ABSTRACT
Joubert syndrome is characterized by unique malformation of the cerebellar vermis. More than thirty Joubert syndrome genes have been identified, including ARL13B. However, its role in cerebellar development remains unexplored. We found that knockdown or knockout of arl13b impaired balance and locomotion in zebrafish larvae. Granule cells were selectively reduced in the corpus cerebelli, a structure homologous to the mammalian vermis. Purkinje cell progenitors were also selectively disturbed dorsomedially. The expression of atoh1 and ptf1, proneural genes of granule and Purkinje cells, respectively, were selectively down-regulated along the dorsal midline of the cerebellum. Moreover, wnt1, which is transiently expressed early in cerebellar development, was selectively reduced. Intriguingly, activating Wnt signaling partially rescued the granule cell defects in arl13b mutants. These findings suggested that Arl13b is necessary for the early development of cerebellar granule and Purkinje cells. The arl13b-deficient zebrafish can serve as a model organism for studying Joubert syndrome.
ABSTRACT
Joubert syndrome is characterized by unique malformation of the cerebellar vermis. More than thirty Joubert syndrome genes have been identified, including ARL13B. However, its role in cerebellar development remains unexplored. We found that knockdown or knockout of arl13b impaired balance and locomotion in zebrafish larvae. Granule cells were selectively reduced in the corpus cerebelli, a structure homologous to the mammalian vermis. Purkinje cell progenitors were also selectively disturbed dorsomedially. The expression of atoh1 and ptf1, proneural genes of granule and Purkinje cells, respectively, were selectively down-regulated along the dorsal midline of the cerebellum. Moreover, wnt1, which is transiently expressed early in cerebellar development, was selectively reduced. Intriguingly, activating Wnt signaling partially rescued the granule cell defects in arl13b mutants. These findings suggested that Arl13b is necessary for the early development of cerebellar granule and Purkinje cells. The arl13b-deficient zebrafish can serve as a model organism for studying Joubert syndrome.
ABSTRACT
El presente estudio se realizó con la finalidad de determinar si la Dipirona altera la agregación plaquetaria. Para ello, se seleccionaron 30 voluntarios sanos, los cuales fueron divididos en dos grupos y asignados al azar a recibir 1 g de Dipirona o 100 mg de Acido Acetilsalicílico. Se determinó la agregación plaquetaria a través del método turbidimétrico; utilizando adenosin difosfato, colágeno y adrenalina. En el grupo Dipirona, se observó una reducción estadísticamente significativa de la agregación plaquetaria a las 72 horas, frente a los 3 estímulos; que revirtió a las 24 horas. En el grupo Acido Acetilsalicílico, disminuyó significativamente la agregación plaquetaria a las 24 horas. Al comparar ambos grupos no hubo diferencia significativa en la muestra basal pero si a las 24 horas. Podemos concluir que la Dipirona, al igual que el resto de los antiinflamatorios no esteroideos, inhibe la agregación plaquetaria de forma reversible, al contrario del Acido Acetilsalicílico.