A carbapenem-resistant (sequence type 5415) strain was isolated from a male patient through routine surveillance in 2018 in Guangzhou, China. Bacteria were isolated from a sputum culture and identified by using the Vitek 2 compact system. The gene was amplified and confirmed by sequencing. Antimicrobial susceptibility testing was determined by a Vitek 2 compact system. The gene was located by Southern blotting. Whole-genome sequencing was carried out using both Illumina MiSeq and Oxford Nanopore MinION. S1-PFGE and Southern blotting showed that the gene was located on a novel 66-kb IncFII [F2A-B-] plasmid. Conjugation assays revealed that the -bearing plasmid was self-transferrable. Genomic sequencing and comparative analysis suggested that plasmid p2947-NDM5 likely originated from a combination of an IncFII-type backbone and the flanking genetic elements. This is the first report of an ST5414 strain expressing an NDM-5 β-lactamase. This study highlights the genetic complexity of carrying plasmids and the urgent need for continuous active monitoring. This is the first report of an ST5414 E. coli strain expressing an NDM-5 β-lactamase. This study highlights the genetic complexity of blaNDM-5 carrying plasmids and the urgent need for continuous active monitoring.Non-O1/non-O139 Vibrio cholerae (NOVC) are increasingly being recognized as causes of sporadic cases of gastroenteritis and extra-intestinal invasive infections, such as bacteremia as well as skin and wound infections in immunosuppressed hosts. However, oral infections caused by these microorganisms have rarely been reported. We present a case of oral infection caused by NOVC in a patient undergoing chemoradiotherapy after esophagectomy for esophageal cancer. The patient recovered well after antibiotic treatment. The isolate from the patient was screened for phenotypic and genetic characteristics with reference to their major virulence genes. https://www.selleckchem.com/products/verubecestat.html Our report provides supporting evidence for oral infection due to NOVC in a patient with esophageal cancer and suggests that some putative accessory virulence factors may be crucial in the pathogenicity of this strain. To the best of our knowledge, this is the first documented case of oral infection due to NOVC.A linezolid-resistant E.faecalis strain harboring optrA and cfr resistance genes were isolated from a patient in china, which had no mutations in rplC, rplD, rplV, and 23S rRNA gene. Transformation indicated that optrA and cfr were located on two different plasmids and both could be transferred to recipient strain, resulting in the increase of MICs of linezolid and chloramphenicol. Cfr, carried by an 11,872-bp plasmid, was enclosed with an IS110 transposase in upstream and an IS3-like transposase in downstream, while optrA was on an 8357-bp plasmid. As far as we know, this is the first report of an E.faecalis clinical strain co-harboring optrA and cfr in China. is reported to function as a tumor suppressor of various cancers. However, the role of in the development of osteosarcoma (OS) has not been elaborated. The purpose of this study was to investigate the functional effects of on OS progression and the underlying mechanism. The expression of protein and mRNA in OS cells was evaluated by Western blotting and quantitative real-time polymerase chain reaction. Cellular proliferation was investigated by cell counting kit-8, colony formation and apoptosis assays. Bioinformatics methods were used to predict target genes. The relationship between and was demonstrated by dual-luciferase reporter assay. Metabolic changes in OS cells were monitored using an XF96 metabolic flux analyzer. We found that was downregulated in OS and that lower expression of promoted proliferation and contributed to the Warburg effect in OS cells. Furthermore, we showed that silencing inhibited proliferation and reduced aerobic glycolysis while overexpression of reduced the anti-tumor function of in OS cells. Mechanistically, acted as a tumor suppressor in OS and reduced the expression of by directly targeting its 3'UTR. The / axis regulated OS proliferation by controlling the Warburg effect. Our results revealed a previously undiscovered function of in OS, which strongly linked metabolic alterations with cancer progression. Targeting may become a promising therapeutic approach for OS. The miR-1297/PFKFB2 axis regulated OS proliferation by controlling the Warburg effect. Our results revealed a previously undiscovered function of miR-1297 in OS, which strongly linked metabolic alterations with cancer progression. Targeting miR-1297 may become a promising therapeutic approach for OS. Long noncoding RNAs (lncRNAs) have been shown to play an important role in the development and progression of esophageal carcinoma (EC). Recently, lncRNA LOC441178 was shown to be dysregulated in many cancer types; however, the role of LOC441178 in EC remains unclear. Flow cytometry, transwell and wound healing assays were used to measure the apoptosis and migration in esophageal squamous cell carcinoma (ESCC) cells. RT-qPCR was used to detect the level of miR-182 in LOC441178-overexpressed EC cells. In addition, DNA methylation status of miR-182 promoter in LOC441178-overexpressed ESCC cells was detected by methylation-specific PCR (MSP) and bisulfite sequencing PCR. In this study, we found that LOC441178 negatively regulated miR-182 expression in ESCC cells. In addition, overexpression of LOC441178 inhibited the proliferation and migration and induced apoptosis in ESCC cells via downregulation of miR-182. Moreover, overexpression of LOC441178 markedly inhibited the phosphorylation of Akt and phosphorylation FOXO3a and increased the expression of FOXO3a in ESCC cells via downregulation of miR-182. Mechanistically, LOC441178 overexpression epigenetically suppressed miR-182 expression via DNA methylation. In vivo experiments revealed that overexpression of LOC441178 inhibited ESCC tumor growth in mouse xenograft model. Collectively, our data suggested that LOC441178 overexpression epigenetically inhibited tumorigenesis of ESCC via DNA methylation of miR-182. These data indicated that the LOC441178/miR-182 axis might represent a novel therapeutic option for the treatment of ESCC. Collectively, our data suggested that LOC441178 overexpression epigenetically inhibited tumorigenesis of ESCC via DNA methylation of miR-182. These data indicated that the LOC441178/miR-182 axis might represent a novel therapeutic option for the treatment of ESCC.