目的 基于深度学习的端到端场景文本识别任务已经取得了很大的进展。然而受限于多尺度、任意形状以及背景干扰等问题,大多数端到端文本识别器依然会面临掩码提议不完整的问题,进而影响模型的文本识别结果。为了提高掩码预测的准确率,提...目的 基于深度学习的端到端场景文本识别任务已经取得了很大的进展。然而受限于多尺度、任意形状以及背景干扰等问题,大多数端到端文本识别器依然会面临掩码提议不完整的问题,进而影响模型的文本识别结果。为了提高掩码预测的准确率,提出了一种基于软注意力的掩码嵌入模块(soft attention mask embedding,SAME),方法 利用Transformer更好的全局感受野,将高层特征进行编码并计算软注意力,然后将编码特征与预测掩码层级嵌入,生成更贴近文本边界的掩码来抑制背景噪声。基于SAME强大的文本掩码优化及细粒度文本特征提取能力,进一步提出了一个健壮的文本识别框架SAME-Net,开展无需字符级注释的端到端精准文本识别。具体来说,由于软注意力是可微的,所提出的SAME-Net可以将识别损失传播回检测分支,以通过学习注意力的权重来指导文本检测,使检测分支可以由检测和识别目标联合优化。结果 在多个文本识别公开数据集上的实验表明了所提方法的有效性。其中,SAME-Net在任意形状文本数据集Total-Text上实现了84.02%的H-mean,相比于2022年的GLASS(global to local attention for scene-text spotting),在不增加额外训练数据的情况下,全词典的识别准确率提升1.02%。所提方法在多向数据集ICDAR 2015(International Conference on Document Analysis and Recognition)也获得了与同期工作相当的性能,取得83.4%的强词典识别结果。结论 提出了一种基于SAME的端到端文本识别方法。该方法利用Transformer的全局感受野生成靠近文本边界的掩码来抑制背景噪声,提出的SAME模块可以将识别损失反向传输到检测模块,并且不需要额外的文本校正模块。通过检测和识别模块的联合优化,可以在没有字符级标注的情况下实现出色的文本定位性能。展开更多
As a sensor of cytosolic DNA, the role of cyclic GMP-AMP synthase (cGAS) in innate immune response is well established, yet how its functions in different biological conditions remain to be elucidated. Here, we identi...As a sensor of cytosolic DNA, the role of cyclic GMP-AMP synthase (cGAS) in innate immune response is well established, yet how its functions in different biological conditions remain to be elucidated. Here, we identify cGAS as an essential regulator in inhibiting mitotic DNA double-strand break (DSB) repair and protecting short telomeres from end-to-end fusion independent of the canonical cGAS-STING pathway. cGAS associates with telomeric/subtelomeric DNA during mitosis when TRF1/TRF2/POT1 are deficient on telomeres. Depletion of cGAS leads to mitotic chromosome end-to-end fusions predominantly occurring between short telomeres. Mechanistically, cGAS interacts with CDK1 and positions them to chromosome ends. Thus, CDK1 inhibits mitotic non-homologous end joining (NHEJ) by blocking the recruitment of RNF8. cGAS-deficient human primary cells are defective in entering replicative senescence and display chromosome end-to-end fusions, genome instability and prolonged growth arrest. Altogether, cGAS safeguards genome stability by controlling mitotic DSB repair to inhibit mitotic chromosome end-to-end fusions, thus facilitating replicative senescence.展开更多
文摘目的 基于深度学习的端到端场景文本识别任务已经取得了很大的进展。然而受限于多尺度、任意形状以及背景干扰等问题,大多数端到端文本识别器依然会面临掩码提议不完整的问题,进而影响模型的文本识别结果。为了提高掩码预测的准确率,提出了一种基于软注意力的掩码嵌入模块(soft attention mask embedding,SAME),方法 利用Transformer更好的全局感受野,将高层特征进行编码并计算软注意力,然后将编码特征与预测掩码层级嵌入,生成更贴近文本边界的掩码来抑制背景噪声。基于SAME强大的文本掩码优化及细粒度文本特征提取能力,进一步提出了一个健壮的文本识别框架SAME-Net,开展无需字符级注释的端到端精准文本识别。具体来说,由于软注意力是可微的,所提出的SAME-Net可以将识别损失传播回检测分支,以通过学习注意力的权重来指导文本检测,使检测分支可以由检测和识别目标联合优化。结果 在多个文本识别公开数据集上的实验表明了所提方法的有效性。其中,SAME-Net在任意形状文本数据集Total-Text上实现了84.02%的H-mean,相比于2022年的GLASS(global to local attention for scene-text spotting),在不增加额外训练数据的情况下,全词典的识别准确率提升1.02%。所提方法在多向数据集ICDAR 2015(International Conference on Document Analysis and Recognition)也获得了与同期工作相当的性能,取得83.4%的强词典识别结果。结论 提出了一种基于SAME的端到端文本识别方法。该方法利用Transformer的全局感受野生成靠近文本边界的掩码来抑制背景噪声,提出的SAME模块可以将识别损失反向传输到检测模块,并且不需要额外的文本校正模块。通过检测和识别模块的联合优化,可以在没有字符级标注的情况下实现出色的文本定位性能。
文摘As a sensor of cytosolic DNA, the role of cyclic GMP-AMP synthase (cGAS) in innate immune response is well established, yet how its functions in different biological conditions remain to be elucidated. Here, we identify cGAS as an essential regulator in inhibiting mitotic DNA double-strand break (DSB) repair and protecting short telomeres from end-to-end fusion independent of the canonical cGAS-STING pathway. cGAS associates with telomeric/subtelomeric DNA during mitosis when TRF1/TRF2/POT1 are deficient on telomeres. Depletion of cGAS leads to mitotic chromosome end-to-end fusions predominantly occurring between short telomeres. Mechanistically, cGAS interacts with CDK1 and positions them to chromosome ends. Thus, CDK1 inhibits mitotic non-homologous end joining (NHEJ) by blocking the recruitment of RNF8. cGAS-deficient human primary cells are defective in entering replicative senescence and display chromosome end-to-end fusions, genome instability and prolonged growth arrest. Altogether, cGAS safeguards genome stability by controlling mitotic DSB repair to inhibit mitotic chromosome end-to-end fusions, thus facilitating replicative senescence.
