97 research outputs found

    Relationship between maternal obesity and infant feeding-interactions

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    BACKGROUND: There are no data regarding the relationship between maternal adiposity and interaction and feeding of infants and possible contribution to childhood obesity. In this study we determined the relationship between maternal body weight and composition and infant feeding patterns and maternal-infant interaction during 24-hour metabolic rate measurements in the Enhanced Metabolic Testing Activity Chamber (EMTAC). METHODS: The amount of time four obese (BMI = 33.5 ± 5.3 kg/m(2)) and three normal weight (BMI = 23.1 ± 0.6 kg/m(2)) biological mothers, spent feeding and interacting with their infants, along with what they ingested, was recorded during 24-hour metabolic rate measurements in the EMTAC. The seven infants were 4.9 ± 0.7 months, 69 ± 3 cm, 7.5 ± 0.8 kg, 26 ± 3 % fat and 29 ± 25 percentile for weight for length. Energy and macronutrient intake (kcal/kg) were assessed. Maternal body composition was determined by air displacement plethysmorgraphy and that of the infants by skin-fold thicknesses. Pearson correlations and independent t-tests were utilized for statistical analysis (p < 0.05). RESULTS: Infants born to obese biological mothers consumed more energy (87.6 ± 18.9 vs. 68.1 ± 17.3) and energy as carbohydrate (25 ± 6 vs.16 ± 3; p < 0.05) than their normal weight counterparts. Most of the increased intake was due to complementary feedings. Twenty-four hour infant energy intake increased with both greater maternal body weight (r = 0.73;p < 0.06) and percent body fat. Furthermore, obese biological mothers spent less total time interacting (570 ± 13 vs. 381 ± 30 minutes) and feeding (298 ± 32 vs.176 ± 22 minutes) (p < 0.05) their infants than their normal weight counterparts. Twenty-four hour interaction time negatively correlated with both maternal body weight (r = -0.98; p < 0.01) and percent body fat (r = -0.92; p < 0.01). Moreover, infants of obese mothers slept more (783 ± 38 vs. 682 ± 32 minutes; p < 0.05) than their normal weight counterparts. However, there were no differences in total 24-hour energy expenditure, resting and sleeping metabolic rates (kcal/kg) for infants born to obese and normal weight biological mothers. CONCLUSION: Greater maternal body weight and percent body fat were associated with greater infant energy intakes. These infants were fed less frequently and consumed more carbohydrates in a shorter period of time as compared to infants from normal weight biological mothers. These variations in feeding patterns may predispose certain infants to obesity

    Pre-symptomatic development of lower motor neuron connectivity in a mouse model of severe spinal muscular atrophy

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    The childhood motor neuron disease spinal muscular atrophy (SMA) results from reduced expression of the survival motor neuron (SMN) gene. Previous studies using in vitro model systems and lower organisms have suggested that low levels of Smn protein disrupt prenatal developmental processes in lower motor neurons, influencing neuronal outgrowth, axon branching and neuromuscular connectivity. The extent to which these developmental pathways contribute to selective vulnerability and pathology in the mammalian neuromuscular system in vivo remains unclear. Here, we have investigated the pre-symptomatic development of neuromuscular connectivity in differentially vulnerable motor neuron populations in Smn(-/-);SMN2 mice, a model of severe SMA. We show that reduced Smn levels have no detectable effect on morphological correlates of pre-symptomatic development in either vulnerable or stable motor units, indicating that abnormal pre-symptomatic developmental processes are unlikely to be a prerequisite for subsequent pathological changes to occur in vivo. Microarray analyses of spinal cord from two different severe SMA mouse models demonstrated that only minimal changes in gene expression were present in pre-symptomatic mice. In stark contrast, microarray analysis of late-symptomatic spinal cord revealed widespread changes in gene expression, implicating extracellular matrix integrity, growth factor signalling and myelination pathways in SMA pathogenesis. Taken together, these data suggest that reduced Smn levels induce SMA pathology by instigating rapidly progressive neurodegenerative pathways in lower motor neurons around the time of disease onset rather than by modulating pre-symptomatic neurodevelopmental pathways

    Segment-scale volcanic episodicity : evidence from the North Kolbeinsey Ridge, Atlantic

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    The upper oceanic crust is produced by magmatism at mid-ocean ridges, a process thought to be characterized by cyclic bouts of intense magmatic activity, separated by periods when faulting accommodates most or even all of the plate motion. It is not known whether there is a distinct periodicity to such magmatic–tectonic cycles. Here we present high-resolution sidescan sonar data from the neovolcanic zone of the North Kolbeinsey Ridge, a shallow slow-spreading ridge where high glacial and steady post-glacial sedimentation rates allow relative flow ages to be determined with a resolution of around 2 kyr using backscatter amplitude as a proxy for sediment thickness and hence age. We identify 18 lava flow fields covering 40% of the area surveyed. A group of 7 flow fields showing the highest (and similar) backscatter intensity are scattered along 75 km of axial valley surveyed, suggesting that at least this length of the segment was magmatically active within a 1.2 kyr time window. Based on conservative age estimates for all datable flows and estimated eruption volumes, the post-glacial volcanic activity imaged is insufficient to maintain crustal thickness, implying that episode(s) of enhanced activity must have preceded the volcanism we image

    Three individuals, three stories, three burials from medieval Trondheim, Norway

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    This article presents the life stories of three individuals who lived in Trondheim, Norway, dur- ing the 13th century. Based on skeletal examinations, facial reconstructions, genetic analy- ses, and stable oxygen isotope analyses, the birthplace, mobility, ancestry, pathology, and physical appearance of these people are presented. The stories are discussed within the relevant historical context. These three people would have been ordinary citizens, without any privileges out of the ordinary, which makes them quite rare in the academic literature. Through the study of individuals one gets a unique look into the Norwegian medieval society

    Finishing the euchromatic sequence of the human genome

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    The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead
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