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BACKGROUND Long non-coding RNA (lncRNA) cancer susceptibility candidate 9 (CASC9) is reported to be linked to cancers. This research aims to explore the role and possible mechanism of CASC9 in lung injury induced by sepsis. METHODS Lipopolysaccharide (LPS) induced human small airway epithelial cells (HSAECs) were established in vitro to mimic sepsis-induced lung injury. The effects of CASC9 and miR-195-5p on HSAECs viability were studied by CCK-8 assay. Interactions between CASC9 and miR-195-5p were determined by bioinformatics analysis, RT-PCR, dual luciferase reporter assay, and RNA immunoprecipitation assay. Pyruvate dehydrogenase kinase 4 (PDK4) and apoptosis-related molecules including Bcl2 and Bad were detected by western blot. Additionally, sepsis-induced lung injury model in rats was established by intraperitoneal injection of LPS in vivo to validate the demonstrations of in vitro studies. RESULTS CASC9 was markedly down-regulated while miR-195-5p was significantly up-regulated in HSAECs treated by LPS and lung tissues of rats with sepsis. CASC9 interacted with miR-195-5p, and negatively regulated its expression level. Overexpression of CASC9 or transfection of miR-195-5p inhibitors significantly promoted the viability of HSAECs. The transfection of miR-195-5p mimics effected oppositely. For mechanism, miR-195-5p targeted the 3’UTR of pyruvate dehydrogenase kinase 4 (PDK4) gene and depressed the protein level, and PDK4 was regulated indirectly by CASC9. Restoration of CASC9 in the lung tissues of rats with sepsis ameliorated lung injury. CONCLUSION CASC9 protects lung epithelial cells from sepsis-induced injury via regulating miR-195-5p/PDK4 axis.OBJECTIVE The importance of human host defense peptide LL-37 in vascular innate immunity is not understood. Here, we assess the impact of LL-37 on double-stranded RNA (dsRNA) signaling in human vascular smooth muscle cells. MATERIALS AND METHODS Cellular import of LL-37 and synthetic dsRNA (poly IC) were investigated by immunocytochemistry and fluorescence imaging. Transcript and protein expression were determined by qPCR, ELISA and Western blot. Knockdown of TLR3 was performed by siRNA. RESULTS LL-37 was rapidly internalized, suggesting that it has intracellular actions. Co-stimulation with poly IC and LL-37 enhanced pro-inflammatory IL-6 and MCP-1 transcripts several fold compared to treatment with poly IC or LL-37 alone. Poly IC increased IL-6 and MCP-1 protein production, and this effect was potentiated by LL-37. LL-37-induced stimulation of poly IC signaling was not associated with enhanced import of poly IC. Treatment with poly IC and LL-37 in combination increased expression of dsRNA receptor TLR3 compared to stimulation with poly IC or LL-37 alone. In TLR3 knockdown cells, treatment with poly IC and LL-37 in combination had no effect on IL-6 and MCP-1 expression, showing loss of function. CONCLUSIONS LL-37 potentiates dsRNA-induced cytokine production through up-regulation of TLR3 expression representing a novel pro-inflammatory mechanism.MOTIVATION Comparing the organization of gene, gene clusters, and their flanking genomic contexts is of critical importance to the determination of gene function and evolutionary basis of microbial traits. Currently, user-friendly and flexible tools enabling to visualize and compare genomic contexts for numerous genomes are still missing. RESULTS We here present Gcluster, a stand-alone Perl tool that allows researchers to customize and create high-quality linear maps of the genomic region around the genes of interest across large numbers of completed and draft genomes. Importantly, Gcluster integrates homologous gene analysis, in the form of a built-in orthoMCL, and mapping genomes onto a given phylogeny to provide superior comparison of gene contexts. AVAILABILITY AND IMPLEMENTATION Gclusteris written in Perl and released under GPLv3. The source code is freely available at https//github.com/Xiangyang1984/Gcluster. Gcluster can also be installed through conda “conda install -c bioconda gcluster”. SUPPLEMENTARY INFORMATION Supplementary data are available at Bioinformatics online. © The Author(s) (2020). Published by Oxford University Press. All rights reserved. For Permissions, please email journals.permissions@oup.com.BACKGROUND Potassium (K+) is essential for cells functions and alterations of the normal plasmatic levels can be life-threatening. The kidney is crucial in maintaining K+ homeostasis, mainly by regulating its secretion in the urine. Hypokalemia is influenced by acid-base status and can be associated to both metabolic alkalosis or acidosis. In adults, drug-induced hypokalemia is the most common form, however, genetically undiagnosed conditions should always be investigated. CASE REPORT We present the case of a 50-year old male patient with asthenia and hypokalemia treated with a Direct Acting Antiviral (DAA). Hypokalemia was ascribed to DAA therapy and potassium salt supplementation was started without improvement. Blood gas analysis revealed the presence of hypokalemic metabolic alkalosis. Since DAA-induced hypokalemia has been reported as secondary to proximal renal tubular acidosis(RTA), the role of entecavir was questioned. Urinalysis was negative for glycosuria and phosphaturia, while the presence of hypocalciuria raised the hypothesis of a Gilteman-like tubulopathy. Thus, a thiazide administration test was performed. Blasticidin S chemical structure Delta FeCl- failed to increase above 2.3% in all studied time points supporting the diagnosis of Gitelman Syndrome that was afterward confirmed by the genetic test, that showed the presence two in trans SLC12A3 mutations. CONCLUSION This case report suggests that genetically determined tubulopathies can be underdiagnosed and should always be considered in the differential diagnosis of non-hypertensive, hypokalemic metabolic alkalosis. © The Author(s) 2020. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. For Permissions, please email journals.permissions@oup.com.The influence of tertiary x-radiation on the radiological staff is widely unknown. Tertiary radiation is caused as the scattered radiation of the patient impacts the walls, floor, ceiling and surrounding air. The question that arises is does tertiary x-radiation provide a relevant contribution to the staff doses. The impact of tertiary radiation was investigated by means of measurements of the personal dose equivalent Hp(10) on an anthropomorphic Alderson Rando male phantom and also on operators/assistants staying in clinical practice. Further, the protective effect of lead foils, especially under tertiary radiation was also investigated. Correlations could be derived for clinical angiographic/interventional procedures between dose area products (DAPs) and dose length products (DLPs) vs. dorsal doses of staff persons. Generally, the staff doses that are a result of tertiary radiation depend on the x-ray energy and range from 0.15 to 0.55% of the scattered radiation impact caused by irradiation of the patient.