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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 77 (1988), S. 47-54 
    ISSN: 1432-0533
    Keywords: Status epilepticus ; Substantia nigra ; Pathology ; Convulsions ; Convulsants
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Neuropathological studies of rats were made after seizures of different durations. Seizures were produced by mercaptopropionic acid in paralyzed, ventilated rats that were perfusion-fixed immediately (acute) or after 2–7 days of recovery (chronic). Analysis of chronic rats, which had only 20-min seizures, showed that damage occurred to several structures including: the substantia nigra pars reticulata, the hypothalamus, the diagonal band of Broca, and the globus pallidus; the damage was worse with longer seizures. In rats perfused acutely no changes were detected in paraffin sections in the aforementioned structures if the length of seizures was 45 min or less. It was concluded that: (1) mercaptopropionic acid-induced seizures cause permanent lesions to specific brain areas, with the most pronounced effect in the substantia nigra pars reticulata; (2) the lesions result from the seizures, and they are roughly proportional to the seizures duration; and (3) permanent lesions may begin within 20 min but require longer times to become visible on light microscopy.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 586 (1990), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 23 (1974), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— A method is described by which the rate of glucose utilization by whole brain of conscious rats may be measured. The basis is the uptake of 14C derived front [2-14C] glucose into the acid-soluble metabolite pool of brain. Catheters are placed in the femoral artery and vein under light ether anesthesia. After full recovery of consciousness a single intravenous injection of [2-14C] glucose is given and arterial blood samples taken at intervals. Simultaneous with the last sample the brain is removed and frozen within 1 s. The accumulation of 14C into the acid-soluble metabilite pool is measured and the rate of glucose utilization is calculated according to the equation: 〈displayedItem type="mathematics" xml:id="mu1" numbered="no"〉〈mediaResource alt="image" href="urn:x-wiley:00223042:JNC917:JNC_917_mu1"/〉 The integral is calculated from the plasma glucose specific activity curve and evidence is presented to justify this procedure. The rate of glucose utilization measured by this method was 0·62 μmol/min per g in conscious rats and 0·28 μmol/min per g in sodium pentobarbital anesthetized rats.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 20 (1973), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— –A method is described by which inorganic phosphate may be extracted from brain when bone fragments are present. Inorganic phosphate is extracted into 80% methanol and this does not hydrolyse phosphate esters of brain or dissolve bone. The inorganic phosphate content of brain was 217 μmol/g in both fed and 24 h starved rats.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 25 (1975), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: —(1) The effects of exposure of rats to increased atmospheric concentrations of CO2 on brain metabolism in vivo were studied. (2) After 2·5 min exposure to an atmosphere of 20% CO2, the rate of glucose utilization by brain decreased from 0·61 μmol/min per g to 0·32 μmol/min per g and remained between 0·3 and 0·4 μmol/min per g for 60 min, the longest interval studied. O2 utilization, calculated from the arteriovenous difference of O2 across the brain and blood flow, was 3·5 μmol/min per g in controls and was 4·7 μmol/min per g after 5 min in the 20% CO2 atmosphere. (3) The concentrations of glucose, glucose 6-phosphate and aspartate were increased during the first 10 min of CO2 exposure whereas the concentrations of other glycolytic intermediates, tricarboxylic acid cycle intermediates and glutamate were decreased. The amount of endogenous substrate which disappeared during the first 10 min was sufficient, if used to supplement glucose as a fuel, to maintain the O2 consumption at, or slightly above, the control level. Glutamate and lactate were quantitatively the most important energy sources. (4) The mechanism whereby‘CO2 decreased the rate of glucose utilization is uncertain. The initial rise in glucose 6-phosphate and fall in fructose 1,6-diphosphate concentrations suggested that an inhibition of phosphofructokinase was responsible. However, after 60 min in 20% CO2, the concentrations of both of these metabolites returned to normal while the rate of glucose utilization remained depressed.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 20 (1973), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The use of the glutamate dehydrogenase (EC 1.4.1.3) and β-hydroxybutyrate dehydrogenase (EC 1.1.1.30) reactions for the calculation of the mitochondrial redox state of brain has been examined. To prevent post-mortem anoxic metabolism, brains were frozen in less than a second by using a new technique. Levels of ketone bodies in brain were so low relative to the contamination by blood and extracellular fluid that calculation of the mitochondrial redox state using the β-hydroxybutyrate dehydrogenase reaction was not practical. The concentrations of the non-nucleotide substrates of the glutamate dehydrogenase reaction could be accurately measured in brain and themitochondrial [NAD+]/[NADH] ratio calculated from the ratio [α-oxoglutarate] [NH4+]/[glutamate]. The calculation is valid if the ratio [α-oxoglutarate] [NH4+]/[glutamate] in mitochondria is the same as that measured in whole tissue. The evidence supporting this conclusion is the near-equilibrium of the aspartate aminotransferase (EC 2.6.1.l) reaction in brain and the observation by others that the distribution of label between α-oxoglutarate and glutamate in brain, after administration of labelled precursors, conforms to expectation. The alanine aminotransferase (EC 2.6.1.2) reaction was not near equilibrium in brain, probably because of the low in vivo activity of the enzyme.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 315 (1978), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Breast cancer research and treatment 2 (1982), S. 239-242 
    ISSN: 1573-7217
    Keywords: cellularity ; DNA ; estrogen receptor ; protein ; wet weight
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Fifty estrogen receptor (ER)-positive breast cancers have been studied to determine the best way of correcting for differences in cellularity when expressing ER concentration. ER concentration expressed on wet weight and tumour cytosol protein bases showed a positive correlation with tumour cellularity. In contrast, ER concentrations expressed on a DNA basis were not significantly related to cellularity. Although such a mode of correcting for differences in cellularity was imperfect, it did yield a receptor concentration which was less dependent upon tissue cellularity and which may reflect more accurately the inherent receptor status of the tumour cells.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-1300
    Keywords: Biomedical imaging ; Multimedia database applications ; PACS ; Imaging systems architecture
    Source: Springer Online Journal Archives 1860-2000
    Topics: Information Science and Librarianship
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1434-0879
    Keywords: Interferon-γ ; Receptors ; Bladder cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Previously we have shown a differential biological response of three human bladder cancer cell lines (RT4, RT112 and MGH-U1) to gamma interferon (IFN-γ). The present study examines the relationship between the biological response and the expression of the interferon-γ receptor on the tumour cell surface. Using a competitive radioligand binding assay and Scatchard analysis, we measured the number and affinity of the IFN-γ receptors on each of the above cell lines. Individual cells from each line expressed large numbers (29,100–41,800) of high-affinity receptors (k d =2.4–3.9×1010M). There was no statistically significant difference in either of these parameters between the three lines. We therfore conclude that the biological response of these bladder lines to IFN-γ does not relate to the number or affinity of its receptor on the plasma membrane of these tumour cells.
    Type of Medium: Electronic Resource
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