Avaliação longitudinal do desenvolvimento motor e da habilidade de sentar em crianças nascidas prematuras

Os bebês prematuros apresentam maior risco para atrasos na aquisição das habilidades neuromotoras. O objetivo do estudo foi detectar atrasos no desenvolvimento motor de crianças prematuras com baixo peso, analisar a evolução da habilidade do sentar e verificar a associação entre essa habilidade com outras aquisições motoras até os 8 meses de idade corrigida (IC). Foram avaliadas 10 crianças nascidas pré-termo, de ambos os sexos, dos 4 aos 8 meses de IC, pela escala motora infantil de Alberta AIMS (Alberta Infant Motor Scale). Cada criança foi avaliada três vezes, aos 4 para 5 meses, 5 para 6 meses, e 7 para 8 meses; os escores foram comparados para verificar alterações ao longo do tempo e identificação de possíveis atrasos no desenvolvimento motor. Os resultados mostram que, aos 7 para 8 meses, 30% das crianças apresentaram desenvolvimento motor atrasado e foram encaminhadas para tratamento fisioterapêutico. A habilidade de sentar foi melhorando progressiva e significativamente com a idade, tendo se mostrado fortemente correlacionada com outras posturas do desenvolvimento motor e com o escore total na AIMS.Preterm-born infants present higher risks of delayed neuromotor development. This study aimed at detecting delayed motor development in preterm, low-birthweight infants, by analysing development of the sitting skill in association to other motor development acquisitions until corrected age (CA) of 8 months. Ten preterm infants of both sexes were assessed by the AIMS - Alberta Infant Motor Scale from ages 4 to 8 months. Each child was evaluated three times, at 4-to-5 months, 5-to-6 months, and at 7-to-8 months CA; their scores were compared to verify changes over time and identify possible delays in motor development. Results show that at the age of 7-to-8 months, 30% of the children had delayed motor development and were referred for physical therapy treatment. The pace of sitting skill development increased gradually and significantly along the age; and strong correlations were found between the ability to sit and other motor development postures, and the total AIMS score

WAKO - ein Programm zur Berechnung von Komplexionsgleichgewichten in waesserigen Loesungen - Einfuehrung und Beispiel. Protonenverbrauch durch Silikatverwitterung in norddeutschen Loessboeden. Indol-3-Essigsaeure - moegliche Strukturen und Metabolismus

TIB: RO 4548(16) / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekSIGLEDEGerman

Liver-restricted repin1 deficiency improves whole-body insulin sensitivity, alters lipid metabolism, and causes secondary changes in adipose tissue in mice.

Replication initiator 1 (Repin1) is a zinc finger protein highly expressed in liver and adipose tissue and maps within a quantitative trait locus (QTL) for body weight and triglyceride (TG) levels in the rat. The QTL has further been supported as a susceptibility locus for dyslipidemia and related metabolic disorders in congenic and subcongenic rat strains. Here, we elucidated the role of Repin1 in lipid metabolism in vivo. We generated a liver-specific Repin1 knockout mouse (LRep1(-/-)) and systematically characterized the consequences of Repin1 deficiency in the liver on body weight, glucose and lipid metabolism, liver lipid patterns, and protein/mRNA expression. Hyperinsulinemic-euglycemic clamp studies revealed significantly improved whole-body insulin sensitivity in LRep1(-/-) mice, which may be due to significantly lower TG content in the liver. Repin1 deficiency causes significant changes in potential downstream target molecules including Cd36, Pparγ, Glut2 protein, Akt phosphorylation, and lipocalin2, Vamp4, and Snap23 mRNA expression. Mice with hepatic deletion of Repin1 display secondary changes in adipose tissue function, which may be mediated by altered hepatic expression of lipocalin2 or chemerin. Our findings indicate that Repin1 plays a role in insulin sensitivity and lipid metabolism by regulating key genes of glucose and lipid metabolism