Here, we identified mcr-4.3 in Acinetobacter baumannii , which had not been previously observed to carry an mcr gene. The mcr-4.3 -harboring A. baumannii strain AB18PR065 was isolated from pig feces from a slaughterhouse in Guangdong Province of China.

Purpose: The discovery of the plasmid-mediated colistin resistance genes, mcr, revealed a mechanism of transmission of colistin resistance, which is a major, global public health concern especially among individuals infected with carbapenem-resistant Gram-negative bacteria. To monitor the spread and epidemiology of mcr genes, a convenient and reliable method to detect mcr genes in clinical isolates is needed, especially in the primary care institutions. This study aimed to establish a restriction endonuclease-based multiplex loop-mediated isothermal amplification (multi-LAMP) assay to detect mcr genes (mcr-1 to mcr-5) harbored by colistin-resistant bacteria. Methods: A triple-LAMP assay for mcr-1, mcr-3, and mcr-4 and a double-LAMP assay for mcr-2 and mcr-5 were established. The sensitivity and specificity of the LAMP reactions were determined via electrophoresis and visual detection. Results: The sensitivity of the LAMP assay was 10-fold greater than that of PCR, with high specificity among the screened primers. Specific mcr genes were distinguished in accordance with band numbers and the fragment length of the digested LAMP amplification products. Furthermore, the LAMP assay was confirmed as a rapid and reliable diagnostic technique upon application for clinical samples, and the results were consistent with those of conventional PCR assay. Conclusion: The multi-LAMP assay is a potentially promising method to detect mcr genes and will, if implemented, help prevent infections by drug-resistant bacteria in primary-care hospitals due to rapid and reliable surveillance. To our knowledge, this is the first study to report the application of LAMP to detect mcr-2 to mcr-5 genes and the first time that multi-LAMP has been applied to detect mcr genes.

Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by joint swelling, joint tenderness and destruction of synovial joints, leading to severe disability. Anti‐inflammatory drugs and disease‐modifying anti‐rheumatic drugs (DMARDs) may improve RA process. However, in most patients the treatment effect is still not satisfactory. Cyclin‐dependent kinase 7 (CDK7) plays a well‐established role in the regulation of the eukaryotic cell division cycle, and recent studies indicated that it exerted anti‐inflammatory effect. In our previous research, we found that inhibition of CDK7 by highly selective inhibitor BS‐181 significantly impeded the development of collagen‐induced arthritis (CIA) mice. However, the underlying mechanism of CDK7 in RA remains to be explored. We elucidated the molecular mechanism of CDK7 inhibition in RA inflammation by administration of CDK7 highly selective inhibitor BS‐181 and siRNA‐CDK7. We found that both IL‐1β, IL‐6, IL‐8 and RANKL transcript levels and IL‐1β/IL‐6 secretion were effectively suppressed by BS‐181 treatment as well as CDK7 knockdown. Furthermore, CDK7 inhibition prevented NF‐κB signalling pathway activation and restrained p65 nuclear translocation. Moreover, CDK7 selective inhibitor BS‐181 also blocked phosphorylation of p65 in MH7A cells. These results strongly indicate that CDK7 inhibition by BS‐181 and siRNA‐CDK7 significantly suppresses rheumatoid arthritis inflammation, which may be via blockage of NF‐κB signalling pathway and IL‐1β/IL‐6 secretion.

Urine specimens are detected by conventional culture method and colonies with more than 10⁴ are identified by MALDI-TOF MS. Meanwhile, we analyze urine samples using FTA cards for simple DNA extraction and UDG-assisted LAMP.