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We further mapped our genome to the p17-84 OXA plasmid (accession number: CP059478) (Figure 1B), which is located in an ST63 pandrug-resistant I A. pittii i .[15] High nucleotide sequence identity was observed for some of the contigs in the TCM2 genome with p17-84 OXA (Figure 1C). Identified resistance genes were correlated with the actual antimicrobial resistance phenotype of the strain and a I bla i SB OXA-58 sb -bearing plasmid should be harbored by the TCM2 strain. Consequently, we concluded that there was a I bla i SB OXA-58 sb -bearing plasmid in the TCM2 strain, which was probably obtained from other I A. pittii i and I A. nosocomialis i strains collected in China in 2012 and 2014, respectively (Supplementary Table 2). [Extracted from the article]

Abstract Aims Salidroside is a major functional component of Rhodiola rosea L. with a lot of pharmacological effects, including anti-tumor. The present work aimed to explore whether Salidroside could also exhibit anti-tumor functions in Wilms' tumor. Main methods WIT49 and RM1 cells were treated by various doses of Salidroside. CCK-8 assay, flow cytometry detection, colony formation assay, Transwell assay, RT-qPCR and Western blot analysis were conducted to measure WIT49 and RM1 cells proliferation, apoptosis, migration and invasion. The expression changes of miR-891b in response to Salidroside treatment were tested by RT-qPCR. Rescue assays were performed to test whether miR-891b was a downstream effector of Salidroside. Finally, the involvement of PI3K/AKT/mTOR and NF-κB signaling pathways was studied. Key findings Salidroside with concentration of 80 μM significantly reduced WIT49 and RM1 cells viability, survival capacity, migration and invasion, and significantly induced apoptosis. Meanwhile, down-regulation of Cyclin D1, MMP-2 and Vimentin, up-regulations of p53 and p21, as well as cleavage of caspase-3 and -9 were observed in Salidroside-treated cell. miR-891b was down-regulated by Salidroside. And Salidroside did not suppress WIT49 and RM1 cells growth, migration and invasion when miR-891b was overexpressed. Also, the deactivation of PI3K/AKT/mTOR and NF-κB pathways induced by Salidroside was reversed by miR-891b overexpression. Significance Salidroside inhibits Wilms' tumor cells growth, migration and invasion via down-regulating miR-891b, which leads to the deactivation of PI3K/AKT/mTOR and NF-κB signaling pathways. Highlights • Salidroside suppresses Wilms' tumor cells proliferation, migration and invasion. • Salidroside induces Wilms' tumor cells apoptosis. • Salidroside down-regulates miR-891b and blocks PI3K/AKT/mTOR and NF-κB signaling. • Salidroside confers its anti-tumor function via down-regulating miR-891b. [ABSTRACT FROM AUTHOR]

Summary: The length–weight relationships (LWRs) for six species were estimated. Fish were captured in the mangroves of Qinzhou Harbour, China, but also some specimens were purchased from fishermen. The sampling was undertaken monthly between May 2011 and April 2012 using seines (mesh size 5–10 mm; height 4 m; length 400 m) and traps (mesh size 8.5 mm; 35 cm2 × 10 m for one unit) at seven sampling sites. Standard length was measured (precision 0.1 cm) and weight determined (precision 0.01 g) after preservation in formaldehyde (10%). Besides the equation parameters a (intercept) and b (slope) we determined also the 95% confidence limits for both parameters as well as the coefficient of correlation. [ABSTRACT FROM AUTHOR]

Hypervirulent carbapenem-resistant Klebsiella pneumoniae (hv-CRKP) has been widely reported and poses a global threat. However, the comprehensive genetic structure of ST11-KL64 hv-CRKP and the possible evolutionary mechanisms from a genetic structure perspective of this high-risk clone remain unclear. Here, a bla KPC-2 - bla NDM-1 -positive ST11-KL64 hv-CRKP isolate was obtained from a human bloodstream infection (BSI). Whole-genome sequencing and bioinformatics analyses revealed that it contained a fusion plasmid, pKPTCM2–1. pKPTCM2–1 is a conjugative plasmid composed of an oriT -positive pLVPK-like virulence plasmid and a type IV secretion system-produced bla NDM-1 -bearing IncX3 plasmid mediated by IS 26 -based co-integration. This progress generated 8-bp target site duplications (TGAAAACC) on both sides. The fusion plasmid possessed self-transferability and could be transferred to bla KPC-2 -harboring ST11-KL64 CRKP to form the ST11-KL64 hv-CRKP clone. The pLVPK-like-positive ST11-KL64 strain exhibited virulence levels similar to those of the typical hypervirulent K. pneumoniae NTUH-2044. The mutation, Tet(A) (A276S), which was believed to lead to tigecycline resistance was observed. Overall, this high-risk clone has emerged as a tremendous threat in fatal BSIs and thus, targeted surveillance is an urgent need to contain the hv-CRKP clones. • One bla KPC-2 - bla NDM-1 -positive ST11-KL64 hv-CRKP in human bloodstream infection. • oriT -positive pLVPK-like virulence plasmid and bla NDM-1 -bearing IncX3 plasmid fusion. • One mutation of Tet(A) (A276S) maybe lead to tigecycline resistance. [ABSTRACT FROM AUTHOR]

Competing Interests: The authors report no conflicts of interest in this work.