3 research outputs found

    Frequencies of feline blood types in Hungary

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    Feline blood group determination is done as a routine diagnostic method in numerous countries. Blood transfusion reactions and feline neonatal isoerythrolysis (FNI) can be avoided with the identification of different feline blood groups. The present study is the first investigation in Hungary during which 100 cats have been examined from all over the country. These cats were out of six breeds: European domestic shorthair, Persian mix, Persian, Abyssinian, Siamese and British shorthair. In the Hungarian feline population European domestic shorthair are most common but other breeds also occur. European domestic shorthair, Persian mix, Abyssinian, Siamese and British shorthair individuals all belonged to blood type A (100%). Blood type B was found very rarely and only in Persian cats. One-third of the Persian cats were categorised into blood type B, whilst type AB was not found during the study

    A point mutation in the dynein heavy chain gene leads to striatal atrophy and compromises neurite outgrowth of striatal neurons

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    The molecular motor dynein and its associated regulatory subunit dynactin have been implicated in several neurodegenerative conditions of the basal ganglia, such as Huntington's disease (HD) and Perry syndrome, an atypical Parkinson-like disease. This pathogenic role has been largely postulated from the existence of mutations in the dynactin subunit p150Glued. However, dynactin is also able to act independently of dynein, and there is currently no direct evidence linking dynein to basal ganglia degeneration. To provide such evidence, we used here a mouse strain carrying a point mutation in the dynein heavy chain gene that impairs retrograde axonal transport. These mice exhibited motor and behavioural abnormalities including hindlimb clasping, early muscle weakness, incoordination and hyperactivity. In vivo brain imaging using magnetic resonance imaging showed striatal atrophy and lateral ventricle enlargement. In the striatum, altered dopamine signalling, decreased dopamine D1 and D2 receptor binding in positron emission tomography SCAN and prominent astrocytosis were observed, although there was no neuronal loss either in the striatum or substantia nigra. In vitro, dynein mutant striatal neurons displayed strongly impaired neuritic morphology. Altogether, these findings provide a direct genetic evidence for the requirement of dynein for the morphology and function of striatal neurons. Our study supports a role for dynein dysfunction in the pathogenesis of neurodegenerative disorders of the basal ganglia, such as Perry syndrome and HD
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