hindbrain – French Translation – Keybot Dictionary

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  www.nserc-crsng.gc.ca  
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regulators of hindbrain sensory neurons, 1501, 5, $26,000.00. ...
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Le présent rapport comprend des tableaux et des figures ...
  4 Hits greencubator.info  
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Hindbrain Integrative Neurobiology
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Génétique Moléculaire des Rythmes Circadiens
  web-japan.org  
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, as soon as the fish is taken out of the sea, a special hooked tool is used to crush its hindbrain. The heart keeps beating and pumping blood. The idea is to get the fish to pump out its own blood by cutting arteries in the gills and tail.
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est supérieur à tout autre art culinaire. La découpe est si importante dans notre métier, que nous avons besoin d’un jeu de couteaux tout à fait impressionnant. Ce sont là nos outils de base, aussi faut-il en prendre grand soin ; les miens sont si bien aiguisés que je pourrais presque me raser avec ! Chaque jour, une part importante de ma journée de travail est consacrée uniquement à leur affûtage.
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To explore the potential pathophysiological interaction between LRRK2 and α-synuclein in vivo, the group of Prof. Darren Moore(Laboratory of Molecular Neurodegenerative Research) modulated LRRK2 expression in a well-established human A53T α-synuclein transgenic mouse model with transgene expression driven by the hindbrain-selective prion protein promoter.
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Mutations in the genes encoding LRRK2 and α-synuclein cause autosomal dominant forms of familial Parkinson's disease (PD). Fibrillar forms of α-synuclein are a major component of Lewy bodies, the intracytoplasmic proteinaceous inclusions that are a pathological hallmark of idiopathic and certain familial forms of PD. LRRK2 mutations cause late-onset familial PD with a clinical, neurochemical and, for the most part, neuropathological phenotype that is indistinguishable from idiopathic PD. Importantly, α-synuclein-positive Lewy bodies are the most common pathology identified in the brains of PD subjects harboring LRRK2 mutations. These observations may suggest that LRRK2 functions in a common pathway with α-synuclein to regulate its aggregation. To explore the potential pathophysiological interaction between LRRK2 and α-synuclein in vivo, the group of Prof. Darren Moore(Laboratory of Molecular Neurodegenerative Research) modulated LRRK2 expression in a well-established human A53T α-synuclein transgenic mouse model with transgene expression driven by the hindbrain-selective prion protein promoter. They failed to provide support for a pathophysiological interaction of LRRK2 and α-synuclein in vivo, at least within neurons of the mouse hindbrain.