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  • 1970-1974  (6)
  • 1
    Electronic Resource
    Electronic Resource
    PERMEABILITY OF THE BLOOD-BRAIN BARRIER TO FRUCTOSE AND THE ANAEROBIC USE OF FRUCTOSE IN THE BRAINS OF YOUNG MICE (1972)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 19 (1972), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: —Fructose levels were determined in plasma and brain of 8- to 12-day-old mice at intervals after the injection of 30 mmol/kg intraperitoneally; controls received NaCl, 15 mmol/kg. In normal animals brain fructose increased very slowly despite a rapid rise in plasma levels (120 times the control value in 5 min). At 40 min the cerebral level was 1.54 ± 0.23 mmol/kg; the corresponding plasma level was 47.1 ± 4.8 mM. The data suggest that fructose can serve as a source of energy to the brain in times of critical need: during insulin hypoglycemia brain fructose increased to only 0.88 ± 0.05 mmol/kg during the same interval (40 min) despite plasma fructose values equal to those in control animals; also 30 s after cerebral ischemia (decapitation) brain fructose fell from a zero time value of 1.19 ± 0.09 mmol/kg (20 min after fructose injection) to 0.76 ± 0.06 mmol/kg (P= 0.005). Under both circumstances (hypoglycemia and ischemie anoxia) an apparent threshold concentration of fructose for utilization was observed—0.6–0.7 mmol/kg. The most likely explanation for this finding appears to be that this level of fructose was in the extracellular space of the brain. Hexokinase activity in brain homogenates of 8- to 12-day-old mice with fructose and ATP at concentrations found in vivo and during ischemie anoxia did not appear to be rate-limiting. We concluded that the major handicap to the use of fructose by the brain was the limited penetration of fructose from the blood to the brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1972.tb06213.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    SUPPRESSIVE ACTIVITY OF PREGNANCY PLASMA ON THE MIXED LYMPHOCYTE REACTION (1973)
    Oxford, UK : Blackwell Publishing Ltd
    BJOG 80 (1973), S. 0 
    Details
    ISSN: 1471-0528
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Complement inactivated plasma obtained from patients in late pregnancy, or at delivery, had a suppressive effect on in vitro mixed lymphocyte reactivity (MLR) between unrelated individuals. In contrast, complement inactivated plasma obtained in the early stages of pregnancy did not suppress mixed lymphocyte reactivity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-0528.1973.tb16033.x
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  • 3
    Electronic Resource
    Electronic Resource
    THE IMMUNOLOGICAL REACTIVITY OF MATERNAL LYMPHOCYTES IN PREGNANCY (1973)
    Oxford, UK : Blackwell Publishing Ltd
    BJOG 80 (1973), S. 0 
    Details
    ISSN: 1471-0528
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Mixed lymphocyte reactions were performed using lymphocytes from women at various stages of pregnancy, and these were compared to mixed lymphocyte reactions between cells from non-pregnant adult volunteers. Immunological reactivity of lymphocytes at all stages of pregnancy was significantly reduced compared to the reactivity of lymphocytes from non-pregnant donors. There was, however, no significant difference between lymphocyte reactivity at 12 to 16, 28, and 36 to 40 weeks of pregnancy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-0528.1973.tb16034.x
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  • 4
    Electronic Resource
    Electronic Resource
    Blocking one-way maternal-foetal MLR (1974)
    [s.l.] : Nature Publishing Group
    Nature 250 (1974), S. 791-791 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] SIR,?The results of animal experiments1,2 show that enhancing or blocking antibodies may be at least partly responsible for the apparent lack of maternal immunological response to the paternally derived histocompatability factors of the foetus. Youtananukorn and Matang-kasombut3 used peripheral ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/250791a0
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  • 5
    Electronic Resource
    Electronic Resource
    Mutations affecting levels of tetrahydrofolate interconversion enzymes in Saccharomyces cerevisiae (1973)
    Springer
    Molecular genetics and genomics 123 (1973), S. 209-218 
    Details
    ISSN: 1617-4623
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary The ADE15, ade3-41 and ser2 markers have been mapped with respect to one another and with respect to the SUC1-MAL1 locus on chromosome VII of Saccharomyces cerevisiae. Three methods have been used for this mapping, viz. conventional tetrad analysis, analysis of single site conversion asci, and analysis of double site conversion asci. The physical distance separating ade3-41 and ADE15, two mutations affecting synthesis of tetrahydrofolate interconversion enzymes, has been estimated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00271239
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  • 6
    Electronic Resource
    Electronic Resource
    Mutations affecting levels of tetrahydrofolate interconversion enzymes in Saccharomyces cerevisiae (1973)
    Springer
    Molecular genetics and genomics 123 (1973), S. 199-208 
    Details
    ISSN: 1617-4623
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary The ADE15 mutation causes a requirement for adenine. It is dominant to its wild type allele as measured by growth of the heterozygous diploid. The mutation results in altered levels of three tetrahydrofolate interconversion enzymes. The presence of ade3-41, which itself causes reduction in the levels of the same three interconversion enzymes, in cis position to the ADE15 mutation eliminates dominance of the ADE15 mutation. The simplest explanation of the cis epistasis of ade3-41 to ADE15 is that the two mutations lie in the same transcriptional unit.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00271238
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