Prevalence and risk analysis of mobile colistin resistance and extended-spectrum ß-lactamase genes carriage in pet dogs and their owners: a population based cross-sectional study.

Mobile colistin resistance gene mcr-1 and extended-spectrum ß-lactamase gene bla CTX-M are highly prevalent in human - and pet-derived bacteria. Isolation of identical strains of mcr-1-positive Escherichia coli (MCRPEC) or bla CTX-M-positive E. coli (CTX-MPEC) from pets and humans highlighted the potential for co-colonization of antibiotic-resistant bacteria which can be a risk for dissemination of resistance genes. In this study, the prevalence of mcr-1 and bla CTX-M carriage from rectal swabs in 299 families (dogs and their owners) were 2.7 and 5.3%, respectively. We identified a significant association of mcr-1 carriage between dogs and their owners. Whilst antibiotic use in the previous three months was associated with bla CTX-M carriage in dogs. Only one instance of dog and owner carrying identical CTX-MPEC was observed. Although the prevalence of identical strains in one family is rare, the huge number of dog ownership worldwide suggest that this threat should not be underestimated.

The lncRNA CCAT1 Upregulates Proliferation and Invasion in Melanoma Cells via Suppressing miR-33a.

It is increasingly evident that various long noncoding RNAs (lncRNAs) participate in the tumorigenesis of multiple tumors, including melanoma. lncRNAs have been validated as oncogenic factors in various tumors; however, the potential regulatory mechanism of CCAT1 in melanoma is still unclear. The purpose of this study was to investigate the regulation of CCAT1 on melanoma genesis. The expression of CCAT1 in melanoma tissue and cell lines was measured using qRT-PCR. Interference oligonucleotide or mimic sequences were applied to up- or downregulate RNA expression. CCK-8 and colony formation assays were performed to detect the proliferation capability. Transwell assay was used to assess the migration and invasion capacities. Bioinformatics analysis was performed to predict the target miRNAs of CCAT1. Expression of CCAT1 was significantly upregulated in melanoma tissue and cell lines. CCAT1 knockdown observably suppressed the proliferation, migration, and invasion abilities. Bioinformatics analysis predicted that miR-33a acted as a target of CCAT1, which was confirmed by dual-luciferase reporter assay. CCAT1 knockdown reversed the tumor-promoting ability of the miR-33a inhibitor. CCAT1 acts as an oncogenic factor in the genesis of melanoma and exerts tumor-promoting roles via sponging miR-33a, providing a novel insight for competing endogenous RNA (ceRNA) in the tumorigenesis of melanoma.