BackgroundIndividuals with schizophrenia are prone to higher rates of hospital readmission， presenting significant clinical challenges and imposing considerable social burdens within the mental health domain. In recent years， various risk prediction models have been developed to forecast readmission in patients with schizophrenia and support clinical decision-making， but their predictive performance and clinical applicability require comprehensive evaluation. ObjectiveTo systematically evaluate the risk prediction models for readmission in patients with schizophrenia， so as to provide insights for the development of high-performance and highly applicable readmission risk prediction models for patients with schizophrenia. MethodsOn July 5， 2025， a systematic literature search was conducted across multiple electronic databases， including PubMed， Embase， Cochrane Library， Web of Science， CINAHL， CNKI， China Biomedical Literature Database， Wanfang Database， and VIP Database， to identify risk prediction models for readmission in patients with schizophrenia. The search period was from the establishment of the databases to July 1， 2025. Two researchers independently performed literature screening， data extraction， risk of bias assessment， and applicability assessment. ResultsA total of 9 studies were included in this review， encompassing 18 risk prediction models for readmission in patients with schizophrenia. Among them， 4 models reported the area under the receiver operating characteristic （ROC） curve （AUC）， ranging from 0.734 to 0.820， 16 models provided AUC values of 0.642–0.879 for internal validation， and 1 model demonstrated an AUC of 0.841 for external validation. Key predictors included disease duration and the concomitant therapy of antipsychotic medications. The risk of bias was assessed as "high" in all included studies. ConclusionThe development of risk prediction models for readmission in patients with schizophrenia remains in an exploratory stage. Although the model exhibits favorable predictive performance， it is associated with a high risk of bias and insufficient performance evaluation.

OBJECTIVES: To explore the therapeutic mechanism of compound Centella asiatica formula (CCA) for alleviating Schistosoma japonicum (Sj)-induced liver fibrosis in mice. METHODS: The active components and targets of CCA were identified using the TCMSP database with cross-analysis of Sj-related liver fibrosis targets. A "drug-component-target-pathway-disease" network was constructed using Cytoscape 3.9.1. Functional enrichment analysis (GO/KEGG) was performed using DAVID. Molecular docking study was carried out to validate interactions between the core targets and the key compounds. For experimental validation of the results, 36 mice were divided into control group, Sj-infected model group, and CCA-treated groups. In the latter two groups, liver fibrosis was induced via abdominal infection with Sj cercariae for 8 weeks, followed by 8 weeks of daily treatment with CCA decoction or saline. Hepatic pathology of the mice was assessedwith HE and Masson staining, and hepatic expressions of collagen-I and collagen-III were detected using immunohistochemistry; serum IL-6 and TNF-α levels were determined with ELISA. Hepatic expressions of TLR4 and MyD88 proteins were analyzed with Western blotting. RESULTS: We identified a total of 107 bioactive CCA components and 791 targets, including 37 intersection targets linked to Sj-induced fibrosis. The core targets included TNF, TP53, JUN, MMP9, and CXCL8, involving the IL-17 signaling, lipid metabolism, TLR4/MyD88 axis, and cancer pathways. Molecular docking study confirmed strong binding affinity between quercetin (a primary CCA component) and TNF/TP53/JUN/MMP9. In Sj-infected mouse models, CCA treatment significantly attenuated hepatic inflammatory cell infiltration, reduced collagen-I and collagen-III deposition, improved tissue architecture, reduced serum IL-6 and TNF-α levels, and downregulated TLR4 and MyD88 expressions in the liver. CONCLUSIONS CCA mitigates Sj-induced liver fibrosis by targeting TNF, TP53, JUN, and MMP9 to modulate the TLR4/MyD88 pathway, thereby suppressing pro-inflammatory cytokine release, inhibiting hepatic stellate cell activation, reducing collagen deposition, and preventing granuloma formation in the liver.
Animals ; Toll-Like Receptor 4/metabolism* ; Mice ; Myeloid Differentiation Factor 88/metabolism* ; Schistosoma japonicum ; Liver Cirrhosis/parasitology* ; Schistosomiasis japonica ; Signal Transduction ; Molecular Docking Simulation ; Inflammation ; Centella/chemistry* ; Drugs, Chinese Herbal/pharmacology* ; Tumor Necrosis Factor-alpha/metabolism*

Objective:To explore the relationship between tumor necrosis factor-like weak inducer of apoptosis(TWEAK),kidney injury molecule 1(KIM-1),RBC distribution width/platelet ratio(RPR)and disease activity,renal injury in children with sys-temic lupus erythematosus(SLE).Methods:A total of 42 children with newly diagnosed SLE in Xiangyang Central Hospital were en-rolled as SLE group between February 2020 and February 2022,while another 40 healthy children undergoing physical examination during the same period were enrolled as control group.According to scores of systemic lupus erythematosus disease activity index(SLEDAI),SLE children were divided into low disease activity group(≤9 points)24 cases and high disease activity group(>9 points)18 cases.According to presence or absence of renal injury,SLE children were divided into LN group 31 cases and non-LN group 11 cases.The red blood cell distribution width(RDW)and platelet count(PLT)in all objects were detected.RPR was calculated.The levels of serum TWEAK and KIM-1 were detected by ELISA.Results:The levels of serum TWEAK,KIM-1 and RPR in SLE group were significantly higher than those in control group(P<0.05).The levels of serum TWEAK,KIM-1 and RPR in high disease activity group were significantly higher than those in low disease activity group(P<0.05),which were significantly higher in LN group than non-LN group(P<0.05).Correlation analysis showed that RPR was significantly positively correlated with SLEDAI score(P<0.05),TWEAK and KIM-1 were significantly positively correlated with 24 h urinary protein(P<0.05).AUC of RPR for assessing high disease activity of SLE was 0.744(95%CI:0.657～0.818),significantly greater than that of TWEAK and KIM-1[0.678(95%CI:0.588～0.760),0.598(95%CI:0.505～0.686),P<0.05].AUC values of TWEAK and KIM-1 for predicting LN 0.847(95%CI:0.773～0.905)and 0.773(95%CI:0.690～0.842),significantly greater than that of RPR AUC values[0.645(95%CI:0.555～0.727),P<0.05].Conclusion:The levels of TWEAK,KIM-1 and RPR are changed in children with SLE.RPR has higher diagnostic efficiency for SLE activity,while TWEAK and KIM-1 have higher predictive value for LN.

To construct a recombinant fowl adenovirus 4(FAdV-4)expressing the Cap protein of goose astrovirus genotype 2(GoAstV-2),the expression cassette of Cap gene was inserted into the natural 1 966 bp deletion region of the FAdV-4 genome in the infectious clone p15A-cm-FAdV4-HNJZ.The resulted recombinant plasmid p15A-cm-FAdV4-HNJZ-Cap/GoAstV-2 was linearized with restriction enzyme and transfected into chicken hepatoma cell line(LMH)to rescue the recombinant FAdV-4 expressing the Cap protein of GoAstV-2,rF Ad V4-Cap/GoAstV-2.After 15 passages in LMH cells,the recombinant rFAdV4-Cap/GoAstV-2 was identified by PCR using primers flanking the insertion site of the Cap gene expression cassette and using viral genome DNA extracted from rFAdV4-Cap/GoAstV-2 infected LMH cells as template.LMH cells were in-fected with 15th passage rFAdV4-Cap/GoAstV-2 and indirect immunofluorescence was performed with a polyclonal antibody against Cap protein as the primary antibody.Western blot was carried out with lysates of rFAdV4-Cap/GoAstV-2 infected LMH cells.The in vitro replication dynamic of the 15th passage of the rFAdV4-Cap/GoAstV-2 was also investigated in LMH cells.The results demonstrated that the Cap gene of GoAstV-2 was presented in the genome of the recombinant vi-rus rF AdV4-Cap/Go Ast V-2,and could be expressed stably.The prepared recombinant virus in this study will lay a foundation for developing inactivated bivalent vaccine candidate against co-in-fection of FAdV-4 and GoAstV-2 in goose.

There is significant inter-individual variation of pharmacokinetics and pharmacody-namics in patients receiving tacrolimus(TAC)for an-ti-rejection therapy,which cause the rejection or toxic action.Based on results of therapeutic drug monitoring and pathophysiological index of trans-plant patients,the individualized dosing regimen can be designed and adjusted by using model in-formed precision dosing(MIPD).The patients'clini-cal outcome can be improved.In the consensus,the different methods of MIPD used for patients re-ceived TAC for anti-rejection therapy were intro-duced,which can be used for the designing and ad-justing doing regimen,predicting adverse drug reac-tion,improving medication adherence and econom-ics during therapy.

AIM:To clarify the molecular mechanism by which astragaloside Ⅳ(AS-Ⅳ)suppresses oxida-tive stress and alleviates cerebral ischemia-reperfusion injury(CIRI)via the PTEN-induced kinase 1(PINK1)/parkin mi-tophagy-associated pathway.METHODS:A middle cerebral artery occlusion/reperfusion(MCAO/R)model was estab-lished in Sprague-Dawley rats.The animals were allocated to sham,MCAO/R,AS-Ⅳ,and mitochondrial division inhibi-tor-1(Mdivi-1)treatment groups.The rats in AS-Ⅳ and Mdivi-1 groups were intraperitoneally injected once daily with AS-Ⅳ(20 mg/kg)for 7 d,while those in Midivi-1 group also received intraperitoneal injection of Mdivi-1(1.2 mg·kg-1·d-1).The rats in sham and MCAO/R groups were given equivalent volume of distilled water.Neurological deficits were as-sessed using Zea Longa scoring,infarcted area volumes were measured using TTC staining,and brain tissue pathology was examined using hematoxylin and eosin staining.The levels of malondialdehyde(MDA)and superoxide dismutase(SOD)were assessed by ELISA,while those of reactive oxygen species(ROS)were measured using flow cytometry.The expres-sion levels of PINK1,parkin and microtubule-associated protein 1 light chain 3(LC3)were quantified using Western blot and RT-qPCR.RESULTS:AS-Ⅳ administration significantly alleviated neuronal and mitochondrial damage in MCAO/R model rat brains(P＜0.05),together with significant reductions in the cerebral infarct volume and neurological dysfunc-tion(P＜0.05).Significant increases in PINK1,parkin and LC3 protein and mRNA levels were observed in response to AS-Ⅳ(P＜0.05),SOD activity rose,and ROS and MDA levels declined significantly(P＜0.05).The co-administration of Mdivi-1 abrogated the protective benefits of AS-Ⅳ,inhibited activation of the PINK1/parkin pathway,down-regulated LC3 at the mRNA and protein levels,and significantly increased mitochondrial damage.Mdivi-1 also markedly reduced autophagosome formation and SOD activity level,but increased both ROS and MDA levels,cerebral infarct volume,and the severity of neurological deficits(P＜0.05).CONCLUSION:Astragaloside Ⅳ activates the PINK/parkin-mediated mitophagy pathway,inhibits oxidative stress and alleviates CIRI in rats.

Objective To construct the training program for the digital and intelligent capabilities of specialized nurses in the Central Sterile Supply Department(CSSD),and conduct preliminary practice to provide talent support for the intelligent development of CSSD.Methods From February to April 2024,based on the core technologies of digital intelligence and related core capabilities,a training program for digital intelligence-related competencies of CSSD specialized nurses was constructed using literature review and the Delphi expert consultation method.From July to August 2024,the program was initially implemented in the training of CSSD specialized nurses.The nurses'information competency before and after the training was compared,and the nurses' satisfaction with the digital intelligence-related training program was assessed.Results This study conducted 2 rounds of expert consultation via questionnaire.The effective recovery rate of the questionnaires in both rounds was 100％.The expert authority coefficients were 0.790 and 0.800,respectively,and the variation coefficients ranged from 0 to 0.229 and 0 to 0.105.Ultimately,a training program for the digital-related competencies of CSSD specialty nurses was established,which includes 4 components:training objectives,training content,training methods,and assessment methods.Specifically,there were 3 indicators at the first level and 14 at the second level for training objectives,6 indicators at the first level and 32 at the second level for training content,and 6 indicators at the first level for training methods and assessment methods.After the implementation of the training program,the information competency of the nurses in all dimensions and the total score were significantly higher than those before training(P＜0.05).Moreover,the average scores for the training content,training methods,and assessment methods were all above 3 points,indicating a high overall satisfaction among the nurses.Conclusion The construction process of the training program for the digital and intelligent capabilities of CSSD specialty nurses is scientific and reliable.The content is highly practical and distinctive in its specialty.The training methods and assessment approaches are diverse.This program can enhance nurses' information competency and provide a reference for the implementation of digital and intelligent training for CSSD specialty nurses.

Acute symptomatic osteoporotic thoracolumbar compression fracture (ASOTLF) can lead to chronic low back pain, kyphosis deformity, pulmonary dysfunction, loss of mobility, and even life-threatening complications. Vertebral augmentation is currently the mainstream treatment method for this condition. In 2019, the Editorial Board of Chinese Journal of Trauma and the Spinal Trauma Group of Orthopedic Surgeons Branch of Chinese Medical Doctor Association collaboratively led the development of Clinical guideline for vertebral augmentation for acute symptomatic osteoporotic thoracolumbar compression fractures. Six years later, with advances in clinical diagnosis and treatment techniques as well as accumulating evidence in related fields, the 2019 guideline requires updating. To this end, the Spinal Trauma Group of Orthopedic Surgeons Branch of Chinese Medical Doctor Association, the Spinal Health Professional Committee of China Human Health Science and Technology Promotion Association, and the Minimally Invasive Orthopedics Professional Committee of Shaanxi Medical Doctor Association have organized experts in the field to develop the Clinical guideline for vertebral augmentation of acute symptomatic osteoporotic thoracolumbar compression fractures ( version 2025) , based on the latest evidence-based medical researches. This guideline incorporates 3 recommendations retained from the 2019 version with updated strength of evidence, along with 12 new recommendations. It provides recommendations from six aspects of diagnosis, pain management, treatment option selection, prevention of postoperative complications, anti-osteoporosis therapy, and postoperative rehabilitation, aiming to provide a reference for standard treatment of vertebral augmentation for ASOTLF in hospitals at all levels.

Objective:To explore the correlation between clinical and CT imaging features and epidermal growth factor receptor (EGFR) gene mutation in patients with non-small cell lung cancer (NSCLC) and screening of mutation prediction indicators.Methods:A retrospective case-control study was conducted. The clinical data of 178 NSCLC patients who were confirmed by pathology and underwent pre-treatment chest-enhanced CT scan and EGFR gene mutation testing in General Hospital of Ningxia Medical University from January 2015 to December 2019 were retrospectively analyzed. Patients were classified into EGFR mutation-positive and mutation-negative groups based on genetic testing results, and the clinical and CT imaging features were compared between the two groups; the multivariate logistic regression model was used to identify the independent influencing factors for EGFR gene mutation in NSCLC patients.Results:Among 178 NSCLC patients, 115 cases (64.6%) were EGFR gene mutation-positive and 63 cases (35.4%) were mutation-negative. Among the 115 EGFR gene mutation-positive patients, there were 61 cases (53.0%) of exon 19 deletion (19del) mutation, 45 cases (39.1%) of exon 21 L858R mutation, 8 cases (7.0%) of exon 20 mutation, and 1 case (0.9%) of exon 18 mutation. The proportions of female patients [60.0% (69/115) vs. 30.2% (19/63)] and patients with out smoking history [74.8% (86/115) vs. 36.5% (23/63)] in EGFR gene mutation-positive group were higher than those in the mutation-negative group, and the differences were statistically significant (both P < 0.001), while the proportions of patients with different pathological types and clinical stages in the two groups showed no statistically significant differences (both P > 0.05). The median maximum diameter of tumor [ M ( Q1, Q3)] detected by CT in the EGFR gene mutation-positive group was 3.70 (2.90, 4.70) cm, while in the mutation-negative group it was 5.30 (3.40, 6.80) cm, and the difference was statistically significant ( Z = -3.66, P < 0.001). The proportions of patients with air bronchogram [27.8% (32/115) vs. 7.9% (5/63)] and without emphysema [83.5% (96/115) vs. 55.6% (35/63)] in the EGFR gene mutation-positive group were higher than those in the mutation-negative group, and the differences were statistically significant (both P < 0.01). The results of multivariate logistic regression analysis showed that no smoking history (yes vs. no, OR = 0.218, 95% CI: 0.073-0.647), short maximum diameter of tumor detected by CT ( OR = 0.814, 95% CI: 0.676-0.981), air bronchogram (yes vs. no, OR = 5.354, 95% CI: 1.782-16.090), and no emphysema (yes vs. no, OR = 0.289, 95% CI: 0.128-0.653) were independent risk factors for EGFR gene mutation in NSCLC patients (all P < 0.05). Conclusions:Clinical and CT imaging features may relate to EGFR gene mutation status in NSCLC patients, and no smoking history, short maximum diameter of tumor detected by CT, air bronchogram and no emphysema may predict EGFR gene mutation.

Objective To screening and validation of key genes for programmed cell death(PCD)in gout through bioinformatics and machine learning and immunoinfiltration analysis.Methods Gout-related datasets were obtained from the Gene Expression Omnibus(GEO)database,comprising the human gout dataset GSE160170 and murine gout dataset GSE190138,which served as the training cohort.Differentiall expression genes(DEGs)were screened with difference factor>2 and P<0.05.The DEGs of two data sets were intersected to obtain the common DEGs(co-DEGs).The co-DEGs were enriched by GO function and KEGG pathway analysis.The combination of co-DEGs and PCD related gene set was used to obtain PCD related DEGs.A PPI network was built in the STRING database.The key module genes were screened in Cytoscape's MCODE,the hub genes were screened in 12 algorithms built into the Cytohubba plugin,including Degree,MCC,DMNC,MCN,EPC,BottleNeck,EcCentricity,closness,Radiality,Betweeness,Stress and Clusteringcoefficoent,the common genes of the two was as candidate genes.The regression model of least absolute shrinkage and selection operator(LASSO)was used to screen key genes in the GSE160170 and GSE190138 data sets respectively,and the intersection of the two was adopted to obtain key genes.The diagnostic value of key genes in gout was evaluated by receiver operating characteristic(ROC)curve.The expression difference of gout related immune cells was investigated by single sample gene set enrichmemt analysis(ssGSEA)immunoinfiltration analysis.Finally,blood samples from 30 gout patients admitted to the Department of Rheumatology,Xi'an Fifth Hospital from February to April 2024 were collected as the experimental group,while blood samples from 30 healthy subjects were collected as the control group.RNA was extracted from the Peripheral blood mononuclear cell(PBMC).Quantitative real time polymerase chain reaction(RT-qPCR)was used to validate the expression of key genes in clinical samples.Results 53 common DEGs of GSE160170 and GSE190138 were obtained,among which 43 genes were up-regulated and 10 were down-regulated.GO and KEGG indicated that most genes were involved in cell death,apoptosis,interlenkin(IL)-17 signaling pathway,tumor necrosis facter(TNF)signaling pathway and nucleotide-binding oligomerization domain-(NOD)-like receptor signaling pathway.12 co-DEGs of programmed cell death and gout were obtained.A total of 7 candidate genes were screened.LASSO regression model screened 5 genes and 4 genes respectively in two datasets,and 3 key genes were abtained by the intersection of the two datasets,which were IL-6,plasminogen activator urokinase receptor(PLAUR)and NOD-like receptor thermal protein domain associated protein3(NLRP3).Validation within the training set revealed that all three genes attained perfect diagnostic performance for gout,with area under the ROC(AUC-ROC)curve values of 1.00.Immunoinfiltration analysis showed that the changes of activated CD4+T cells,activated CD8+T cells and natural killer cells were closely related to the occurrence and development of gout.In the clinical samples,compared with the control group,PLAUR,NLRP3 and IL-6 were highly expressed in gout patients,and the differences were statistically significant(t=18.852,9.633,8.293,all P＜0.05).Conclusion IL-6,PLAUR and NLRP3 provide potential biomarkers and therapeutic targets for the diagnosis and treatment of gout,offering new directions in this field.