The mechanisms by which antibiotic growth promoters (AGP) enhance growth rates, feed efficiencies, and disease resistance in poultry need to be understood for designing safer and alternative strategies to replace AGP. Avilamycin has been widely used as an AGP in poultry, but its impact on the structure and function of the gut microbiome of broiler chickens has not been fully elucidated. In this study, we investigated the bacterial communities of the ileum and cecum in broiler chickens fed with an avilamycin-supplemented diet, by high-throughput sequencing of bacterial 16S rRNA genes. Alpha diversity metrics indicated that the ileal bacterial diversity was higher in avilamycin-fed chickens than in the control group, whereas the opposite was true for the cecum. Multivariate analyses revealed that the ileal microbiota of the avilamycin-fed group were clearly distinguished from those of the control group, whereas the cecal bacterial communities were apparently not influenced by feeding diets containing avilamycin. In the ilea, 2 operational taxonomic units (OTU) that matched Lactobacillus reuteri and Clostridium were enriched (P = 0.016 and P = 0.007, respectively) in the avilamycin-fed group, and an OTU belonging to Lactobacillus crispatus was decreased (P = 0.016). In the cecal microbiota showing much higher diversity with 1,286 non-singleton OTU, 12 OTU were decreased, and 3 were increased in response to avilamycin treatment (P = 0.005-0.047). Functional profiling of bacterial communities based on PICRUSt analysis revealed that 10 functional categories were enriched by avilamycin treatments, and 4 functional categories were decreased. In conclusion, our results demonstrated that the influence of avilamycin supplementation on the diversity, taxonomic composition, and functional profiles of the microbiota was evidently different in the ileum and cecum. These results further our understanding of the impact of AGP on the composition and activity of commensal bacteria in the chicken gastrointestinal tract to develop novel feeding strategies for improving animal health and performance.
The aim of this study was to assess changes in bone mineral density (BMD) and cadmium (Cd) levels in blood and urine in individuals living in a Cd-contaminated area according to the type of osteoporosis medication over a three-year period. This follow-up study included 204 residents living in the vicinity of a closed copper refinery, who had been found to have elevated urinary or blood Cd levels. Cd levels in the blood and urine, as well as BMD, were measured every 6 months. After the first BMD measurement, individuals were prescribed antiresorptives such as alendronate or vitamin D and calcium, according to their BMD. Subjects were classified according to the type of medicine provided over the previous 6 months. General linear models controlling for other factors were used to evaluate the effects of each type of medication on the participants' Cd levels and BMD. Spinal BMD showed a significant increase in the antiresorptive group compared to the nontreatment group. Significant decreases in blood Cd levels were found in the vitamin D and calcium group, in comparison to the nontreatment group, as well as a marginally significant decrease in the antiresorptive group. The vitamin D and calcium group showed a significantly greater decrease in urinary Cd levels than the nontreatment group. In contrast, antiresorptive medication was found to have a negative effect on urinary Cd excretion. These results suggest that vitamin D and calcium treatment for osteoporosis lowers blood Cd levels more effectively and improves urinary Cd excretion.
Viral vectors and electroporation (EP)-mediated gene transfers are efficient means of inducing somatic mosaicismin mice, but they lack the exquisite control over transgene copy number, gene zygosity, and genomic-locus specificity that genetically engineered mouse models (GEMMs) provide. Here, we develop and demonstrate a simple and generalizable in vivo method, mosaic analysis by dual recombinase-mediated cassette exchange (MADR). MADR allows for stable labeling of mutant cells express transgenic elements from a precisely-defined chromosomal locus. To test our method, we generated reporter-labeled lineages from stem and progenitor cells in a well-defined Rosa26 mTmG mouse. We demonstrate the power and versatility of MADR by creating novel glioma models with mixed, reporter-defined zygosity or with "personalized" driver mutations from pediatric glioma-each manipulation altering the profile of resulting tumors. Thus, MADR provides a high-throughput genetic platform for the dissection of development and disease, and this rapid method can be applied to the thousands of existing gene-trap mice.
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