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Selenium-Enriched Mushroom Powder Enhances Intestinal Health and Growth Performance in the Absence of Zinc Oxide in Post-Weaned Pig Diets
SIMPLE SUMMARY: The imminent ban on zinc oxide in pig diets within the European Union is a major challenge facing the swine industry. Commercial weaning is associated with abrupt dietary, environmental and social changes resulting in stress, reduced feed intake and gut developmental issues in the post-weaned pig. Mushrooms are rich in natural bioactives and have long been regarded as a health-promoting food due to their immunomodulatory and antioxidant effects and their ability to modulate the gut microbiota. Mushrooms can become abundant in organic selenium when grown under certain conditions. The present study aimed to determine the optimum Se level, using Se-enriched mushrooms and selenite, in weaned pig diets to enhance intestinal health, performance and antioxidant capacity. Our study demonstrated that 0.3 ppm selenium inclusion, using selenium-enriched mushroom powder, led to positive effects on faecal scores and had similar pig performance compared to zinc oxide during the first 21 days post-weaning. The selenium inclusion level of 0.6 ppm, using selenium-enriched mushroom powder and selenite, enhanced pig performance and aspects of gastrointestinal health during days 21 and 39 post-weaning. ABSTRACT: This study was conducted to examine the effects of varying selenium (Se) inclusion levels, in the form of Se-enriched mushroom powder (SeMP) and selenite, on post-weaning growth performance (Period 1; day 1–21), intestinal health and antioxidant capacity (Period 2; day 21–39). Weaned pigs were blocked according to live weight, sex and litter of origin and randomly assigned to the following experimental groups: basal (basal + selenite (0.3 ppm Se)); ZnO (basal + ZnO + selenite (0.3 ppm Se)); 0.15 SeMP (basal + SeMP (0.15 ppm Se)); 0.3 SeMP (basal + SeMP (0.3 ppm Se)) and 0.6 SeMP/Sel (basal + SeMP (0.3 ppm Se) + selenite (Sel) (0.3 ppm Se)) with eight replicates/experimental group. After 21 days, the ZnO experimental group was removed from the experiment and the remaining pigs continued on their respective ...
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The Effect of the Neurogranin Schizophrenia Risk Variant rs12807809 on Brain Structure and Function
In: Twin research and human genetics: the official journal of the International Society for Twin Studies (ISTS) and the Human Genetics Society of Australasia, Band 15, Heft 3, S. 296-303
ISSN: 1839-2628
A single nucleotide polymorphism rs12807809 located upstream of the neurogranin (NRGN) gene has been identified as a risk variant for schizophrenia in recent genome-wide association studies. To date, there has been little investigation of the endophenotypic consequences of this variant, and our own investigations have suggested that the effects of this gene are not apparent at the level of cognitive function in patients or controls. Because the impact of risk variants may be more apparent at the level of brain, the aim of this investigation was to delineate whether NRGN genotype predicted variability in brain structure and/or function. Healthy individuals participated in structural (N= 140) and/or functional (N= 36) magnetic resonance imaging (s/fMRI). Voxel-based morphometry was used to compare gray and white matter volumes between carriers of the non-risk C allele (i.e., CC/CT) and those who were homozygous for the risk T allele. Functional imaging data were acquired during the performance of a spatial working memory task, and were also analyzed with respect to the difference between C carriers and T homozygotes. There was no effect of the NRGN variant rs12807809 on behavioral performance or brain structure. However, there was a main effect of genotype on brain activity during performance of the working memory task, such that while C carriers exhibited a load-independent decrease in left superior frontal gyrus/BA10, TT individuals failed to show a similar decrease in activity. The failure to disengage this ventromedial prefrontal region, despite preserved performance, may be indicative of a reduction in processing efficiency in healthy TT carriers. Although it remains to be established whether this holds true in larger samples and in patient cohorts, if valid, this suggests a potential mechanism by which NRGN variability might contribute to schizophrenia risk.