As the core vehicle for preserving and transmitting traditional Chinese medicine（TCM） academic thought and clinical experience， the establishment of a robust quality evaluation system for TCM clinical case reports is a crucial component in the current standardization and modernization of TCM. Based on the practical experience of constructing the China Clinical Cases Library of Traditional Chinese Medicine by the China Association of Chinese Medicine， this study conducted a comprehensive analysis of critical challenges， including insufficient authenticity and unfocused evaluation criteria. It proposed a three-dimensional evaluation framework grounded in the structure-process-outcome logic， encompassing three dimensions of authenticity and standardization， characteristics and advantages， application and translational impact. This framework integrated 12 key evaluation indicators in a systematic manner. The model preserved the academic characteristics of TCM syndrome differentiation and treatment， while aligning with modern scientific research standards， achieving a balance between individualized TCM experience and standardized evaluation. Concurrently， this study provided theoretical foundations and methodological guidance for evaluating the quality of TCM clinical cases， contributing significantly to the inheritance of TCM knowledge， evidence-based practice， and the reform of talent evaluation mechanisms.

Objective To analyze the characteristics of hearing loss at different frequencies among noise-exposed workers in a lithium battery manufacturing enterprise. Methods A total of 1 954 noise-exposed workers from a large lithium battery manufacturing enterprise were selected as the study subjects using the judgmental sampling method. Pure-tone audiometry, individual noise exposure level monitoring, and workplace noise intensity measurement were conducted. Results The overall detection rate of hearing loss among the study subjects was 39.0%. The detection rates of unilateral and bilateral hearing loss were 21.0% (410/1 954) and 18.0% (352/1 954), respectively. The detection rate of hearing loss in the right ear was higher than that in the left ear (30.1% vs 26.9%, P<0.05). The detection rates of elevated hearing thresholds at high frequencies and speech frequencies were 38.8% and 1.1%, respectively. Comparisons of the detection rates of elevated hearing thresholds across different frequencies between the left and right ears showed significant differences (all P<0.01); specifically, the detection rate at 4.0 kHz in the right ear was higher than that in the left ear (P<0.01). The detection rates of elevated hearing thresholds at 2.0, 4.0, and 6.0 kHz increased with longer duration of noise exposure (all P<0.05). Except at 1.0 kHz, the detection rates of elevated hearing thresholds at 0.5, 2.0, 3.0, 4.0, and 6.0 kHz showed increasing trends with age (all P<0.05). Conclusion Hearing loss among noise-exposed workers in the lithium battery manufacturing industry is predominant in the high-frequency type, with the highest sensitivity at 4.0 kHz and greater susceptibility in the right ear. The detection rate of high frequency hearing loss increases with longer noise exposure duration and advacing age. Health surveillance should focus on workers with longer noise exposure duration and older age. Noise control measures should be strengthened.

With the rapid development of generative artificial intelligence(GAI)technologies,their widespread application in academic research and writing is continuously expanding the boundaries of sci-entific inquiry.However,this trend has also raised a series of ethical and regulatory challenges,inclu-ding issues related to authorship,content authenticity,citation accuracy,and accountability.In light of the growing involvement of AI in generating academic content,establishing an open,controllable,and trustworthy ethical governance framework has become a key task for safeguarding research integrity and maintaining trust within the academic community.This expert consensus outlines ethical requirements across key stages of AI-assisted academic writing-including topic selection,data management,citation practices,and authorship attribution.It aims to clarify the boundaries and ethical obligations surrounding AI use in academic writing,ensuring that technological tools enhance efficiency without compromising in-tegrity.The goal is to provide guidance and institutional support for building a responsible and sustainable research ecosystem.

AIM To establish a rapid quantitative analysis model for saponins in Paris polyphylla var.yunnanensis(PPY)by near infrared spectroscopy.METHODS The contents of polyphyllins Ⅰ,Ⅱ,Ⅶ and there total content in PPY were determined by HPLC,while spectral data within the range of 10 000 to 4 000 cm-1 were collected.A quantitative analysis model was established by combining these data with partial least squares regression(PLSR).Multivariate scatter correction(MSC)and vector normalization(SNV)were applied prior to further preprocessing the spectra with original,first-order derivative(1stD),or second-order derivative(2ndD)treatments.Lastly,the model was optimized through non-smoothing(NS),Norris Derivative filtering(Nd),and Savitzky-Golay filtering(S-G)method.Model stability was evaluated based on correlation coefficients and variance.The predicted contents of each saponin component in the validation set samples were calculated.RESULTS The contents of polyphyllins Ⅰ,Ⅱ,Ⅶ were 0.42-17.98,0.46-10.44,0.23-3.86 mg/g,respectively.The total content ranged from 2.91 to 22.1 mg/g.The optimal parameters of three saponins were achieved when selecting the MSC+2ndD+S-G pretreatment method.The corresponding ratio of line segment length to segment gap was 13∶5,15∶5,11∶5,with correlation coefficients of 0.982,0.930,0.958,respectively.The root mean square errors of calibration(RMSEC)were 0.702,0.797,0.238,and the root mean square errors of prediction(RMSEP)were 1.120,0.835,0.304,respectively.The optimal parameters for the total content were obtained when selecting the MSC+2ndD+NS pretreatment method,with a correlation coefficient of 0.970,a RMSEC of 1.090,and a RMSEP of 1.740.CONCLUSION This accurate and rapid method can be used for detection of saponin contents in P.Polyphylla.

Objective To explore the role of sevoflurane(SEV)in sepsis-induced acute lung injury(ALI)and observe its impact on the Wnt/β-catenin signaling pathway.Methods Forty C57 mice were randomly divided into 4 groups(n=10 each):Sham,CLP,SEV,and SEV+XAV(β-catenin inhibitor).A sepsis model was established via cecal ligation and puncture.Lung injury was evaluated using HE staining,lung wet/dry weight ratio,and TUNEL staining.Levels of inflammatory factors(TNF-α,IL-1β,IL-6)were detected by ELISA.Oxidative stress indices(SOD,MDA,ROS)were measured by colorimetry and flow cytometry.Hindlimb blood perfusion and oxygenation were assessed with laser speckle flowmetry.Expressions of key Wnt pathway molecules and down-stream target genes(c-Myc,Cyclin D1)were detected by RT-qPCR and Western blot.Co-localization of β-catenin and SP-C(a marker of type Ⅱ alveolar epithelial cells)in lung tissues was determined by immunofluorescence staining.Results Compared with the Sham group,the CLP group exhibited significant increases in sepsis severity,lung pathological damage including alveolar structure destruction,inflammatory infiltration,and apoptosis,elevation in pro-inflammatory cytokine levels,and significant decrease in SOD and increase in MDA and ROS.Additionally,lower limb blood flow and oxygenation levels were significantly reduced,while the expression of β-catenin and its downstream target genes,as well as the co-localization signal and fluorescence intensity of β-catenin with SP-C,were significantly downregulated(all P<0.05).Compared with the CLP group,the SEV group showed significant improvements in all these indicators.However,compared with the SEV group,the SEV+XAV group demon-strated a reversed protective effect,with all indicators approaching the levels observed in the CLP group(all P<0.05).Conclusion Sevoflurane alleviates sepsis-induced ALI by activating Wnt/β-catenin signaling pathway,exerting anti-inflammatory and antioxidant effects,and enhancing the expression and localization of β-catenin in type Ⅱ alveolar epithelial cells.

Based on ultra-high performance liquid chromatography-quadrupole-Exactive Orbitrap mass spectrometry(UPLC-Q-Exactive Orbitrap-MS) technology and network pharmacology, this study explored the pharmacodynamic substances and potential mechanisms of Huazhuo Sanjie Chubi Decoction in the treatment of gouty arthritis(GA). UPLC-Q-Exactive Orbitrap-MS technology was used to identify the components in Huazhuo Sanjie Chubi Decoction, and the qualitative analysis of its active ingredients was carried out, with a total of 184 active ingredients identified. A total of 897 active ingredient targets were screened through the PharmMapper database, and 491 GA-related disease targets were obtained from the OMIM, GeneCards, CTD databases. After Venn analysis, 60 intersecting targets were obtained. The component target-GA target network was constructed through the Cytoscape platform, and the STRING database was used to construct a protein-protein interaction network, with 16 core targets screened. The core targets were subjected to Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analyses, and the component-target-pathway network was constructed. It was found that the main active ingredients of the formula for the treatment of GA were phenols, flavonoids, alkaloids, and terpenoids, and the key targets were SRC, MMP3, MMP9, REN, ALB, IGF1R, PPARG, MAPK1, HPRT1, and CASP1. Through GO analysis, it was found that the treatment of GA mainly involved biological processes such as lipid response, bacterial response, and biostimulus response. KEGG analysis showed that the pathways related to the treatment of GA included lipids and atherosclerosis, neutrophil extracellular traps(NETs), IL-17, and so on. In summary, phenols, flavonoids, alkaloids, and terpenoids may be the core pharmacodynamic substances of Huazhuo Sanjie Chubi Decoction in the treatment of GA, and the pharmacodynamic mechanism may be related to SRC, MMP3, MMP9, and other targets, as well as lipids and atherosclerosis, NETs, IL-17, and other pathways.
Drugs, Chinese Herbal/therapeutic use* ; Network Pharmacology ; Arthritis, Gouty/metabolism* ; Chromatography, High Pressure Liquid/methods* ; Humans ; Mass Spectrometry/methods* ; Protein Interaction Maps/drug effects*

OBJECTIVES: To investigate the molecular epidemiology of children with phenylketonuria (PKU) in Gansu, China, providing foundational data for intervention strategies. METHODS: A retrospective analysis was conducted on 1 159 PKU families who attended Gansu Provincial Maternity and Child Care Hospital from January 2012 to December 2024. Sanger sequencing, multiplex ligation-dependent probe amplification, whole exome sequencing, and deep intronic variant analysis were used to analyze the PAH gene. RESULTS: For the 1 159 children with PKU, 2 295 variants were identified in 2 318 alleles, resulting in a detection rate of 99.01%. The detection rates were 100% (914/914) in 457 classic PKU families, 99.45% (907/912) in 456 mild PKU families, and 96.34% (474/492) in 246 mild hyperphenylalaninemia families. The 2 295 variants detected comprised 208 distinct mutation types, among which c.728G>A (14.95%, 343/2 295) had the highest frequency, followed by c.611A>G (4.88%, 112/2 295) and c.721C>T (4.79%, 110/2 295). The cumulative frequency of the top 23 hotspot variants reached 70.28% (1 613/2 295), and most variant alleles were detected in exon 7 (29.19%, 670/2 295). CONCLUSIONS Deep intronic variant analysis of the PAH gene can improve the genetic diagnostic rate of PKU. The development of targeted detection kits for PAH hotspot variants may enable precision screening programs and enhance preventive strategies for PKU.
Humans ; Phenylketonurias/epidemiology* ; Female ; Male ; Retrospective Studies ; Phenylalanine Hydroxylase/genetics* ; Mutation ; Child, Preschool ; China/epidemiology* ; Child ; Infant

BACKGROUND: Double-stranded RNA-specific adenosine deaminase 1 (ADAR1) binds to double-stranded RNA and catalyzes the deamination of adenosine (A) to inosine (I). The functional mechanism of ADAR1 in non-small cell lung cancer (NSCLC) remains incompletely understood. This study aimed to investigate the prognostic significance of ADAR1 in NSCLC and to elucidate its potential role in regulating tumor cell proliferation and migration. METHODS: Data from The Cancer Genome Atlas (TCGA) and cBioPortal were analyzed to assess the correlation between high ADAR1 expression and clinicopathological features as well as prognosis in lung cancer. We performed Western blot (WB), cell proliferation assays, Transwell invasion/migration assays, and nude mouse xenograft modeling to examine the phenotypic changes and molecular mechanisms induced by ADAR1 knockdown. Furthermore, the ADAR1 p150 overexpression model was utilized to validate the proposed mechanism. RESULTS: ADAR1 expression was significantly elevated in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) tissues compared with adjacent non-tumor tissues (LUAD: P=3.70×10-15, LUSC: P=0.016). High ADAR1 expression was associated with poor prognosis (LUAD: P=2.03×10-2, LUSC: P=2.81×10-2) and distant metastasis (P=0.003). Gene Set Enrichment Analysis (GSEA) indicated that elevated ADAR1 was associated with mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway activation, matrix metalloproteinase-9 (MMP-9) expression, and cell adhesion. ADAR1 and MMP-9 levels showed a strongly positive correlation (P=6.45×10-34) in 10 lung cancer cell lines, highest in H1581. Knockdown of ADAR1 in H1581 cells induced a rounded cellular morphology with reduced pseudopodia. Concomitantly, it suppressed cell proliferation, invasion, migration, and in vivo tumorigenesis. It also suppressed ERK phosphorylation and downregulated cellular Finkel-Biskis-Jinkins murine osteosarcoma viral oncogene homolog (c-FOS), MMP-9, N-cadherin, and Vimentin. Conversely, ADAR1 p150 overexpression in PC9 cells enhanced ERK phosphorylation and increased c-FOS and MMP-9 expression. CONCLUSIONS High ADAR1 expression is closely associated with poor prognosis and distant metastasis in NSCLC patients. Mechanistically, ADAR1 may promote proliferation, invasion, migration, and tumorigenesis in lung cancer cells via the ERK/c-FOS/MMP-9 axis.
Humans ; Lung Neoplasms/physiopathology* ; Adenosine Deaminase/genetics* ; Matrix Metalloproteinase 9/genetics* ; Cell Proliferation ; Carcinoma, Non-Small-Cell Lung/physiopathology* ; Cell Movement ; Animals ; Mice ; RNA-Binding Proteins/genetics* ; Female ; Male ; Cell Line, Tumor ; Proto-Oncogene Proteins c-fos/genetics* ; Middle Aged ; MAP Kinase Signaling System ; Gene Expression Regulation, Neoplastic ; Mice, Nude ; Extracellular Signal-Regulated MAP Kinases/genetics*

OBJECTIVE: To investigate the effect of miR-483-5p on hepatocellular carcinoma (HCC) cells proliferation and stemness, as well as the attenuating effect of Pien Tze Huang (PZH). METHODS: Differentially expressed miRNA between HepG2 cells and hepatic cancer stem-like cells (HCSCs) were identified by a miRNA microarray assay. miR-483-5p mimics were transfected into HepG2 cells to explore the effects of miR-483-5p on cell proliferation and stemness. HepG2 cells and HCSCs were treated with PZH (0, 0.25, 0.50 and 0.75 mg/mL) to explore the effects of PZH on the proliferation and stemness, both in non-induced state and the state induced by miR-483-5p mimics. RESULTS: miR-483-5p was significantly up-regulated in HCSCs and its overexpression increased cell proliferation and stemness in HepG2 cells (P<0.05). PZH not only significantly inhibited proliferation in HepG2 cells, but also significantly suppressed the cell proliferation and self-renewal of HCSCs (P<0.05). The effects of miR-483-5p mimics on proliferation and stemness of HepG2 cells were partially abolished by PZH. CONCLUSIONS miR-483-5p promotes proliferation and enhances stemness of HepG2 cells, which were attenuated by PZH, demonstrating that miR-483-5p is a potential molecular target for the treatment of HCC and provide experimental evidence to support clinical use of PZH for patients with HCC.
Humans ; MicroRNAs/metabolism* ; Cell Proliferation/drug effects* ; Liver Neoplasms/drug therapy* ; Carcinoma, Hepatocellular/drug therapy* ; Hep G2 Cells ; Neoplastic Stem Cells/metabolism* ; Drugs, Chinese Herbal/therapeutic use* ; Gene Expression Regulation, Neoplastic/drug effects*