Current Medical Science最新文献

{"title":"Erratum to: Stereotactic Injection of shRNA GSK-3β-AAV Promotes Axonal Regeneration after Spinal Cord Injury.","authors":"Yu-Chao Zuo, Nan-Xiang Xiong, Hong-Yang Zhao","doi":"10.1007/s11596-025-00012-8","DOIUrl":"10.1007/s11596-025-00012-8","url":null,"abstract":"","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"154-155"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143448340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Avocado Oil: Recent Advances in Its Anti-diabetic Potential.","authors":"Dorji Drakpa, Taniya Paul, Sukriti Chakrabarty, Karma Jigdrel, Prasun Mukherjee, Jeena Gupta","doi":"10.1007/s11596-025-00010-w","DOIUrl":"10.1007/s11596-025-00010-w","url":null,"abstract":"<p><strong>Background: </strong>Diet plays a crucial role in insulin resistance and diabetes, with high-fat and high-carbohydrate diets being major contributors. However, the type of fat consumed is critical, as different fatty acids impact insulin sensitivity differently.</p><p><strong>Objective: </strong>This review examines the potential benefits of avocado oil, which is rich in monounsaturated fatty acids (MUFAs), in improving glycaemic control and lipid metabolism. It also explores variations in avocado oil composition across different avocado cultivars.</p><p><strong>Methods: </strong>Experimental and clinical studies were analysed to assess the metabolic effects of avocado oil. The impact of MUFAs on insulin sensitivity, lipid profiles, and metabolic health was reviewed, alongside the influence of fruit quality, maturity, and cultivar differences.</p><p><strong>Results: </strong>Avocado oil may enhance glycaemic control and lipid metabolism, benefiting individuals with diabetes and hypercholesterolemia. However, its composition varies significantly across avocado variants such as Hass, Reed, Ettinger, and Fuerte, influencing its therapeutic properties.</p><p><strong>Conclusion: </strong>Avocado oil's high MUFA content offers promising metabolic benefits. Further research is needed to standardize its therapeutic application, considering cultivar-dependent variations in composition.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"11-24"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143491075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Helicobacter pylori Eradication on Clinical and Laboratory Parameters in Non-alcoholic Fatty Liver Disease Patients: A Systematic Review and Meta-analysis of Randomized Controlled Trials.","authors":"Fouad Jaber, Saqr Alsakarneh, Azizullah Beran, Tala Alsharaeh, Ahmed-Jordan Salahat, Abdelrahman Abdelshafi, Islam Mohamed, Willie Johnson, Khaled Elfert, Mohammad Jaber, Mohammad Almeqdadi, Mohamed Ahmed, Hassan Ghoz, Wendell K Clarkston, John H Helzberg","doi":"10.1007/s11596-025-00001-x","DOIUrl":"10.1007/s11596-025-00001-x","url":null,"abstract":"<p><strong>Objective: </strong>Helicobacter pylori (HP) infection is associated with non-alcoholic fatty liver disease (NAFLD) and insulin resistance; however, the correlation between HP eradication and NAFLD remains controversial. This systematic review and meta-analysis examined the effect of HP treatment on clinical and laboratory parameters in NAFLD patients.</p><p><strong>Methods: </strong>We conducted a literature search of the PubMed, Embase, Scopus, and Web of Science databases through September 2023 for randomized controlled trials (RCTs) examining the effect of HP treatment on NAFLD patients versus lifestyle changes alone. The primary outcome was the change in steatosis parameters. The secondary endpoints were changes in anthropometric parameters, inflammatory markers (TNF-α), and metabolic parameters (fasting blood glucose, homeostasis model assessment of insulin resistance, AST/ALT, and lipid profile). The random effects model was used to calculate the standardized mean difference (SMD) with associated 95% confidence intervals (CIs) for our desired outcome.</p><p><strong>Results: </strong>Four RCTs met our inclusion criteria. A total of 453 patients were included (mean age 42.8 years, 58.5% males), 228 (50.3%) of whom were in the HP eradication group and 225 (49.7%) of whom were in the lifestyle modification group. Compared with lifestyle modification alone, HP eradication had a significant effect on reducing liver steatosis and TNF-α levels (SMD: - 0.9; 95% CI - 14.67, - 3.82, I² = 0% and SMD: - 6.3; 95% CI - 9.04, - 3.56, I² = 0%, respectively). No significant effect on other metabolic parameters was found.</p><p><strong>Conclusions: </strong>HP eradication significantly reduced liver steatosis and TNF-α levels in NAFLD patients. However, HP eradication did not significantly affect other metabolic indices compared to lifestyle changes alone.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"1-10"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143491107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overexpression of Circ-Astn1 Suppresses Hyperglycemia-Induced Endothelial Cell Damage via the miR-138-5p/SIRT1 Axis.","authors":"Hong-Bin Yu, Li-Yun Wang, Xiao-Ning Yan, Xue-Yan Wu, Jian-Long Wu, Da-Wei Liu, Si-Yang Liu","doi":"10.1007/s11596-025-00011-9","DOIUrl":"10.1007/s11596-025-00011-9","url":null,"abstract":"<p><strong>Objective: </strong>To elucidate the regulatory mechanism of circRNAs in diabetic retinopathy.</p><p><strong>Methods: </strong>Next-generation sequencing (NGS) was employed to identify circRNAs that are abnormally expressed in endothelial progenitor cells (EPCs) under hyperglycemia (HG) conditions. The regulatory mechanism and predicted targets of this circRNA were also studied via bioinformatics analysis, luciferase reporter assays, angiogenic differentiation experiments, flow cytometry, and RT-qPCR.</p><p><strong>Results: </strong>Circ-astrotactin 1 (circ-Astn1) expression was decreased in EPCs under HG conditions, and circ-Astn1 overexpression inhibited HG-induced endothelial damage. The miR-138-5p and silencing information regulator 2 related enzyme 1 (SIRT1) were identified as circ-Astn1 downstream targets, which were further verified through luciferase reporter assays. SIRT1 silencing or miR-138-5p overexpression reversed the protective effect of circ-Astn1 on HG-induced endothelial cell dysfunction, as evidenced by increased apoptosis, abnormal vascular differentiation, and inflammatory factor secretion. SIRT1 overexpression reversed miR-138-5p-induced endothelial cell dysfunction under HG conditions. In vivo experiments confirmed that circ-Astn1 overexpression promoted skin wound healing through the regulation of SIRT1.</p><p><strong>Conclusions: </strong>These findings suggest that circ-Astn1 promotes SIRT1 expression by sponging miR-138-5p. Circ-Astn1 overexpression suppresses HG-induced endothelial cell damage via miR-138-5p/SIRT1 axis.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"93-103"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11906496/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Casr Inhibition-Mediated M2 Microglial Transformation in Ischemic Preconditioning Against Stroke.","authors":"Zhi-Hao Zhai, Zuo-Yu Huang, Kai-Xun Huang, Yuan-Qiang Zhong, En-Xiang Tao, Yun-Feng Yang","doi":"10.1007/s11596-025-00003-9","DOIUrl":"10.1007/s11596-025-00003-9","url":null,"abstract":"<p><strong>Objective: </strong>Stroke is a main cause of disability and mortality worldwide. It has been reported that ischemic preconditioning (IP) has neuroprotective effects against stroke. This study aimed to verify the mechanism by which calcium-sensing receptor (Casr) inhibition-mediated M2 microglial transformation in the IP protects against stroke, which will provide a potential therapeutic target for stroke.</p><p><strong>Methods: </strong>Middle cerebral artery occlusion (MCAO) rats and oxygen-glucose deprivation (OGD) neurons were used in this study. IP was induced via the transient MCAO and OGD methods. RNA sequencing (RNA-Seq) was used to explore the underlying key molecules. Western blotting and immunohistochemistry were performed to detect the expression of Casr and the M1 and M2 microglial markers. CCK8 was used to detect cell viability. The calcium concentration was detected via the use of Fluo-4 AM, a fluorescence probe. The Casr inhibitor NPS2143 and the Casr activator R568 were used to explore the role of Casr in M2 microglial transformation and neuroprotection.</p><p><strong>Results: </strong>We first revealed that IP induced M2 microglial transformation in ischemic injury. In addition, MCAO injury increased Casr expression and the calcium concentration, which was inhibited by IP. Furthermore, Casr activation inhibited the M2 microglial transformation induced by IP. Finally, we found that Casr inhibition improved the survival rate, alleviated neurological deficits, and reduced the infarct volume induced by MCAO.</p><p><strong>Conclusions: </strong>We confirmed that Casr-related neuroprotection induced by IP is associated with the transformation of M2 microglia. These findings can be used to understand the protective mechanisms of IP against ischemic stroke.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"82-92"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum to: Electroacupuncture Alleviates Memory Deficits in APP/PS1 Mice by Targeting Serotonergic Neurons in Dorsal Raphe Nucleus.","authors":"Chao-Chao Yu, Xiao-Fei Wang, Jia Wang, Chu Li, Juan Xiao, Xue-Song Wang, Rui Han, Shu-Qin Wang, Yuan-Fang Lin, Li-Hong Kong, Yan-Jun Du","doi":"10.1007/s11596-025-00014-6","DOIUrl":"10.1007/s11596-025-00014-6","url":null,"abstract":"","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"156"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143491103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Salidroside Enhances the Sensitivity of Lung Cancer Cells to Paclitaxel by Regulating the Wnt/β-catenin Signaling Pathway.","authors":"Guo-Liang Pi, Liang-Hao Cheng, Bin-Feng Li, Fei Ming","doi":"10.1007/s11596-025-00005-7","DOIUrl":"10.1007/s11596-025-00005-7","url":null,"abstract":"<p><strong>Objective: </strong>Chemoresistance, such as paclitaxel (PTX) resistance, has become a great obstacle in non-small cell lung cancer (NSCLC) treatment. The natural agent salidroside (SAL) has been shown to exert an antitumor effect on NSCLC. Nonetheless, it is unclear whether SAL can decrease the resistance of NSCLC to PTX.</p><p><strong>Methods: </strong>PTX-resistant NSCLC cells (H1299/PTX and A549/PTX) were generated. Cell Counting Kit-8 (CCK-8) assay was used to detect cell viability. Colony formation assay and flow cytometry were utilized to assess cell proliferation and apoptosis, respectively. Immunofluorescence staining and TOP/FOP flash luciferase assay were employed to estimate β-catenin activation. Western blotting was implemented to estimate the protein levels of apoptosis-, proliferation-, and Wnt/β-catenin signaling-associated markers. A xenograft mouse model was established to investigate the impact of SAL on PTX resistance in vivo.</p><p><strong>Results: </strong>SAL increased PTX-induced suppression of proliferation and promoted apoptosis in PTX-resistant NSCLC cells. SAL blocked the Wnt/β-catenin signaling in A549/PTX cells and in tumor-bearing mice. Activating Wnt/β-catenin signaling reversed the SAL-mediated increase in the sensitivity of NSCLC cells to PTX. SAL attenuated PTX resistance in NSCLC in the xenograft mouse model.</p><p><strong>Conclusion: </strong>SAL enhances the sensitivity of NSCLC cells to PTX by blocking the Wnt/β-catenin signal transduction.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"104-113"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ANP Increases Zn^2⁺ Accumulation During Reperfusion in Ex Vivo and In Vivo Hearts.","authors":"Yu-Ting Ma, Tong Laga, Chong-Ning Zhong, Bing-Qi Zhuang, Hai-Lian Quan, Lan Hong","doi":"10.1007/s11596-025-00019-1","DOIUrl":"10.1007/s11596-025-00019-1","url":null,"abstract":"<p><strong>Objective: </strong>Atrial natriuretic peptide (ANP) and Zn^2⁺ have been shown to confer cardioprotection against ischemia/reperfusion (I/R) injury. Zn^2⁺ alleviates myocardial hypertrophy and pulmonary hypertension by regulating ANP expression, but its precise role in ANP-mediated cardioprotection remains unclear. This study aimed to investigate whether ANP protects the heart during reperfusion by modulating Zn^2⁺ levels and to explore the underlying mechanisms involved.</p><p><strong>Methods: </strong>In this study, we utilized an isolated reperfused heart model in rats, as well as wild-type (WT) and ANP knockout (ANP^-/-) mouse models, for in vivo I/R experiments. For clinical investigations, plasma samples were collected from 216 patients with ischemia-related diseases. Evans blue and TTC staining, radioimmunoassay, ICP‒OES, echocardiography, Hydro-Cy3-mediated ROS detection, and Western blotting were employed to evaluate the effect of ANP on Zn^2⁺ homeostasis.</p><p><strong>Results: </strong>Plasma ANP levels were significantly elevated in patients with ST-elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI), and heart failure (HF). ANP secretion increased during reperfusion, rather than infarction, both ex vivo and in vivo, promoting Zn^2⁺ accumulation in reperfused tissue. ANP and Zn^2⁺ protected mitochondria and reduced infarct size; these effects were reversed by the Zn^2⁺ chelator TPEN. In WT and ANP^-/- mice, EF% and FS% decreased after reperfusion, with ANP^-/- mice exhibiting significantly worse cardiac function. ANP pretreatment alone improved cardiac function, but combined pretreatment with ANP and TPEN decreased EF% and FS% while increasing LVID. Reperfusion increased ROS levels in both WT and ANP^-/- hearts, which were reduced by ANP pretreatment. I/R injury elevated Zn^2⁺ transporter 8 (ZnT8) expression, an effect that was counteracted by ANP, although this effect was reversed by TPEN. Hypoxia-inducible factor 1-alpha (HIF-1α) expression was elevated in I/R rats and ANP^-/- mice, and it was inhibited by both Zn^2⁺ and ANP pretreatment. However, the HIF-1α inhibitor 2-Me did not reverse the effect of ANP on ZnT8 expression. Additionally, ANP increased PI3K expression in both WT and ANP^-/- I/R mice, but this effect was blocked by the PI3K inhibitor LY294002.</p><p><strong>Conclusions: </strong>ANP modulates Zn^2⁺ homeostasis during reperfusion injury by downregulating ZnT8 through the PI3K signalling pathway, thereby reducing myocardial I/R injury.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"35-50"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting Glycolytic Enzymes with 3-Bromopyruvic Acid to Enhance the Efficacy of Interventional Embolization in Hepatocellular Carcinoma.","authors":"Min Wang, Xiao-Ning Wu, Xu Cheng, Xiao-Peng Guo, Zhuang-Lin Zeng, Song-Lin Song, Ai-Ping Cheng","doi":"10.1007/s11596-025-00009-3","DOIUrl":"10.1007/s11596-025-00009-3","url":null,"abstract":"<p><strong>Objective: </strong>Tumour cells in a hypoxic state are more invasive, have stronger self-renewal capabilities, and are difficult to treat because of their ability to promote tumour recurrence and metastasis. The glycolysis inhibitor 3-bromopyruvic acid (3-BrPA) can completely inactivate glycolytic enzymes at extremely low drug concentrations, thereby exerting a strong inhibitory effect on the glucose energy metabolism of tumor cells. Therefore, we tested the inhibitory effect of 3-BrPA on hepatocellular carcinoma cells (HepG2) in vitro; then, we used the VX2 liver cancer model to study the antitumour effect of 3-BrPA combined with interventional embolization on liver cancer.</p><p><strong>Methods: </strong>In vitro, a CCK-8 assay was used to detect the inhibitory effect of different concentrations of 3-BrPA on HepG2 cells, and light microscopy confirmed that the HepG2 cells were completely dead. Western blotting was used to detect the expression of key proteins involved in apoptosis. A total of 30 New Zealand white rabbits were used to establish a liver cancer model and were randomly divided into 3 groups 2 weeks after tumor establishment: the control group was perfused with saline in the hepatic artery; the transcatheter arterial embolization (TAE) group was given TAE; and the experimental group was perfused with 3-BrPA combined with TAE. The tumor-bearing rabbits were killed one week after surgery. The tumor volume and tumor necrosis ratio were calculated via the histopathological examination.</p><p><strong>Results: </strong>In vitro, the inhibitory effect of 3-BrPA on HepG2 cells increased with increasing concentration. 3-BrPA (100 μmol/L) could induce the necrosis of HepG2 cells. Stimulation with 50 μmol/L 3-BrPA could activate the tumor cell apoptosis pathway. 3-BrPA combined with TAE treatment could significantly inhibit tumor growth and cause more complete tumor necrosis.</p><p><strong>Conclusion: </strong>3-BrPA not only has antitumour effects in vitro but can also significantly improve antitumour effects in the hypoxic microenvironment after embolization in vivo.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"114-121"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dual-Stream Attention-Based Classification Network for Tibial Plateau Fractures via Diffusion Model Augmentation and Segmentation Map Integration.","authors":"Yi Xie, Zhi-Wei Hao, Xin-Meng Wang, Hong-Lin Wang, Jia-Ming Yang, Hong Zhou, Xu-Dong Wang, Jia-Yao Zhang, Hui-Wen Yang, Peng-Ran Liu, Zhe-Wei Ye","doi":"10.1007/s11596-025-00008-4","DOIUrl":"10.1007/s11596-025-00008-4","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to explore a novel method that integrates the segmentation guidance classification and the diffusion model augmentation to realize the automatic classification for tibial plateau fractures (TPFs).</p><p><strong>Methods: </strong>YOLOv8n-cls was used to construct a baseline model on the data of 3781 patients from the Orthopedic Trauma Center of Wuhan Union Hospital. Additionally, a segmentation-guided classification approach was proposed. To enhance the dataset, a diffusion model was further demonstrated for data augmentation.</p><p><strong>Results: </strong>The novel method that integrated the segmentation-guided classification and diffusion model augmentation significantly improved the accuracy and robustness of fracture classification. The average accuracy of classification for TPFs rose from 0.844 to 0.896. The comprehensive performance of the dual-stream model was also significantly enhanced after many rounds of training, with both the macro-area under the curve (AUC) and the micro-AUC increasing from 0.94 to 0.97. By utilizing diffusion model augmentation and segmentation map integration, the model demonstrated superior efficacy in identifying Schatzker I, achieving an accuracy of 0.880. It yielded an accuracy of 0.898 for Schatzker II and III and 0.913 for Schatzker IV; for Schatzker V and VI, the accuracy was 0.887; and for intercondylar ridge fracture, the accuracy was 0.923.</p><p><strong>Conclusion: </strong>The dual-stream attention-based classification network, which has been verified by many experiments, exhibited great potential in predicting the classification of TPFs. This method facilitates automatic TPF assessment and may assist surgeons in the rapid formulation of surgical plans.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"57-69"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143491077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}