Patients with melanoma should be informed of the importance of conducting systematic TSSE and using a partner during examination; however, some patients may prefer skin examination by healthcare providers. Measurement of TSSE self-report merits further study.

The poor prognosis of gastric adenocarcinoma is partly due to chemotherapy failure, especially the oxaliplatin-based chemotherapy. However, the specific mechanism of oxaliplatin resistance is unclear. We aim to find the roles that LINC00641 and miR-582-5p play in regulating oxaliplatin resistance. Quantitative reverse transcriptase-PCR was used to evaluate the expression of LINC00641 and microRNA-582-5p (miR-582-5p) in gastric cancer both in vivo and in vitro. Transwell and CCK-8 assays were performed; and LC3 I/II and p62 were detected by western blot to evaluate the activation of autophagy. LINC00641 expression was associated with prognosis and oxaliplatin resistance in patients with gastric adenocarcinoma. The expression of LINC00641 was higher in gastric cancer tissues; whereas miR-582-5p was down-regulated in gastric cancer tissues. Moreover, LINC00641 was highly expressed in oxaliplatin-resistant cell lines and miR-582-5p was down-regulated. In addition, LINC00641 negatively regulated the expression of miR-582-5p. With regard to biological functions, down-regulation of LINC00641 suppressed cell migration and proliferation. Further experiments indicated that down-regulation of LINC00641 inhibited the autophagy process, making gastric cancer cells more sensitive to oxaliplatin. LINC00641 and miR-582-5p are biomarkers for predicting overall survival, as they were involved in regulating oxaliplatin resistance by altering autophagy in gastric adenocarcinoma.

Influenced by Georgia's settlement agreement with the United States Department of Justice relating to the enforcement of the Americans with Disabilities Act, an increasing number of individuals with intellectual and developmental disabilities (IDD) are transitioning from institutions to community living. In this study we evaluate the pattern of medication use among individuals who recently transitioned to the community (IRTC), comparing results to the IDD population already residing in the community (comparison group). Average use and prevalence rates were trended over time, between January 1, 2010, and December 31. 2012. Findings indicate a significant increase in medication use in the IRTC and comparison group, with a greater and faster increase in the IRTC population. We suggest the transition process should be examined and revised, ensuring adequate preparation time and training for each person and relevant staff, particularly on medications and challenging behaviors. Several demographic trends were also significant and are discussed.

Objective Rheumatoid arthritis (RA) is a nonspecific, chronic, systemic autoimmune disease characterized by symmetric polyarticular synovitis. Bioinformatics analysis of potential biomarkers, mRNA–miRNA–lncRNA axes, and signaling pathways in the pathogenesis of RA provides potential targets and theoretical basis for further research on RA. Methods The GSE1919 and GSE77298 datasets were downloaded from the Gene Expression Omnibus database ( http://www.ncbi.nlm.nih.gov/geo ). Perl was used to perform data merging, and R was used to perform batch correction. The “limma” package of R was used to screen differentially expressed genes, and the “clusterProfiler” package was used to perform enrichment analysis of the Gene Ontology and Kyoto Encyclopedia of Genes and Genomes. Search Tool for the Retrieval of Interacting Genes/Proteins was used to construct the protein–protein interaction network, Cytoscape was used for module analysis, and R was used to screen for hub genes. GraphPad Prism was used to plot the receiver operating characteristic curve of the hub genes. Gene set enrichment analysis and competitive endogenous RNA network analysis were performed on hub genes with the greatest diagnostic values. The hub gene with the greatest diagnostic value was verified using immunohistochemical staining. Results We obtained nine hub genes ( ITGB2, VAMP8, HLA-A, PTAFR, SYK, FCER1G, HLA-DPB1, LCP2 , and ACTR2 ) and four mRNA–miRNA–lncRNA axes (ITGB2-hsa-miR-486-3p-SNHG3, ITGB2-hsa-miR-338-5p-XIST, ITGB2-hsa-miR-5581-3p-XIST, and ITGB2-hsa-miR-1226-5p-XIST) related to the pathogenesis of RA. The nine hub genes were highly expressed, and ITGB2 had the highest diagnostic value for RA. We also identified signaling pathways related to the pathogenesis of RA: Fc epsilon Rl and chemokine signaling pathways. The immunohistochemical results showed that ITGB2 expression was significantly upregulated in RA. Conclusion The hub genes, mRNA–miRNA–lncRNA axes, and signaling pathways related to RA pathogenesis identified in this study provide a new research direction for the mechanism, diagnosis, and treatment of RA.

The development of multidrug resistance is the major obstacle to successful lung cancer chemotherapy. Cancer cells gain resistance through increased levels of P-glycoprotein (P-gp), which is encoded by the multidrug resistance-associated protein 1 (MDR1) gene. Leucine-rich PPR motif-containing protein (LRPPRC), a member of the PPR family, has been verified to regulate the transcription of MDR1. This regulation is influenced by the methylation status of the GC -100 box in the MDR1 promoter. The present study aimed to investigate the effect of LRPPRC on cisplatin (DDP) resistance in lung cancer cells and explore the underlying mechanism. DDP-resistant non-small cell lung cancer cell lines (A549/DDP, H1299/DDP) were generated. The expression levels of LRPPRC and P-gp/MDR1, investigated by qPCR and western blot analysis, were increased in the A549/DDP and H1299/DDP cells compared with that in the parental cells. LRPPRC silencing with shRNA increased DDP sensitivity in vitro and in vivo. LRPPRC silencing inhibited the level of LRPPRC binding with the MDR1 promoter, investigated by chromatin immunoprecipitation-qPCR, and the corresponding MDR1 expression. Demethylation treatment rescued the decrease in the level of LRPPRC binding with MDR1 and the corresponding expression of MDR1 and the increase in DDP sensitivity due to LRPPRC silencing. Our study suggests that LRPPRC contributes to DDP resistance in lung cancer cells by regulating MDR1 transcription. Thus, LRPPRC may serve as a potential molecular target for chemo-resistance reversal in lung cancer.