1.Society of Critical Care Medicine 2024 Guidelines on Adult ICU Design: An Interpretation
Hui ZHANG ; Jianhua SUN ; Wanchen ZHAO ; Lingli XIE ; Cong MA ; Yifan FANG ; Jing CAI ; Na GUO
Medical Journal of Peking Union Medical College Hospital 2026;17(2):421-428
This article provides a systematic interpretation and review of the
2.Surgical treatment of hepatic alveolar echinococcosis: challenges and innovations
Pei ZHANG ; Lu ZHAO ; Yunfei FANG ; Hui YANG ; Yifan WANG ; Yanqiong MA ; Yu MENG
Organ Transplantation 2026;17(3):512-518
Hepatic alveolar echinococcosis is a highly invasive zoonotic parasitic disease with poor prognosis. Surgical intervention serves as the pivotal approach to achieve radical cure and improve the prognosis of hepatic alveolar echinococcosis patients. In recent years, with the popularization of the concept of precision surgery and the development of the multidisciplinary diagnosis and treatment model, the surgical treatment strategies for hepatic alveolar echinococcosis have been continuously enriched, and the selection of surgical procedures has become increasingly diversified. Although key surgical techniques such as radical hepatectomy, autologous liver transplantation and allogeneic liver transplantation have achieved remarkable progress in clinical application, many insurmountable challenges still remain. Therefore, by sorting out the latest evidence-based advances in the field of surgical treatment for hepatic alveolar echinococcosis, this article focuses on discussing the application status and bottlenecks of radical hepatectomy, autologous liver transplantation and allogeneic liver transplantation in hepatic alveolar echinococcosis, aiming to provide a reference for the clinical treatment of hepatic alveolar echinococcosis.
3.Interleukin-33 Knockout Promotes High Mobility Group Box 1 Release from Astrocytes by Acetylation Mediated by P300/CBP-Associated Factor in Experimental Autoimmune Encephalomyelitis.
Yifan XIAO ; Liyan HAO ; Xinyi CAO ; Yibo ZHANG ; Qingqing XU ; Luyao QIN ; Yixuan ZHANG ; Yangxingzi WU ; Hongyan ZHOU ; Mengjuan WU ; Mingshan PI ; Qi XIONG ; Youhua YANG ; Yuran GUI ; Wei LIU ; Fang ZHENG ; Xiji SHU ; Yiyuan XIA
Neuroscience Bulletin 2025;41(7):1181-1197
High mobility group box 1 (HMGB1), when released extracellularly, plays a pivotal role in the development of spinal cord synapses and exacerbates autoimmune diseases within the central nervous system. In experimental autoimmune encephalomyelitis (EAE), a condition that models multiple sclerosis, the levels of extracellular HMGB1 and interleukin-33 (IL-33) have been found to be inversely correlated. However, the mechanism by which IL-33 deficiency enhances HMGB1 release during EAE remains elusive. Our study elucidates a potential signaling pathway whereby the absence of IL-33 leads to increased binding of P300/CBP-associated factor with HMGB1 in the nuclei of astrocytes, upregulating HMGB1 acetylation and promoting its release from astrocyte nuclei in the spinal cord of EAE mice. Conversely, the addition of IL-33 counteracts the TNF-α-induced increase in HMGB1 and acetylated HMGB1 levels in primary astrocytes. These findings underscore the potential of IL-33-associated signaling pathways as a therapeutic target for EAE treatment.
Animals
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Encephalomyelitis, Autoimmune, Experimental/metabolism*
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Astrocytes/metabolism*
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Interleukin-33/metabolism*
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HMGB1 Protein/metabolism*
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Acetylation
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Mice, Knockout
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Mice, Inbred C57BL
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p300-CBP Transcription Factors/metabolism*
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Mice
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Spinal Cord/metabolism*
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Cells, Cultured
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Female
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Signal Transduction
4.Analysis of Potential Active Components and Molecular Mechanism of Baoxin Granules Regulating Ferroptosis in Treatment of Heart Failure
Yu CHEN ; Maolin WANG ; Yun WANG ; Yifan ZHAO ; Jing XU ; Hongwei WU ; Fang WANG ; Xiaoang ZHAO ; Youming LI ; Jixiang TIAN
Chinese Journal of Experimental Traditional Medical Formulae 2025;31(12):202-209
ObjectiveBased on ultra performance liquid chromatography-quadrupole-time-of-flight mass spectrometry(UPLC-Q-TOF-MS), network pharmacology, molecular docking and cell experiments, the active ingredients, possible targets and molecular mechanisms of Baoxin granules(BXG) regulating ferroptosis in the treatment of heart failure(HF) were explored. MethodsBXG intestinal absorption fluid was prepared by everted gut sac and the chemical composition contained therein were identified by UPLC-Q-TOF-MS. According to the obtained components, the potential targets of BXG were predicted, and the HF-related targets and related genes of ferroptosis were retrieved at the same time, and the intersecting targets were obtained by Venn diagram. In addition, the protein-protein interaction(PPI) network and the component-target network were constructed, and the core components and core targets were obtained by topological analysis. Then Gene Ontology(GO) function and Kyoto Encyclopedia of Genes and Genomes(KEGG) enrichment analysis were performed on the core targets, and molecular docking validation of the key targets and main components was carried out by AutoDockTools 1.5.7. H9c2 cells were used to establish a oxygen-glucose deprivation model, and the protective effect of BXG on cells was investigated by detecting cell viability, cell survival rate and reactive oxygen species(ROS) level. The protein expression levels of signal transducer and activator of transcription 3(STAT3), phosphorylation(p)-STAT3 and glutathione peroxidase 4(GPX4) were detected by Western blot to clarify the regulatory effect of BXG on ferroptosis. ResultsA total of 61 chemical components in BXG intestinal absorption fluid were identified, and network pharmacology obtained 27 potential targets of BXG for the treatment of HF, as well as 139 signaling pathways. BXG may act on core targets such as STAT3, tumor protein p53(TP53), epidermal growth factor receptor(EGFR), JUN and prostaglandin-endoperoxide synthase 2(PTGS2) through core components such as glabrolide and limonin, which in turn intervene in lipid and atherosclerosis, phosphatidylinositol 3-kinase/protein kinase B(PI3K/Akt), endocrine resistance and other signaling pathways to exert therapeutic effects on HF. Molecular docking showed that the docking results of multiple groups of targets and compounds were good. In vitro cell experiments showed that compared with the blank group, the cell viability and survival rate of the model group were significantly decreased, the level of ROS was significantly increased(P<0.01), the expression levels of STAT3, p-STAT3, p-STAT3/STAT3 and GPX4 proteins were significantly decreased(P<0.05, P<0.01). Compared with the model group, the cell viability and survival rate of the BXG group were significantly increased, the ROS level was significantly decreased(P<0.01), the STAT3, p-STAT3, p-STAT3/STAT3 and GPX4 protein levels were significantly increased(P<0.05, P<0.01). ConclusionBXG may inhibit the occurrence of ferroptosis by up-regulating the expression of STAT3 and GPX4, thus exerting a therapeutic effect on HF, and flavonoids may be the key components of this role.
5.Analysis of Potential Active Components and Molecular Mechanism of Baoxin Granules Regulating Ferroptosis in Treatment of Heart Failure
Yu CHEN ; Maolin WANG ; Yun WANG ; Yifan ZHAO ; Jing XU ; Hongwei WU ; Fang WANG ; Xiaoang ZHAO ; Youming LI ; Jixiang TIAN
Chinese Journal of Experimental Traditional Medical Formulae 2025;31(12):202-209
ObjectiveBased on ultra performance liquid chromatography-quadrupole-time-of-flight mass spectrometry(UPLC-Q-TOF-MS), network pharmacology, molecular docking and cell experiments, the active ingredients, possible targets and molecular mechanisms of Baoxin granules(BXG) regulating ferroptosis in the treatment of heart failure(HF) were explored. MethodsBXG intestinal absorption fluid was prepared by everted gut sac and the chemical composition contained therein were identified by UPLC-Q-TOF-MS. According to the obtained components, the potential targets of BXG were predicted, and the HF-related targets and related genes of ferroptosis were retrieved at the same time, and the intersecting targets were obtained by Venn diagram. In addition, the protein-protein interaction(PPI) network and the component-target network were constructed, and the core components and core targets were obtained by topological analysis. Then Gene Ontology(GO) function and Kyoto Encyclopedia of Genes and Genomes(KEGG) enrichment analysis were performed on the core targets, and molecular docking validation of the key targets and main components was carried out by AutoDockTools 1.5.7. H9c2 cells were used to establish a oxygen-glucose deprivation model, and the protective effect of BXG on cells was investigated by detecting cell viability, cell survival rate and reactive oxygen species(ROS) level. The protein expression levels of signal transducer and activator of transcription 3(STAT3), phosphorylation(p)-STAT3 and glutathione peroxidase 4(GPX4) were detected by Western blot to clarify the regulatory effect of BXG on ferroptosis. ResultsA total of 61 chemical components in BXG intestinal absorption fluid were identified, and network pharmacology obtained 27 potential targets of BXG for the treatment of HF, as well as 139 signaling pathways. BXG may act on core targets such as STAT3, tumor protein p53(TP53), epidermal growth factor receptor(EGFR), JUN and prostaglandin-endoperoxide synthase 2(PTGS2) through core components such as glabrolide and limonin, which in turn intervene in lipid and atherosclerosis, phosphatidylinositol 3-kinase/protein kinase B(PI3K/Akt), endocrine resistance and other signaling pathways to exert therapeutic effects on HF. Molecular docking showed that the docking results of multiple groups of targets and compounds were good. In vitro cell experiments showed that compared with the blank group, the cell viability and survival rate of the model group were significantly decreased, the level of ROS was significantly increased(P<0.01), the expression levels of STAT3, p-STAT3, p-STAT3/STAT3 and GPX4 proteins were significantly decreased(P<0.05, P<0.01). Compared with the model group, the cell viability and survival rate of the BXG group were significantly increased, the ROS level was significantly decreased(P<0.01), the STAT3, p-STAT3, p-STAT3/STAT3 and GPX4 protein levels were significantly increased(P<0.05, P<0.01). ConclusionBXG may inhibit the occurrence of ferroptosis by up-regulating the expression of STAT3 and GPX4, thus exerting a therapeutic effect on HF, and flavonoids may be the key components of this role.
6.Standardization of electronic medical records data in rehabilitation
Yifan TIAN ; Fang XUN ; Haiyan YE ; Ye LIU ; Yingxin ZHANG ; Yaru YANG ; Zhongyan WANG ; Meng ZHANG ; Xiaoxie LIU ; Yanyan YANG ; Bin ZENG ; Mouwang ZHOU ; Yuxiao XIE ; Guangxu XU ; Jiejiao ZHENG ; Mingsheng ZHANG ; Xiangming YE ; Fubiao HUANG ; Qiuchen HUANG ; Yiji WANG ; Di CHEN ; Zhuoying QIU
Chinese Journal of Rehabilitation Theory and Practice 2025;31(1):33-44
ObjectiveTo explore the data standard system of electronic medical records in the field of rehabilitation, focusing on the terminology and coding standards, data structure, and key content categories of rehabilitation electronic medical records. MethodsBased on the Administrative Norms for the Application of Electronic Medical Records issued by the National Health Commission of China, the electronic medical record standard architecture issued by the International Organization for Standardization and Health Level Seven (HL7), the framework of the World Health Organization Family of International Classifications (WHO-FICs), Basic Architecture and Data Standards of Electronic Medical Records, Basic Data Set of Electronic Medical Records, and Specifications for Sharing Documents of Electronic Medical Records, the study constructed and organized the data structure, content, and data standards of rehabilitation electronic medical records. ResultsThe data structure of rehabilitation electronic medical records should strictly follow the structure of electronic medical records, including four levels (clinical document, document section, data set and data element) and four major content areas (basic information, diagnostic information, intervention information and cost information). Rehabilitation electronic medical records further integrated information related to rehabilitation needs and characteristics, emphasizing rehabilitation treatment, into clinical information. By fully applying the WHO-FICs reference classifications, rehabilitation electronic medical records could establish a standardized framework, diagnostic criteria, functional description tools, coding tools and terminology index tools for the coding, indexing, functional description, and analysis and interpretation of diseases and health problems. The study elaborated on the data structure and content categories of rehabilitation electronic medical records in four major categories, refined the granularity of reporting rehabilitation content in electronic medical records, and provided detailed data reporting guidance for rehabilitation electronic medical records. ConclusionThe standardization of rehabilitation electronic medical records is significant for improving the quality of rehabilitation medical services and promoting the rehabilitation process of patients. The development of rehabilitation electronic medical records must be based on the national and international standards. Under the general electronic medical records data structure and standards, a rehabilitation electronic medical records data system should be constructed which incorporates core data such as disease diagnosis, functional description and assessment, and rehabilitation interventions. The standardized rehabilitation electronic medical records scheme constructed in this study can support the improvement of standardization of rehabilitation electronic medical records data information.
7.A Cross-sectional Survey on the Use of Non-Vitamin K Antagonist Oral Anticoagulants in Elderly Patients with Non-Valvular Atrial Fibrillation
Yifan NA ; Junpeng LIU ; Yatong ZHANG ; Zinan ZHAO ; Tianqi ZHANG ; Yuhao WAN ; Min ZENG ; Ning SUN ; Cheng WU ; Jun WANG ; Fang WANG ; Jiefu YANG
Chinese Journal of Geriatrics 2025;44(4):458-464
Objective:To investigate the use of non-vitamin K antagonist oral anticoagulants(NOACs)and their associated comorbidities in patients aged 80 years and older with non-valvular atrial fibrillation(NVAF), as well as to understand the challenges faced by elderly patients receiving NOAC therapy.Methods:We retrospectively enrolled elderly patients(≥80 years old)with NVAF who were treated with NOACs at a hospital in Beijing from January 2018 to August 2023.Patients were categorized into two age groups: 80-89 years and ≥90 years.We collected baseline data, including demographic characteristics, details of atrial fibrillation, comorbidities, laboratory test results, and medication combinations, for descriptive statistical analysis and intergroup comparisons.Results:A total of 695 elderly patients with NVAF receiving NOACs were included in the study, with a median age of 84 years.Among these patients, there were 328 males(47.19%, 328/695)and 422 cases of paroxysmal atrial fibrillation(60.72%, 422/695).The age group of 80-89 years comprised 640 cases(92.09%, 640/695), while the group aged 90 years and above included 55 cases(7.91%, 55/695).The use of NOACs in patients aged 90 and older exhibited an increasing trend over the years.Inter-group comparisons indicated that the ≥90 years group had lower body mass index, longer hospital stays, increased bedridden time, poorer renal function, lower levels of albumin and hemoglobin, and higher D-dimer levels.Inappropriate dosing of DOACs occurred in 49.64%(345/695)of cases, with 90.72%(313/345)receiving doses lower than recommended.Lower-than-recommended doses were more prevalent in the ≥90 years group, while higher-than-recommended doses were more common in the 80-89 years group.Polypharmacy was noted in 61.29%(426/695)of patients.The concurrent use of antiplatelet drugs, rhythm control medications, and ventricular rate control drugs was observed in 12.52%(87/695), 19.57%(136/695), and 54.53%(379/695)of patients, respectively, with no significant differences between groups.Conclusions:Inappropriate dosing and polypharmacy are prevalent issues among elderly NVAF patients.Therefore, it is essential to enhance multidisciplinary collaboration to optimize anticoagulation treatment strategies.
8.Clinical characteristics and molecular function of ubiquitin-like containing PHD and RING finger domains 1 in soft tissue sarcoma
Yijin YAN ; Huan WANG ; Yifan DING ; Haoran XU ; Weihua HU ; Huang FANG
Journal of Clinical Surgery 2025;33(7):735-740
Objective To explore the expression pattern and molecular function of ubiquitin-like containing PHD and RING finger domains 1(UHRF1)gene in soft tissue sarcoma(STS),as well as its correlation with clinical characteristics and prognosis of STS.Methods RNA data and related clinical data of 263 STS tissues were obtained from Cancer Genome Atlas(TCGA).Wilcoxon rank-sum test was used to analyze correlation between two groups of data;Spearman correlation coefficient analyzed the top 35 co-expressed genes positively and negatively correlated with UHRF1 expression in STS database,ggplot2 statistical package displayed co-expressed gene heatmap,Pearson correlation coefficient showed correlation between UHRF1 expression and expression of the top 10 genes in the heatmap;different UHRF1 gene expression groups in STS were analyzed using DESeq2 package,ggplot2 package was used to draw volcano plots,gene ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)enrichment analyzed differentially expressed genes(DEGs)and protein functions,ggplot2 package for visualization,and cluster Profiler package for statistical analysis;STRING web was used to establish PPI network of DEGs,and the MCC algorithm in CytoHubba of Cytoscape was used to analyze hub genes.Results In STS,UHRF1 gene was significantly correlated with its histological type(liposarcoma 22.2%,synovial sarcoma 3.8%,leiomyosarcoma 40.7%,malignant peripheral nerve sheath tumor 3.8%,myxofibrosarcoma 9.6%,pleomorphic sarcoma 19.9%,P=0.001),tumor necrosis(none 38.8%,focal necrosis 20.8%,moderate necrosis 33.8%,extensive necrosis 6.6%,P=0.010),and tumor metastasis(no metastasis 67%,metastasis 33%,P<0.001).In different clinical subgroups(age,gender,histological type,residual tumor,tumor necrosis,tumor depth,margin status,tumor multifocality,radiotherapy),high expression of UHRF1 led to poor prognosis of overall survival(OS),disease-specific survival(DSS),and progression-free interval(PFI);Three prognostic factors above were simultaneously shortened in the following five subgroups:namely residual tumor R0 and R1,tumor necrosis extensive,focal and moderate,tumor depth deep,positive margin status,tumor without multifocality.Analysis of the top 10 co-expressed genes associated with UHRF1 expression revealed that the associated positive genes were PAGE5,LINC01425,LCEP3,SERPINB7,AC074031.1,LCE3A,LCE2A,PAGE2B,MYF5,and AC037486.1(P<0.05);the associated negative genes were CDH19,CSN1S1,TAC3,AC103563.7,SAA1,CHST8,PRLHR,MIR202HG,IGHV1-24,and ART4(P<0.05).A total of 3 029 DEGs of UHRF1 in STS were obtained with a threshold of|log2 fold-change(FC)|>1.0 and adjusted P value<0.05,in which 1 228 genes were up-regulated and 1 801 genes were down-regulated;GO enrichment analyed primary biological processes(BP),original cellular components(CC),and original molecular functions(MF),and KEGG enrichment analyed signaling pathways.A total of 343 DEGs including 133 up-regulated genes and 210 down-regulated genes,were obtained with a threshold of|log2 fold-change(FC)|>2.0 and adjusted P value<0.05.The top 10 hub genes were analyzed.The top 3 hub genes were GCG,SST and SHH,respectively.Conclusion UHRF1 is significantly correlated with histological type,tumor necrosis,metastasis,OS,DSS,and PFI events in STS.In co expressed genes model and molecular functions of related positive and negative genes involved in multiple biological processes;The network of differentially expressed genes and protein product interactions involved in mechanisms of occurrence and development of the disease,and provided new ideas for in-depth researches on STS.
9.A cross-lagged study of relationship between natural contact,executive function,and generalized anxiety symptoms in college students
Yuanxiu YE ; Yifan ZHANG ; Fang FAN
Chinese Mental Health Journal 2025;39(12):1074-1080
Objective:To investigate the relationship between natural contact,executive function,and general-ized anxiety symptoms among college students.Methods:A total of 3 243 college students completed three assess-ments over a 10-month period(T1,T2,T3),using the Green Space Contact(GSC)items of the Natural Contact Questionnaire(NCQ),Web-based Executive Function Questionnaire(WEFQ),and Generalized Anxiety Disorder-7 Scale(GAD-7).Cross-lagged panel and longitudinal mediation analyses were conducted.Results:At all three time points,GSC,WEFQ,and GAD-7 scores were significantly correlated with each other(|r|=0.06-0.59,Ps<0.01).Cross-lagged analysis showed that GSC scores and GAD-7 scores revealed bidirectional predictive effects(β=-0.04--0.03,Ps<0.05).Longitudinal mediation analysis indicated that T2 WEFQ scores mediated the rela-tionship between T1 GSC and T3 GAD-7 scores.The mediating effect was-0.01(95%CI=-0.010--0.001),accounting for 12.82%of the total effect.Furthermore,T2 WEFQ scores also mediated the relationship between T1 GAD-7 scores and T3 GSC scores.The mediating effect was-0.01(95%CI=-0.019--0.005),accounting for 48.00%of the total effect.Conclusion:Higher frequency of natural contact is associated with lower generalized anxiety symptoms in college students.Executive function plays a bidirectional mediating role in the as-sociation between natural contact and generalized anxiety symptoms.
10.Tryptanthrin inhibits the malignant growth of glioma cells by regulating the MAPK/ERK signaling pathway
Jing WEI ; Han ZHOU ; Fangzheng JIAO ; Zihan YUAN ; Yifan QIAO ; Yan FANG
Chinese Journal of Clinical and Experimental Pathology 2025;41(5):618-626
Purpose To explore whether tryptanthrin(TRYP)can inhibit the malignant behavioral ability of glio-ma cells,and to elucidate the specific mechanism of its action.Methods MTT assay was performed to detect the effect of TRYP on the proliferation of glioma cells;Transwell assay was performed to detect the effect of TRYP on the migration and invasion of glioma cells;AnnexinV-FITC/PI apoptosis assay was performed to detect the effect of TRYP on the apoptosis of glioma cells;PI/RNase cell cycle assay was performed to detect the effect of TRYP on the cell cycle distribution of glioma cells;Western blot assay was performed to detect the effect of TRYP on the protein expressions of p-ERK and c-Myc in glioma cells.The effect of TRYP on the proliferation of glioma cells in vivo was verified by con-structing a subcutaneous transplantation tumor model in nude mice,and the effect of TRYP on the apoptotic ability of cells in the transplantation tumor was detected by TUNEL assay.Immunohistochemistry was used to detect the effect of TRYP on the expression of Ki67,BRAF,c-Myc,and p-ERK proteins in transplanted tumor tissues.Results MTT assay showed that TRYP could effectively inhibit the proliferation of glioma cells(P<0.001).Transwell assay showed that TRYP could inhibit the invasion and migration of glioma cells(P<0.001).AnnexinV-FITC/PI cell apoptosis as-say showed that TRYP could promote the apoptosis of glioma cells(P<0.001).The results of PI/RNase cell cycle as-say showed that TRYP was able to promote the G2 phase block of glioma cells(P<0.001).Western blot results showed that the expression levels of c-Myc and p-ERK proteins in the glioma cells were significantly reduced after TR-YP treatment(P<0.001).The results of subcutaneous transplantation tumor model in nude mice showed that TRYP could effectively inhibit the growth rate(P<0.01)and weight(P<0.05)of transplanted tumor.TUNEL assay showed that TRYP could promote the apoptosis of tumor cells in transplanted tumor(P<0.001).Immunohistochemis-try results showed that TRYP could effectively inhibit the protein expression of Ki67(P<0.01),BRAF,c-Myc,and p-ERK(P<0.001).Conclusion TRYP can inhibit the proliferation,invasion,and migration ability of glioma cells,promote apoptosis of glioma cells,and block the cell cycle of glioma cells.TRYP may inhibit the malignant pro-gression of glioma cells by suppressing the protein expression of BRAF,c-Myc and p-ERK1/2 in the MAPK/ERK sig-naling pathway.

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