针对传统粮堆体积测量方法中设备成本高、依赖相机标定、复杂形态适配性差等问题,提出一种基于密集无约束体三维重建(dense and unconstrained stereo 3D reconstruction,DUSt3R)点云的散装粮堆体积智能估算方法。该方法利用DUSt3R的注...针对传统粮堆体积测量方法中设备成本高、依赖相机标定、复杂形态适配性差等问题,提出一种基于密集无约束体三维重建(dense and unconstrained stereo 3D reconstruction,DUSt3R)点云的散装粮堆体积智能估算方法。该方法利用DUSt3R的注意力机制与稠密匹配技术,实现端到端生成三维点云。构建基于粮堆特性的点云优化模块,结合统计滤波与RANSAC平面检测技术,提升点云噪声去除能力,并通过DBSCAN聚类实现粮堆与地面的精准分割。结果表明:该方法有效克服了对相机标定的依赖,显著提升了点云噪声处理与分割精度;通过动态网格投影与Alpha Shape曲面重建技术自适应拟合复杂粮堆形态,在保证测量准确性的同时大幅降低硬件成本,具备良好的工程适用性;在6种典型粮堆形态上开展试验验证,平均测量误差约为5%,仅需普通摄像头即可完成数据采集。该体积测量方法可与平粮机器人作业设备高效集成,为散装粮堆体积测量与自动化作业引导提供了低成本、高精度的技术解决方案。展开更多
Hans Zempel1,2 TAU,a microtubule-associated protein,encoded by the microtubule-associated protein tau(MAPT)gene,is a central regulator of microtubule stability and axonal function in the human brain,with its pathologi...Hans Zempel1,2 TAU,a microtubule-associated protein,encoded by the microtubule-associated protein tau(MAPT)gene,is a central regulator of microtubule stability and axonal function in the human brain,with its pathological aggregation representing a hallmark of Alzheimer’s disease and related tauopathies.Despite extensive research into the role of TAU in neurodegeneration,its essentiality for human brain development has remained unclear.This perspective synthesizes recent genetic,molecular,and cellular evidence to demonstrate that the human brain-specific TAU isoform 0N3R is indispensable for proper neurodevelopment,pointing to loss-of-function of this isoform as a novel paradigm for TAU-associated disease.Alternative splicing of MAPT generates six brain-specific TAU isoforms,with 0N3R being exclusively expressed during fetal brain development.Analysis of large-scale human genetic datasets(gnomAD v4.0.0)reveals a high probability of loss-of-function intolerance(pLI=0.96)for the 0N3R isoform.This is in stark contrast to the canonical Matched Annotation from the NCBI and EMBL-EBI(MANE)transcript and peripheral“Big TAU,”both of which are tolerant to loss-of-function mutations.This intolerance is further supported by the scarcity of loss-of-function mutations in 0N3R-encoding exons and high missense constraint scores,suggesting strong evolutionary selection against disruption of this isoform.Functional studies using human induced pluripotent stem cell-derived cortical neurons with CRISPR-Cas9-mediated MAPT knockout reveal that,unlike in murine models where compensation by other microtubule-associated proteins occurs,loss of TAU in human neurons leads to deficits in neurite outgrowth,axon initial segment shortening,and a trend toward hyperexcitability,accompanied by broad transcriptomic changes affecting genes involved in microtubule organization and synaptic structure.Remarkably,re-expression of any of the six human brain-specific TAU isoforms rescues these phenotypes,underscoring their functional redundancy during development.These findings position the 0N3R isoform as essential for human brain development and suggest that loss-of-function mutations affecting this isoform likely result in neurodevelopmental impairment,potentially manifesting as intellectual disability without overt dysmorphic features.This contrasts with the apparent tolerance to MAPT loss-of-function in mice and peripheral tissues,highlighting a critical species-and isoform-specific requirement for TAU in human neurodevelopment.The hypothesis of 0N3R-TAU loss-of-function intolerance opens new avenues for understanding neurodevelopmental disorders and refines the conceptual framework of TAU-associated disease mechanisms beyond toxic gain-of-function.展开更多
文摘针对传统粮堆体积测量方法中设备成本高、依赖相机标定、复杂形态适配性差等问题,提出一种基于密集无约束体三维重建(dense and unconstrained stereo 3D reconstruction,DUSt3R)点云的散装粮堆体积智能估算方法。该方法利用DUSt3R的注意力机制与稠密匹配技术,实现端到端生成三维点云。构建基于粮堆特性的点云优化模块,结合统计滤波与RANSAC平面检测技术,提升点云噪声去除能力,并通过DBSCAN聚类实现粮堆与地面的精准分割。结果表明:该方法有效克服了对相机标定的依赖,显著提升了点云噪声处理与分割精度;通过动态网格投影与Alpha Shape曲面重建技术自适应拟合复杂粮堆形态,在保证测量准确性的同时大幅降低硬件成本,具备良好的工程适用性;在6种典型粮堆形态上开展试验验证,平均测量误差约为5%,仅需普通摄像头即可完成数据采集。该体积测量方法可与平粮机器人作业设备高效集成,为散装粮堆体积测量与自动化作业引导提供了低成本、高精度的技术解决方案。
文摘Hans Zempel1,2 TAU,a microtubule-associated protein,encoded by the microtubule-associated protein tau(MAPT)gene,is a central regulator of microtubule stability and axonal function in the human brain,with its pathological aggregation representing a hallmark of Alzheimer’s disease and related tauopathies.Despite extensive research into the role of TAU in neurodegeneration,its essentiality for human brain development has remained unclear.This perspective synthesizes recent genetic,molecular,and cellular evidence to demonstrate that the human brain-specific TAU isoform 0N3R is indispensable for proper neurodevelopment,pointing to loss-of-function of this isoform as a novel paradigm for TAU-associated disease.Alternative splicing of MAPT generates six brain-specific TAU isoforms,with 0N3R being exclusively expressed during fetal brain development.Analysis of large-scale human genetic datasets(gnomAD v4.0.0)reveals a high probability of loss-of-function intolerance(pLI=0.96)for the 0N3R isoform.This is in stark contrast to the canonical Matched Annotation from the NCBI and EMBL-EBI(MANE)transcript and peripheral“Big TAU,”both of which are tolerant to loss-of-function mutations.This intolerance is further supported by the scarcity of loss-of-function mutations in 0N3R-encoding exons and high missense constraint scores,suggesting strong evolutionary selection against disruption of this isoform.Functional studies using human induced pluripotent stem cell-derived cortical neurons with CRISPR-Cas9-mediated MAPT knockout reveal that,unlike in murine models where compensation by other microtubule-associated proteins occurs,loss of TAU in human neurons leads to deficits in neurite outgrowth,axon initial segment shortening,and a trend toward hyperexcitability,accompanied by broad transcriptomic changes affecting genes involved in microtubule organization and synaptic structure.Remarkably,re-expression of any of the six human brain-specific TAU isoforms rescues these phenotypes,underscoring their functional redundancy during development.These findings position the 0N3R isoform as essential for human brain development and suggest that loss-of-function mutations affecting this isoform likely result in neurodevelopmental impairment,potentially manifesting as intellectual disability without overt dysmorphic features.This contrasts with the apparent tolerance to MAPT loss-of-function in mice and peripheral tissues,highlighting a critical species-and isoform-specific requirement for TAU in human neurodevelopment.The hypothesis of 0N3R-TAU loss-of-function intolerance opens new avenues for understanding neurodevelopmental disorders and refines the conceptual framework of TAU-associated disease mechanisms beyond toxic gain-of-function.
