Purpose: To evaluate the clinical outcomes of endovascular treatment for ruptured vertebral artery dissecting aneurysms (VADAs), with a focus on endovascular protocols tailored to different anatomical subtypes. Materials and Methods: We retrospectively analyzed 44 consecutive patients with ruptured VADAs treated from December 2014 to October 2024. Treatment strategies were guided by aneurysm location: parent artery occlusion (PAO) was used for lesions in non-dominant VAs, while stent-assisted coiling (SAC) reconstruction was used for aneurysms in dominant VAs. Patients were stratified by modified Rankin Scale (mRS) scores at 3-month follow-up (favorable: mRS 0–2; unfavorable: mRS 3–6). Results: All procedures were technically successful, including 12 single SAC, 13 overlapping SAC, and 19 with PAO (2 involving posterior inferior cerebellar artery preservation). Immediate complete occlusion was achieved in 50.0% of single SAC cases, 76.9% overlapping SAC, and 100% in the PAO group. Six (13.6%) procedure-related complications occurred, including 2 hemorrhagic and 4 ischemic events. Thirty patients (68.2%) had favorable outcomes, and the unfavorable outcomes group showed a higher incidence of ischemic events (P=0.012). An initial poor Hunt–Hess grade (≥IV) was an independent risk factor for unfavorable outcomes (odds ratio 6.35, 95% confidence interval 1.24–32.59; P=0.027). Angiographic follow-up was performed for 34 aneurysms, with complete occlusion achieved in 32 (94.1%); the remaining 2 patients were retreated. Conclusion Endovascular management is safe and effective for ruptured VADAs. Anatomical stratification—PAO for non-dominant VA lesions and SAC for dominant VA aneurysms—may help achieve favorable outcomes.

ObjectiveTo explore the mechanism of the anti-cancer compound formula Feiyanning in inhibiting epithelial-mesenchymal transition （EMT） and invasion and metastasis of non-small cell lung cancer （NSCLC）. MethodsCell proliferation and activity were assessed using the cell counting kit-8（CCK-8） assay to evaluate the effect of Feiyanning on the proliferation of A549 and H1299 cells. Wound healing and Transwell assays were conducted to examine Feiyanning's impact on the metastasis of A549 and H1299 cells. The effects of Feiyanning on EMT and the transforming growth factor-β₁ （TGF-β₁）/Smad signaling pathway proteins in A549 and H1299 cells were detected by Western blot. Exogenous TGF-β₁ was used to induce EMT in A549 and H1299 cells. The effects of Feiyanning on TGF-β₁-induced NSCLC cell metastasis， EMT， and the TGF-β₁/Smad pathway proteins were assessed by wound healing assay， Transwell assay， and Western blot. In vivo， an A549 lung metastasis model was established via tail vein injection in nude mice. A total of 28 SPF male nude mice were randomly divided into four groups： Model （NC） group， Feiyanning low-dose （FYN1） group， Feiyanning high-dose （FYN2） group， and the positive control group （TGF-β receptor kinase inhibitor SB431542 group）. The corresponding interventions were performed. After 40 days， the mice were euthanized， and lung metastases were analyzed. The expression of E-cadherin， N-cadherin， p-Smad2， and p-Smad3 in each group was detected by immunohistochemistry （IHC）. ResultsAfter Feiyanning intervention， compared to the blank group， Feiyanning inhibited the proliferation of A549 and H1299 cells in a concentration-dependent manner （P<0.01）. The metastasis ability of Feiyanning-treated cells was significantly decreased compared to the blank group （P<0.01）. The expression of EMT marker proteins N-cadherin and zinc finger transcription factors （Zeb1， Snail， Slug） was significantly reduced in the Feiyanning groups compared to the blank group （P<0.05， P<0.01）. The expression of p-Smad2/3， Smad2/3， TβRI， and TβRⅡ， key proteins in the TGF-β₁/Smad signaling pathway， was also significantly decreased （P<0.01）. In the TGF-β₁-induced EMT model， compared to the TGF-β₁ group， the cell metastasis ability in the Feiyanning groups was reduced （P<0.01）， and the expression levels of N-cadherin， Zeb1， Snail， and Slug were significantly lower （P<0.01）. The expression levels of p-Smad2/3， Smad2/3， TβRI， and TβRⅡ were also significantly reduced （P<0.01）. In vivo results showed that compared to the model group， the number of lung metastases in the FYN1， FYN2， and SB431542 groups was reduced （P<0.01）， and the range of cell infiltration was narrowed. Immunohistochemical results showed that compared to the model group， the expression of E-cadherin in the FYN1， FYN2， and SB431542 groups was increased （P<0.01）， the expression of N-cadherin decreased （P<0.05， P<0.01）， and the expression of p-Smad2 and p-Smad3， key proteins of the TGF-β₁/Smad pathway， was reduced （P<0.01）. ConclusionFeiyanning inhibits the invasion and metastasis of NSCLC cells and EMT. The mechanism is related to the inhibition of TGF-β₁/Smad signaling pathway.

ObjectiveTo explore the mechanism of the anti-cancer compound formula Feiyanning in inhibiting epithelial-mesenchymal transition （EMT） and invasion and metastasis of non-small cell lung cancer （NSCLC）. MethodsCell proliferation and activity were assessed using the cell counting kit-8（CCK-8） assay to evaluate the effect of Feiyanning on the proliferation of A549 and H1299 cells. Wound healing and Transwell assays were conducted to examine Feiyanning's impact on the metastasis of A549 and H1299 cells. The effects of Feiyanning on EMT and the transforming growth factor-β₁ （TGF-β₁）/Smad signaling pathway proteins in A549 and H1299 cells were detected by Western blot. Exogenous TGF-β₁ was used to induce EMT in A549 and H1299 cells. The effects of Feiyanning on TGF-β₁-induced NSCLC cell metastasis， EMT， and the TGF-β₁/Smad pathway proteins were assessed by wound healing assay， Transwell assay， and Western blot. In vivo， an A549 lung metastasis model was established via tail vein injection in nude mice. A total of 28 SPF male nude mice were randomly divided into four groups： Model （NC） group， Feiyanning low-dose （FYN1） group， Feiyanning high-dose （FYN2） group， and the positive control group （TGF-β receptor kinase inhibitor SB431542 group）. The corresponding interventions were performed. After 40 days， the mice were euthanized， and lung metastases were analyzed. The expression of E-cadherin， N-cadherin， p-Smad2， and p-Smad3 in each group was detected by immunohistochemistry （IHC）. ResultsAfter Feiyanning intervention， compared to the blank group， Feiyanning inhibited the proliferation of A549 and H1299 cells in a concentration-dependent manner （P<0.01）. The metastasis ability of Feiyanning-treated cells was significantly decreased compared to the blank group （P<0.01）. The expression of EMT marker proteins N-cadherin and zinc finger transcription factors （Zeb1， Snail， Slug） was significantly reduced in the Feiyanning groups compared to the blank group （P<0.05， P<0.01）. The expression of p-Smad2/3， Smad2/3， TβRI， and TβRⅡ， key proteins in the TGF-β₁/Smad signaling pathway， was also significantly decreased （P<0.01）. In the TGF-β₁-induced EMT model， compared to the TGF-β₁ group， the cell metastasis ability in the Feiyanning groups was reduced （P<0.01）， and the expression levels of N-cadherin， Zeb1， Snail， and Slug were significantly lower （P<0.01）. The expression levels of p-Smad2/3， Smad2/3， TβRI， and TβRⅡ were also significantly reduced （P<0.01）. In vivo results showed that compared to the model group， the number of lung metastases in the FYN1， FYN2， and SB431542 groups was reduced （P<0.01）， and the range of cell infiltration was narrowed. Immunohistochemical results showed that compared to the model group， the expression of E-cadherin in the FYN1， FYN2， and SB431542 groups was increased （P<0.01）， the expression of N-cadherin decreased （P<0.05， P<0.01）， and the expression of p-Smad2 and p-Smad3， key proteins of the TGF-β₁/Smad pathway， was reduced （P<0.01）. ConclusionFeiyanning inhibits the invasion and metastasis of NSCLC cells and EMT. The mechanism is related to the inhibition of TGF-β₁/Smad signaling pathway.

Objective To explore the safety of Yttrium-90 resin microsphere selective internal radiation therapy (⁹⁰Y-SIRT) on malignant liver tumors. Methods A retrospective analysis was conducted on 64 patients with malignant liver tumors who underwent ⁹⁰Y-SIRT from February 2023 to November 2024 at Weifang People’s Hospital. The clinical characteristics of the patients and the occurrence of adverse reactions after treatment were analyzed to assess the safety of ⁹⁰Y-SIRT. Results Among the 64 patients, there were 52 males (81.25%) and 12 females (18.75%); the average age was (56.29±11.08) years. Seven patients (10.94%) had tumors with maximum diameter of less than 5 cm, 38 patients (59.38%) had tumors with maximum diameter of 5-10 cm, and 19 patients (29.68%) had tumors with maximum diameter of greater than 10 cm. There were 47 cases (73.44%) of solitary lesions and 17 cases (26.56%) of multiple lesions; 53 cases (82.81%) were primary liver cancers and 11 cases (17.19%) were metastatic liver cancers. Of the 64 patients, 63 successfully completed the Technetium-99m macroaggregated albumin (^99mTc-MAA) perfusion test and received the ⁹⁰Y-SIRT; one patient received ⁹⁰Y-SIRT after the second ^99mTc-MAA perfusion test due to a work error. The most common adverse reactions included grade 1 alanine aminotransferase (ALT) elevation in 26 cases (40.62%) and grade 2 in 2 cases (9.37%), grade 1 aspartate aminotransferase (AST) elevation in 27 cases (42.18%) and grade 2 in 7 cases (10.93%); grade 1 nausea in 17 cases (26.56%) and grade 2 in 6 cases (9.37%); grade 1 abdominal pain in 12 cases (18.75%), grade 2 in 5 cases (7.81%), and grade 3 in 1 case (1.56%); grade 1 vomiting in 11 cases (17.18%), grade 2 in 5 cases (7.81%), and grade 3 in 1 case (1.56%). Conclusion The adverse reactions of ⁹⁰Y-SIRT for treating malignant liver tumors are mild, indicating good safety.

Traditional Chinese medicine (TCM) represents a paradigmatic approach to personalized medicine, developed through the systematic accumulation and refinement of clinical empirical data over more than 2000 years, and now encompasses large-scale electronic medical records (EMR) and experimental molecular data. Artificial intelligence (AI) has demonstrated its utility in medicine through the development of various expert systems (e.g., MYCIN) since the 1970s. With the emergence of deep learning and large language models (LLMs), AI's potential in medicine shows considerable promise. Consequently, the integration of AI and TCM from both clinical and scientific perspectives presents a fundamental and promising research direction. This survey provides an insightful overview of TCM AI research, summarizing related research tasks from three perspectives: systems-level biological mechanism elucidation, real-world clinical evidence inference, and personalized clinical decision support. The review highlights representative AI methodologies alongside their applications in both TCM scientific inquiry and clinical practice. To critically assess the current state of the field, this work identifies major challenges and opportunities that constrain the development of robust research capabilities-particularly in the mechanistic understanding of TCM syndromes and herbal formulations, novel drug discovery, and the delivery of high-quality, patient-centered clinical care. The findings underscore that future advancements in AI-driven TCM research will rely on the development of high-quality, large-scale data repositories; the construction of comprehensive and domain-specific knowledge graphs (KGs); deeper insights into the biological mechanisms underpinning clinical efficacy; rigorous causal inference frameworks; and intelligent, personalized decision support systems.
Medicine, Chinese Traditional/methods* ; Artificial Intelligence ; Humans ; Precision Medicine ; Decision Support Systems, Clinical

Objective To explore the mediating effect of sleep quality between somatic symptoms and severity of depression in patients with depression. Methods A total of 384 drug-naive patients diagnosed with depression were recruited from the Department of Psychological Medicine of Zhongshan Hospital, Fudan University, during the period from February to August 2024. The severity of depression, somatic symptoms, and sleep quality were assessed using Patient Health Qusetionaire (PHQ)-9, PHQ-15, and Pittsburgh sleep quality index (PSQI), respectively. Based on the PHQ-15 scores, all participants were stratified into two groups: a mild somatic symptoms group（＜10 points, n＝136）and a moderate-to-severe somatic symptoms group（≥10 points, n＝248）. Comparisons of sleep quality between the two groups were conducted, and partial correlation analysis was performed to examine the correlation between sleep quality and somatic symptoms. Additionally, linear regression and mediation analyses were conducted to investigate the mediating effect of sleep quality between somatic symptoms and severity of depression. Results The PSQI scores in moderate-to-severe somatic symptoms group were significantly higher than those in mild somatic symptoms group (P＜0.001). Partial correlation analysis indicated that, after controlling for depression severity, the positive correlation between PSQI and PHQ-15 scores remained significant in both groups (P＜0.01). Regression analysis identified both sleep quality and somatic symptoms as predictors of severity of depression (P＜0.001). Additionally, mediation analysis demonstrated that sleep quality partially mediated the relationship between somatic symptoms and severity of depression, accounting for 26.63% (0.090/0.338) of the total effect. Conclusions In patients with depression, sleep quality is associated with somatic symptoms, and both contribute to an increased risk of the severity of depression. Moreover, sleep quality plays a partial mediating effect between somatic symptoms and severity of depression, highlighting the importance of addressing sleep-related issues in the management of depression.

Objective Based on the clinical data and imaging manifestations of patients with ischemic stroke to establish a simple clinical prediction model that is used for identifying intracranial atherosclerotic stenosis-acute large vessel occlusion(ICAS-LVO in posterior circulation before surgery.Methods The clinical data of patients with acute large vessel occlusion(LVO in the posterior circulation,who received endovascular intervention at the First Affiliated Hospital of Nanjing Medical University of China from January 2019 to September 2022,were retrospectively analyzed.According to the intraoperative angiographic findings,the patients were divided into ICAS-LVO group and non-ICAS-LVO group.Univariate analysis and multivariate logistic regression analysis were used to analyze the patient's demographic characteristics,clinical history,imaging findings,and laboratory results,based on which a clinical prediction model for ICAS-LVO was established,and according to the relevant parameters a nomogram prediction model was plotted.Results A total of 110 patients with LVO in the posterior circulation who received endovascular treatment were included in the final analysis.In 51 patients(49.6％)the cause of vascular occlusion was the atherosclerotic stenosis of the intracranial arteries.Compared with non-ICAS-LVO group,in ICAS-LVO group the patients were younger,the incidence of atrial fibrillation was lower,and the level of plasma D-dimer was lower.Three factors,including atrial fibrillation,occlusion site and collateral circulation status,were finally screened out to establish the prediction model for ICAS-LVO.This model demonstrated acceptable calibration(Hosmer-Lemeshow test,P=0.562)and good discrimination ability(AUC=0.956;95％CI:0.906-0.986).Conclusion The clinical prediction model for ICAS-LVO,which is established on the three predictive factors(absence of atrial fibrillation,occlusion located at the V4 segment of the vertebral artery or at the proximal to mid segment of the basilar artery,and a favorable collateral circulation),carries high sensitivity and accuracy.This model can help neurointervention physicians to make early identification of ICAS-LVO and to promptly formulate vascular recanalization treatment strategies.

Objective To discuss the prediction value of the early efficacy of hepatic arterial infusion chemotherapy(HAIC)in treating stage Ⅱ-Ⅲ hepatocellular carcinoma(HCC).Methods The clinical data of 81 patients with stage Ⅱ-Ⅲ HCC,who received at least 3 times of HAIC at the Nanchang Municipal Central Hospital of China from November 2021 to March 2024,were retrospectively analyzed.CT or MRI was used to compare patient's local tumor response after each treatment cycle.Based on modified Response Evaluation Criteria in Solid Tumors(mRECIST),the curative effects of patients after receiving the first,the second,and the last HAIC treatment were compared between each other.The prediction value of the early efficacy of HAIC in treating patients with stage Ⅱ-Ⅲ HCC was analyzed.Results In the 67 patients,the efficacy of the last time HAIC was equal or similar to that of the first time HAIC,and in the remaining 14 patients the efficacy of the last time HAIC was different from that of the first time HAIC,with an efficacy prediction rate of 82.72％.The efficacy of the last time HAIC was equal or similar to that of the second time HAIC in 71 patients,and in the remaining 10 patients the efficacy of the last time HAIC was different from that of the second time HAIC,with an efficacy prediction rate of 87.65％.Conclusion In treating stage Ⅱ-Ⅲ HCC with HAIC,the early efficacy can be used to predict the final efficacy after completion of the total treatment course.

Objective To explore the mechanism of Kangliu Zengxiao Jiandu Prescription(KLJD)in enhancing the efficacy of cisplatin chemotherapy in non-small cell lung cancer(NSCLC)through network pharmacology and in vivo/in vitro experiments.Methods Components of KLJD were screened via the TCMSP database to identify active components and potential targets.Lung cancer-related genes were obtained from the GeneCards and OMIM databases.GO and KEGG pathway enrichment analysis was performed on drug-disease intersection targets using the Metascape database;molecular docking was performed between core target proteins and main active components.A Lewis lung cancer mouse model was established,and intervened with KLJD and cisplatin.Organ indexes and tumor inhibition rate were counted,and Western blot and RT-PCR were used to detect the expressions of key pathway target proteins and mRNA;A549 and H1299 cells were intervened with KLJD,and Western blot was used to detect key target protein expressions.Results Network pharmacology identified 74 active components and 20 key targets of KLJD,primarily involved in biological processes such as cell proliferation and inflammatory response,and pathways in cancer and PI3K/AKT signaling pathway;molecular docking revealed stable binding between EGFR and major compounds.Animal experiments demonstrated that,compared with the model group,the KLJD group showed significantly higher tumor inhibition rate(P<0.01)and downregulation of EGFR,AKT and PI3K protein and mRNA expression in tumor tissues(P<0.05).Compared with the cisplatin group,the combination group exhibited significantly enhanced tumor inhibition rate(P<0.01),elevated thymic and splenic indices(P<0.01),and decreased EGFR,PI3K and AKT protein and mRNA expressions(P<0.01).Cell experiments showed that KLJD concentration-dependently inhibited A549 and H1299 cell proliferation(IC50:14.72 mg/mL and 14.68 mg/mL,respectively).Combined with cisplatin,KLJD synergistically down-regulated EGFR PI3K and AKT protein expressions(P<0.01).Conclusion KLJD effectively enhances cisplatin's chemotherapeutic efficacy in NSCLC by inhibiting the EGFR/PI3K/AKT pathway while improving immune organ function.Its mechanism likely involves multi-target regulation,including suppression of tumor proliferation,promotion of apoptosis,and modulation of the immune microenvironment.