Second People's Hospital of Nanning

Kidney stone disease (KSD) is a common disorder of the urinary system and is closely related to genetic polymorphisms. However, the relationship between OSBPL8 polymorphisms and kidney stones has not been thoroughly investigated.

Six OSBPL8 polymorphisms (rs17042391,rs17042409,rs4761431,rs7303892,rs4761434, and rs17042390) were analyzed in a Chinese case-control cohort containing 923 nephrolithiasis patients and 945 healthy controls.The association of these OSBPL8 gene polymorphisms with KSD susceptibility was analyzed using logistic regression, and examined by calculating the odds ratios (ORs) and 95% confidence intervals (CIs).

The OSBPL8 polymorphisms (GG for rs17042391, rs17042409, rs4761431, rs7303892; AA for rs4761434; and G for rs17042390) were significantly associated with a decreased risk of KSD in females.The protected alleles (G allele of rs17042391, G allele of rs17042409, G allele of rs4761431, A allele of rs4761434, and G allele of rs17042390) were related to decreased BMI levels in KSD patients; female patients with these alleles also exhibited lower BMI, HDL, and LDL levels,the G allele of rs7303892 was linked to reduced serum cholesterol levels in these females.Additionally, the haplotype ACAAGA was associated with decreased KSD risk in females, but haplotype GGGGAG presented an opposing effect.

Our research shows that the OSBPL8 gene polymorphisms reduced the risk of KSD in females, and were also associated with lipid-related metabolic traits.

Several observational studies have suggested a possible link between gout, serum uric acid (UA) levels, and erectile dysfunction (ED). Nonetheless, the current body of evidence does not allow for a conclusive determination regarding the influence of gout and serum UA on the likelihood of developing ED. The primary aim of this research was to explore the potential causal relationship between gout and serum UA levels in relation to ED utilizing Mendelian randomization (MR) analysis. The principal analytical method employed was inverse variance weighting (IVW). Following this, a sensitivity analysis was performed using Cochran Q-test, funnel plots, MR-Egger regression, and the leave-one-out method. The findings from the IVW analysis revealed no significant association between gout and ED (odds ratio [OR] = 1.004, 95% confidence interval [CI]: 0.948–1.063, P = .888), nor between serum UA levels and ED (OR = 1.013, 95% CI: 0.775–2.126, P = .333). The results from the supplementary methods corroborated those obtained from the IVW approach. This study confirmed the absence of heterogeneity and horizontal pleiotropy, with consistent results across all sensitivity analyses. The MR analysis did not yield genetic-level evidence to substantiate a direct causal relationship between gout, serum UA, and ED.

Gliomas, the most prevalent primary brain tumors, exhibit a poor five-year survival rate despite advances in various treatments, necessitating further studies to understand tumor progression and develop new therapies, particularly targeting EphA2, which is implicated in vasculogenic mimicry and glioma progression.Dihydroartemisinin (DHA) has shown anti-glioma effects through mechanisms such as PERK-related ferroptosis and inhibition of proliferation and angiogenesis, although its interaction with EphA2 in mediating these effects requires further investigation.In this study, we revealed that DHA significantly inhibits the formation of vasculogenic-like networks, the stemness of C6 glioma stem cells and the growth of glioma by inhibiting the expression of EphA2.Mechanistic investigations indicated that PI3K/Akt pathway at least partly mediated this function, since overexpression of EphA2 reversed the anti-tumor effects of DHA.Conclusively, the current report provides evidence that DHA, PI3K/Akt/EphA2 blockage, and VM inhibition are promising therapies for glioma.