Relationship between gout, hyperuricemia, and obesity-does central obesity play a significant role?-a study based on the NHANES database.

BACKGROUND: Our objective was to evaluate how various measures of obesity, such as body mass index(BMI), body roundness index(BRI), and weigh adjusted waist index(WWI), influence urate levels, prevalence of gout and to compare the disparities among these obesity indicators. METHODS: By analyzing the 2001-2018 National Health and Nutrition Examination Survey (NHANES), we assessed the relationship between BMI, WWI, and BRI indices and urate levels, hyperuricemia, and the prevalence of gout. Smoothed curve fitting was used to determine whether there was a nonlinear relationship between BMI,WWI, and BRI indices and urate levels, hyperuricemia, and the prevalence of gout, and threshold effects analysis was used to test this relationship. We also used ROC curves to determine the diagnostic efficacy of BMI, WWI, and BRI on the prevalence of hyperuricemia and gout. RESULTS: The study incorporated a total of 29,310 participants aged over 20 years, out of which 14,268 were male. Following the adjustment for the pertinent confounding factors, it was observed that higher levels of BMI, WWI, and BRI were significantly associated with a gradual and dose-dependent increase in urate levels. In the sensitivity analysis, each unit increment in BMI, WWI, and BRI levels exhibited an 8%, 72%, and 26% respective elevation in the risk of hyperuricemia, as well as a 5%, 31%, and 15% respective increase in the risk of gout. Dose-response curves provided evidence of a linear positive correlation between BMI, WWI, BRI, and urate levels, as well as the prevalence of hyperuricemia and gout. Based on the response from the ROC curve, overall, the diagnostic efficacy of BRI for hyperuricemia and gout surpasses that of BMI. CONCLUSION: The central obesity indices WWI and BRI levels are superior to BMI in detecting the prevalence of urate levels, hyperuricemia, and gout, and although a clear causal relationship has not yet been established, it is important to recognize the impact of central obesity on uric acid levels and to give it due attention.

[Decreased DNase1L3 secretion and associated antibodies induce impaired degradation of NETs in patients with sporadic SLE].

Objective To evaluate the correlation between alterations in DNase1 and DNase1L3 enzyme activities and impairment of NET degradation in patients with sporadic SLE, and to investigate the underlying mechanism. Methods 46 sporadic SLE patients and 30 age- and sex-matched healthy individuals were recruited. Serum levels of DNase1, DNase1L3 and corresponding autoantibodies were detected by ELISA. DNase1 and DNase1L3 were isolated by immunoprecipitation; NETs and enzyme degradation activities were detected using a modified immunofluorescence. DNase1L3 secretion by PBMCs was analyzed by ELISPOT, Western blotting and reverse transcription PCR. Results Levels of H3-dsDNA and Ela-dsDNA complexes were significantly elevated in SLE patients. LDGs in SLE population was significantly higher than in the control group, and LDGs was positively correlated with H3-dsDNA and Ela-dsDNA NETs complexes. The ability of SLE patients to degrade NET in vitro was significantly lower than that of the control group. Degradation experiments of DNase1 and DNase1L3 in different proportions showed that the decrease in DNase1L3 activity was the primary contributor to the elevated NET residue level. The concentration of DNase1L3 autoantibodies in SLE patients was significantly elevated compared to the control group. In addition, the capacity of PBMCs to secrete DNase1L3 was significantly lower in the SLE patients compared to the control group. Conclusion Decreased secretion of DNase1L3 and the presence of relevant autoantibodies notably impede NET degradation in patients with SLE, offering new directions for the monitoring and treatment of SLE patients.

Knockdown of BUB1 inhibits tumor necrosis factor-α-induced proliferation and migration of rheumatoid arthritis synovial fibroblasts by regulating PI3K/Akt pathway.

BACKGROUND: Rheumatoid arthritis (RA) is a common disease with joint cartilage destruction. BUB1 Mitotic Checkpoint Serine/Threonine Kinase (BUB1) is abnormally expressed in synovial tissues of RA patients, but its effect on RA remains unclear. In this study, we explored the role of BUB1 in RA. METHODS: An RA cell model was constructed by treating MH7A cells with tumor necrosis factor-α (TNF-α). The levels of BUB1, GAPDH, phosphorylated phosphatidylinositol 3 kinase (p-PI3K)/PI3K, and phosphorylated serine/threonine kinase (p-Akt)/Akt in MH7A cells were examined by Western blot. The MH7A cell proliferation was examined by colony formation assay. Wound healing assay and transwell assay were carried out to detect MH7A cell migration and invasion. The mRNA levels of proinflammatory cytokines were assessed by quantitative reverse transcription polymerase chain reaction. RESULTS: The results showed that knockdown BUB1 inhibited TNF-α-induced MH7A cell proliferation, migration, and invasion. Silencing BUB1 repressed the PI3K/Akt pathway in TNF-α-induced MH7A cells. We also found that the TNF-α-induced MH7A cell proliferation, migration, and invasion were repressed by si-BUB1 transfection, whereas these effects were attenuated by 740Y-P (an activator of the PI3K pathway) co-treatment. Knockdown of BUB1 reduced the expression of the proinflammatory cytokines. CONCLUSION: Knockdown BUB1 repressed TNF-α-induced MH7A cell proliferation, migration and invasion through the PI3K/Akt pathway.

Systemic evaluation of lymphocyte-bound C4d and immunoglobulins for diagnosis and activity monitoring of systemic lupus erythematosus.

OBJECTIVE: To investigate the role of lymphocyte-bound C4d (LB-C4d: T-C4d, B-C4d) and immunoglobulins (LB-Igs: T-IgG, T-IgM, B-κ and B-λ) in the diagnosis and monitoring of SLE. DESIGN & METHODS: The levels of C4d and Igs on peripheral lymphocytes were measured in 172 patients with SLE, 174 patients with other non-SLE inflammatory diseases and 100 healthy individuals. Immunobinding and blocking experiments were performed to characterize Igs from SLE patients to generate LB-C4d/Igs in vitro. Sixty-five patients with SLE were followed up longitudinally. Disease activity was assessed for each SLE patient. RESULTS: Patients with SLE had the highest median LB-C4d/Igs levels. LB-C4d had a significant but weak positive association with LB-Igs, with correlation coefficients ranging from 0.008 to 0.316. Anti-cardiolipin IgG and anti-ß2GP1 IgG, but not C3 and C4, were found to be closely associated with LB-C4d/Igs formation, with correlations as high as 0.337. Compared to anti-dsDNA, LB-C4d performed better in SLE diagnosis, while B-κ and B-λ performed better in disease activity monitoring. CONCLUSIONS: Both autoantibodies and receptors on lymphocytes contribute to LB-C4d/Igs formation. LB-C4d/Igs could be used as reliable indicators for SLE diagnosis and activity monitoring.

Efficacy and safety of Xinfeng capsule in patients with rheumatoid arthritis: a multi-center parallel-group double-blind randomized controlled trial.

OBJECTIVE: To evaluate the efficacy. and safety of Xinfeng capsule in patients suffering rheumatoid arthritis (RA). METHODS: A multi-center parallel-group designed, double-blind, randomized, controlled trial was conducted. Totally 304 RA patients were assigned to two groups: one group was administered Xinfeng capsule (XFC) plus the placebo of leflunomide and the other given leflunomide (LEF) plus the placebo of XFC for twelve weeks. The clinical and laboratory parameters were compared at baseline and fourth, eighth, and twelfth weeks. RESULTS: After twelve-week treatment, patients in two groups all showed some trend of effectiveness when compared in terms of American Rheumatism Association (ACR) recommended 20%, 50%, 70% improvement criteria, but it was insignificant. The validity in ameliorate modified disease activity score (DAS28) and laboratory indexes as erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), rheumatoid factor (RF) were also found no difference. The score of health assessment questionnaire (HAQ), self-rating anxiety scale (SAS), self-rating depression scale (SDS) and quality of life questionnaire with rheumatoid arthritis (RAQOL) both lower than the first week and the changes showed no difference. However, the score of SDS dropped more in XFC group than in the other. A total of 147 adverse reaction cases were reported, which shows no difference between the two groups. The most common adverse reactions were hepatic impairment, anemia, leukocytopenia, epigastric discomfort and phalacrosis. CONCLUSION: XFC demonstrated better improvement in the scores of SDS and compared with those of LEF group.

[Effect of purple sweet potato on lipid metabolism and oxidative stress in hyperlipidemic rats].

OBJECTIVE: To investigate the effect of purple sweet potato on lipid metabolism and oxidative stress in hyperlipidemic rats. METHODS: Forty male SD rats were randomly divided into 4 groups: normal control group, high-fat control group, high purple sweet potato groups, low purple sweet potato group. The rats were fed with different diets for 6w respectively. RESULTS: Serum TC, TG levels were significantly lower in high dosage group than in high-fat control group; while only serum TG was significantly lower in low dosage group than in high-fat control group, these changes started at the third week and lasted to the end of experiment. Serum LDL-C and AI levels were significantly lower in high and low dosage group than in high-fat control group, whereas, serum HDL-C was significantly higher than that in high-fat control group at w3 and lasted to the end of experiment. Serum SOD was significantly higher in high and low dosage group than in high-fat control group, whereas, serum MDA was significantly lower than that in high-fat control group at w6. CONCLUSION: Purple sweet potato can decrease serum lipids and reduce hepatic oxidative stress in hyperlipidemic rats.