Objective:To explore the clinical characteristics, diagnosis and treatment strategies, and prognosis of pulmonary embolism (PE) complicating childhood rheumatic diseases.Methods:A retrospective case series study was performed on the demographic data, laboratory indicators, imaging features, treatment regimens, and follow-up data of 8 children with rheumatic diseases complicated by PE who were admitted to the Department of Rheumatology and Immunology, Capital Center for Children′s Health, Capital Medical University from January 2014 to October 2023.Results:Among the 8 children, there were 4 boys and 4 girls, with an age of 12.0 (7.5, 13.0) years. Among the primary diseases, there were 3 cases of systemic lupus erythematosus, 2 cases of Beh?et′s disease, 2 cases of Takayasu arteritis, and 1 case of antiphospholipid syndrome. All children developed PE during the active phase of the primary disease. PE was detected at the onset of the primary disease in 3 cases, and the median time from the diagnosis of the primary disease to the development of PE was 10.0 (6.0, 25.0) months in the remaining 5 cases. Fever was present in all 8 children, 4 cases were accompanied by chest tightness, dyspnea, etc., and 2 cases only presented with fever. Laboratory examinations revealed the following results: erythrocyte sedimentation rate was 42.0 (17.0, 78.0) mm/1 h, high-sensitivity C-reactive protein was 12.7 (2.6, 78.7) mg/L, white blood cell count was 9.6 (7.2, 18.7)×10 9/L; D-dimer was 2.3 (0.9, 6.2) mg/L; and hemoglobin was (109±16) g/L.Imaging examinations revealed that 5 cases had involvement of the bilateral lower pulmonary arteries, 5 cases had peripheral embolism, and 3 cases had central PE. Complications included 3 cases of deep vein thrombosis, 2 cases of intracranial venous sinus thrombosis, and 1 case of mild pulmonary hypertension.In terms of treatment, 7 cases received anticoagulation with heparin followed by warfarin. Immunomodulation was mainly based on glucocorticoids combined with immunosuppressants, and 4 cases were combined with biological agents. The follow-up time of 4.17 (1.75, 7.17) years, the time for complete absorption of PE was 10.5 (6.0, 18.0) months; all 8 children had no target events, with no recurrence or chronic thromboembolic pulmonary hypertension, and the pulmonary artery remodeling was good. Conclusions:PE complicating childhood rheumatic diseases is closely related to the activity of the primary disease. The clinical manifestations are insidious, with fever as the main symptom. Imaging examination is the key to diagnosis.Early adoption of heparin followed by warfarin anticoagulation and glucocorticoids combined with immunosuppressants and (or) biological agents to control the primary disease can achieve a favorable prognosis.

Objective:To explore the clinical characteristics, diagnosis and treatment strategies, and prognosis of pulmonary embolism (PE) complicating childhood rheumatic diseases.Methods:A retrospective case series study was performed on the demographic data, laboratory indicators, imaging features, treatment regimens, and follow-up data of 8 children with rheumatic diseases complicated by PE who were admitted to the Department of Rheumatology and Immunology, Capital Center for Children′s Health, Capital Medical University from January 2014 to October 2023.Results:Among the 8 children, there were 4 boys and 4 girls, with an age of 12.0 (7.5, 13.0) years. Among the primary diseases, there were 3 cases of systemic lupus erythematosus, 2 cases of Beh?et′s disease, 2 cases of Takayasu arteritis, and 1 case of antiphospholipid syndrome. All children developed PE during the active phase of the primary disease. PE was detected at the onset of the primary disease in 3 cases, and the median time from the diagnosis of the primary disease to the development of PE was 10.0 (6.0, 25.0) months in the remaining 5 cases. Fever was present in all 8 children, 4 cases were accompanied by chest tightness, dyspnea, etc., and 2 cases only presented with fever. Laboratory examinations revealed the following results: erythrocyte sedimentation rate was 42.0 (17.0, 78.0) mm/1 h, high-sensitivity C-reactive protein was 12.7 (2.6, 78.7) mg/L, white blood cell count was 9.6 (7.2, 18.7)×10 9/L; D-dimer was 2.3 (0.9, 6.2) mg/L; and hemoglobin was (109±16) g/L.Imaging examinations revealed that 5 cases had involvement of the bilateral lower pulmonary arteries, 5 cases had peripheral embolism, and 3 cases had central PE. Complications included 3 cases of deep vein thrombosis, 2 cases of intracranial venous sinus thrombosis, and 1 case of mild pulmonary hypertension.In terms of treatment, 7 cases received anticoagulation with heparin followed by warfarin. Immunomodulation was mainly based on glucocorticoids combined with immunosuppressants, and 4 cases were combined with biological agents. The follow-up time of 4.17 (1.75, 7.17) years, the time for complete absorption of PE was 10.5 (6.0, 18.0) months; all 8 children had no target events, with no recurrence or chronic thromboembolic pulmonary hypertension, and the pulmonary artery remodeling was good. Conclusions:PE complicating childhood rheumatic diseases is closely related to the activity of the primary disease. The clinical manifestations are insidious, with fever as the main symptom. Imaging examination is the key to diagnosis.Early adoption of heparin followed by warfarin anticoagulation and glucocorticoids combined with immunosuppressants and (or) biological agents to control the primary disease can achieve a favorable prognosis.

Objective:To analyze the clinical features of patients with traumatic optic neuropathy (TON) and to explore its clinical patterns and treatment outcomes.Methods:A retrospective analysis was conducted on data from 323 patients (334 eyes) with TON, who were treated in the Department of Otorhinolaryngology Head and Neck Surgery, the Affiliated Hospital of Qingdao University from April 1999 to October 2024. Among these patients, 288 were male and 35 were female, with ages ranging from 4 to 70 years. All patients were followed up for a period of 6 to 24 months, with the final follow-up visual acuity recorded as the ultimate visual outcome. The visual acuity evaluation criteria were classified into five levels: no light perception, light perception, hand movement in front of the eye, counting fingers at 1 meter, and "chart-visible acuity". A treatment outcome was deemed effective if the post-treatment visual acuity improved by one level or more compared to pre-treatment, or if the chart-visible acuity improved by two lines or more on the logMAR chart. The clinical characteristics of patients, causes of injury, complications, treatment methods, and changes in visual acuity before and after treatment were summarized. Logistic regression analyses were performed to identify the influencing factors affecting treatment efficacy.Results:TON occurred mostly in young (215/323, 66.56%) males (288/323, 89.16%), the majority of patients came from villages and towns (236/323, 73.07%). Traffic accidents (232/323, 71.83%) remained the main etiology. Most patients had craniofacial injuries and other bodily injuries. The effective rate of vision improvement was 50.30% (168/334). Multiple logistic regression analyses identified that residual vision (light perception or better) at presentation ( OR=3.26, P<0.001) and receiving treatment within 7 days after injury ( OR=2.04, P=0.008) were protective factors on visual acuity recovery, while the presence of orbital wall fracture was a risk factor for visual acuity recovery ( OR=0.26, P<0.001). Additionally, undergoing surgical treatment was a protective factor for visual improvement in patients with no light perception ( OR=2.94, P=0.007). For patients with residual vision at presentation, orbital wall fracture was a significant risk factor ( OR=0.28, P=0.009). Conclusions:TON is more prevalent in young males and is primarily caused by traffic accidents, leading to a poor prognosis. Timely medical intervention following injury significantly influences prognostic outcomes. Early surgical intervention (within 7 days) is recommended, particularly for patients with no light perception at presentation.

Objective To develop a risk prediction model for ischemic stroke in symptomatic intracranial atherosclerotic stenosis(ICAS)patients based on high-resolution magnetic resonance imaging(HR-MRI)and arterial spin labeling(ASL)imaging.Methods A total of 142 patients were included and divided into acute ischemic stroke(AIS)and transient ischemic attack(TIA)groups based on stroke occurrence.Clinical risk factors,plaque characteristics,and arterial transit artifact(ATA)presence on ASL images were compared between the two groups.Multivariate logistic regression analysis was performed,incorporating clinical risk factors,plaque characteristics,and double post labeling delay(PLD)ATA presence.The predictive value of different models was compared using receiver operating characteristic(ROC)curve and DeLong tests.Results Hypertension,positive lumen remodeling,plaque enhance-ment rate,1.5 s-ATA presence,and 2.5 s-ATA presence were independent risk factors for AIS(P＜0.05).The combination of HR-MRI and ASL imaging predicted AIS most effectively[area under the curve(AUC)=0.908;95％ confidence interval(CI)0.862-0.954].No significant difference was found between the prediction performances of HR-MRI and ASL(95％CI-0.041-0.082,Z=0.659,P=0.509).Conclusion ASL is more convenient than HR-MRI for predicting ischemic stroke in ICAS patients.A model combining plaque characteristics and ATA presence effectively predicts AIS occurrence.

Objective To develop a risk prediction model for ischemic stroke in symptomatic intracranial atherosclerotic stenosis(ICAS)patients based on high-resolution magnetic resonance imaging(HR-MRI)and arterial spin labeling(ASL)imaging.Methods A total of 142 patients were included and divided into acute ischemic stroke(AIS)and transient ischemic attack(TIA)groups based on stroke occurrence.Clinical risk factors,plaque characteristics,and arterial transit artifact(ATA)presence on ASL images were compared between the two groups.Multivariate logistic regression analysis was performed,incorporating clinical risk factors,plaque characteristics,and double post labeling delay(PLD)ATA presence.The predictive value of different models was compared using receiver operating characteristic(ROC)curve and DeLong tests.Results Hypertension,positive lumen remodeling,plaque enhance-ment rate,1.5 s-ATA presence,and 2.5 s-ATA presence were independent risk factors for AIS(P＜0.05).The combination of HR-MRI and ASL imaging predicted AIS most effectively[area under the curve(AUC)=0.908;95％ confidence interval(CI)0.862-0.954].No significant difference was found between the prediction performances of HR-MRI and ASL(95％CI-0.041-0.082,Z=0.659,P=0.509).Conclusion ASL is more convenient than HR-MRI for predicting ischemic stroke in ICAS patients.A model combining plaque characteristics and ATA presence effectively predicts AIS occurrence.

Single-cell assay for transposase-accessible chromatin sequencing(scATAC-seq)is a power-ful technique for studying cellular heterogeneity and gene regulatory networks,widely applied in epigenet-ic research.However,the complexity of data analysis workflows and high programming requirements have limited its broader adoption among non-programmer researchers.To address this issue,we developed Sig-nac.UIO,a modular and visual scATAC-seq analysis platform based on the R Shiny framework,integra-ting mainstream tools such as Signac and Seurat.The platform includes ten key modules covering quality control,cell filtering,dimensionality reduction,clustering,differential analysis,cell annotation,path-way enrichment,motif analysis,and transcription factor footprinting.Through a graphical user interface,users can perform full analyses and obtain interactive visualization results.The platform's stability and u-tility have been validated using a public PBMC dataset and it is currently deployed online(https://xula-bgdpu.org.cn/Signac.UIO),providing an efficient and user-friendly tool for single-cell epigenomics re-search.

Aim To investigate the effect of cordycepin(COR)on gentamicin(GEN)-induced nephrotoxicity and the molecular mechanism of inhibiting oxidative stress and ferroptosis induced by GEN.Methods The oral SD rats were divided into a control group,GEN group,and GEN+COR group.Following the success-ful setting up of the animal model,the serum creatinine(CR)and urea nitrogen(BUN)levels of rats were measured,and renal tissue injury was assessed using HE staining.In addition,the contents of malondialde-hyde and glutathione in kidney tissues of SD rats in each group were detected,and the expressions of fer-roptosis markers GPX4 and SLC7A11 were analyzed by Western blot.Results Compared with the control group,CR and BUN in GEN-stimulated group signifi-cantly increased(P＜0.01),and the level of CR and BUN was effectively reduced after 50 mg·kg-1 COR oral administration.HE results also showed that COR could alleviate the kidney tissue damage caused by GEN.COR could reverse the increase of malondialde-hyde level and the decrease of glutathione level caused by GEN in rat kidney tissue,and COR could restore the decrease of GPX4 and SLC7A11 protein levels induced by GEN.Conclusion COR can reduce GEN-induced kidney injury by inhibiting oxidative stress and ferrop-tosis.

Aim To investigate the role and underlying mechanisms of transient receptor potential cation chan-nel 6(TRPC6)in epileptogenesis using a kainic acid(KA)-induced mouse model.Methods C57BL/6 and TRPC6-KO(KO)mice were divided into two groups and implanted with cannulas for microinjection of KA(0.03 g·L-1,5 μL)into the lateral ventricle to establish the acute epilepsy model group,with saline injection serving as the control group.The Racine score was used to record the uninterrupted seizure grade of mice within two hours after KA administration.Immunohistochemistry was used to detect neuronal loss and tissue damage in the hippocampus brain region of mice.Immunofluorescence staining,Western blot and qPCR were used to detect the expressions of TRPC6,NLRP3,ASC,Caspase-1,p62,Atg7,Atg5,Beclin-1,LC3b-Ⅱ/LC3b-Ⅰ.in the hippocampus.Results KA induced significant neuronal loss and tissue damage in the hippocampal CA3 brain region of epilep-sy mice,while the expression levels of TRPC6,NL-RP3,ASC and Caspase-1 and other proteins in the hippocampus brain area of epilepsy mice increased,and the protein expression of autophagy-related proteins Atg7,Atg5,Beclin-1,LC3b-Ⅱ/LC3b-Ⅰ increased,while the expression of p62 protein decreased.TRPC6 knockout exacerbated KA-induced epileptogenesis,neuronal injury,inflammatory response and autophagy activation.Conclusion TRPC6 is involved in KA-in-duced epileptigenesis,and the mechanism may be re-lated to the activation of NLRP3 inflammasome-autoph-agy signaling caused by TRPC6 deletion.

Aim To investigate the role and underlying mechanisms of transient receptor potential cation chan-nel 6(TRPC6)in epileptogenesis using a kainic acid(KA)-induced mouse model.Methods C57BL/6 and TRPC6-KO(KO)mice were divided into two groups and implanted with cannulas for microinjection of KA(0.03 g·L-1,5 μL)into the lateral ventricle to establish the acute epilepsy model group,with saline injection serving as the control group.The Racine score was used to record the uninterrupted seizure grade of mice within two hours after KA administration.Immunohistochemistry was used to detect neuronal loss and tissue damage in the hippocampus brain region of mice.Immunofluorescence staining,Western blot and qPCR were used to detect the expressions of TRPC6,NLRP3,ASC,Caspase-1,p62,Atg7,Atg5,Beclin-1,LC3b-Ⅱ/LC3b-Ⅰ.in the hippocampus.Results KA induced significant neuronal loss and tissue damage in the hippocampal CA3 brain region of epilep-sy mice,while the expression levels of TRPC6,NL-RP3,ASC and Caspase-1 and other proteins in the hippocampus brain area of epilepsy mice increased,and the protein expression of autophagy-related proteins Atg7,Atg5,Beclin-1,LC3b-Ⅱ/LC3b-Ⅰ increased,while the expression of p62 protein decreased.TRPC6 knockout exacerbated KA-induced epileptogenesis,neuronal injury,inflammatory response and autophagy activation.Conclusion TRPC6 is involved in KA-in-duced epileptigenesis,and the mechanism may be re-lated to the activation of NLRP3 inflammasome-autoph-agy signaling caused by TRPC6 deletion.

Single-cell assay for transposase-accessible chromatin sequencing(scATAC-seq)is a power-ful technique for studying cellular heterogeneity and gene regulatory networks,widely applied in epigenet-ic research.However,the complexity of data analysis workflows and high programming requirements have limited its broader adoption among non-programmer researchers.To address this issue,we developed Sig-nac.UIO,a modular and visual scATAC-seq analysis platform based on the R Shiny framework,integra-ting mainstream tools such as Signac and Seurat.The platform includes ten key modules covering quality control,cell filtering,dimensionality reduction,clustering,differential analysis,cell annotation,path-way enrichment,motif analysis,and transcription factor footprinting.Through a graphical user interface,users can perform full analyses and obtain interactive visualization results.The platform's stability and u-tility have been validated using a public PBMC dataset and it is currently deployed online(https://xula-bgdpu.org.cn/Signac.UIO),providing an efficient and user-friendly tool for single-cell epigenomics re-search.