It is proposed that the pathogenesis of rheumatoid arthritis （RA） is centered on deficiency， dampness， and blood stasis， which interact with and evolve into one another during the onset and progression of the disease. The development of RA is closely associated with insufficiency of healthy qi and the interbinding of dampness and blood stasis. Accordingly， treatment emphasizes an integrated approach that combines tonifying deficiency， eliminating dampness， and resolving blood stasis， and is implemented in three main stages. In the initial stage， therapy focuses on supporting healthy qi， dispelling dampness， and relieving impediment， with modified Huangqi Guizhi Wuwu Decoction （黄芪桂枝五物汤） combined with Yiyiren Decoction （薏苡仁汤）. In the active stage， treatment aims to eliminate dampness， resolve blood stasis， and unblock the collaterals， using modified Wutou Decoction （乌头汤） or Guizhi Shaoyao Zhimu Decoction （桂枝芍药知母汤）. In the remission stage， therapy emphasizes strengthening the spleen and reple-nishing qi to prevent recurrence， with modified Shenling Baizhu Powder （参苓白术散） combined with Guipi Decoction （归脾汤）.

ObjectiveTo evaluate the efficacy and safety of Janus kinase （JAK） inhibitors combined with Chinese herbal medicine （CHM） in treating rheumatoid arthritis （RA）. MethodsClinical data from 169 RA patients were retrospectively collected. Among them， 71 cases received JAK inhibitors as the control group， while 98 cases received JAK inhibitors plus CHM as the observation group， both treated for 24 weeks. The rheumatoid factor （RF）， cyclic citic peptide antibody （anti-CCP）， erythrocyte sedimentation rate （ESR）， C-reactive protein （CRP）， and white blood cell count （WBC） were recorded before and after treatment. Databases including CNKI， Wanfang， VIP， PubMed and Web of Science were searched from inception till August 31st， 2025 for randomized controlled trials （RCTs） on the combined use of JAK inhibitors and CHM for RA. The methodological quality of the included studies was evaluated using the risk of bias assessment tool. Meta-analyses were performed for RF， anti-CCP， ESR， CRP， 28-joint disease activity score （DAS28）， overall clinical effective rate， and incidence of adverse events. Sensitivity analysis were also performed. ResultsThe retrospective study demonstrated that after treatment， ESR， CRP， and anti-CCP levels decreased in the observation group， while ESR and CRP levels decreased in the control group （P＜0.05）. Moreover， ESR and RF levels in the observation group were lower than those in the control group （P＜0.05）. A total of 9 RCTs involving 770 patients were included in the meta-analysis. The results indicated that the JAK inhibitors plus CHM group was superior to the JAK inhibitors group in reducing RF （MD=-8.97， 95%CI -15.01 to -2.94， P=0.004）， CRP （MD=-3.34， 95%CI -3.82 to -2.86， P＜0.001）， ESR （MD=-5.33， 95%CI -7.98 to -2.69， P＜0.001）， and DAS28 score （MD=-0.54， 95%CI -0.74 to -0.34， P＜0.001）， as well as in improving the overall clinical effective rate （OR=4.53， 95%CI 2.55 to 8.03， P＜0.001）. No statistically significant differences were observed between groups in anti-CCP levels （SMD=-2.08， 95%CI -4.41 to 0.24， P=0.080） or incidence of adverse events （OR=0.93， 95%CI 0.55 to 1.57， P=0.790）. ConclusionThe combination of JAK inhibitors and CHM demonstrates remarkable efficacy in treating RA， contributing to improved disease activity and reduced inflammatory markers with a favorable safety profile.

Disrupted bone morphogenetic protein type 2 receptor (BMPR2) signaling in endothelial cells drives pulmonary arterial hypertension (PAH). However, targeted recovery of this signaling pathway by lipid nanoparticles (LNPs) has not been explored as a therapy. Here, we employed Design of Experiments to optimize the delivery efficiency of LNPs targeting pulmonary endothelial cells developed by our laboratory, resulting in a remarkable 35-fold increase in a simplified three-component formulation without helper lipids. Administration of BMPR2 mRNA LNPs effectively reversed established PAH in two experimental rat models (monocrotaline or SU5416-hypoxia) by reversing pulmonary vascular remodeling. Specifically, BMPR2 mRNA LNPs replenished the expression of BMPR2 protein and subsequently activated downstream pathways, as confirmed by elevated levels of p-SMAD1/5/9 and ID1 proteins. The relief of pulmonary arterial occlusion was demonstrated by thinned pulmonary arterial media and decreased proportion of full muscularized vessels. Alleviation of right ventricular hypertrophy was indicated by declined Fulton index, the cross-sectional area of right ventricular cardiomyocytes as well as collagen deposition. Effective recovery of right ventricular function was evidenced by increased pulmonary artery flow acceleration time/pulmonary artery flow ejection time ratio. These findings underscore the potential of restoring BMPR2 signaling through pulmonary endothelial cell-specific LNPs for treating PAH.

A matrix solid phase dispersion ( MSPD) method was developed for the simultaneous preparation of samples of 15 mycotoxin biomarkers including deoxynivalenol, aflatoxins and zearalenone from eggs, which were subsequently determined by liquid chromatography-electrospray ionization tandem mass spectrometry ( LC-ESI-MS/MS) under the multiple reaction monitoring ( MRM) mode. For the analysis, the samples were first mixed with C18 particles and loaded into an empty column, then 20 mL of acetonitrile/methanol (1:1, V/V) containing 1 mmol/L ammonium formate was used to elute the sample. The eluent was then dried with nitrogen flow and redissolved into the mobile phase. After filtration, samples were brought into vials and used for analysis. Different from other methods, no extra complicated purification and centrifugation steps were required in the procedure of MSPD. This method had good linearity in the range of 0. 2-100 ng/mL, with the correlation coefficient (r2) greater than 0. 9931. The limits of detection (LODs, S/N=3) and limits of quantification ( LOQs, S/N=3 ) of this method were 0. 05-2 μg/kg and 0. 2-4 μg/kg respectively. Comprehensive extraction recoveries of the 15 compounds ranged from 61% to 90%.

Objective Previous studies have shown that genetic variants in the interferons regulatory factor 5 (IRF5) gene are associated with rheumatoid arthritis (RA) in European and Japanese, but not found in Han Chinese. We conducted this study to investigate whether genetic variants in the IRF5 gene are associated with RA in ShaanXi Han Chinese population. Methods This study was collected 576 RA patients and 768 normal controls. Six IRF5 gene polymorphisms (rs729302, rs2004640, rs752637, rs3807306, rs10954213 and rs2280714) were genotyped by the SNaPshot method. T-test and χ2 test were used for statistic analysis. The genotype and allele frequencies were evaluated using the chi square tests. Genotyping data were adjusted by Logistic regression method by age and gender. The linkage disequilibrium (LD) block structure was examined using Hapview 4.2 software. Results Six SNPs inspected complied with Hardy-weinberg equilibrium (P>0.05). Two SNPs were significantly associated with RA: rs729302 A risk allele [OR=1.29, 95%CI (1.10, 1.50), P=5.57×10-3];dominant model [OR=1.58, 95%CI (1.10, 2.27), P=0.024], recessive model [OR=1.31, 95%CI (1.17, 1.64), P=0.028]. rs2004640 T risk allele [OR=1.28, 95%CI (1.08, 1.54), P=0.039]; dominant model [OR=1.27, 95%CI (1.03, 1.58), P=0.036]. In addition, there was no significant difference in rs752637, rs3807306, rs10954213 and rs2280714 SNPs between RA group and control and genotyped polymorphisms were significantly associated with RA susceptibility. Conclusion The present study confirm that rs729302 and rs2004640 in the IRF5 gene is significantly associated with increased risk of RA in ShaanXi Han Chinese population.