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[Macrocephaly as the initial manifestation of glutaryl-CoA-dehydrogenase deficiency (glutaric aciduria type I)].

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Glutaric aciduria type I is due to an impaired glutaryl-CoA-dehydrogenase with an increased urinary excretion of glutaric and 3-OH glutaric acid. Typically, the clinical course until the sixth month or even 3rd year of life is symptom free, and only later an encephalopathic crisis develops. The only

Glutaric aciduria type 1 (glutaryl-CoA-dehydrogenase deficiency): advances and unanswered questions. Report from an international meeting.

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Infants with macrocephaly, young children with acute disease resembling encephalitis, and children with truncal hypotonia, ataxia, or dystonia may be affected by glutaric aciduria type I (GA 1, glutaryl-CoA-dehydrogenase deficiency), a not-so-rare autosomal recessive neurometabolic disease.

[Glutaric aciduria type 1: an example of the importance of early detection of so-called cerebral organic aciduria].

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Glutaric aciduria type 1 (GA 1) is a preventable cause of acute brain damage in early childhood, leading to a severe dystonic-dyskinetic disorder. Typically between 6 and 18 months of age, a non-specific illness such as respiratory or gastrointestinal infection or immunization leads to

Selective inhibition of skin fibroblast elastase elicits a concentration-dependent prevention of ultraviolet B-induced wrinkle formation.

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We previously reported that wrinkle formation in the skin following long-term ultraviolet B irradiation is accompanied by decreases in skin elasticity and the curling of elastic fibers in the dermis. We further showed that wrinkles could be repaired by treatment with retinoic acid and that this was

The role of elastases secreted by fibroblasts in wrinkle formation: implication through selective inhibition of elastase activity.

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We have previously demonstrated that decreases in skin elasticity, accompanied by increases in the tortuosity of elastic fibers, are important early events in wrinkle formation. In order to study the role of elastases in the degeneration of elastic fibers during wrinkle formation we examined the

Neuroinflammation and microglia/macrophage phenotype modulate the molecular background of post-stroke depression: A literature review

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Increasing evidence hints to the central role of neuroinflammation in the development of post-stroke depression. Danger signals released in the acute phase of ischemia trigger microglial activation, along with the infiltration of neutrophils and macrophages. The increased secretion of

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