Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Barbiturate  (1)
  • Energy metabolism  (1)
Source
Material
Years
Keywords
  • 1
    Electronic Resource
    Electronic Resource
    Over-expression of glucose transporter isoform GLUT1 and hexokinase I in rat renal oncocytic tubules and oncocytomas (1994)
    Springer
    Virchows Archiv 425 (1994), S. 63-68 
    Details
    ISSN: 1432-2307
    Keywords: Renal carcinogenesis ; Epithelial kidney tumours ; Energy metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Renal oncocytomas, which have previously been shown to originate from the collecting duct system, were induced in male Sprague-Dawley rats by oral administration of N-nitrosomorpholine (NNM) for 7 weeks. The expression of glucose transporter isoforms GLUT1 and GLUT2, and of several enzymes involved in glucose metabolism [hexokinase (HK), pyruvate kinase (PK), lactate dehydrogenase (LDH), malate dehydrogenase (MDH)] were studied by cytochemical approaches in serial cryostat sections of the kidney 12, 23 and 34 weeks after withdrawal of NNM. Oncocytic tubules connected with collecting ducts were first observed 23 weeks, and oncocytomas 34 weeks after withdrawal. The cytochemical pattern of oncocytic tubules and oncocytomas was similar, but differed markedly from that of normal collecting ducts in nearly all variables studied; expression of GLUT1 and hexokinase I proteins were strongly increased; activities of HK, PK and MDH were elevated, while LDH activity was reduced. These results suggest that oncocytic transformation is associated with fundamental changes in energy metabolism which differ from those in cell lineages leading to other types of renal cell tumours, such as clear/acidophilic and basophilic cell tumours. The characteristic over-expression of GLUT1 may be used as a diagnostic criterion for the discrimination between oncocytes and acidophilic (granular) cells in clear/acidophilic renal cell tumours which show a reduced expression of this glucose transporter protein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00193950
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Einfluß von Aethanol auf die Neurotransmitter Glutamat und GABA (1982)
    Springer
    European archives of psychiatry and clinical neuroscience 232 (1982), S. 183-189 
    Details
    ISSN: 1433-8491
    Keywords: Ethanol ; Barbiturate ; Cortex ; GABA ; Glutamate ; Hippocampus ; Nigra ; Striatum ; Aethanol ; Barbiturat ; Cortex ; GABA ; Glutamat ; Hippocampus ; Nigra ; Striatum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung In zwei Versuchsserien wurde der Einfluß von chronischer Aethanolgabe (5 g/kg täglich) über 2 bzw. 4 Wochen auf die Neurotransmitter Glutamat und GABA bei Ratten untersucht. Dabei fand sich ein durch Barbiturat maskierter Anstieg der GABA-Konzentration in Striatum, Hippocampus und Substantia nigra, 8 bzw. 12 Stunden nach der letzten Aethanolgabe. Für Glutamat konnte ebenfalls ein Anstieg in den untersuchten Hirnregionen gefunden werden, der mit den für Dopamin bekannten Veränderungen unter Aethanol vereinbar ist. Die Bedeutung für die Pathogenese hirnorganischer Anfälle und psychotischer Symptome nach chronischem Alkoholmißbrauch wird diskutiert.
    Notes: Summary The effect of chronic ethanol administration, 5 g/kg per day for 2 or 4 weeks, on the neurotransmitters glutamate and GABA was investigated in rats. An increase in GABA was found in the striatum, hippocampus, and substantia nigra, 8 or 12 h after the last ingestion of ethanol, this being masked by injection of barbiturate. In addition an increase of glutamate has been found in the examined brain areas. This is consistent with the known effect of ethanol on brain Dopa metabolism and release. Finally, the relevance of the results for the pathogenesis of withdrawal seizures and delirious states is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00343699
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...