Background: and Purpose Live cell-based assays (LCBA) are increasingly used for serological antibody detection due to their ability to preserve antigen conformation, offering moderately higher sensitivity than fixed cell-based assays. However, the clinical necessity of prioritizing LCBA for the detection of aquaporin-4 immunoglobulin G (AQP4-IgG) in neuromyelitis optica spectrum disorder (NMOSD) remains unclear, especially when compared to its established role in diagnosing myelin oligodendrocyte glycoprotein antibody-associated disease. Methods: We compared the performance of live cell-based assays using immunofluorescence (LCBA-IF) and fixed cell-based assays using immunofluorescence (FCBA-IF) in detecting AQP4-IgG in 90 cases of NMOSD meeting 2015 International Panel for Neuromyelitis Optica Diagnosis criteria, alongside 40 controls. Additionally, we further investigated the relationship between AQP4-IgG titers as measured by LCBA-IF and FCBA-IF and clinical parameters in NMOSD patients. Results: Results showed 96.9% agreement between LCBA-IF and FCBA-IF (Cohen’s κ=0.935), with a strong Spearman correlation (0.977, p<0.001). Both methods demonstrated 100% specificity, with LCBA-IF showing slightly higher sensitivity compared to FCBA-IF. Within LCBAIF-tested groups, statistically significant differences in annualized relapse rates were observed across all pairwise comparisons (low-titer vs. moderate-titer, low-titer vs. high-titer, and moderate-titer vs. high-titer; all p<0.050). However, this association reached statistical significance in some FCBA-IF-tested groups. Conclusions Overall, there is a strong concordance between LCBA-IF and FCBA-IF in detecting AQP4-IgG, where LCBA-IF shows slightly higher sensitivity. Furthermore, there is a potential link between elevated AQP4-IgG titers and an increased risk of relapse, and this correlation may appear more pronounced when using LCBA-IF.

Tissue repair requires the reconstruction of functional vascular networks to restore oxygen and nutrient delivery, eliminate metabolic waste, and maintain tissue homeostasis. Although biochemical factors such as growth factors and cytokines have been extensively studied in vascular regeneration, increasing evidence indicates that mechanical signals from the extracellular matrix (ECM) are equally important regulators of angiogenesis. Matrix stiffness, as a major biomechanical property of the tissue microenvironment, provides critical information that influences endothelial cell (EC) behavior and vascular remodeling through mechanotransduction. However, the biological effects of matrix stiffness are not universally defined as either pro- or anti-angiogenic, but are highly dependent on tissue context, cellular composition, disease progression, and the dynamic changes occurring during tissue repair. Therefore, understanding how matrix stiffness regulates vascular regeneration is essential for developing more precise strategies for tissue engineering and regenerative medicine. In this review, we summarize recent advances in the regulation of angiogenesis by matrix stiffness during tissue repair from multiple perspectives. First, we discuss the direct effects of matrix stiffness on EC behaviors, including differentiation, morphological remodeling, migration, proliferation, barrier maintenance, and vascular network formation. ECs sense mechanical alterations in the surrounding matrix through various mechanosensitive structures, including integrins, focal adhesion complexes, and mechanosensitive ion channels such as Piezo1 and TRPV proteins. These mechanical signals are subsequently transmitted through intracellular pathways involving FAK, RhoA/ROCK, MAPK, and Hippo-YAP/TAZ signaling, leading to cytoskeletal reorganization and transcriptional regulation. Through these mechanisms, matrix stiffness regulates endothelial functional states and determines the balance between regenerative vascular formation and pathological vascular remodeling. Beyond the direct regulation of ECs, we further highlight the importance of stiffness-mediated intercellular communication within the regenerative microenvironment. Matrix stiffness can regulate the behavior and secretory profiles of vascular-associated cells, including mesenchymal stem cells and macrophages, thereby indirectly affecting endothelial function through paracrine mechanisms. Changes in matrix mechanics influence the secretion of angiogenic factors, inflammatory cytokines, and extracellular vesicles from these cells, creating a mechanical regulation network that coordinates vascular regeneration. This perspective extends the traditional concept of matrix stiffness from a physical support structure to an active regulatory signal that integrates multiple cellular responses during tissue repair. Furthermore, we discuss the tissue-specific effects of matrix stiffness in vascular regeneration across different organs, including the aorta, lung, liver, and heart. Although excessive matrix stiffening is frequently associated with fibrosis and vascular dysfunction, the consequences of mechanical changes vary considerably among tissues. Moderate stiffness alterations may support endothelial activation and vascular stabilization in certain regenerative contexts, whereas persistent pathological stiffening can promote inflammation, endothelial dysfunction, and impaired vascular repair. These findings emphasize that the biological meaning of “soft” and “stiff” microenvironments should be interpreted according to specific tissue and experimental conditions rather than as universal mechanical classifications. Finally, we summarize current challenges and future perspectives in this field. A major limitation is the lack of standardized mechanical characterization among different studies, as stiffness measurements are influenced by material properties, testing methods, and experimental conditions, limiting direct comparison across research systems. Moreover, most existing models fail to fully reproduce the dynamic and viscoelastic properties of native ECM during tissue regeneration. Future studies should combine advanced biomaterials with standardized mechanical analysis, organoid models, and multi-omics approaches to establish more accurate mechanical regulatory maps. Overall, this review proposes that matrix stiffness is not merely a structural feature of tissues, but an active biological signal that regulates vascular regeneration through coordinated mechanotransduction and multicellular interactions. A deeper understanding of stiffness-mediated vascular regulation will provide new theoretical insights and therapeutic opportunities for improving tissue repair outcomes.

Objective To establish a chromatography-tandem mass spectrometry method for detecting chlorfenapyr and its metabolite tralopyril in blood,and to investigate the toxicokinetics in rats.Methods Chlorfenapyr(8 mg/kg)was administered orally to rats,and blood samples were collected from rats'canthus vein at 5 min,15 min,30 min,1 h,3 h,6 h,12 h,24 h and 48 h after administration.The blood samples were extracted using 100 μL of 5%formic acid solution and 400 μL of acetonitrile.Chlorfena-pyr was qualitatively and quantitatively detected by triple quadrupole gas chromatography-tandem mass spectrometry(GC-MS/MS)and tralopyril was detected by triple quadrupole liquid chromatography-tandem mass spectrometry(LC-MS/MS).The DAS 3.0 software was used to fit the toxicokinetic equa-tions and calculate the toxicokinetic parameters.Results Chlorfenapyr was detectable from 5 min to 24 h with a peak time of 1 h.Tralopyril was detectable from 15 min to 48 h with a peak time of 3 h.The toxicokinetic process of chlorfenapyr in rat blood conformed to a first-order absorption one-compartment open model,with the toxicokinetic equation described as C=e-0.265t-e-0.175t.Tralopyril con-formed to the first-order absorption three-compartment model,and the toxicokinetic equation was C=47 361.069e-2.209t-35 404.962e-1.486t+11 956.363e-0.512t.In the equations,C stands for the concentration of the target substance in the blood,e is the natural constant(≈2.718 28),and t stands for time.Conclu-sion This study optimized the detection method for chlorfenapyr and its metabolite tralopyril in blood.The toxicokinetic equations and parameters of chlorfenapyr and tralopyril can provide a reference for the estimation of oral intake time of chlorfenapyr.

China has become the country with the highest global burden of heart failure(HF).Despite the widespread use of prognostic-improving medications today,the mortality rate of HF remains high,reaching 13.7％at one year-particularly among patients with heart failure with reduced ejection fraction(HFrEF).HF interventional device therapy(structural intervention)targets the structural factors underlying HF,including atrial pressure,ventricular remodeling,and valvular intervention.It leverages the heart's intrinsic physiological properties and pathological progression mechanisms to deliver treatments through interventions without external active forces,achieving anatomical or functional repair.This field has emerged as a rapidly growing area and plays an increasingly critical role in HF management.This article provides a comprehensive review and summary of the latest advancements in HF and cardiomyopathy interventional therapy over the past year.It covers various novel technologies and products currently in the research phase,aiming to provide an in-depth analysis of the current status and future directions of HF interventional therapy,and further advance the development of this discipline.

Objective:To explore the advantages of internet-based smart healthcare for full-cycle transcatheter edge-to-edge repair (TEER) management in reducing postoperative adverse events rate, improving cardiac function, and enhancing quality of life.Methods:This retrospective study enrolled patients with mitral regurgitation who underwent transcatheter TEER at Beijing Anzhen Hospital Valve Intervention Center between June 2021 and September 2023. Patients were classified into degeneration mitral regurgitation (DMR) and functional mitral regurgitation (FMR) according to etiology, with further stratification by enrollment period into usual care group (June 2021 to October 2022) and full-cycle management group (November 2022 to September 2023). The 1-year postoperative follow-up data were collected and compared between subgroups with the same etiology. Kaplan-Meier survival curves were plotted, and log-rank tests were used to compare the differences in major endpoint event-free survival rates between the two groups. Univariate and multivariate Cox regression and logistic regression analyses were performed to evaluate the impact of the full-cycle management system on patients′ outcomes.Results:A total of 130 patients were included, aged (72.0±8.6) years, including 82 (63%) males. DMR was identified in 84 cases (40 in the usual care group and 44 in the full-cycle management group), while FMR was observed in 46 cases (27 in the usual care group and 19 in the full-cycle management group). Kaplan-Meier analysis demonstrated higher 1-year major endpoint event-free survival rates in the full-cycle management group compared to the usual care group, though the difference was not statistically significant (log-rank P>0.05). Compared to the usual care group, the full-cycle management group showed significantly higher proportions of New York Heart Association classification Ⅰ-Ⅱ patients (DMR: 67% vs. 52%, P=0.031; FMR: 68% vs. 52%, P=0.021), greater 6-minute walking distances (DMR: (346.39±70.41) m vs. (294.11±60.47) m, P=0.012; FMR: (356.60±54.68) m vs. (318.55±39.02) m, P=0.004), and superior Kansas City Cardiomyopathy Questionnaire scores (DMR: 81.50 (74.50, 85.00) points vs. 71.00 (66.00, 82.25) points, P=0.014; FMR: 83.00 (76.00, 85.00) points vs. 74.00 (70.75, 80.00) points, P=0.030). Multivariate logistic regression confirmed the full-cycle management system as an independent predictor for the above improved outcomes (all P<0.05). Conclusion:Smart healthcare-based full-cycle management improves cardiac function and quality of life in mitral regurgitation patients after TEER, demonstrating lower rates of major endpoint events compared to usual care.

Spine fracture and dislocation are common traumatic spinal conditions that often require surgical intervention due to compromised spinal stability. Surgical approaches include anterior, posterior, and combined anterior-posterior spinal procedures. According to the specific surgical requirements, patients may be placed in the prone position or repositioned between prone and supine positions during surgery. Intraoperative repositioning has become an essential step in patient positioning. However, during repositioning, patients with spinal fracture and dislocation are at increased risk for complications such as hemodynamic instability, nerve injury, and pressure injuries to the skin and soft tissue. Notably, due to the instability of the spinal cord, even minor manipulations can further exacerbate the damage, potentially leading to severe outcomes like paraplegia. Although the current clinical guidelines provide instructive recommendations for standard position, there remains no specific protocols for intraoperative repositioning in patients with spine fracture and dislocation. With a concern for the lack of clinical studies on positioning techniques, risk prevention, and operational norms for special patients, no applicable guidelines or standards are available. A consensus was required to provide clinical reference, meet the requirements of surgical treatment, and minimize the safety risks of patients caused by improper placement of positions. Professional Committee of Operating Room Nursing of Shaanxi Nursing Association organized experts in nursing management and operating room nursing from major hospitals across China to formulate Expert consensus on intraoperative repositioning for patients with spinal fracture and dislocation ( version 2025). The consensus provides 11 recommendations covering pre-repositioning preparation, intraoperative maneuvers, and post-repositioning observation, aiming to provide references for clinical standardization of the intraoperative repositioning process and protection of patients′ safety.

Objective:To investigate the clinical and pathological characteristics of primary thoracic synovial sarcoma (PTSS).Methods:Forty-two PTSS cases diagnosed at the Department of Pathology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China from October 2011 to April 2024 were analyzed. All cases were retrospectively studied using hematoxylin-eosin staining and immunohistochemistry. Their clinicopathological features were also reviewed. SS18 rearrangement was assessed in 28 cases using fluorescence in situ hybridization (FISH). Next generation sequencing (NGS) was performed on 8 cases.Results:Among the 42 cases, there were 23 biopsies and 19 surgically-removed specimens. One case was a specimen resected after neoadjuvant chemotherapy. There were 22 males and 20 females, with an age ranging from 6 to 68 years. Twenty-nine cases occured in the lung, 6 in mediastinum, 4 in pericardium, 1 in visceral pleura, and 1 in right atrium. One case did not show any unequivocal primary site. Computed tomography showed the tumors were manifested as a cystic mass, a solid mass, or thickening of the pleura and pericardium. Thirty-two cases had respiratory symptoms, while 19 had pleural effusion. One case had a history of radiotherapy for papillary thyroid carcinoma. Nineteen patients were treated with surgery, while 19 were treated with chemotherapy without surgery. Four patients were diagnosed and discharged, without specific treatment on the record. Morphologically, 1 case was biphasic type, 39 cases were monophasic type, and 2 cases were poorly differentiated type. In addition to the typical morphology of synovial sarcoma, tumors also showed pulmonary bullous changes, stromal collagen hyalinization, hemangiopericytoma-like vasculature, stromal edematous myxoid changes, and microcystic structure. Immunohistochemically, all cases were diffusely positive for TRPS1 (22/22), TLE1 (21/22), CD99 (26/26), SS18-SSX (25/25) and INI1 (12/12), including 3 cases with decreased expression of INI1. Twenty-one cases were focally positive for EMA (21/30), 4 cases for SMA (4/23), 2 cases for S-100 (2/28), and 2 cases (2/35) for CKpan. Twenty-eight cases (28/28) had SS18 rearrangement displaying a split signal on FISH analysis. Eight cases were found to have mutations in SMC1A, NOTCH2, CDK12, SPRY4, BRCA1, STK11, NF2, and PDGFRα genes using NGS. Eighteen of the 29 patients survived and 16 showed disease progression.Conclusions:PTSS is more commonly found in the lungs than other sites and has non-classical morphological features of various types, which need to be differentiated from other tumors. TRPS1 is highly expressed in PTSS and has certain diagnostic values. The diagnosis of PTSS also requires combination of patient′s medical history with thorough imaging studies.

Objective:To summarize the clinical manifestations of anti-synthetase syndrome (ASS) with interstitial lung disease (ILD) patients with different antibody subtypes and the skeletal muscle pathology of ASS.Methods:A total of 106 ASS-ILD patients admitted to the First Medical Center of Chinese People′s Liberation Army General Hospital from May 11, 2015 to June 25, 2023 were included. Their intramuscular and extramuscular clinical manifestations were collected. The correlation between different antibody subtypes in patients with ASS and the various subtypes of ILD was investigated. The skeletal muscle pathological characteristics of 13 ASS patients were also summarized.Results:Among the 106 ASS-ILD patients, 56 (52.8%) were anti-JO-1 antibody positive, 19 (17.9%) were anti-PL-7 antibody positive, 11 (10.4%) were anti-PL-12 antibody positive, 14 (13.2%) were anti-EJ antibody positive, and 6 (5.7%) were anti-OJ antibody positive. All the patients had ILD [including nonspecific interstitial pneumonia (NSIP), usual interstitial pneumonia (UIP), organizing pneumonia (OP), mixed pneumonia]. In all the patients, 46.2% (49/106) had cardiac damage, 37.7% (40/106) had arthritis, 29.2% (31/106) had myasthenia gravis, 24.5% (26/106) had myalgia, and 19.8% (21/106) had Raynaud′s phenomenon. The incidence of NSIP was 75.0% (42/56) in the anti-JO-1 antibody-positive group, significantly higher than other groups (anti-PL-7 antibody-positive group, 8/19;anti-PL-12 antibody-positive group, 3/11;anti-EJ antibody-positive group, 5/14;anti-OJ antibody-positive group, 2/6; P=0.001). UIP was most common in the anti-PL-7 antibody-positive group (8/19). OP was most frequent in the anti-PL-12 antibody-positive group (5/11). The incidence of arthritis was highest in the anti-JO-1 antibody-positive group (51.8%, 29/56). The anti-Ro-52 antibody-positive rate was significantly higher in the anti-EJ antibody-positive group (12/14) than in the other 4 groups [anti-JO-1 antibody-positive group, 33.9% (19/56); anti-PL-7 antibody-positive group, 10/19; anti-PL-12 antibody-positive group, 6/11; anti-OJ antibody-positive group, 0/6; P=0.001]. ASS skeletal muscle pathology was manifested as necrotizing myopathy pattern (6/13), inflammatory myopathy pattern (4/13), and nonspecific myopathy pattern (3/13). All the 106 patients received methylprednisolone as the basic treatment. Among them, 69 patients (65.1%) received methylprednisolone alone, while 37 patients (34.9%) received combination therapy involving immunosuppressants, whose symptoms improved after treatment. Conclusions:A discernible correlation exists between the clinical manifestations of ASS with ILD and specific antibody subtypes. ASS patients generally respond well to immunotherapy. ASS can manifest as 3 distinct skeletal muscle pathological patterns: necrotizing myopathy pattern, inflammatory myopathy pattern, and nonspecific myopathy pattern.

Objective:To investigate lipid metabolism gene mutations and pathogenicity of hypertriglyceridemia acute pancreatitis (HTG-AP) patients.Methods:Clinical data of 495 HTG-AP patients admitted from June 2018 to June 2020 in the center for severe acute pancreatitis of Eastern Theater General Hospital were retrospectively analyzed. Whole-exome sequencing and mutation verification were performed by next-generation sequencing technology and Sanger sequencing. The pathogenicity of gene mutation was analyzed by population mutation ratio, pathogenicity prediction software, conservation scoring software, protein structure prediction, and in vitro experiments. Results:The mutation ratio of lipid metabolism-related genes, namely LPL, APOA5, LMF1, GPIHBP1, and APOC2, were 14.81%, 55.78%, 43.61%, 1.62%, and 0.61%, respectively. Among them, 44 heterozygous mutations in LPL gene were detected including 36 missense mutations, 5 nonsense mutations and 3 frameshift mutations, which were all rarely carried in single patient. Six HTG-AP patients carried the LPL gene heterozygous mutation c.835C>G (p.Leu279Val). The mean level of serum triglyceride at the onset of HTG-AP was 27.4 mmol/L. All of them had a history of recurrent HTG-AP, and most of them had severe acute pancreatitis. The serum LPL concentration and activity were lower than the normal level. The pathogenicity analysis results suggested that the LPL p.Leu279Val was a rare, highly possible pathogenic and highly conserved gene mutation. The in vitro results showed that the LPL p.Leu279Val could significantly reduce the synthesis and secretion ability of LPL as well as its enzymatic activity. Conclusions:The mutation ratio of lipid metabolism-related genes, including LPL, APOA5, LMF1, GPIHBP1, and APOC2, are relatively high in the HTG-AP patients. The LPL p.Leu279Val is a rare and highly possible pathogenic gene mutation, which may lead to recurrent episodes of HTG-AP.

Objective:To investigate the impact of plasmapheresis therapy on the clinical efficacy in predicted severe hypertriglyceridemia-associated acute pancreatitis (HTG-AP) patients.Methods:The clinical data of 500 HTG-AP patients admitted to 36 medical centers across China in the Chinese Acute Pancreatitis Clinical Trials Group-PERFORM database from November 2020 to June 2023 were retrospectively analyzed. Besides the inclusion and exclusion criteria from PERFORM study, patients who had acute physiology and chronic health evaluation Ⅱ (APACHEⅡ) score ≥8 or CRP>150 mg/L on admission were included in the final analyses ( n=189). Patients were categorized into the plasmapheresis group ( n=51) and the routine treatment group ( n=138) according to the triglyceride-lowering therapies they received. General data, laboratory findings, AP severity, and clinical outcomes were recorded. Results:Patients undergoing plasmapheresis had higher initial triglyceride levels, APACHEⅡ score, SOFA score, and more organ failure than those receiving routine medical treatment. Results of multivariable logistic regression models showed that the plasmapheresis group, as compared to the routine treatment group, was neither associated with decreased risk of persistent organ failure within 14 days [54.9% (28/51) vs 37.7% (52/138), OR=0.89, 95% CI 0.36-2.21, P=0.810], nor with reduced incidence of organ failure on day 7 [17.7% (9/51) vs 15.9% (22/138), OR=0.60, 95% CI 0.19-1.88, P=0.378]. There was no significant difference on the dynamic changes of serum triglyceride within the first three days of admission ( P=0.108). Conclusions:Early plasmapheresis is not associated with reduced incidence of persistent organ failure in predicted severe HTG-AP patients.