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  • 1995-1999  (1)
  • 1980-1984  (1)
  • Cerebral cortex  (1)
  • Coxsackievirus A5  (1)
  • 21.10.Ft Charge distribution
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Neurochemical research 23 (1998), S. 1485-1491 
    ISSN: 1573-6903
    Keywords: Cerebral cortex ; energy metabolism ; enzymes ; L-acetylcarnitine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The maximum rate (Vmax) of some mitochondrial enzymatic activities related to the energy transduction (citrate synthase, α-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, cytochrome oxidase) and amino acid metabolism (glutamate dehydrogenase, glutamate-pyruvate-transaminase, glutamate-oxaloacetate-transaminase) was evaluated in non-synaptic (free) and intra-synaptic mitochondria from rat brain cerebral cortex. Three types of mitochondria were isolated from rats subjected to i.p. treatment with L-acetylcarnitine at two different doses (30 and 60 mg·kg−1, 28 days, 5 days/week). In control (vehicle-treated) animals, enzyme activities are differently expressed in non-synaptic mitochondria respect to intra-synaptic “light” and “heavy” ones. In fact, α-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, glutamate-pyruvate-transaminase and glutamate-oxaloacetate-transaminase are lower, while citrate synthase, cytochrome oxidase and glutamate dehydrogenase are higher in intra-synaptic mitochondria than in non-synaptic ones. This confirms that in various types of brain mitochondria a different metabolic machinery exists, due to their location in vivo. Treatment with L-acetylcarnitine decreased citrate synthase and glutamate dehydrogenase activities, while increased cytochrome oxidase and α-ketoglutarate dehydrogenase activities only in intra-synaptic mitochondria. Therefore in vivo administration of L-acetylcarnitine mainly affects some specific enzyme activities, suggesting a specific molecular trigger mode of action and only of the intra-synaptic mitochondria, suggesting a specific subcellular trigger site of action.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1590-3478
    Keywords: Reye syndrome ; influenza B virus ; Coxsackievirus A5 ; mixed infection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Sommario Abbiamo studiato da un punto di vista clinico e virologico un caso di sindrome di Reye verificatosi in una bambina di 16 mesi pochi giorni dopo un episodio di influenza. La diagnosi di sindrome di Reye è stata posta sulla base di dati clinici e di laboratorio. Le indagini virologiche sono state condotte su campioni di feci, tampone faringeo, liquor e su una coppia di sieri. Dal liquor è stato isolato un virus coxsackie A5. Nella coppia di sieri è stata stata evidenziata una sieroconversione verso la variante del virus influenzale di tipo B in circolazione nella regione a quell'epoca e verso il ceppo di virus coxsackie A5 isolato. L'isolamento dal SNC del virus coxsackie A5 e la dimostrazione di una concomitante infezione da virus influenzale B nel caso da noi studiato depongono a favore dell'ipotesi che una infezione virale mista possa scatenare la sindrome di Reye.
    Notes: Abstract A 16 month old girl developed Reye syndrome a few days after an episode of influenza. The diagnosis of RS was made on clinical and laboratory data. Virological examinations were done on specimens of stools, throat swab, spinal fluid and two samples of serum. A coxsackievirus A5 was isolated from the spinal fluid. A seroconversion was found against the variant of influenza type B virus circulating in our region at that time and the isolated coxsackie A5 strain. The involvement in the CNS of coxsackie A5 and the demonstration of a simultaneous infection with influenza B virus supports the hypothesis that a mixed viral infection could trigger the Reye syndrome.
    Type of Medium: Electronic Resource
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