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  <Article>
    <Journal>
      <PublisherName/>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn/>
      <Volume>125</Volume>
      <Issue>16</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1998</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>The ich1 gene of the mushroom Coprinus cinereus is essential for pileus formation in fruiting</ArticleTitle>
    <FirstPage LZero="delete">3133</FirstPage>
    <LastPage>3141</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Hajime</FirstName>
        <LastName>Muraguchi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Kamada</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>&lt;p&gt;The formation of the pileus in homobasidiomycete fungi is essential for sexual reproduction, because the pileus bears the hymenium, a layer of cells that includes the specialised basidia in which nuclear fusion, meiosis and sporulation occur. The developmental mutant ichijiku of Coprinus cinereus fails to develop a differentiated pileus at the apex of the primordial shaft, which is the basal part of the fruit-body primordia and formed in an early stage of fruit-body differentiation. Genetic analysis indicates that this phenotype is caused by a recessive mutation in a single gene (ich1). The ich1 gene was mapped to chromosome XII using restriction fragment length polymorphism markers and the marker chromosome method, and cloned by complementation using a chromosome-XII-specific cosmid library. The ich1 gene encodes a novel protein of 1,353 amino acids. The Ich1 amino-acid sequence contains nuclear targeting signals, suggesting that the Ich1 protein would function in the nucleus. Northern blot analysis indicates that the ich1 gene is specifically expressed in the pileus of the wild-type fruit-body. No ich1 mRNA was detected in the ichijiku mutant, consistent with loss of the promoter region of ich1 in the mutant genome. These data demonstrate that the ick1 gene product is essential for pileus formation.&lt;/p&gt;
</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Developmental mutant</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Ich1</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Pileus</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Fruit-body</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">morphogenesis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Basidiomycete</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Coprinus</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn/>
      <Volume>17</Volume>
      <Issue>6</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1963</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Post mortem activation of human blood fibrinolytic enzyme in sudden and natural deaths</ArticleTitle>
    <FirstPage LZero="delete">279</FirstPage>
    <LastPage>288</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Kyoichi</FirstName>
        <LastName>Haba</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Osamu</FirstName>
        <LastName>Kumano</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masao</FirstName>
        <LastName>Mohri</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideo</FirstName>
        <LastName>Takemaru</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kohichi</FirstName>
        <LastName>Kawanishi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shohei</FirstName>
        <LastName>Tobe</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Kamada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Seishi</FirstName>
        <LastName>Ueno</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/32596</ArticleId>
    </ArticleIdList>
    <Abstract>&lt;p&gt;With the purpose to elucidate the cause and difference of blood fluidity in sudden death and natural one, we have observed the fibrinolysis of the blood in medico-legal and pathological autopsies by means of Fibrin Plate Method, a
routine method devised in our laboratory. As the result it has been found that in the blood serum of sudden death and
in some of natural deaths from tumors, leukemias, etc., the decrease in fibrinolytic activity is equivalent to the amount of proactivator that combined with the SK-like substance liberated into blood. On the other hand, in the blood of most of natural deaths, and in that bled from vessels and stored in body cavities, no natural fibrinolysis is observable and the same fibrinolytic activity with SK as normal one is demonstrated. Thus it is concluded that the cause of blood fluidity in sudden death is due to the fibrinolysis.&lt;/p&gt;
</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList/>
    <ReferenceList/>
  </Article>
</ArticleSet>
