RESUMEN
OBJECTIVE: Dietary habits have long been known to be a critical factor influencing cognitive health, especially among older adults. Despite extensive research on various dietary components, the impact of omega-3 polyunsaturated fatty acids (PUFAs) on cognitive function has not yet been thoroughly investigated. This research seeks to determine whether more intake of omega-3 PUFAs correlates with improved cognitive function in older adults. METHODS: Data were analyzed from the National Health and Nutrition Examination Survey (NHANES), which included 2430 elderly participants aged 60 and above. The association between omega-3 consumption and cognitive outcomes was evaluated using linear regression models. Smoothing curves and threshold effect analysis were employed to examine nonlinear associations. Subgroup studies were conducted to demonstrate the strength and reliability of the correlation and factors affecting them. RESULTS: The fully adjusted model demonstrated significant positive correlations between omega-3 intake and scores on all 3 cognitive assessments performed. Specifically, in the final model, the beta coefficients for the CERAD Word Learning test, Animal Fluency Test, and Digit Symbol Substitution Test were 0.53 (95% CI: 0.33-0.72; P < 0.0001), 0.29 (95% CI: 0.12-0.47; P = 0.001), and 0.61 (95% CI: 0.19-1.03; P = 0.0045), respectively. CONCLUSION: Increased intake of omega-3 was positively and independently associated with cognitive function in older adults, suggesting that consumption of omega-3 PUFAs may help to prevent cognitive decline with aging. Prospective studies are needed to determine the direct of effect in this association.
RESUMEN
BACKGROUND: Acute myeloid leukemia (AML) is a type of hematological tumor caused by malignant clone hematopoietic stem cells. The relationship between lncRNAs and tumor occurrence and progression has been gaining attention. Research has shown that Smooth muscle and endothelial cell-enriched migration/differentiation-associated lncRNA (SENCR) is abnormally expressed in various diseases, whereas its role in AML is still poorly understood. METHODS: The expression of SENCR, microRNA-4731-5p (miR-4731-5p) and Interferon regulatory factor 2 (IRF2) were measured using qRT-PCR. The proliferation, cycle and apoptosis of AML cells with or without knockdown of SENCR were detected by CCK-8 assay, EdU assay, flow cytometry, western blotting and TUNEL assay, respectively. Consistently, SENCR knockdown was impaired the AML progression in immunodeficient mice. In addition, the binding of miR-4731-5p to SENCR or IRF2 was confirmed by luciferase reporter genes assay. Finally, rescue experiments were conducted to confirm the role of SENCR/miR-4731-5p/IRF2 axis in AML. RESULTS: SENCR is highly expressed in AML patients and cell lines. The patients with high SENCR expression had poorer prognosis compared with those with low SENCR expression. Interestingly, knockdown of SENCR inhibits the growth of AML cells. Further results demonstrated that the reduction of SENCR slows the progression of AML in vivo. SENCR could function as a competing endogenous RNA (ceRNA) to negatively regulate miR-4731-5p in AML cells. Furthermore, IRF2 was validated as a direct target gene of miR-4731-5p in AML cells. CONCLUSIONS: Our findings underscore the important role of SENCR in regulating the malignant phenotype of AML cells by targeting the miR-4731-5p/IRF2 axis.