现有的视网膜血管分割算法存在特征提取能力不足和分割效率低等问题。针对该问题,对UNet网络进行改进,提出一种基于多尺度特征提取的U型网络(Multi-scale feature extraction based on UNet, MF-UNet)。该算法在编码和解码部分构建反卷...现有的视网膜血管分割算法存在特征提取能力不足和分割效率低等问题。针对该问题,对UNet网络进行改进,提出一种基于多尺度特征提取的U型网络(Multi-scale feature extraction based on UNet, MF-UNet)。该算法在编码和解码部分构建反卷积分割模块替代传统卷积块,使网络保留更多的血管细节信息。之后,在编码和解码中间连接部引入混合池化(Mix Pooling Moudle, MPM)和模板卷积(Template convolution, TConv),提升网络对多尺度特征的提取能力,从而提升血管的分割质量和分割效率。在两个眼底数据库DRIVE和STARE上进行实验验证,结果表明,MF-UNet算法在准确性、灵敏度、特异性和AUC表现优异,更优于UNet与其他视网膜血管分割算法。展开更多
Hepatocellular carcinoma(HCC)is a highly malignant tumor with significant global health implications.The role of CD4+T cells,particularly conventional CD4+T cells(Tconvs),in HCC progression remains unexplored.Furtherm...Hepatocellular carcinoma(HCC)is a highly malignant tumor with significant global health implications.The role of CD4+T cells,particularly conventional CD4+T cells(Tconvs),in HCC progression remains unexplored.Furthermore,epigenetic factors are crucial in immune regulation,yet their specific role in HCC-infiltrating Tconv cells remains elusive.This study elucidates the role of MATR3,an epigenetic regulator,in modulating Tconv activity and immune evasion within the HCC microenvironment.Reanalysis of the scRNA-seq data revealed that early activation of CD4+T cells is crucial for establishing an antitumor immune response.In vivo and in vitro experiments revealed that Tconv enhances cDC1-induced CD8+T-cell activation.Screening identified MATR3 as a critical regulator of Tconv function,which is necessary for antitumour activity but harmful when overexpressed.Excessive MATR3 expression exacerbates Tconv exhaustion and impairs function by recruiting the SWI/SNF complex to relax chromatin in the TOX promoter region,leading to aberrant transcriptional changes.In summary,MATR3 is an HCC-specific epigenetic checkpoint that bidirectionally regulates Tconv antitumour immunity,suggesting new therapeutic strategies targeting epigenetic regulators to enhance antitumour immunity in HCC.展开更多
基金supported by the Key Program,National Natural Science Foundation of China(No.81930016)National Key Research and Development Program of China(No.2021YFA1100500)+5 种基金Key Research&Development Plan of Zhejiang Province(No.2019C03050)Construction Fund of Key Medical Disciplines of Hangzhou(OO20200093)Key Research&Development Plan of Zhejiang Province(No.2021C03118),Projects of Medical and Health Technology Program in Zhejiang Province(WKJ-ZJ-2120)National Natural Science Foundation of China(No.82273177,No.12304256)Natural Science Foundation of Zhejiang Province(LY22H160046,LQ24C050005)Key Research and Development Plan of Zhejiang Province(2022C03108).Joint Funds of the National Natural Science Foundation of China(No.U23A20451).
文摘Hepatocellular carcinoma(HCC)is a highly malignant tumor with significant global health implications.The role of CD4+T cells,particularly conventional CD4+T cells(Tconvs),in HCC progression remains unexplored.Furthermore,epigenetic factors are crucial in immune regulation,yet their specific role in HCC-infiltrating Tconv cells remains elusive.This study elucidates the role of MATR3,an epigenetic regulator,in modulating Tconv activity and immune evasion within the HCC microenvironment.Reanalysis of the scRNA-seq data revealed that early activation of CD4+T cells is crucial for establishing an antitumor immune response.In vivo and in vitro experiments revealed that Tconv enhances cDC1-induced CD8+T-cell activation.Screening identified MATR3 as a critical regulator of Tconv function,which is necessary for antitumour activity but harmful when overexpressed.Excessive MATR3 expression exacerbates Tconv exhaustion and impairs function by recruiting the SWI/SNF complex to relax chromatin in the TOX promoter region,leading to aberrant transcriptional changes.In summary,MATR3 is an HCC-specific epigenetic checkpoint that bidirectionally regulates Tconv antitumour immunity,suggesting new therapeutic strategies targeting epigenetic regulators to enhance antitumour immunity in HCC.
