To assess the association between dietary magnesium intake and hyperuricemia in United States (US) adults, we extracted 26,796 US adults aged 20–85 years from the National Health and Nutrition Examination Survey (NHANES) in 2001–2014. All dietary intake was measured through 24 h dietary recall method. Multivariable logistic regression analysis was performed to investigate the association between magnesium intake and hyperuricemia after adjusting for several important confounding variables. When compared to the lowest quintile (Q1), for male, adjusted odds ratios (ORs) of hyperuricemia in the second quintile (Q2) to the fifth quintile (Q5) of the magnesium intake were 0.83 (95% CI: 0.72–0.95), 0.74 (0.64–0.85), 0.78 (0.67–0.90), and 0.70 (0.58–0.84, p for trend = 0.0003), respectively. For female, OR was 0.75 (0.62–0.90) in the fourth quintile (Q4) (p for trend = 0.0242). As compared to Q4 of magnesium intake (contains recommended amount), the relative odds of hyperuricemia were increased by 1.29 times in Q1 (OR = 1.29, 1.11–1.50) in male. The ORs were 1.33 (1.11–1.61) in Q1, 1.27 (1.07–1.50) in Q2 in female. Our results indicated that increased magnesium intake was associated with decreased hyperuricemia risk. It also indicated the importance of recommended dietary allowance (RDA) of magnesium and the potential function of magnesium intake in the prevention of hyperuricemia.

We aim to explore the associations between dietary zinc intake and hyperuricemia (HU) in United States (US) adults. 24,975 US adults aged 20 years or older from the National Health and Nutrition Examination Survey (NHANES) from 2001 to 2014 were stratified into quintiles based on zinc intake. All dietary intake measured through 24-h dietary recalls. Multivariable logistic regression analysis was performed to examine the association between zinc intake and HU after adjustment for possible confounders. For males, compared with respondents consuming less than 7.33 mg zinc daily, the adjusted odds ratios (ORs) were 0.83 (95% CI, 0.71, 0.97) among those consuming 10.26–13.54 mg zinc daily, 0.78 (95% CI, 0.63–0.96) among those consuming 18.50 mg or greater, and p for the trend was 0.0134. For females, compared with respondents consuming less than 5.38 mg zinc daily, the OR was 0.78 (95% CI, 0.63, 0.97) among those consuming 9.64–12.93 mg zinc daily, and p for the trend was 0.3024. Our findings indicated that dietary zinc intake is inversely associated with HU in US men and women, independent of some major confounding factors.

A high-purine diet can cause hyperuricemia and destroy the microbial composition of the gut microbiota. Both folic acid and zinc significantly reduce uric acid levels and alleviate hyperuricemia. However, whether the underlying mechanisms are associated with the regulation of the gut microbiota remain unknown. To explore alterations of the gut microbiota related to folic acid and zinc treatment in rats with hyperuricemia in our study. A hyperuricemic rat model was established with a high-purine diet. The effects of folic acid and zinc on uric acid levels were evaluated. Alterations of the gut microbiota related to hyperuricemia and the treatments were evaluated by sequencing using the Illumina MiSeq system. The results demonstrated that uric acid levels dropped observably, and the activities of adenosine deaminase (ADA) and xanthine oxidase (XOD) were downregulated after folic acid or zinc intervention. 16S rRNA gene sequencing-based gut microbiota analysis revealed that folic acid and zinc enhanced the abundance of probiotic bacteria and reduced that of pathogenic bacteria, thus improving intestinal barrier function. PICRUST analysis indicated that folic acid and zinc restored gut microbiota metabolism. These findings indicate that folic acid and zinc ameliorate hyperuricemia by inhibiting uric acid biosynthesis and stimulating uric acid excretion by modulating the gut microbiota. Thus, folic acid and zinc may be new and safe therapeutic agents to improve hyperuricemia.

MicroRNA-132 (miR-132) is a highly conserved molecule that plays a crucial regulatory role in central nervous system (CNS) disorders. The expression levels of miR-132 exhibit variability in various neurological disorders and have been closely linked to disease onset and progression. The expression level of miR-132 in the CNS is regulated by a diverse range of stimuli and signaling pathways, including neuronal migration and integration, dendritic outgrowth, and complexity, synaptogenesis, synaptic plasticity, as well as inflammation and apoptosis activation. The aberrant expression of miR-132 in various central neurodegenerative diseases has garnered widespread attention. Clinical studies have revealed altered miR-132 expression levels in both chronic and acute CNS diseases, positioning miR-132 as a potential biomarker or therapeutic target. An in-depth exploration of miR-132 holds the promise of enhancing our understanding of the mechanisms underlying CNS diseases, thereby offering novel insights and strategies for disease diagnosis and treatment. It is anticipated that this review will assist researchers in recognizing the potential value of miR-132 and in generating innovative ideas for clinical trials related to CNS degenerative diseases.

To assess the association between intake of folate, vitamin B6, and vitamin B12 with hyperuricemia (HU) among adults from the United States (US), we extracted relevant data from 24,975 US adults aged 20–85 years from the National Health and Nutrition Examination Survey (NHANES) in 2001–2014. All dietary intake was evaluated by 24-h dietary recalls. Multivariable logistic regression analysis was performed to explore the associations after adjustment for confounders. Compared to the lowest quintile (Q1), for males, adjusted odds ratios (ORs) of HU in Q2 to Q5 of folate (dietary folate equivalent, DFE) intake were 0.84 (95% CI, 0.73–0.96), 0.84 (0.73–0.97), 0.72 (0.62–0.84), and 0.64 (0.53–0.77), respectively (p for trend <0.0001). In females, adjusted ORs in Q2 to Q4 of folate (DFE) intake were 0.84 (95% CI, 0.71–0.99), 0.81 (0.68–0.96), and 0.82 (0.68–0.99), with a p for trend of 0.1475. Our findings indicated the intakes of total folate, folic acid, food folate, folate (DFE), vitamin B12, but not vitamin B6, were inversely related to the risk of HU in males. A lower risk of HU with higher intakes of total folate, food folate, and folate (DFE) was found in females, but with no association between intakes of folic acid, vitamin B6, B12, and the risk of HU for females.

Background: This study incorporates fundamental research referring to considerable amounts of gene-sequencing data and bioinformatics tools to analyze the pathological mechanisms of diffuse large B-cell lymphoma (DLBCL). Methods: A lncRNA-miRNA-mRNA ceRNA network of DLBCL was constructed through database analysis combining GTEx and TCGA. qPCR was used to detect the expression of LINC00963 and miR-320a in DLBCL cell lines. After LINC00963 or miR-320a overexpression in vitro, western blot was performed to assess the protein levels of UPR sensors (GRP78, p-IRE1, IRE1, active ATF6, ATF4 and XBP1), along with apoptosis markers (Bcl-2, Bax, caspase 3) and autophagy indicators (Beclin1, LC3II, LC3I and p62). Additionally, the expression of LC3 was analyzed through immunofluorescence (IF) assay. Results: Following LINC00963 overexpression in vitro, SUDHL4 cell line showed a marked increase in the level of UPR-related GRP78, p-IRE1 and spliced XBP-1/XBP-1(s), apoptosis-related Bax and cleaved caspase 3, as well as autophagy-related Beclin1 and LC3II, whereas miR-320a mimic greatly diminished the effects of LINC00963 overexpression. Moreover, LINC00963 targeted miR-320a while miR-320a bound to the 3’UTR of XBP1. It was also found that LINC00963 overexpression resulted in significantly delayed tumor growth in a xenograft model of DLBCL. Conclusion: Mechanistically, LINC00963/miR-320a regulated XBP1-apoptosis pathway and autophagy, implying the therapeutic potential of this pathway for selective targeting. The data presented here illustrated the mechanism of LINC00963/miR-320a/XBP1 in DLBCL for the first time.