Background: Extrauterine growth retardation is a major clinical problem in very-low-birth-weight infants. Parenteral nutrition (PN) serves to achieve rapid maximal nutrition in early postnatal life. There is a lack of uniformity with regard to neonatal PN practice. The objective of this study is to ascertain current practice regarding neonatal PN prescription in the early postnatal period in the United Kingdom.
Methods: A study questionnaire was e-mailed to neonatal pharmacists serving level 3 and major level 2 units in the United Kingdom between October 2005 and March 2006. Static numerical information regarding glucose, amino acids, and lipid prescription during the first 10 days of life was collected and compared with current recommendations.
Results: Fifty-two (81%) units responded to the questionnaire; 4 units were excluded for incomplete data. Twenty-six units (54%) initiated PN on day 1. Full PN was achieved by the median age of 6 days. Twelve units (25%) achieved full PN only by day 7 or later. Maximum median amino acids were 2.9 g/kg/d. Only 13 units (27%) prescribed >/=3 g/kg/d, and 2 prescribed more than 3.5 g/kg/d. Nineteen units (39%) initiated lipids on day 1. Eleven units (23%) delayed lipids until day 3, and 2 units delayed lipids until day 4. In comparison to the recommended intake of calories and amino acids, the current median prescription would result in a cumulative deficit over the first 10 days of 420 kcal/kg and 11.9 g/kg, respectively.
Conclusions: Our study suggests diverse practice with regard to neonatal PN prescription in the United Kingdom. Current neonatal PN practice entails a significant calorie and protein deficit during early postnatal life and warrants further review.
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http://dx.doi.org/10.1177/0148607108314373 | DOI Listing |
Neurosci Biobehav Rev
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Douglas Research Centre, McGill University, Montreal, QC, Canada; Department of Psychiatry, Faculty of Medicine, McGill University, Montreal, QC, Canada; Ludmer Centre for Neuroinformatics and Mental Health, McGill University, Montreal, QC, Canada. Electronic address:
Early-life adversity during pre- and early post-natal phases can impact brain development and lead to maladaptive changes in executive behaviors. This increases the risk for a range of psychopathologies and physical diseases. Importantly, exposure to adversities during these periods is also linked to alterations in the orbito-frontal cortex (OFC) which is a key player in these executive functions.
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Eur Thyroid J
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H Heuer, Department of Endocrinology, Diabetes and Metabolism, University of Duisburg-Essen, Essen, Germany.
Objective: Mutations in the thyroid hormone (TH) transporter monocarboxylate transporter 8 (MCT8) cause Allan-Herndon-Dudley syndrome (AHDS), a severe form of psychomotor retardation with muscle hypoplasia and spastic paraplegia as key symptoms. These abnormalities have been attributed to an impaired TH transport across brain barriers and into neural cells thereby affecting brain development and function. Likewise, Mct8/Oatp1c1 (organic anion transporting polypeptide 1c1) double knockout (M/Odko) mice, a well-established murine AHDS model, display a strongly reduced TH passage into the brain as well as locomotor abnormalities.
View Article and Find Full Text PDFBiochem Biophys Res Commun
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Department of Molecular and Cellular Biology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan; Department of Clinical Bioanalysis and Molecular Biology, Graduate School of Medical and Dental Sciences, Institute Science of Tokyo/TMDU, Tokyo, Japan. Electronic address:
Myelin is an electrical insulator that enables saltatory nerve conduction and is essential for proper functioning of the central nervous system (CNS). It is formed by oligodendrocytes (OLs) in the CNS, and during OL development various molecules, including extracellular matrix (ECM) proteins, regulate OL differentiation and myelination; however, the role of ECM proteins in these processes is not well understood. Our present work is centered on the analyses of the expression and function of fibulin-7 (Fbln7), an ECM protein of the fibulin family, in OL differentiation.
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