Publications by authors named "Alexandre S de Mello"

This study aimed to investigate the impact of maternal consumption of a hyperlipid diet and grape juice on global histone H4 acetylation levels in the offsprinǵs hippocampus at different stages of development. During pregnancy and lactation of offspring, dams were divided into 4 groups: control diet (CD), high-fat diet (HFD), control diet and purple grape juice (PGJCD) and purple grape juice and high-fat diet (PGJHFD). Male Wistar rats were euthanized at 21days of age (PN21, adolescents) and at 50days of age (PN50, adults).

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Objectives: Gaucher's disease type 1 (GD1) pathophysiology includes an imbalance on brain-derived neurotrophic factor (BDNF) levels and in the inflammatory system. However, the pathways involved remain poorly understood. The hypothesis of this study is that epigenetic mechanisms might be involved, at least partially, in this phenomenon.

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The objective of this study was to determine the effect of U18666A, an inhibitor of cholesterol synthesis and its intracellular transport, on oxidative stress parameters in cortical astrocytes cultured from Wistar rats (0-3 days old). The cultures were incubated with U18666A (0.25 µg/mL) for 48 h, conditions that are considered ideal to mimic Niemann-Pick type C disease.

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Spinocerebellar ataxias (SCAs) constitute a group of autosomal dominant neurodegenerative disorders with no current treatment. The insulin/insulin-like growth factor 1 (IGF-1) system (IIS) has been shown to play a role in the neurological dysfunction of SCAs and other polyglutamine disorders. We aimed to study the biomarker profile of serum IIS components in SCA3.

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Gaucher disease (GD) is a sphingolipidosis caused by a genetic defect that leads to glucocerebrosidase (beta-glucosidase) deficiency. Between January 1982 and October 2003, 1,081 blood samples from patients suspected of having GD were referred for biochemical analysis. The activities of the enzymes beta-glucosidase (beta-glu) and chitotriosidase (CT) were measured in these samples.

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Background: Gaucher's disease (GD) is a disorder caused by the deficiency of lysosomal beta-glucosidase, an enzyme that participates in the degradation of glycosphingolipids. Deficiency of this enzyme results in the accumulation of glucocerebrosides in macrophage lysosomes. No studies comparing the biochemical and kinetic behavior of this enzyme in leukocytes and fibroblasts from normal individuals and patients with Gaucher's disease are available.

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