The Association of Socioeconomic Status with the Burden of Cataract-related Blindness and the Effect of Ultraviolet Radiation Exposure: An Ecological Study.

OBJECTIVE: To assess the association of socioeconomic status with the burden of cataract blindness in terms of year lived with disability (YLD) rates and to determine whether ultraviolet radiation (UVR) levels modify the effect of socioeconomic status on this health burden. METHODS: National and subnational age-standardized YLD rates associated with cataract-related blindness were derived from the Global Burden of Disease (GBD) study 2017. The human development index (HDI) from the Human Development Report was used as a measure of socioeconomic status. Estimated ground-level UVR exposure was obtained from the Ozone Monitoring Instrument (OMI) dataset of the National Aeronautics and Space Administration (NASA). RESULTS: Across 185 countries, socioeconomic status was inversely associated with the burden of cataract blindness. Countries with a very high HDI had an 84% lower age-standardized YLD rate [95% confidence interval ( CI): 60%-93%, P < 0.001] than countries with a low HDI; for high-HDI countries, the proportion was 76% (95% CI: 53%-88%, P < 0.001), and for medium-HDI countries, the proportion was 48% (95% CI: 15%-68%, P = 0.010; P for trend < 0.001). The interaction analysis showed that UVR exposure played an interactive role in the association between socioeconomic status and cataract blindness burden ( P value for interaction = 0.047). CONCLUSION: Long-term high-UVR exposure amplifies the association of poor socioeconomic status with the burden of cataract-related blindness. The findings emphasize the need for strengthening UVR exposure protection interventions in developing countries with high-UVR exposure.

Identification of hub genes and therapeutic drugs in rheumatoid arthritis patients.

OBJECTIVES: Rheumatoid arthritis (RA) is considered a chronic autoimmune inflammatory disease that causes great morbidity and shortens life expectancy; however, the precise pathogenesis of RA remains unclear. This study aimed to select hub genes correlated with the development of RA. METHODS: Two gene expression profiles, GSE55235 and GSE12021, obtained from the Gene Expression Omnibus (GEO) were used to identify differentially expressed genes (DEGs) in control and RA samples using GEO2R, followed by other bioinformatics methods, including functional enrichment analysis, protein-protein interaction (PPI) networks, miRNA-hub gene network, and drug-hub gene interactions. In addition, qRT-PCR was finally conducted to confirm the reliability and validity of the expression level of the novel DEGs via freshly collected heparinized blood samples of healthy controls and RA patients. RESULTS: A sum of 136 upregulated and 37 downregulated DEGs were selected. Functional enrichment analysis indicated that all the upregulated DEGs were correlated with immune response, B cell receptor signalling pathway, and adaptive immune response. KEGG pathway enrichment analysis revealed that the upregulated DEGs were mostly related to cytokine-cytokine receptor interaction, primary immunodeficiency, chemokine signalling pathways, and cell adhesion molecules (CAMs). In total, 12 hub genes (IL15, KLRK1, GZMA, CXCR6, IGHV4-38-2, IGLL5, CXCL13, CXCL11, MS4A1, SDC1, SLAMF1, and PDCD1LG2) were identified and all these hub genes were upregulated, of which IGLL5 and IGHV4-38-2 were first reported to be correlated with the pathogenic mechanism and prognosis of RA. Furthermore, we also used qRT-PCR to validate the overexpression of IGLL5 and IGHV4-38-2 in RA patients compared to the healthy controls. In the miRNA-hub gene network, hsa-miR-1185-5p and hsa-miR-3679-5p might inhibit the expression of IGLL5 during the progression of RA. The 15 most promising candidate drugs, which were all approved by the Food and Drug Administration, may assist with the treatment of RA. CONCLUSIONS: Overall, these findings may assist with developing diagnostic, prognostic, and therapeutic biomarkers for RA. Key Points • IGLL5 and IGHV4-38-2 were first reported to be correlated with the pathogenic mechanism and prognosis of RA. • Besides, hsa-miR-1185-5p and hsa-miR-3679-5p may inhibit the expression of IGLL5 during the progression of RA.