Development and validation of a Systemic Sclerosis Health Literacy Scale.

Background and aim: Health literacy levels are strongly associated with clinical outcomes and quality of life in patients with chronic diseases, and patients with limited health literacy often require more medical care and achieve poorer clinical outcomes. Among the large number of studies on health literacy, few studies have focused on the health literacy of people with systemic sclerosis (SSc), and there is no specific tool to measure health literacy in this group. Therefore, this study plans to develop a health literacy scale for patients with SSc. Methods: This study included 428 SSc patients from the outpatient and inpatient departments of the Department of Rheumatology and Immunology, the first affiliated Hospital of Anhui Medical University and the first affiliated Hospital of University of Science and Technology of China. The formulation of the scale was completed by forming the concept of health literacy of SSc patients, establishing the item pool, screening items, and evaluating reliability and validity. Classical measurement theory was used to screen items, factor analysis was used to explore the construct validity of the scale, and Cronbach's alpha coefficient was used to assess the internal consistency. Results: Our study population was predominantly middle-aged women, with a male to female ratio of 1:5.7 and a mean age of 51.57 ± 10.99. A SSc Health Literacy scale with 6 dimensions and 30 items was developed. The six dimensions are clinic ability, judgment/evaluation information ability, access to information ability, social support, treatment compliance and application information ability. The Cronbach's alpha coefficient of the scale is 0.960, retest reliability is 0.898, split-half reliability is 0.953, content validity is 0.983, which has good reliability and validity. Conclusion: The Systemic Sclerosis Health Literacy Scale may become a valid tool to evaluate the health literacy level of patients with SSc.

Bioinformatics analysis of markers based on m6 A related to prognosis combined with immune invasion of renal clear cell carcinoma.

The incidence rate of renal cell carcinoma (RCC) is about 3% of all adult cancers. Of these, the Kidney clear cell renal cell carcinoma (KIRC) is the most common type, accounting for about 70%-75% of RCC. KIRC is difficult to be detected in time clinically. KIRC still has no effective treatment at this stage. We combined high-throughput bioinformatics analysis to obtained the structural sequence transcriptome data, relevant clinical information, and m6 A gene map of KIRC patients from genomics TCGA database. Pearson's correlation analysis was used to explore m6 A related gene long noncoding RNAs (lncRNAs), and then univariate Cox regression analysis was performed to screen the prognostic role of KIRC patients. Lasso-Cox regression was performed to establish the lncRNAs risk model associated with m6 A.LINC02154 and AC016773.2, Z98200.2, AL161782.1, EMX2OS, AC021483.2, CD27-AS1, AC006213.3 were iidentif. Compared with the low-risk group, the overall survival of patients in the high-risk group was significantly worse. Analyzing whether there are differences in immune cells between high-risk and low-risk subgroups. There were CD4 memory resting, Monocytes, Macrophages M1, Dendritic cells activated, Mast cells resting, which had higher infiltrations in the low-risk group. We performed Go enrichment analysis, Kyoto Encyclopedia of Genes and Genomes enrichment analysis and gene set enrichment analysis enrichment analysis. Overall, our results suggest that the component of m6A-related lncRNAs in the prognostic signal may be a key mediator in the immune microenvironment of KIRC, which represents a promising therapeutic effect.

Long non­coding RNA 00858 knockdown alleviates bladder cancer via regulation of the miR­3064­5p/CTGF axis.

The long non-coding RNA 00858 (LINC00858) has been reported to be an oncogene for various cancer diseases, including osteosarcoma and colorectal cancer. However, the expression pattern and function of LINC00858 in bladder cancer remain largely unknown. The expression level of LINC00858 was measured in tumor tissues and cell lines by RT-qPCR. The role of LINC00858 in bladder cancer cells were studied by gain- and loss-of-function strategies in vitro. Cell proliferation, migration and invasion were assessed by CCK-8, colony formation, wound healing and Transwell chamber assays. At the molecular level, dual luciferase reporter and RNA RIP assays were performed to identify the interaction among LINC00858, microRNA (miR)-3064-5p and cellular communication network factor 2 (CTGF). The results revealed that the expression level of LINC00858 was upregulated in bladder cancer tissues and cell lines including T24, J82 and 5637. Moreover, knockdown of LINC00858 suppressed cell proliferation, migration and invasion in vitro. Mechanistically, LINC00858 functioned as a competitive RNA to increase the expression level of oncogene CTGF by sequestering miR-3064-5p. In conclusion, LINC00858 knockdown inhibited the proliferation, migration and invasion of bladder cancer cells via regulation of the miR-3064-5p/CTGF axis.

Low expression of PDK1 inhibits renal cell carcinoma cell proliferation, migration, invasion and epithelial mesenchymal transition through inhibition of the PI3K-PDK1-Akt pathway.

As the most commonly occurring form of primary renal tumor, renal cell carcinoma (RCC) is a malignancy accompanied by a high mortality rate. 3-phosphoinositide-dependent protein kinase 1 (PDK1) has been established as a protein target and generated considerable interest in both the pharmaceutical and academia industry. The aim of the current study was to investigate the effect of si-PDK1 on the RCC cell apoptosis, proliferation, migration, invasion and epithelial mesenchymal transition (EMT) in connection with the PI3K-PDK1-Akt pathway. Microarray analysis from the GEO database was adopted to identify differentially expressed genes (DEGs) related to RCC, after which the positive expression of the PDK1 protein in tissue was determined accordingly. The optimal silencing si-RNA was subsequently selected and RCC cell lines 786-O and A498 were selected and transfected with either a si-PDK1 or activator of the PI3K-PDK1-Akt pathway for grouping purposes. The mRNA and protein expressions of PDK1, the PI3K-PDK1-Akt pathway-, EMT- and apoptosis-related genes were then evaluated. The effect of si-PDK1 on cell proliferation, apoptosis, invasion and migration was then analyzed. Through microarray analysis of GSE6344, GSE53757, GSE14762 and GSE781, PDK1 was examined. PDK1 was determined to be highly expressed in RCC tissues. Si-PDK1 exhibited marked reductions in relation to the mRNA and protein expression of PDK1, PI3K, AKT as well as Vimentin while elevated mRNA and protein expressions of E-cadherin were detected, which ultimately suggested that cell migration, proliferation and invasion had been inhibited coupled with enhanced levels of cell apoptosis. While a notable observation was made highlighting that the PI3K-PDK1-Akt pathway antagonized the effect of PDK1 silencing. Taken together, the key observations of this study provide evidence suggesting that high expressions of PDK1 are found in RCC, while highlighting that silencing PDK1 could inhibit RCC cell proliferation, migration, invasion and EMT by repressing the PI3K-PDK1-Akt pathway.