword">
        <Param Name="value">X線所見</Param>
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      <Object Type="keyword">
        <Param Name="value">骨塩量</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>9-10</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>18分間完全全脳虚血犬の脳組織障害に関する実験的研究</ArticleTitle>
    <FirstPage LZero="delete">887</FirstPage>
    <LastPage>899</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Takayuki</FirstName>
        <LastName>Okamoto</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>The neuronal damage of small to medium sized striatal neurons, hippocampal CA1 pyramidal cells and cerebellar Purkinje cells was histologically studied after reperfusion following 18 minutes of global brain ischemia in dogs. Neuronal damage of small to medium sized striatal neurons progressed up to 6 hours after reperfusion, but further damage was not observed from 6 hours to 7 days after reperfusion. Little damage of either the hippocampal CA1 pyramidal cells or cerebellar Purkinje cells was observed 6 hours after reperfusion, but severe delayed damage of those cells was observed from 24 to 48 hours after reperfusion. These results suggest that the delayed onset of neuronal damage of both hippocampal CA1 pyramidal cells and cerebellar Purkinje cells is due to secondary injury factor (s) after reperfusion subsequent to ischemia. The delayed neuronal damage in this model may be prevented or reduced by treatment of secondary injury factor (s).</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">全脳虚血</Param>
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      <Object Type="keyword">
        <Param Name="value">イヌ</Param>
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      <Object Type="keyword">
        <Param Name="value">海馬CA1</Param>
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      <Object Type="keyword">
        <Param Name="value">プルキンエ細胞</Param>
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      <Object Type="keyword">
        <Param Name="value">線条体</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>9-10</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>エンドトキシンによる培養肝細胞内メタロチオネインmRNA発現に関する実験的研究</ArticleTitle>
    <FirstPage LZero="delete">875</FirstPage>
    <LastPage>886</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Motoharu</FirstName>
        <LastName>Matsushita</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>In order to clarify the mechanism of metallothionein (MT) induction by bacterial endotoxin, the induction of MT mRNA in cultured human hepatic (Chang) cells by a human MT cDNA was investigated. Although endotoxin added to the culture medium did not induce MT mRNA, the conditioned medium from endotoxin-activated macrophages induced MT mRNA in Chang cells. Conditioned medium containing actinomycin D inhibited the induction of MT mRNA, while conditioned medium containing cycloheximide did not. The induction of MT mRNA was found to be a primary induction. MT inducibility was also tested with IL-1, IFN, IL-6, and TNF, all of which are substances released from endotoxin-activated macrophages. Since they did not induce MT mRNA in Chang cells, endotoxin-activated macrophages release some other MT inducer (s), which are heat stable and synthesized de novo in endetoxin-activated macrophages. To elucidate the details of MT mRNA induction, the kinetics of MT mRNA induction by conditioned medium in Chang cells was studied and compared with the kinetics of MT mRNA induction by zinc and dexamethasone in Chang cells. MT mRNA was induced by conditioned medium dose dependently, and the level of MT mRNA was increased within 3hr, reached a maximum at 12hr, and then gradually decreased. Since the induction of MTmRNA in regulated by factor (s) released from endotoxin-activated macrophages, MT may be involved in the host defense mechanism.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">メタロチオネイン</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">エンドトキシン</Param>
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      <Object Type="keyword">
        <Param Name="value">マクロファージ</Param>
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      <Object Type="keyword">
        <Param Name="value">メッセンジャーRNA</Param>
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      <Object Type="keyword">
        <Param Name="value">Northern blot hybridization</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>9-10</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1989</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>高齢者に対する全人工股関節置換術の治療成績</ArticleTitle>
    <FirstPage LZero="delete">863</FirstPage>
    <LastPage>874</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Norihei</FirstName>
        <LastName>Tsuchida</LastName>
        <Affiliation/>
      </Author>
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      <ArticleId IdType="doi"/>
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    <Abstract>A follow-up study was performed on 68 total hip replacements (THR) in 62 patients over 65 years of age who were followed for more than 3 years (average, 6 years 9 months). Except in 14 cases of death or 9 incomplete histories at follow-up, 39 cases were investigated both clinically and radiologically. Thirty-four were osteoarthritic patients and others were avascular necrosis of the femoral head and femoral neck fracture. For the operations, Charnley, Müller and New Müller type prosthesis were used. In a prognostic nutritional index, all records were over 45.
Although elderly patients hed various pre-operative complications, hip scores have improved from 44.3 to 79.2 points post-operatively. Radiological study confirmed that osteoporosis in aged patients has little relationship with loosening of the prosthesis. Results of the THR using Müller prosthesis were poor compared with the Charnley or New Müller prosthesis. For elderly patients, THR can be well indicated even if the life span is not so long after the operation.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">追跡調査</Param>
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      <Object Type="keyword">
        <Param Name="value">合併症</Param>
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      <Object Type="keyword">
        <Param Name="value">骨萎縮</Param>
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  </Article>
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