Objective:To construct a "local-systemic" dual-track prediction model integrating the resistance index (RI) score of bilateral sacroiliac joints and the systemic immune-inflammation index (SII), and to evaluate its predictive efficacy for the active stage of ankylosing spondylitis (AS).Methods:A total of 205 patients with ankylosing spondylitis (AS) from the Second Hospital of Lanzhou University between April 2022 and April 2025 were retrospectively enrolled and categorized into an active group ( n=113) and a remission group ( n=92). Hematological parameters and ultrasound data were collected. The resistance index (RI) of the synovial area in bilateral sacroiliac joints was measured by Doppler ultrasound and scored as follows: RI < 0.5: 3 points; RI 0.5~0.55: 2 points; RI > 0.55: 1 point; undetectable blood flow: 0 points. A total bilateral RI score (range 0 to 6) was calculated. The systemic immune-inflammation index (SII) was derived as (neutrophils× platelets)/lymphocytes. Normality was tested for all continuous variables; normally distributed data were compared using the t-test, while non-normally distributed data were analyzed with the Mann-Whitney U test. Categorical variables were compared using the χ2 test or analysis of variance.Variable selection was performed using Lasso regression, and a multivariate logistic regression model was developed to assess predictive performance. Results:The proportion of patients with a bilateral RI total score≥5 was significantly higher in the active group compared to the remission group (50 of 113, 44.3% vs 2 of 92, 2.2%, χ2=55.63, P<0.001). Multivariate logistic regression analysis, after adjustment for confounding variables, identified the SII [ OR(95% CI)=1.01(1.00, 1.01), P<0.001], bilateral RI total score [ OR(95% CI)=1.67(1.29, 2.26), P<0.001], erythrocyte sedimentation rate [ OR(95% CI)=1.19(1.11, 1.30), P<0.001], and mean corpuscular hemoglobin concentration [ OR(95% CI)=1.09(1.03, 1.17), P<0.001] as independent risk factors for active AS. Conversely, lymphocyte count [ OR(95% CI)=0.42(0.18, 0.92), P=0.030] and globulin [ OR(95% CI)=0.89(0.80, 0.99), P=0.040] were significantly associated with protective effects. The bilateral RI total score demonstrated the strongest predictive effect, with each 1-point increase associated with a 67% elevation in the risk of active disease. ROC curve analysis indicated that the area under the curve (AUC) for predicting whether AS is in the active disease phase was 0.94 for the combined model (SII+bilateral RI total score), compared with 0.93 for the SII-alone model and 0.92 for the bilateral RI total score-alone model, demonstrating superior predictive performance of the combined model (SII+bilateral RI total score). An online prediction tool has been developed based on the combined model. Conclusion:The dual-track prediction model, which integrates local joint hemodynamic characteristics and systemic immune-inflammatory status, facilitates a multidimensional assessment of the risk of active AS and provides an objective basis for early identification.

Objective:To construct a "local-systemic" dual-track prediction model integrating the resistance index (RI) score of bilateral sacroiliac joints and the systemic immune-inflammation index (SII), and to evaluate its predictive efficacy for the active stage of ankylosing spondylitis (AS).Methods:A total of 205 patients with ankylosing spondylitis (AS) from the Second Hospital of Lanzhou University between April 2022 and April 2025 were retrospectively enrolled and categorized into an active group ( n=113) and a remission group ( n=92). Hematological parameters and ultrasound data were collected. The resistance index (RI) of the synovial area in bilateral sacroiliac joints was measured by Doppler ultrasound and scored as follows: RI < 0.5: 3 points; RI 0.5~0.55: 2 points; RI > 0.55: 1 point; undetectable blood flow: 0 points. A total bilateral RI score (range 0 to 6) was calculated. The systemic immune-inflammation index (SII) was derived as (neutrophils× platelets)/lymphocytes. Normality was tested for all continuous variables; normally distributed data were compared using the t-test, while non-normally distributed data were analyzed with the Mann-Whitney U test. Categorical variables were compared using the χ2 test or analysis of variance.Variable selection was performed using Lasso regression, and a multivariate logistic regression model was developed to assess predictive performance. Results:The proportion of patients with a bilateral RI total score≥5 was significantly higher in the active group compared to the remission group (50 of 113, 44.3% vs 2 of 92, 2.2%, χ2=55.63, P<0.001). Multivariate logistic regression analysis, after adjustment for confounding variables, identified the SII [ OR(95% CI)=1.01(1.00, 1.01), P<0.001], bilateral RI total score [ OR(95% CI)=1.67(1.29, 2.26), P<0.001], erythrocyte sedimentation rate [ OR(95% CI)=1.19(1.11, 1.30), P<0.001], and mean corpuscular hemoglobin concentration [ OR(95% CI)=1.09(1.03, 1.17), P<0.001] as independent risk factors for active AS. Conversely, lymphocyte count [ OR(95% CI)=0.42(0.18, 0.92), P=0.030] and globulin [ OR(95% CI)=0.89(0.80, 0.99), P=0.040] were significantly associated with protective effects. The bilateral RI total score demonstrated the strongest predictive effect, with each 1-point increase associated with a 67% elevation in the risk of active disease. ROC curve analysis indicated that the area under the curve (AUC) for predicting whether AS is in the active disease phase was 0.94 for the combined model (SII+bilateral RI total score), compared with 0.93 for the SII-alone model and 0.92 for the bilateral RI total score-alone model, demonstrating superior predictive performance of the combined model (SII+bilateral RI total score). An online prediction tool has been developed based on the combined model. Conclusion:The dual-track prediction model, which integrates local joint hemodynamic characteristics and systemic immune-inflammatory status, facilitates a multidimensional assessment of the risk of active AS and provides an objective basis for early identification.

Objective:To investigate the predictive value of the cancer antigen 125 (CA 125) elimination rate constant K (KELIM) score for no visible residual disease (R0) and prognosis in high-grade serous ovarian carcinoma (HGSOC) patients undergoing neoadjuvant chemotherapy (NACT)+interval debulking surgery (IDS). Methods:A retrospective analysis was conducted on 78 HGSOC patients treated with NACT+IDS at Beijing Hospital, from June 2014 to June 2024. The KELIM score was calculated, and its predictive value for R0 resection, chemotherapy response score (CRS), platinum-free interval (PFI), progression-free survival (PFS) time, and overall survival (OS) time was analyzed.Results:(1) The mean age at diagnosis was (61.9±9.9) years. The mean KELIM score was 1.1±0.4, with 44 patients having KELIM score≥1 and 34 having KELIM score <1. (2) Patients with KELIM score ≥1 had significantly higher rates of R0 resection (84% vs 56%; P=0.006), CRS3 grading (41% vs 0; P<0.001), and PFI ≥6 months (84% vs 53%; P=0.04) compared to those with KELIM score <1. Additionally, the median PFS time (18.7 vs 13.2 months; P<0.001) and OS time (34.8 vs 29.9 months; P=0.007) were significantly longer in the KELIM score ≥1 group. Chemosensitivity: patients with PFI <6 months had a significantly lower median KELIM score than those with PFI ≥6 months (0.8 vs 1.2; P=0.005). Surgical outcome: patients achieving R0 resection had a significantly higher median KELIM score than those without R0 (1.2 vs 0.7; P<0.001). (3) Univariate analysis identified non-R0 resection, CRS3 grading, lack of poly adenosine diphosphate ribose polymerase (PARP) inhibitor maintenance therapy, and KELIM score <1 as significant risk factors for OS time (all P<0.05). Multivariate analysis confirmed non-R0 resection ( HR=3.78,95% CI: 1.13-12.66; P=0.031), no PARP inhibitor maintenance ( HR=7.41,95% CI:1.82-30.15; P=0.005), and KELIM score <1 ( HR=5.14,95% CI:1.41-18.72; P=0.013) as independent risk factors for OS time. Conclusions:The KELIM score may serve as a predictive marker for chemosensitivity, R0 resection, PFS time, and OS time in HGSOC patients undergoing NACT+IDS. KELIM score<1 is an independent risk factor for OS.

Pyroptosis is a novel,inflammatory programmed cell death mediated by gasdermins(GSDMs),which characterized by the formation of membrane pores and the release of pro-inflammatory cytokines.Rheumatoid arthritis(RA)is a chronic,inflamma-tory autoimmune disease characterized by persistent synovitis in multiple joints,progressive destruction of bone and cartilage,and eventually leading to joint deformity and disability.Recently,it has been shown that pyroptosis plays an important role in development of RA.This review summarizes the molecular mechanism of pyroptosis,its pathogenic role and therapeutic strategies in RA,aiming of providing new insights for the mechanism research and new drug development of RA.

Objective:To investigate the predictive value of the cancer antigen 125 (CA 125) elimination rate constant K (KELIM) score for no visible residual disease (R0) and prognosis in high-grade serous ovarian carcinoma (HGSOC) patients undergoing neoadjuvant chemotherapy (NACT)+interval debulking surgery (IDS). Methods:A retrospective analysis was conducted on 78 HGSOC patients treated with NACT+IDS at Beijing Hospital, from June 2014 to June 2024. The KELIM score was calculated, and its predictive value for R0 resection, chemotherapy response score (CRS), platinum-free interval (PFI), progression-free survival (PFS) time, and overall survival (OS) time was analyzed.Results:(1) The mean age at diagnosis was (61.9±9.9) years. The mean KELIM score was 1.1±0.4, with 44 patients having KELIM score≥1 and 34 having KELIM score <1. (2) Patients with KELIM score ≥1 had significantly higher rates of R0 resection (84% vs 56%; P=0.006), CRS3 grading (41% vs 0; P<0.001), and PFI ≥6 months (84% vs 53%; P=0.04) compared to those with KELIM score <1. Additionally, the median PFS time (18.7 vs 13.2 months; P<0.001) and OS time (34.8 vs 29.9 months; P=0.007) were significantly longer in the KELIM score ≥1 group. Chemosensitivity: patients with PFI <6 months had a significantly lower median KELIM score than those with PFI ≥6 months (0.8 vs 1.2; P=0.005). Surgical outcome: patients achieving R0 resection had a significantly higher median KELIM score than those without R0 (1.2 vs 0.7; P<0.001). (3) Univariate analysis identified non-R0 resection, CRS3 grading, lack of poly adenosine diphosphate ribose polymerase (PARP) inhibitor maintenance therapy, and KELIM score <1 as significant risk factors for OS time (all P<0.05). Multivariate analysis confirmed non-R0 resection ( HR=3.78,95% CI: 1.13-12.66; P=0.031), no PARP inhibitor maintenance ( HR=7.41,95% CI:1.82-30.15; P=0.005), and KELIM score <1 ( HR=5.14,95% CI:1.41-18.72; P=0.013) as independent risk factors for OS time. Conclusions:The KELIM score may serve as a predictive marker for chemosensitivity, R0 resection, PFS time, and OS time in HGSOC patients undergoing NACT+IDS. KELIM score<1 is an independent risk factor for OS.

Objective To explore the mechanism of Quhan Zhufeng Mixture on proliferation and apoptosis of rheumatoid arthritis fibroblast-like synoviocyte(RA-FLS)based on NDRG2/JAK2/STAT3 signaling pathway.Methods RA-FLS cells were cultured in vitro,and were divided into ① blank serum group,methotrexate group,Quhan Zhufeng Mixture low-,medium-and high-dosage groups;② blank serum group,AG490 group,Quhan Zhufeng Mixture low-,medium-and high-dosage groups.Different concentrations of drug-containing serum were used to intervene cells.Cell proliferation was detected by CCK-8 method,apoptosis was detected by flow cytometry,and mRNA expressions of Bax,Bcl-2,Caspace-3,Caspace-9,N-myc downstream regulatory gene 2(NDRG2),Janus kinase 2(JAK2)and signal transduction and transcription activator 3(STAT3)were detected by RT-qPCR,Western blot was used to detect the protein expressions of Bax,Bcl-2,Caspace-3,Caspace-9,NDRG2,JAK2,STAT3,p-JAK2 and p-STAT3 in cells.Results Compared with the blank serum group,cell survival rate in methotrexate group,Quhan Zhufeng Mixture all dosage groups significantly decreased(P<0.01),the apoptosis rate significantly increased(P<0.01),the mRNA and protein expressions of Bax and Caspase-9 significantly increased(P<0.05,P<0.01),while the mRNA and protein expression of Bcl-2 significantly decreased(P<0.01),and Caspase-3 mRNA and protein expression in methotrexate group and Quhan Zhufeng Mixture medium-and high-dosage groups significantly increased(P<0.01).Compared with the blank serum group,the mRNA and protein expression of NDRG2 significantly increased in Quhan Zhufeng Mixture all dosage groups(P<0.05,P<0.01),the mRNA and protein expressions of JAK2 and STAT3 were significantly reduced in AG490 group and Quhan Zhufeng Mixture medium-and high-dosage groups(P<0.05,P<0.01),and the expressions of p-JAK2 and p-STAT3 proteins were significantly reduced(P<0.01).Conclusion Quhan Zhufeng Mixture can regulate the proliferation and apoptosis of RA-FLS by regulating the activity of NDRG2/JAK2/STAT3 signaling pathway,playing a role in treating rheumatoid arthritis.

Objective To explore the mechanism of Quhan Zhufeng Mixture on proliferation and apoptosis of rheumatoid arthritis fibroblast-like synoviocyte(RA-FLS)based on NDRG2/JAK2/STAT3 signaling pathway.Methods RA-FLS cells were cultured in vitro,and were divided into ① blank serum group,methotrexate group,Quhan Zhufeng Mixture low-,medium-and high-dosage groups;② blank serum group,AG490 group,Quhan Zhufeng Mixture low-,medium-and high-dosage groups.Different concentrations of drug-containing serum were used to intervene cells.Cell proliferation was detected by CCK-8 method,apoptosis was detected by flow cytometry,and mRNA expressions of Bax,Bcl-2,Caspace-3,Caspace-9,N-myc downstream regulatory gene 2(NDRG2),Janus kinase 2(JAK2)and signal transduction and transcription activator 3(STAT3)were detected by RT-qPCR,Western blot was used to detect the protein expressions of Bax,Bcl-2,Caspace-3,Caspace-9,NDRG2,JAK2,STAT3,p-JAK2 and p-STAT3 in cells.Results Compared with the blank serum group,cell survival rate in methotrexate group,Quhan Zhufeng Mixture all dosage groups significantly decreased(P<0.01),the apoptosis rate significantly increased(P<0.01),the mRNA and protein expressions of Bax and Caspase-9 significantly increased(P<0.05,P<0.01),while the mRNA and protein expression of Bcl-2 significantly decreased(P<0.01),and Caspase-3 mRNA and protein expression in methotrexate group and Quhan Zhufeng Mixture medium-and high-dosage groups significantly increased(P<0.01).Compared with the blank serum group,the mRNA and protein expression of NDRG2 significantly increased in Quhan Zhufeng Mixture all dosage groups(P<0.05,P<0.01),the mRNA and protein expressions of JAK2 and STAT3 were significantly reduced in AG490 group and Quhan Zhufeng Mixture medium-and high-dosage groups(P<0.05,P<0.01),and the expressions of p-JAK2 and p-STAT3 proteins were significantly reduced(P<0.01).Conclusion Quhan Zhufeng Mixture can regulate the proliferation and apoptosis of RA-FLS by regulating the activity of NDRG2/JAK2/STAT3 signaling pathway,playing a role in treating rheumatoid arthritis.

Pyroptosis is a novel,inflammatory programmed cell death mediated by gasdermins(GSDMs),which characterized by the formation of membrane pores and the release of pro-inflammatory cytokines.Rheumatoid arthritis(RA)is a chronic,inflamma-tory autoimmune disease characterized by persistent synovitis in multiple joints,progressive destruction of bone and cartilage,and eventually leading to joint deformity and disability.Recently,it has been shown that pyroptosis plays an important role in development of RA.This review summarizes the molecular mechanism of pyroptosis,its pathogenic role and therapeutic strategies in RA,aiming of providing new insights for the mechanism research and new drug development of RA.

Objective Through a multi-software visual analysis of the literature on the influence of T cells on rheumatoid arthritis(RA)in recent ten years,the research hotspot and frontier development in this field were summarized.Methods The Chinese and English literature on the influence of T cells on RA from 2012 to 2022 years was retrieved from CNKI and Web of Science database as the research object.CiteSpace and VOSviewer software were used to analyze the number of publications,authors and keywords.Results 519 articles in Chinese and 861 in English were retrieved.The results showed that the number of articles in Chinese increased slowly from 2020 to 2022 years,while the overall trend in English was stable.Keyword analysis shows that it is predicted that future research in this field will focus on the pathogenesis of T cells in RA,the mechanism of bone destruction in RA,disease activity,oxidative stress.Conclusion The influence of T cells on RA has attracted much attention in the past,present and future,and has great research value.However,due to the differences in research priorities at home and abroad,the teams should interact positively and communicate with each other to reveal the internal mechanism of RA and provide theoretical basis for targeted therapy.

Rheumatoid arthritis is a common clinical autoimmune disease characterized by persistent synovitis and pannus formation. In late stage， irreversible destruction and deformation of bone and joint may occur. In this paper， the authors believe that kidney deficiency and essence deficiency is the core mechanism of rheumatoid arthritis bone destruction， and its disease evolution law is summarized as "marrow reduction， flesh flaccid， collaterals blocked". On the basis of modern medical understanding of bone destruction in rheumatoid arthritis， it is considered that the mechanism in Chinese medicine of "marrow reduction， flesh flaccid， collaterals blocked" ultimately leads to bone destruction， is similar to that in the western medicine of abnormal differentiation of osteoclasts， high expression of nuclear factor-κB receptor activator of ligand， and abnormal expression of inflammatory factors. This point of view may provide a more comprehensive and scientific understanding of the key pathogenic mechanism of bone destruction in rheumatoid arthritis.