ObjectiveTo observe the short-term and long-term efficacy of traditional Chinese medicine （TCM） surgical operations in treating mixed hemorrhoids. MethodsA multi-center retrospective cohort study was conducted， collecting clinical data from 17，831 mixed hemorrhoid surgery patients in 8 top-tier TCM hospitals in Jiangsu Province. Standardized and structured datasets were obtained through artificial intelligence models. Patients who underwent western surgical treatment were categorized into the western surgery group （11,646 cases）， and those receiving TCM surgical operations were categorized into the TCM surgery group （6185 cases）. Propensity score matching （1∶1 matching） was used to balance baseline data between groups. The primary outcome was the one-year recurrence rate， and secondary outcomes included the main symptoms （rectal bleeding， degree of prolapse） and secondary symptoms （anal distension， anal edema， wound secretion and exudation， anal stenosis， residual skin tags， perianal itching， and anal pain） measured on days 7， 28， and 60 after discharge. ResultsAfter matching， 2194 patients were included in each group. Symptom scores showed that at 28 days after discharge， the TCM surgical group had superior improvement in rectal bleeding ［OR=5.786， 95%CI （3.092，10.827）］， degree of prolapse ［OR=4.510， 95%CI （1.649，12.333）］， and anal edema ［OR=3.188， 95%CI （1.295，7.845）］ compared to the western surgical group. At 60 days post-discharge， the TCM group still showed advantages in improving rectal bleeding ［OR=5.237， 95%CI （1.077，25.464）］ and anal pain ［OR=11.697， 95%CI （1.186，115.336）］ （P＜0.05）. Long-term follow-up showed that the one-year recurrence rate in the TCM surgery group was 1.1% （8/726）， while that in the western surgery group was 2.3% （10/444）， with no statistically significant difference between the two groups （P＞0.05）. ConclusionBased on real-world data， TCM surgical treatment for mixed hemorrhoids shows significant short-term symptom improvement， particularly in terms of hemostasis， reducing swelling， and alleviating prolapse of anal masses.

ObjectiveTo develop a standardized classification model for traditional Chinese medicine （TCM） syndrome patterns of mixed hemorrhoids using multi-center real-world data， and unveil their distribution patterns and core risk factors， thereby providing evidence-based support for standardizing TCM syndrome differentiation and implementing precision interventions. MethodsA multi-center cross-sectional study was conducted， enrolling 13 283 mixed hemorrhoid patients from eight hospitals in Jiangsu Province between September 1st， 2023 and December 31st， 2024. DeepSeek-R1-Distill-Qwen-7B and LLaMA-3.3 large language models （LLM） were integrated with latent class analysis （LCA） to perform unsupervised learning and latent class modeling of TCM symptomatology. Potential risk factors were screened via univariate analysis， followed by logistic regression to identify independent risk factors for each syndrome pattern. ResultsThe model's performance indicators were stable and reliable across different clinical data types，i.e. in the outpatient records， past medical history （F1=99.7%）， current medical history （F1=94.9%）， and specialist examination （F1=90.7%）； in inpatient records， past medical history （F1=98.2%）， current medical history （F1=91.2%）， specialist examination （F1=90.3%）， and discharge status （F1=90.6%）. Latent class mode-ling identified four core TCM syndrome patterns including spleen deficiency and qi sinking syndrome （915 cases， 6.89%）， damp-heat pouring downward syndrome （10 820 cases， 81.46%）， qi stagnation and blood stasis syndrome （1252 cases， 9.43%）， and wind injuring intestinal collaterals syndrome （296 cases， 2.22%）， with respective latent class probabilities of 0.069， 0.815， 0.094， and 0.022. Logistic regression demonstrated that gender， age， disease duration， hypertension， diabetes， hyperlipidemia， constipation， smoking history， and alcohol consumption were independent risk factors for pattern differentiation （P＜0.05）. The efficacy validation evaluation revealed that the cure rates for patients with spleen deficiency and qi sinking syndrome and qi stagnation and blood stasis syndrome were higher than those for patients with damp-heat pouring downward syndrome （adjusted P＜0.05）， with no statistically significant differences among other syndrome patterns. ConclusionDamp-heat pouring downward syndrome is the predominant syndrome in mixed hemorrhoids. Gender， age， disease duration， hypertension， diabetes， hyperlipi-demia， constipation， smoking history， and alcohol consumption are independent risk factors for the differentiation of syndrome types.

This paper has constructed a traditional Chinese medicine （TCM） specialized disease dataset platform for mixed hemorrhoids based on a multimodal large model， and the preliminary application has been validated. The platform uses StarRocks to establish a four-level data warehouse system， enabling the aggregation， cleaning， and standardization of multi-source heterogeneous data. Using DeepSeek-R1-Distill-Qwen-7B as the base model， domain fine-tuning is performed through low-rank adaptation （LoRA） technology. Combined with LLaMA-3.3 natural language processing and reasoning chain techniques， the platform enables intelligent parsing and structured extraction of unstructured TCM medical records. It accurately identifies six major categories and 28 subcategories of entities， including symptoms and syndromes， with a fine-tuned model F1 score of 93.8%. The platform has established a high-quality specialized disease dataset containing more than 50,000 medical records and has been applied in a real-world study involving 17,831 patients， preliminarily verifying the efficacy of TCM heritage surgery.

Objective:To explore the association between childhood trauma and prefrontal cortex functional networks in early adulthood using functional near-infrared spectroscopy(fNIRS).Methods:Twenty-eight individu-als with childhood trauma comprised the trauma group,while 32 without trauma formed the control group.The Childhood Trauma Questionnaire(CTQ)assessed abuse and neglect,the Ruminative Responses Scale(RRS)meas-ured repetitive thinking about negative events,and the Iowa Gambling Task(IGT)evaluated decision-making tend-encies.fNIRS data collected during the IGT were used to calculate degree centrality(DC),betweenness centrality(BC),and local efficiency(LE)in prefrontal networks.Mediation analysis explored relationships among childhood trauma,brain function(DC,BC,LE),and ruminative thinking.Results:Compared to controls,the trauma group had decreased DC in bilateral dorsolateral prefrontal cortices,increased DC,BC,and LE in the right inferior frontal gy-rus,and elevated LE in the bilateral frontal poles.BC and LE in the right inferior frontal gyrus partially mediated the relationship between CTQ sexual abuse and RRS scores(48.57％and 41.43％,respectively).Conclusion:Child-hood trauma is significantly associated with changes in prefrontal network properties in early adulthood.Sexual a-buse,in particular,may influence emotional regulation and cognitive functions by altering the network attributes of the right inferior frontal gyrus.

With the extensive application of nuclear technology in industry, agriculture, and medicine, the safety issues associated with neutron radiation have become increasingly prominent. Due to their high penetrability and strong ionization effect, neutrons can cause serious health risks by directly damaging DNA or inducing secondary γ radiation. Therefore, the neutron radiation protection has become a core challenge in radiation protection, especially the research and development of neutron shielding materials. To ensure the safe development of nuclear technology, neutron shielding materials are indispensable and constitute a fundamental core technology for radiation protection. This paper reviews the theory of neutron radiation protection and the research progress of neutron shielding materials, with a focus on the current application status and existing problems of neutron shielding materials. This article also discusses the future development trends. This review aims to provide theoretical support and technical references for the safe application and development of nuclear technology.

OBJECTIVES: To investigate the mechanism through which salidroside inhibits proliferation of gastric cancer (GC) cells focusing on glucose metabolic reprogramming pathways. METHODS: High-throughput sequencing combined with bioinformatics analysis was employed to identify the potential targets of salidroside in human GC MGC-803 cells. Liposome-mediated transfection experiments were carried out to validate the functional and mechanistic roles of these targets. CCK-8 and colony formation assays were used to assess the effects of salidroside on GC cell viability and clonogenic ability. qRT-PCR, Western blotting, and biochemical assay kits were used to analyze the regulatory effects of salidroside on the miR-1343-3p-OGDHL/PDHB enzyme complex-pyruvate metabolic pathway in GC cells. RESULTS: Bioinformatics analysis suggested that the tumor-suppressive factor miR-1343-3p negatively regulated the key glycolytic enzyme gene oxoglutarate dehydrogenase-like (OGDHL) in GC cells, and OGDHL and pyruvate dehydrogenase E1 subunit beta (PDHB) were both significantly upregulated in GC tissues, which was close by correlated with reduced survival rates of GC patients. In MGC-803 cells, salidroside treatment significantly enhanced the expression level of miR-1343-3p and downregulated OGDHL expression, resulting in disruption of the stability of PDHB, reduced pyruvate oxidative decarboxylation, and consequently decreased production of acetyl-CoA and ATP. CONCLUSIONS Salidroside inhibits GC cell proliferation possibly by regulating the miR-1343-3p-OGDHL/PDHB enzyme complex-pyruvate metabolic pathway, which provides new insights into its anti-tumor mechanisms and suggests new strategies for targeted therapy for GC.
Humans ; Stomach Neoplasms/pathology* ; MicroRNAs/genetics* ; Cell Proliferation/drug effects* ; Glucosides/pharmacology* ; Phenols/pharmacology* ; Cell Line, Tumor ; Glucose/metabolism* ; Pyruvate Dehydrogenase (Lipoamide)/metabolism*

Loss-of-function variants in CSDE1 have been strongly linked to neuropsychiatric disorders, yet the precise role of CSDE1 in neurogenesis remains elusive. In this study, we demonstrate that knockout of Csde1 during cortical development in mice results in impaired neural progenitor proliferation, leading to abnormal cortical lamination and embryonic lethality. Transcriptomic analysis revealed that Csde1 upregulates the transcription of genes involved in the cell cycle network. Applying a dual thymidine-labelling approach, we further revealed prolonged cell cycle durations of neuronal progenitors in Csde1-knockout mice, with a notable extension of the G1 phase. Intersection with CLIP-seq data demonstrated that Csde1 binds to the 3' untranslated region (UTR) of mRNA transcripts encoding cell cycle genes. Particularly, we uncovered that Csde1 directly binds to the 3' UTR of mRNA transcripts encoding Cdk6, a pivotal gene in regulating the transition from the G1 to S phases of the cell cycle, thereby maintaining its stability. Collectively, this study elucidates Csde1 as a novel regulator of Cdk6, sheds new light on its critical roles in orchestrating brain development, and underscores how mutations in Csde1 may contribute to the pathogenesis of neuropsychiatric disorders.
Animals ; Neurogenesis/genetics* ; Cell Cycle/genetics* ; Mice, Knockout ; Mice ; Neural Stem Cells/metabolism* ; DNA-Binding Proteins/metabolism* ; Cyclin-Dependent Kinase 6/genetics* ; Cell Proliferation ; 3' Untranslated Regions ; Cerebral Cortex/embryology* ; RNA-Binding Proteins ; Mice, Inbred C57BL

Objective To investigate the molecular mechanism by which salidroside inhibits the proliferation of gastric cancer(GC)cells through upregulation of miR-1343-3p.Methods RNA databases were used to screen for mRNAs associated with tumor proliferation and with miR-1343-3p,and exhibiting significant changes in their expression levels after salidroside treatment of human GC cells.Gene matching and immunoprecipitation of RNA-binding proteins were conducted to analyze the association between miR-1343-3p and SOX18.Immunocytochemistry was performed to determine the localization of SOX18 protein.The effect of salidroside on the proliferation of human GC cells(MGC-803 and AGS)was determined by CCK-8 assay.Human GC cells were divided into a blank control group and low-and high-dose salidroside groups.The expression of miR-1343-3p and SOX18 mRNA was measured by real-time quantitative fluorescence PCR(qPCR).The protein expression of SOX18 was measured by Western blot.GC cells were co-transfected with miR-1343-3p mimic and miR-1343-3p inhibitor,respectively,via LipofectamineTM 2000 liposomes.The expression of miR-1343-3p and SOX18 mRNA was measured by qPCR,and the protein expression of SOX18 was measured by Western blot.Results Through bioinformatic analysis,SOX18 was identified as a downstream target of miR-1343-3p.Gene alignment confirmed the presence of specific binding sites between the two genes,and immunoprecipitation of RNA-binding proteins validated the targeting relationship between them(P<0.05).Immunocytochemistry demonstrated the nuclear localization of SOX18 protein.CCK-8 assay findings demonstrated that salidroside significantly inhibited the proliferation of GC cells in a time-and dose-dependent manner.Compared with the blank control group,salidroside-treated GC cells showed decreased expression of both SOX18 mRNA and protein(P<0.05)and an increased miR-1343-3p expression(P<0.05).Compared with the control group,GC cells in the miR-1343-3p mimic group exhibited increased expression of miR-1343-3p and decreased expression of SOX18 mRNA and protein.In contrast,GC cells in the miR-1343-3p inhibitor group showed decreased expression of miR-1343-3p and increased expression of SOX18 mRNA and protein(all P<0.05).Conclusion Salidroside may inhibit the proliferation of GC cells by regulating the miR-1343-3p/SOX18 signaling axis and these regulators may present new potential therapeutic targets or biomarkers for gastric cancer.

Objective To explore the impact of obstructive sleep apnea(OSA)on cognitive impairment in post-stroke patients,to explore its underlying mechanism and to evaluate potential diagnostic value by dynamically moni-toring the level of brain-derived neurotrophic factor(BDNF)and Tau protein in serum.Methods Totally 96 stroke patients admitted to Mianyang third People's Hospital from February 2022 to June 2024 were selected.They were divided into the groups complicated with OSA and control one without OSA following up of neuropsychological scales for 1 week,1 month,3 months,and 6 months after stroke for evaluating cognitive function.Enzyme-linked immunosorbent assay(ELISA)was applied to detect the level of BDNF and Tau protein in serum.The correlation of test results and the degree of cognitive impairment as well as their diagnostic value were analyzed.Results The AHI in the OSA group was significantly higher than that of control group,while LSaO2 and MSaO2 were significantly lower in the OSA group(P＜0.05).One week and 1,3,6 month months after the onset of the disease,the MMSE and MoCA scores in the OSA group were significantly lower than those in the control group,BDNF level was signifi-cantly lower while Tau protein level was significantly higher as compare to those in control group(P＜0.05).Pear-son correlation analysis showed that the serum BDNF level was positively correlated with both MMSE score(r=0.654,P＜0.001)and MoCA score(r=0.689,P＜0.001).However,the serum Tau protein level was nega-tively correlated with both MMSE score(r=-0.623,P＜0.001)and MoCA score(r=-0.667,P＜0.001).The ar-ea under the curve(AUC)of the combined detection of BDNF and Tau protein was greater than that of the individ-ual detection.The diagnostic value of the combined detection of BDNF and Tau protein for cognitive impairment in post-stroke patients was greater than that of the individual detection(P＜0.05).Conclusions OSA significantly exacerbates patients'cognitive impairment after stroke.Elevated serum BDNF level and decreased Tau protein level may be the underlying mechanisms of cognitive impairment.Serum BDNF and Tau protein may function as potential biomarkers for diagnosis of cognitive impairment after stroke.

Objective:To investigate the effect of protein tyrosine phosphatase D(PTPRD)demethylation on the proliferation,migration,and chemoresistance of gastric cancer(GC)cells through the phosphatidyl inositol 3 kinase/protein kinase B/mammalian target of rapamycin(PI3K/Akt/mTOR)pathway.Methods:The gastric cancer MKN-74 and MKN-45 cells,as well as human gastric mucosal epithelial GES-1 cells,GES-1 were cultured in vitro and PTPRD expression was detected.MKN-45 cells and their drug-resistant variant MKN-45/5-FU cells were routinely cultured and transfected with various vectors:PTPRD empty vector(NC group,NC/5-FU group),PTPRD overexpressing adenovirus(PTPRD group,PTPRD/5-FU group),shRNA empty vector(sh-NC group,sh-NC/5-FU group),shRNA PTPRD lentivirus(sh-PTPRD group,sh-PTPRD/5-FU group),and PTPRD overexpressing adenovirus+10 μmol/L 740Y-P treatment(PTPRD+740Y-P group,PTPRD+740Y-P/5-FU group).MTT assay and wound healing assay were used to assess cell proliferation and migration.Cell autophagy levels were assessed using autophagy assay,and the expression of epithelial-mesenchymal transition(EMT)and PI3K/Akt/mTOR pathway related proteins was detected using western blot(WB).MKN-45 cells were treated with 0,2.5,5,10,20 and 40 μmol/L 5-aza solutions,and the PTPRD mRNA expression and cell proliferation in MKN-45 cells were detected using qPCR and MTT assays.Results:PTPRD mRNA and protein were significantly downregulated in gastric cancer cells(P<0.05).Compared with the MKN-45 group,the numbers of autophagosomes and autophagosomes,as well as the protein expression of PTPRD,E-cadherin,and BAX significantly increased in the PTPRD group(all P<0.05),while cell proliferation,migration rate,and protein expression of p-PI3K,vimentin,p-Akt,and p-mTOR decreased significantly(all P<0.05);However,in the sh-PTPRD group,cell proliferation activity,migration rate,and protein expression of p-PI3K,vimentin,p-Akt,and p-mTOR increased notably,while the quantity of autophagosomes,autophagosomes,and protein expression of PTPRD,E-cadherin,and BAX decreased(all P<0.05).Compared with the PTPRD group,the PTPRD+740Y-P group showed an increase in cell proliferation activity,migration rate,protein expression of p-PI3K,vimentin,p-Akt,and p-mTOR(all P<0.05),and a decrease in number of autophagosomes,autophagosomes,and protein expression of PTPRD,E-cadherin,and BAX(all P<0.05).With the increase of 5-aza concentration,the mRNA expression of PTPRD in MKN-45 cells increased(P<0.05),while the cell proliferation activity decreased(P<0.05).Compared with the MKN-45/5-FU group,the cell migration rate and proliferation activity decreased in PTPRD/5-FU group,while the sh-PTPRD/5-FU group showed an increase in cell migration rate and proliferation activity(all P<0.05).Compared with the PTPRD/5-FU group,the PTPRD+740Y-P/5-FU group showed an increase in cell migration rate and proliferation activity(all P<0.05).Conclusion:PTPRD is downregulated in GC cells,and its demethylation may inhibit proliferation and migration of GC cells and enhance chemosensitivity by suppressing the PI3K/Akt/mTOR pathway.