ObjectiveTo investigate the mechanism by which Wumeiwan suppresses the development and progression of colorectal cancer（CRC） through the regulation of fatty acid metabolic reprogramming， thereby providing new experimental evidence for the prevention and treatment of CRC. MethodsA total of 120 C57BL/6 mice were randomly divided into the blank group， model group， Wumeiwan high-， medium-， and low-dose groups（54， 27， 13.5 g·kg^-1）， and the mesalazine group（0.01 g·kg^-1）， with 20 mice in each group. Except for the blank group， all mice were subjected to azoxymethane（AOM）/dextran sulfate sodium（DSS） treatment to establish an inflammation-associated CRC model. One week after AOM injection， mice in the treatment groups received intragastric administration of the designated drugs， while the blank and model groups received an equal volume of purified water， continuing until 20 d after the intervention endpoint. Hematoxylin-eosin（HE） staining was used to observe colonic histopathological alterations， and immunohistochemistry for vascular endothelial growth factor（VEGF） was performed to evaluate neovascularization and tumor invasion. Metabolomics combined with Kyoto Encyclopedia of Genes and Genomes（KEGG） and metabolite set enrichment analysis（MSEA） was applied to identify key CRC-related metabolic pathways， which were further validated by transcriptomic Gene Ontology（GO） enrichment and gene heatmap analysis. Subsequently， Western blot was performed to determine the expression levels of core proteins in these pathways， and immunofluorescence was used to analyze their localization and co-expression patterns in tissues， thereby elucidating the mechanism of Wumeiwan from multiple biological dimensions. ResultsCompared with the blank group， mice in the model group exhibited a significant decrease in body weight and a significant increase in the disease activity index（DAI） score（P<0.05）， with pronounced colonic mucosal damage accompanied by aggravated tumor invasion. Compared with the model group， Wumeiwan intervention markedly improved body weight loss and reduced DAI score， attenuated mucosal injury， and significantly decreased VEGF expression level（P<0.05）. Multi-omics analysis revealed that differential metabolites and genes across groups were commonly enriched in fatty acid metabolism， fatty acid biosynthesis， and other lipid-related pathways. Relative to the blank group， the model group showed significant upregulation levels of fatty acid synthesis-related genes， including sterol regulatory element-binding protein 1（SREBP1）， fatty acid synthase（FASN）， stearoyl-CoA desaturase 1（SCD1）， as well as saturated fatty acids（P<0.05）. Compared with the model group， treatment with Wumeiwan significantly reduced the expression of key genes involved in fatty acid metabolic pathways， including SREBP1， FASN， and SCD1（P<0.05）. Western blot results further confirmed that proteins in this pathway were significantly elevated in the model group， whereas they were markedly downregulated following Wumeiwan treatment（P<0.05）. Immunofluorescence analysis demonstrated enhanced co-localization of SREBP1 with the cancer-associated fibroblast（CAF） marker α-smooth muscle actin（SMA） in the model group， whereas this co-localization signal was attenuated after Wumeiwan intervention（P<0.05）. ConclusionWumeiwan can improve survival outcomes and alleviate colonic pathological damage in CRC mice， its therapeutic mechanism may be closely associated with the regulation of fatty acid metabolic reprogramming mediated by the SREBP1/FASN/SCD1 signaling pathway.

This paper systematically summarizes the practical experience of the 2025 Dingri earthquake emergency medical rescue in Tibet. It analyzes the requirements for earthquake medical rescue under conditions of high-altitude hypoxia, low temperature, and low air pressure. The paper provides a detailed discussion on the strategic layout of earthquake medical rescue at the national level, local government level, and through social participation. It covers the construction of rescue organizational systems, technical systems, material support systems, and information systems. The importance of building rescue teams is emphasized. In high-altitude and cold conditions, rapid response, scientific decision-making, and multi-party collaboration are identified as key elements to enhance rescue efficiency. By optimizing rescue organizational structures, strengthening the development of new equipment, and promoting telemedicine technologies, the precision and effectiveness of medical rescue can be significantly improved, providing important references for future similar disaster rescues.

Sleep deprivation (SD) has emerged as a significant modifiable risk factor for Alzheimer’s disease (AD), with mounting evidence demonstrating its multifaceted role in accelerating AD pathogenesis through diverse molecular, cellular, and systemic mechanisms. SD is refined within the broader spectrum of sleep-wake and circadian disruption, emphasizing that both acute total sleep loss and chronic sleep restriction destabilize the homeostatic and circadian processes governing glymphatic clearance of neurotoxic proteins. During normal sleep, concentrations of interstitial Aβ and tau fall as cerebrospinal fluid oscillations flush extracellular waste; SD abolishes this rhythm, causing overnight rises in soluble Aβ and tau species in rodent hippocampus and human CSF. Orexinergic neurons sustain arousal, and become hyperactive under SD, further delaying sleep onset and amplifying Aβ production. At the molecular level, SD disrupts Aβ homeostasis through multiple converging pathways, including enhanced production via beta-site APP cleaving enzyme 1 (BACE1) upregulation, coupled with impaired clearance mechanisms involving the glymphatic system dysfunction and reduced Aβ-degrading enzymes (neprilysin and insulin-degrading enzyme). Cellular and histological analyses revealed that these proteinopathies are significantly exacerbated by SD-induced neuroinflammatory cascades characterized by microglial overactivation, astrocyte reactivity, and sustained elevation of pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) through NF‑κB signaling and NLRP3 inflammasome activation, creating a self-perpetuating cycle of neurotoxicity. The synaptic and neuronal consequences of chronic SD are particularly profound and potentially irreversible, featuring reduced expression of critical synaptic markers (PSD95, synaptophysin), impaired long-term potentiation (LTP), dendritic spine loss, and diminished neurotrophic support, especially brain-derived neurotrophic factor (BDNF) depletion, which collectively contribute to progressive cognitive decline and memory deficits. Mechanistic investigations identify three core pathways through which SD exerts its neurodegenerative effects: circadian rhythm disruption via BMAL1 suppression, orexin system hyperactivity leading to sustained wakefulness and metabolic stress, and oxidative stress accumulation through mitochondrial dysfunction and reactive oxygen species overproduction. The review critically evaluates promising therapeutic interventions including pharmacological approaches (melatonin, dual orexin receptor antagonists), metabolic strategies (ketogenic diets, and Mediterranean diets rich in omega-3 fatty acids), lifestyle modifications (targeted exercise regimens, cognitive behavioral therapy for insomnia), and emerging technologies (non-invasive photobiomodulation, transcranial magnetic stimulation). Current research limitations include insufficient understanding of dose-response relationships between SD duration/intensity and AD pathology progression, lack of long-term longitudinal clinical data in genetically vulnerable populations (particularly APOE ε4 carriers and those with familial AD mutations), the absence of standardized SD protocols across experimental models that accurately mimic human chronic sleep restriction patterns, and limited investigation of sex differences in SD-induced AD risk. The accumulated evidence underscores the importance of addressing sleep disturbances as part of multimodal AD prevention strategies and highlights the urgent need for clinical trials evaluating sleep-focused interventions in at-risk populations. The review proposes future directions focused on translating mechanistic insights into precision medicine approaches, emphasizing the need for biomarkers to identify SD-vulnerable individuals, chronotherapeutic strategies aligned with circadian biology, and multi-omics integration across sleep, proteostasis and immune profiles may delineate precision-medicine strategies for at-risk populations. By systematically examining these critical connections, this analysis positions sleep quality optimization as a viable strategy for AD prevention and early intervention while providing a comprehensive roadmap for future mechanistic and interventional research in this rapidly evolving field.

In clinical practice,the diagnosis of hepatocellular carcinoma primarily relies on imaging findings.For cases with atypical imaging features or insufficient diagnostic specificity,pathological analysis remains essential.With the advancement of precision medicine,research focus has expanded from pure diagnostic evaluation to therapeutic efficacy prediction.Imaging-based prognostic biomarkers have emerged as a key research frontier in hepatocellular carcinoma management.Although accurate diagnosis remains paramount,current investigations increasingly prioritize the identification of biomarkers for treatment response prediction and outcome stratification.Recent studies demonstrate that radiological characteristics not only reflect tumor heterogeneity but also carry prognostic implications for hepatocellular carcinoma.These imaging biomarkers enable non-invasive outcome prediction and provide objective evidence to optimize therapeutic decision-making.This comprehensive review summarizes MRI-derived imaging features associated with hepatocellular carcinoma prognosis,aiming to guide personalized treatment strategies and ultimately improve survival outcomes for hepatocellular carcinoma patients.

OBJECTIVE To explore the effect of Astragali Radix-Curcuma Zedoaria-Paridis Rhizoma(Qi-Zhu-Zao)combina-tion on inhibiting the growth and metastasis of colon cancer based on the PINK1/Parkin/EMT signaling pathway.METHODS Thirty male BALB/c mice were randomly assigned to five groups:sham operation group,model group,positive control group,high-dose Qi-Zhu-Zao group(5.85 g·kg-1),and low-dose Qi-Zhu-Zao group(2.925 g·kg-1),with six mice in each group.An orthotopic colon cancer model was established in the mice using CT26.WT cells.After 15 days of treatment,tumor and liver tissues were collected from each group.Hematoxylin and eosin(HE)staining was performed to assess tumor metastasis,and transmission electron microscopy was used to observe mitochondrial autophagy in tumor tissues.The expression of mitochondrial autophagy-related proteins PINK1,Parkin,p62,and LC3-Ⅱ/LC3-Ⅰ was analyzed using Western blot and immunohistochemistry(IHC).Additionally,the expression levels of epithelial-mesenchymal transition(EMT)-related proteins and mRNA,including E-cadherin,N-cadherin,Vimentin,and Snail,were detected using Western blot,qPCR,and IHC staining.RESULTS Compared to the model group,mice in the treatment groups exhibited significantly reduced tumor volumes and fewer metastatic foci.Additionally,liver tissues showed pathological changes,and the overall growth condition of the mice was markedly improved;the tumor tissues in the treatment groups displayed selective mitochon-drial autophagy,accompanied by the formation of autophagosomes.The treatment influenced the PINK1/Parkin pathway-mediated mi-tochondrial autophagy biological process,with PINK1,Parkin,p62,and LC3-Ⅱ/LC3-Ⅰ levels being significantly upregulated(P<0.05,P<0.01),the high-dose group exhibited a more significant impact than the low-dose group(P<0.05,P<0.01).Furthermore,the treatment groups also showed significant reductions in the protein and mRNA levels of N-cadherin,Vimentin,and Snail(P<0.05,P<0.01),along with significant increases in the protein and mRNA levels of E-cadherin(P<0.05,P<0.01),these effects were more pronounced in the high-dose group compared to the low-dose group(P<0.05,P<0.01).CONCLUSION The herbal combination of Qi-Zhu-Zao inhibits tumor growth and metastasis to a certain extent in a mouse model of orthotopic transplantation of colon cancer.The underlying mechanism may involve the restoration of mitochondrial function through the PINK1/Parkin signaling pathway and the inhibition of the epithelial-mesenchymal transition(EMT)process,thereby achieving a therapeutic effect on colon cancer.

Objective:To investigate the related factors of cognitive impairment in middle-aged and old-aged patients with type 2 diabetes mellitus(T2DM).Methods:A total of 970 patients with T2DM(585 middle-aged group and 385 old-aged group)were selected from residents of a large community in Beijing from September to December 2018.The Mini-Mental State Examination(MMSE)was used to assess the cognitive func-tion.Multivariate logistic regression was used to analyze the related factors.Results:The detection rates of cognitive impairment were 12.0％and 13.5％in middle-aged and old-aged patients with T2DM,respectively.Among mid-dle-aged patients with T2DM,work(OR=0.22,95％CI:0.03-0.77)and education at the junior college or un-dergraduate level and above(OR=0.18,95％CI:0.04-0.55)were protective factors for cognitive impair-ment.Myocardial infarction(OR=4.13,95％CI:1.26-13.63)was a risk factor for cognitive impairment.Among old-aged patients with T2DM,drinking tea 1-2 times a week(OR=0.11,95％CI:0.01-0.58)and education at the junior college or undergraduate level and above(OR=0.19,95％CI:0.05-0.54)were protective factors for cognitive impairment.Stroke(OR=3.64,95％CI:1.55-8.39)and good sleep self-assessment(OR=2.75,95％CI:1.13-7.35)were risk factors for cognitive impairment.Conclusion:Cognitive impairment in middle-aged pa-tients with T2DM is related to work,education level and myocardial infarction,and cognitive impairment in old-aged patients with T2DM is related to lifestyle,education level and stroke.

AIM To study the chemical constituents from Asteris Radix et Rhizoma and their anti-inflammatory activities.METHODS The extract from Asteris Radix et Rhizoma was isolated and purified by column chromatography and high performance liquid chromatography,then the structures of obtained compounds were identified by physicochemical properties and spectral data.Their anti-inflammatory activities were evaluated by RAW264.7 model.RESULTS Thirteen compounds were isolated and identified as(Z)-9,10,11-trihydroxy-12-octadecenoic acid(1),tianshic acid(2),6,6-dimethyl-2-methlenebicyclo[3.1.1]hept-3-O-(6-O-apiofuranosyl)-β-D-glucopyranoside(3),ent-16β,17-dihydroxy-kauran-19-oic acid(4),ent-17-hydroxy-19-kauranoic acid(5),7β,17-dihydroxy-16α-ent-kauran-19-oic acid 19-O-β-D-glucopyranoside ester(6),paniculoside Ⅳ(7),thomimarine A(8),cyclo-(S-Pro-R-Leu)(9),4,5-di-O-caffeoylquinic acid 1-methyl ether(10),methyl 3,5-di-O-caffeoyl quinate(11),5-acetyl-3β-hydroxy-2β-(1-hydroxyisopropyl)-2,3-dihydrobenzofurane(12),4-ally-2,6-dimethoxyphenyl glucoside(13).Compounds 1 and 3-12 had inhibition on the release of NO in RAW264.7 cells,and 4-6,8,10-12 were better than the positive control.CONCLUSION Compounds 1,6,8-9 are isolated from Compositae family for the first time,and 2-5,7,10 and 11-13 are first isolated from this plant.Compounds 1,3-12 have anti-inflammatory activities.

Purpose To analyze and compare the impact of incorporating molecular classification into the new FI-GO(2023)staging system for endometrial cancer(EC).Methods A retrospective analysis was conducted on 332 ca-ses of EC diagnosed and molecular subtyped by Department of Pathology Tianjin Central Hospital of Gynecology Obstet-rics in 2023.All cases were staged according to the FIGO(2023)staging criteria for EC.Results The median age of the 332 EC patients was 56 years(range:27-76 years).Molecular subtypes included 30 POLE mutation(POLE-mut),80 mismatch repair deficiency(MMRd),194 no specific molecular profile(NSMP),and 28 p53 abnormal(p53abn).Significant differences were observed among the four molecular subtypes regarding age,FIGO stage,patho-logical type,and lymph node metastasis rate(P＜0.05).However,no significant differences were found in the depth of myometrial invasion or lymphovascular space invasion.In the POLEmut group,19 cases(63.33％)were of non-ag-gressive histological types and 11(36.67％)were aggressive.After incorporating molecular subtyping,all 11 stage Ⅱ patients were downgraded to stage Ⅰ AmPOLEmut,increasing the proportion of stage Ⅰ patients from 62.07％to 100％.In the p53abn group,9 cases(32.14％)were non-aggressive and 19(67.86％)were aggressive.Molecular integra-tion led to the upstaging of 4 stage Ⅰ patients with myometrial invasion to stage Ⅱ Cmp53abn,increasing the proportion of stage Ⅱ patients from 34.61％to 50％.Conclusion Molecular subtypes p53abn and POLEmut are associated with distinct alterations in EC staging,specifically leading to tumor upstaging or downstaging.Our findings underscore the critical importance of comprehensive molecular subtyping in EC staging,as it refines prognostic risk stratification and provides valuable guidance for adjuvant treatment decisions.

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.

Objective To explore the incidence and its influencing factors of transient severe motion(TSM)in the arterial phase of gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid(Gd-EOB-DTPA)enhanced MRI.Methods The databases of China National Knowledge Network(CNKI),VIP,Wanfang,PubMed,and Embase were searched for studies on the incidence and influencing factors of TSM,and the search time was from the establishment of the databases to October 2024.Meta-analysis was performed via Stata 17.0 software.Results A total of 30 papers(33 studies)were finally included,totaling 12 565 patients.Meta-analysis results showed that the incidence of TSM in the arterial phase of Gd-EOB-DTPA enhanced MRI was 13.0％.The risk factors for TSM included age[odds ratio(OR)=1.03;95％confidence interval(CI)1.02-1.05;P＜0.001),chronic obstructive pulmonary disease(COPD)(OR=4.21;95％CI 1.76-10.09;P=0.001),and moderate-to-severe pleural effusion(OR=3.34;95％CI 1.69-6.63;P=0.001),while a previous usage history of Gd-EOB-DTPA(OR=0.56;95％CI 0.39-0.81;P=0.002)was a protective factor of TSM.Conclusion The incidence of TSM in the arterial phase of Gd-EOB-DTPA enhanced MRI is relatively high.Age,COPD,moderate-to-severe pleural effusion are risk factors for TSM,while the previous usage history of Gd-EOB-DTPA is a protective factor for TSM.