117,553 research outputs found

    Early nutrition patterns and diseases of adulthood : a plausible link?

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    In the last decades several studies tested the hypothesis that at early development stages certain foods or nutrients, in specific amounts, fed during limited sensitive periods, may determine an endocrine metabolic asset leading to clinical alterations that take place decades later (early nutritional programming of long term health). Evidence is mounting for programming effects of infant feeding. Observational studies indicate that breast feeding, relative to formula feeding, reduces the risk for obesity at school age by about 20% even after adjustment for biological and sociodemographic confounders. Moreover, breastfeeding is constantly associated with increased neurodevelopmental scores up to early adulthood, while its outcome in terms of delayed decay of brain function is still unknown. Besides the environment surrounding breastfeeding, specific nutrients within human milk may play a direct role. With the introduction of solids the major changes in diet are represented by the sudden decrease of fat intake from 50 to 30% of total energy. A protein excess, commonly found throughout all European Countries, has been associated to a higher risk of adiposity in early childhood, as confirmed by first reports from a large European trial. The amount of fat does not seem to be associated with later adiposity, while its quality may affect blood lipoproteins, blood pressure and neurodevelopmental performance. Early intake of dietary fibers might also have beneficial effects. Epidemiologic data show that episodes of rapid growth (growth acceleration hypothesis), whichever the dietary habits, are associated with later unfavorable health conditions and should be prevente

    Genetics of nonalcoholic fatty liver disease : a 2018 update

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    Nonalcoholic fatty liver disease (NAFLD), now the leading cause of liver damage worldwide, is epide-miologically associated with obesity, insulin resistance and type 2 diabetes, and is a potentially progressive condition to advanced liver fibrosis and hepatocellular carcinoma. However, there is huge interindividual variability in liver disease susceptibility. Inherited factors also play an important role in determining disease predisposition. During the last years, common variants in PNPLA3, TM6SF2, MBOAT7 and GCKR have been demonstrated to predispose to the full spectrum of NAFLD pathology by facilitating hepatic fat accumulation in the presence of environmental triggers. Other variants regulating inflammation and fibrogenesis then modulate liver disease progression in those at higher risk. Evidence is also accumulating that rare variants are involved in disease predisposition. In the future, evaluation of genetic risk factors may be exploited to stratify the risk of liver-related complications of the disease, and to guide hepatocellular carcinoma surveillance and choose pharmacological therapy

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed

    Signal averaging of pre- and post-extrasystolic beats in patients with ventricular arrhythmias

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    To evaluate the effects of premature ventricular beats on the impulse conduction of adjacent sinus cycles, we compared the high amplification signal-averaged electrocardiogram parameters of the pre- and post-extrasystolic beats with those of the remaining sinus cycle. According to the duration of filtered QRS (fQRS), to the voltage of root mean square of the terminal 40 ms (RMS 40) and to the duration of low amplitude terminal components of the sinus cycles, ventricular late potentials were detected in nine out of 29 subjects. Patients with an abnormal signal-averaged electrocardiogram exhibited a longer fQRS (146 ± 6 versus 116 ± 2 ms), a reduced RMS40 voltage (18 ± 2 versus 80 ± 10 μV) and a prolonged duration of <40 μV components (42 ± 4 versus 17± 2 ms). Analysis of the pre-extrasystolic beats did not reveal any signifcant variation in the above parameters, showing a mean difference of 0.44 ± 2.4 ms; 0.02 ± 1.14 μV; 1 ± 1.9 ms and of -1.45 ± 1.02 ms; 3.5 ± 8.6 μV; -0.7 ± 0.84 ms respectively, for patients with and without ventricular late potentials. In addition, no significant variation was observed when the post-extrasystolic beats were considered. These results indicate that the sinus cycles adjacent to premature ventricular discharges do not present variations of signal-averaged electrocardiogram parameters that may suggest an influence of the ectopic beats on their intramyocardial inmpulse propagation

    High-dimensional ICA analysis detects wthin-network functional connectivity damage of default-mode and sensory-motor networks in Alzheimer's disease

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    High-dimensional independent component analysis (ICA), compared to low-dimensional ICA, allows to conduct a detailed parcellation of the resting-state networks. The purpose of this study was to give further insight into functional connectivity (FC) in Alzheimer's disease (AD) using high-dimensional ICA. For this reason, we performed both low- and high-dimensional ICA analyses of resting-state fMRI data of 20 healthy controls and 21 patients with AD, focusing on the primarily altered default-mode network (DMN) and exploring the sensory-motor network. As expected, results obtained at low dimensionality were in line with previous literature. Moreover, high-dimensional results allowed us to observe either the presence of within-network disconnections and FC damage confined to some of the resting-state subnetworks. Due to the higher sensitivity of the high-dimensional ICA analysis, our results suggest that high-dimensional decomposition in subnetworks is very promising to better localize FC alterations in AD and that FC damage is not confined to the DMN
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