Both cathartic colon （CC） and cathartic-dependent constipation （CDC） are caused by the abuse of stimulant laxatives， while their concepts are not completely the same.Starting from the disease name of CC， this article traced the origin and evolution of the concept of CC， summarizes and compared the similarities and differences between CC， CDC， and slow transit constipation （STC）， and called for strict differentiation among the three.Furthermore， this article explored the specific contents of Western medicine clinical subtypes and traditional Chinese medicine （TCM） syndrome differentiation of CDC and delved into the TCM pathogenesis of CDC according to both literature and clinical practice.The relationship between clinical subtypes and TCM syndromes was established， and the syndrome characteristics of CDC of different clinical subtypes and TCM syndromes were summarized.The recommended prescriptions for corresponding syndromes were listed.A systematic CDC diagnosis and treatment approach of "clinical subtypes-syndrome differentiation-syndrome characteristics-recommended prescriptions" was thus formed.Additionally， the paper provides an overview of current research on CDC in both Western medicine and TCM contexts， identifies future research directions， and suggests research pathways for refining and advancing CDC studies.

ObjectiveTo observe the clinical efficacy of the Yiqi Yangyin Huoxue prescription （YYHP） in the treatment of cathartic colon （CC） and its effects on fecal short-chain fatty acids （SCFAs）， and to explore the correlations among CC severity indicators and between these indicators and patient history. MethodsAccording to the inclusion and exclusion criteria， 98 patients meeting the diagnostic criteria of both traditional Chinese and Western medicine for CC with the syndrome of Qi-Yin deficiency complicated by blood stasis were randomly assigned to an observation group and a control group. The observation group received YYHP granules， while the control group received lactulose. Both medications were administered twice daily， one sachet each time， half an hour after breakfast and dinner， with a treatment course of 8 weeks. The primary constipation symptom score， Patient Assessment of Constipation Quality of Life （PAC-QOL） score， and TCM syndrome score were assessed before and after treatment and at the 8^th week after the end of treatment. The overall clinical effective rate， as well as the efficacy attenuation index and degree， were evaluated. Fecal SCFA levels were measured using gas chromatography-mass spectrometry （GC-MS）. Spearman correlation analysis was performed to explore the correlations among CC severity indicators and between these indicators and patient history. ResultsThe overall clinical effective rate in the observation group （95.83%） was higher than that in the control group （78.72%） （P<0.05）. After treatment， the total scores for primary constipation symptoms， PAC-QOL， and TCM syndromes decreased in both groups （P<0.05）， with more significant reductions in the observation group （P<0.05）. The severity of all primary constipation symptoms was alleviated in both groups （P<0.05）. In terms of "excessive straining and difficult defecation"， "anal heaviness， incomplete evacuation， and bloating sensation"， "abdominal distension"， and "defecation frequency"， the observation group showed better efficacy than the control group （P<0.05）. Scores of the four PAC-QOL dimensions and the scores and severity of primary and secondary TCM symptoms were reduced in both groups （P<0.05）， with more significant reductions in the observation group （P<0.05）. After treatment， acetic acid， propionic acid， butyric acid， and total SCFAs in the observation group increased significantly （P<0.05）. The efficacy attenuation index and degree in the observation group were lower than those in the control group （P<0.05）. No severe adverse reactions occurred in either group， and there was no statistically significant difference in the incidence of adverse reactions between the two groups. Positive correlations of varying degrees were observed among the total scores of primary constipation symptoms， PAC-QOL， and TCM syndromes， as well as between these scores and the history of stimulant laxative use， disease duration， and age. ConclusionYYHP can effectively alleviate the primary constipation symptoms in CC patients， improve quality of life， and ameliorate TCM syndromes， with good safety. It also has the advantage of a lower rebound degree after drug withdrawal， and its mechanism may be related to increasing fecal SCFA levels. Long-term abuse of stimulant laxatives may aggravate the severity of CC and prolong the disease course.

[摘 要] 目的：探讨lncRNA核内富集丰富转录本1（NEAT1）调控miR-1287-5p/DNA损伤诱导转录本4（DDIT4）轴对卵巢癌SKOV3细胞增殖、凋亡和侵袭的影响及其机制。方法：收集2023年6月至2024年6月期间湖北医药学院附属随州医院手术切除的27例卵巢癌患者的癌及癌旁组织标本，以及正常人卵巢上皮细胞IOSE80和卵巢癌细胞系SKOV3、CAOV3和A2780，RT-qPCR检测卵巢癌组织与细胞中lncRNA NEAT1、miR-1287-5p及DDIT4 mRNA表达。将SKOV3细胞分为Ctrl组、si-NC组、si-NEAT1组、si-NEAT1 + anti-miR-NC组、si-NEAT1 + anti-miR-1287-5p组、si-NEAT1 + vector组、si-NEAT1 + OE-DDIT4组。CCK-8法、克隆形成实验、流式细胞术、Transwell实验分别检测各组细胞增殖、凋亡及侵袭能力，WB法检测细胞中DDIT4、细胞周期蛋白D1（cyclin D1）、p53、迁移侵袭增强子1（MIEN1）蛋白水平。双萤光素酶报告基因验证lncRNA NEAT1与miR-1287-5p/DDIT4靶向结合关系，RNA pull-down实验、RNA免疫沉淀实验分别验证lncRNA NEAT1与miR-1287-5p、miR-1287-5p与DDIT4的靶向结合关系。另设pcDNA组（转染空载体pcDNA3.1）和pc-NEAT1 组（转染pcDNA-NEAT1）以验证NEAT1过表达效应。结果：卵巢癌组织中lncRNA NEAT1、DDIT4 mRNA表达水平显著高于癌旁组织（P < 0.05），而miR-1287-5p表达显著低于癌旁组织（P < 0.05）。敲低lncRNA NEAT1后，与Ctrl组和si-NC组相比，si-NEAT1组lncRNA NEAT1表达、DDIT4 mRNA表达均显著降低（均P < 0.05），miR-1287-5p 表达显著升高（P < 0.05）；而过表达lncRNA NEAT1则下调miR-1287-5p表达并上调DDIT4表达，呈现与敲低实验相反的调控效应；敲低lncRNA NEAT1后，克隆形成数、细胞增殖活性、细胞侵袭数均显著降低（均P < 0.05），细胞凋亡率显著升高（P < 0.05）；DDIT4、cyclin D1、MIEN1蛋白表达均显著降低（均P < 0.05），p53蛋白表达显著升高（P < 0.05）。进一步实验证实，anti-miR-1287-5p或OE-DDIT4均可减弱si-NEAT1对SKOV3细胞增殖和侵袭的抑制作用，同时减弱其对细胞凋亡的促进作用。lncRNA NEAT1靶向调控miR-1287-5p/DDIT4。结论：lncRNA NEAT1通过靶向调控miR-1287-5p/DDIT4轴促进SKOV3细胞增殖和侵袭，抑制细胞凋亡。

Objective To explore the effect and mechanism of Gegen Qinlian decoction (GQD) on myocardial injury induced by high-fat diet combined with streptozotocin in type 2 diabetic mice through network pharmacology and animal experiments. MethodsNetwork pharmacology was applied to screen the potential signaling pathways of GQD in the intervention of diabetic heart disease (DHD). A total of 36 specific pathogen-free (SPF) male C57BL/6J mice aged 8 weeks were acclimatized for 1 week and randomly divided into a normal control group (n=6) and a model group (n=30). Mice in the model group were fed a 60% high-fat diet and 5% glucose water for 4 weeks, and were intraperitoneally injected with 100 mg/kg streptozotocin after 12 h of fasting to establish the type 2 diabetes model. Mice in the normal control group were given a conventional diet and drinking water, and were intraperitoneally injected with an equal volume of citrate buffer after 12 h of fasting at the same time point. After successful establishment of the diabetic mouse model, the model mice were randomly divided into five groups according to body weight: model control group, GQD low-dose group, GQD medium-dose group, GQD high-dose group, and metformin positive control group, with 6 mice in each group. After 6 weeks of intragastric administration of corresponding doses of GQD, metformin, and ddH₂O respectively, all mice in the six groups (one normal control group and five model groups) were anesthetized with inhaled 2% isoflurane, blood samples were collected via eyeball enucleation, and heart tissues were harvested after euthanasia by cardiac exsanguination. Hematoxylin-eosin (HE) staining and wheat germ agglutinin (WGA) staining were performed to observe the pathological damage of myocardial tissues and measure the cross-sectional area of cardiomyocytes. Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of pro-inflammatory cytokines in serum. Immunohistochemical staining was adopted to determine the protein expression levels of receptor for advanced glycation end products (RAGE), nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3), and phosphorylated nuclear factor-κB p65 (p-p65) in myocardial tissues. ResultsNetwork pharmacology analysis revealed that the targets of GQD against DHD were significantly enriched in inflammatory pathways, including the advanced glycation end products (AGEs)-RAGE axis, tumor necrosis factor (TNF) and interleukin-17 (IL-17) signaling pathways. HE and WGA staining results showed that, compared with the normal control group, the model control group exhibited myocardial fiber rupture, cardiomyocyte swelling, and significantly increased cardiomyocyte cross-sectional area (P<0.05). Compared with the model control group, GQD intervention significantly ameliorated the pathological changes, including myocardial fiber rupture, cell swelling, and cardiomyocyte hypertrophy. The results of immunohistochemical staining and ELISA indicated that compared with the model control group, GQD intervention markedly downregulated the protein expression of RAGE, NLRP3, and p-p65 in myocardial tissues, as well as the levels of serum pro-inflammatory cytokines (P<0.05). ConclusionGQD can effectively alleviate myocardial pathological injury in diet-induced type 2 diabetic mice, and its mechanism may be related to inhibiting the activation of the RAGE/p-p65/NLRP3 signaling pathway and reducing myocardial inflammatory response.

Objective To develop an artificial intelligence (AI)-driven lung cancer database by structuring and standardizing clinical data, enabling advanced data mining for lung cancer research, and providing high-quality data for real-world studies. Methods Building on the extensive clinical data resources of the Department of Thoracic Surgery at Peking Union Medical College Hospital, this study utilized machine learning techniques, particularly natural language processing (NLP), to automatically process unstructured data from electronic medical records, examination reports, and pathology reports, converting them into structured formats. Data governance and automated cleaning methods were employed to ensure data integrity and consistency. Results As of September 2024, the database included comprehensive data from 18 811 patients, encompassing inpatient and outpatient records, examination and pathology reports, physician orders, and follow-up information, creating a well-structured, multi-dimensional dataset with rich variables. The database’s real-time querying and multi-layer filtering functions enabled researchers to efficiently retrieve study data that meet specific criteria, significantly enhancing data processing speed and advancing research progress. In a real-world application exploring the prognosis of non-small cell lung cancer, the database facilitated the rapid analysis of prognostic factors. Research findings indicated that factors such as tumor staging and comorbidities had a significant impact on patient survival rates, further demonstrating the database’s value in clinical big data mining. Conclusion The AI-driven lung cancer database enhances data management and analysis efficiency, providing strong support for large-scale clinical research, retrospective studies, and disease management. With the ongoing integration of large language models and multi-modal data, the database’s precision and analytical capabilities are expected to improve further, providing stronger support for big data mining and real-world research of lung cancer.

Background and aims:Hepatocellular carcinoma(HCC)is a leading cause of cancer-related mortality worldwide,and its etiology involves a complex interplay of genetic and environmental factors.Despite ad-vancements in our understanding of HCC biology and the development of novel therapeutic strategies,the molecular mechanisms underlying its onset,progression,and resistance to therapy remain largely vague.This study aimed to investigate the role of mechanosensitive ion channel-related genes(MICRGs)in HCC,focusing on their potential as prognostic biomarkers and their involvement in immune modulation and drug resistance.Methods:A comprehensive analysis was conducted using The Cancer Genome Atlas database to identify MICRGs that are upregulated in HCC.Gene expression profiling,bioinformatics tools,and functional experiments were employed to elucidate the role of these channels.In addition,protein-protein interaction(PPI)network analyses and enrichment analyses were performed to explore the biological significance of these genes.An immune cell infiltration analysis was also conducted to understand MICRG-related immune landscape.Single-cell RNA sequencing(scRNA-seq)data were utilized to identify MICRGs in different cell types within the HCC tissue.Deep-learning neural network analysis across patient cohorts was conducted to identify genes associated with sorafenib resistance.Knockdown ex-periments,cell viability assays,and apoptosis assays on HCC cell lines were performed to examine the role of Piezo-type mechanosensitive ion channel component 1(PIEZO1)in sorafenib resistance.Results:The analysis identified a subset of MICRGs,including PIEZO1,that were significantly upregulated in HCC and associated with poor prognosis.The PPI network analysis revealed complex interactions among these genes.Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses proposed the involvement of these genes in calcium signaling pathways.Immune cell infiltration analysis demonstrated distinct associations between MICRGs and various immune subpopulations,highlighting their potential roles in immune modulation.scRNA-seq data indicated the upregulation of MICRGs in various cell types in HCC tissues,particularly in endothelial cells and tumor-associated macrophages.Deep-learning neural network analysis across different patient cohorts identified PIEZO1 as a crucial regulator of sorafenib resistance in HCC,which was further validated by functional assays on HCC cell lines.Conclusions:This study provides evidence that MICRGs,particularly PIEZO1,take on crucial roles in HCC progression and drug resistance.The upregulation of PIEZO1 in HCC cells is associated with poor prog-nosis and resistance to sorafenib.These findings indicate that PIEZO1 could serve as a potential thera-peutic target for overcoming drug resistance and a prognostic biomarker in HCC.Future studies should focus on validating these findings in larger patient cohorts and exploring the functional implications of targeting PIEZO1 in preclinical models.

Objective To observe the clinical efficacy of Fangxiang Wentong Powder(composed of Salviae Miltiorrhizae Radix et Rhizoma,Chuanxiong Rhizoma,Alpiniae Officinarum Rhizoma,Piper Longum,and Corydalis Rhizoma)acupoint application combined with Kuanxiong Aerosol in treating female patients with coronary slow flow(CSF)associated angina.Methods After sample size estimation,119 female inpatients diagnosed as CSF associated angina and differentiated as chest-qi obstruction with yang deficiency and cold accumulation syndrome of traditional Chinese medicine(TCM)were collected from the cardiovascular departments of the Third People's Hospital of Fujian University of Traditional Chinese Medicine,the Second Affiliated Hospital of Guangzhou University of Chinese Medicine(Guangdong Provincial Hospital of Chinese Medicine),Zhanjiang First Traditional Chinese Medicine Hospital,and Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine from November 2023 to March 2024.Using a table of random numbers,the patients were divided into a treatment group(84 cases)and a control group(35 cases)in a ratio of 5∶2.The control group was treated with Isosorbide Monomitrate Sustained-Release Capsules,while the treatment group was treated with application of Fangxiang Wentong Powder on acupoints of Danzhong(CV17),Gaohuang(BL43),and Xinshu(BL15),together with sublingual administration of Kuanxiong Aerosol.The treatment course for both groups covered 7 days.Before and after treatment,the changes in the simplified Seattle Angina Questionnaire(SAQ-7)scores,Chinese Quality of Life Questionnaire for Cardiovascular Patients(CQQC)scores,6-minute walking distance(6MWD),serum C-reactive protein(CRP)level,and white blood cell-to-mean platelet volume ratio(WMR)were observed.The TCM symptom efficacy was compared between the two groups,and adverse reactions were monitored.Results(1)There were 8 patients withdrew in the treatment group for failing in completing the questionnaires,and 2 patients withdrew in the control group for suffering headaches after taking nitrates.Eventually,109 patients completed the trial,including 76 in the treatment group and 33 in the control group.(2)After 7 days of treatment,the total effective rate for TCM symptom efficacy in the treatment group was 86.84%(66/76),and that in the control group was 72.73%(24/33).The intergroup comparison(tested by the chi-square test)showed that the TCM symptom efficacy in the treatment group was significantly superior to that in the control group.(3)After treatment,both groups showed improvements in the scores of activity limitation and angina frequency items of SAQ-7,and the treatment group also showed improvements in the scores of subjective satisfaction item of SAQ-7(P＜0.05).The treatment group's improvements in the scores of activity limitation,angina frequency,and subjective satisfaction items of SAQ-7 were significantly superior to those of the control group(P＜0.05).(4)After treatment,the CQQC scores in the treatment group was significantly improved(P＜0.05),while no significant improvement was observed in the control group(P＞0.05).The improvement of CQQC scores in the treatment group was significantly superior to that in the control group(P＜0.05).(5)After treatment,both groups showed improvements in 6MWD(P＜0.05),and the improvement in the treatment group was significantly superior to that in the control group(P＜0.05).(6)After treatment,the serum levels of inflammatory indicators of CRP and WMR in the treatment group were significantly improved(P＜0.05),while no significant improvements were presented in the control group(P＞0.05).The improvements in serum CRP level and WMR value in the treatment group were significantly superior to those in the control group(P＜0.05).(7)No adverse reactions were found in the treatment group,indicating high safety.Conclusion Fangxiang Wentong Powder acupoint application combined with Kuanxiong Aerosol is more effective than Isosorbide Monomitrate Sustained-Release Capsules,improving exercise tolerance,decreasing inflammatory factor levels,and improving the quality of life to some extent during the treatment of female patients with CSF.

Objective To explore the characteristics and distribution patterns of traditional Chinese medicine(TCM)syndromes in invasive pulmonary aspergillosis(IPA).Methods A retrospective analysis was conducted on 232 IPA patients who were admitted at Dongguan Hospital of Guangzhou University of Chinese Medicine between August 2019 and August 2024.General clinical data and TCM symptom information were collected to establish a database of TCM syndrome for IPA.Factor analysis and cluster analysis were performed,and the results were interpreted by combining with clinical practice to investigate the distribution patterns of TCM syndromes.Results Among 232 IPA patients,42 TCM syndrome factors were identified after excluding the syndrome factors with the frequency below 5%.The common TCM symptoms of IPA were frequent cough,wheezing,dry cough without sputum or with scant sputum,thick or purulent sputum,and chest tightness and distress,all having the frequency above 65%.Integrated factor analysis and cluster analyse revealed five major TCM syndrome patterns:phlegm-heat congesting the lung syndrome(29.74%),phlegm-damp accumulating in the lung syndrome(20.26%),qi-yin deficiency syndrome(23.28%),lung-kidney qi deficiency syndrome(15.09%),and deficient-fire scorching the lung syndrome(11.64%).The fundamental pathogenesis of IPA was characterized by deficiency in the origin and excess in the superficiality,and deficiency interweaved with excess.IPA primarily involved the lung,with secondary involvement of the spleen and kidney.Conclusion Phlegm-heat congesting the lung syndrome is the most common TCM syndrome pattern in IPA patients,reflecting a complexity of deficiency in the origin and excess in the superficiality,and deficiency interweaved with excess.Treatment of IPA should prioritize clearing heat and resolving phlegm,while adjunctive strategies such as drying dampness and resolving phlegm,tonifying qi and nourishing yin,supplementing lung and kidney,or nourishing yin to purge fire,should be tailored to specific syndrome manifestations.

Objective To explore the risk factors for 28-day mortality of sepsis-associated acute kidney injury(SA-AKI)patients and to develop a nomogram risk prediction model.Methods A retrospective cohort study was conducted,involving 184 patients with SA-AKI admitted to the intensive care unit(ICU)of the 940th Hospital of Joint Logistic Support Force of PLA between January 2017 and December 2022.Patients were categorized into survival(n=135)and non-survival(n=49)groups based on 28-day mortality.Clinical data were collected,and statistically significant risk factors were preliminarily screened.Multivariate stepwise logistic regression analysis was performed to identify independent risk factors for 28-day mortality of SA-AKI patients.A nomogram predictive model was constructed using these factors,and internally validated with the Bootstrap method.The receiver operating characteristic curve(ROC curve)was drawn,and the area under the ROC curve(AUC)was calculated to verify the predictive value and accuracy of the model.Results The 28-day mortality rate among 184 SA-AKI patients was 26.6％(49/184).Multivariate stepwise logistic regression analysis identified multiple organ dysfunction syndrome(MODS)(OR=16.393,95％CI 4.317-62.254,P＜0.001),high acute physiology and chronic health evaluation Ⅱ(APACHE Ⅱ)score(OR=1.097,95％CI 1.036-1.161,P=0.002),low oxygenation index(OR=0.992,95％CI 0.986-0.998,P=0.015),low neutrophil count(OR=0.912,95％CI 0.860-0.968,P=0.002)and low fibrinogen concentration(OR=0.733,95％CI 0.549-0.978,P=0.034)as independent risk factors.The prediction model equation was P=1/1+e-logit(P),logit(P)=-1.626+2.797×MODS+0.092×AP ACHE Ⅱ+(-0.311)×fibrinogen+(-0.092)×neutrophil count+(-0.008)×oxygenation index.Internal validation with 1000 Bootstrap resamples showed high consistency between predicted and actual values.ROC analysis showed an AUC of 0.911(95％CI 0.868-0.955,P＜0.05)for the model,with 93.9％sensitivity and 78.5％specificity at a cut-off of 0.194.The Hosmer-Lemeshow test confirmed good calibration(P=0.62),and decision-making curve analysis demonstrated clinical utility within the high-risk threshold range(0.1-0.9).Conclusions MODS,high APACHE Ⅱ score,low oxygenation index,low neutrophil count,and low fibrinogen concentration are independent risk factors for 28-day mortality in SA-AKI patients.The developed nomogram risk prediction model may provide important guidance for predicting 28-day mortality in SA-AKI patients.

Programmed cell death (PCD) is characterized as a cell death pathway governed by specific gene-encoding requirements, plays crucial roles in the homeostasis and innate immunity of organisms, and serves as both a pathogenic mechanism and a therapeutic target for a variety of human diseases. Z-DNA-binding protein 1 (ZBP1) functions as a cytosolic nucleic acid sensor, utilizing its unique Zα domains to detect endogenous or exogenous nucleic acids and its receptor-interacting protein homotypic interaction motif (RHIM) domains to sense or bind specific signaling molecules, thereby exerting regulatory effects on various forms of PCD. ZBP1 is involved in apoptosis, necroptosis, pyroptosis, and PANoptosis and interacts with molecules, such as receptor-interacting protein kinase 3 (RIPK3), to influence cell fate under various pathological conditions. It plays a crucial role in regulating PCD during infections, inflammatory and neurological diseases, cancers, and other conditions, affecting disease onset and progression. Targeting ZBP1-associated PCD may represent a viable therapeutic strategy for related pathological conditions. This review comprehensively summarizes the regulatory functions of ZBP1 in PCD and its interactions with several closely associated signaling molecules and delineates the diseases linked to ZBP1-mediated PCD, along with the potential therapeutic implications of ZBP1 in these contexts. Ongoing research on ZBP1 is being refined across various disease models, and these advancements may provide novel insights for studies focusing on PCD, potentially leading to new therapeutic options for related diseases.