• Nenhum resultado encontrado

Isofagomine in vivo effects in a neuronopathic Gaucher disease mouse.

N/A
N/A
Protected

Academic year: 2017

Share "Isofagomine in vivo effects in a neuronopathic Gaucher disease mouse."

Copied!
12
0
0

Texto

Loading

Imagem

Figure 1. Treatment and phenotypes. (A) IFG treatment regime. IFG was given to pregnant females 3 to 5 days prior birth at 20 mg/kg/d
Figure 2. Life span and body weight. (A) Both treated and untreated 4L;C* mice had normal growth of their body weight till 35 days
Figure 4. Analyses of GC and GS levels in the cortex and liver by LC/MS. (A) Cortex GC and GS levels in IFG treated 4L;C* did not show significant reduction relative to the untreated mice
Figure 5. Analyses of GC and GS levels in the spleen and lung by LC/MS. (A) Spleen GC level in 4L;C* mice was not different from that in the WT
+2

Referências

Documentos relacionados

sí mismo (fragmento 48-49) y que la ciencia consiste en el conocimiento de esto último y no de imitaciones, para luego concluir que Aristóteles tuvo que haber defendido en este

Nota- bly, CXCL9 and CXCL10 are chemoattractants, and the recruitment of immune cells to the site of histone injection in a subcutaneous mouse model supports the concept that low

Sendo assim, a presente investigação além de contribuir para a literatura da imagem percebida do Brasil como destino turístico, realizou uma análise comparativa entre

The brain areas involved in the clinical effects of MPH are the same involved in the different mechanisms of chemical dependence, and the increased levels of dopamine found in

To determine if the effects of uroguany- lin in the kidney are mediated by its receptor, GC-C, we employed the sealed-mouse renal function assay on GC-C deficient mice (12)..

-ATPase activity in the synaptic plasma membrane from cere- bral cortex of adult rats submitted to chronic administration of imipramine and fluoxe- tine.. We also studied the in vitro

in the mouse model. TBI also induced an increase in protein expression of COX1, PGE2, and IL-6, as well as a decline in BDNF, PDGF-BB, synapsin-I, and SYP levels. Administration

(54) also demonstrated that the in vivo and in vitro treatment with PTX increased muscle cAMP levels and induced a decrease in the increased rate of total protein degradation in