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  • 1
    Electronic Resource
    Electronic Resource
    Adenosine uptake in pyrimidine 5′-nucleotidase deficient human erythrocytes via a high affinity transport system (1985)
    Springer
    Cellular and molecular life sciences 41 (1985), S. 366-368 
    Details
    ISSN: 1420-9071
    Keywords: Erythrocytes ; pyrimidine-S′-nucleotidase ; 14C-adenosine uptake
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Using a pulse-labeling technique,14C-adenosine uptake into pyrimidine 5′-nucleotidase (P5N) deficient erythrocytes (RBC) was found to be impaired. The Lineweaver-Burk plot showed Km values of 2.0×10−3 mM and 0.2 ×10−3 mM for normal RBC and P5N deficient RBC, respectively. These results indicate that P5N is one of regulators of the adenosine transport system and/or is associated with adenosine carrier protein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02004508
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Detection of pyrimidine 5′-nucleotidase deficiency using1H-or31P-nuclear magnetic resonance (1986)
    Springer
    Cellular and molecular life sciences 42 (1986), S. 69-72 
    Details
    ISSN: 1420-9071
    Keywords: Pyrimidine 5′-nucleotidase (P5′N) ; nuclear magnetic resonance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary We describe here a further Japanese family with pyrimidine 5′-nucleotidase (P5′N) deficiency diagnosed using a nuclear magnetic resonance (NMR) spectrum, in Kumamoto prefecture where two families having the disease have been reported before. The specific spectra in1H-NMR of P5′N deficient erythrocytes were due to three methyl protons of CDP-choline at 3.22 ppm and to H-2, H-8 and ribose-1′ of pyrimidine nucleotide phosphate(s) in the lower fields (at 5.82 and 8.00 ppm). The other specificities in31P-NMR spectra were due to CDP-choline, CDP-ethanolamine and UDP-glucose. Those spectra were not detected in other types of hemolytic anemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01975900
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Insulin and glucagon therapy of acute hepatic failure (1991)
    Springer
    Digestive diseases and sciences 36 (1991), S. 809-815 
    Details
    ISSN: 1573-2568
    Keywords: insulin ; glucagon ; acute hepatic failure ; liver regeneration ; polyamine ; ornithine decarboxylase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract When insulin and glucagon are administered to rats with severe liver injury, survival is enhanced with an attenuation of the liver injury compared to that of untreated controls. In rats with acute liver injury both hormones produce a rapid normalization of hepatic protein content following initiation of DNA synthesis. When rats receive both hormones after partial hepatectomy, the first burst of DNA synthesis reaches a maximum earlier than that seen in controls. Both hormones enhance the increment of hepatic putrescine essential for DNA synthesis through activation of ornithine decaroxylase and/or spermidine-N1-acetyltransferase. The enhancement of putrescine content by each hormone is additive. Putrescine supplementation promotes hepatic DNA synthesis after hepatectomy. Based on these data, we conclude that a combination of insulin, and glucagon is effective in the therapy of acute hepatic failure in rats. The restoration of liver function as well as the stimulation of liver cell proliferation via putrescine production may contribute to this effect.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01311241
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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