fetal brain malformation

胎儿脑畸形
  • 文章类型: Journal Article
    标准平面(SP)对于胎儿脑畸形的诊断至关重要。然而,由于胎儿姿势的巨大差异和SPs定义的复杂性,准确获取SPs非常耗时且需要丰富的经验.
    这项研究旨在提供一种指导方法,可以帮助超声医师更准确,更快速地获得SP。
    首先,超声医师使用3D探头扫描胎儿头部以获得3D体积数据,然后我们使用仿射变换将3D体数据校准到标准身体位置,并实时建立相应的3D头部模型。当超声医师使用2D探头扫描飞机时,当前平面的位置可以通过我们的RLNet(回归位置网络)在3D头部模型中清楚地显示,这可以指导超声医师更准确地获得三个SP。当找到三个SP时,根据与三个SP的空间关系,可以自动生成矢状面和冠状面。
    在3200个2DUS图像上进行的实验结果表明,RLNet实现了跨丘脑平面的平均角度误差为3.91±2.86°,与其他已发表的数据相比,有明显的改善。自动生成的冠状和矢状SP符合胎儿脑畸形的诊断标准和诊断要求。
    首次提出了一种基于深度学习的超声脑畸形筛查引导扫描方法,具有一定的临床应用价值。
    Standard planes (SPs) are crucial for the diagnosis of fetal brain malformation. However, it is very time-consuming and requires extensive experiences to acquire the SPs accurately due to the large difference in fetal posture and the complexity of SPs definitions.
    This study aims to present a guiding approach that could assist sonographer to obtain the SPs more accurately and more quickly.
    To begin with, sonographer uses the 3D probe to scan the fetal head to obtain 3D volume data, and then we used affine transformation to calibrate 3D volume data to the standard body position and established the corresponding 3D head model in \'real time\'. When the sonographer uses the 2D probe to scan a plane, the position of current plane can be clearly show in 3D head model by our RLNet (regression location network), which can conduct the sonographer to obtain the three SPs more accurately. When the three SPs are located, the sagittal plane and the coronal planes can be automatically generated according to the spatial relationship with the three SPs.
    Experimental results conducted on 3200 2D US images show that the RLNet achieves average angle error of the transthalamic plane was 3.91±2.86°, which has a obvious improvement compared other published data. The automatically generated coronal and sagittal SPs conform the diagnostic criteria and the diagnostic requirements of fetal brain malformation.
    A guiding scanning method based deep learning for ultrasonic brain malformation screening is firstly proposed and it has a pragmatic value for future clinical application.
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  • 文章类型: Journal Article
    由于据报道,在巴西感染ZIKV的孕妇的胎儿中,小头畸形是一致的结果,最近涉及寨卡病毒(ZIKV)-小头症的病因机制关系。研究人员,然而,仍在努力为这个有趣的因果手铐建立胚胎学基础。本研究揭示了有力的证据,有利于合理的ZIKV-小头症因果关系联系。基本原理基于:(1)ZIKV基因组与人类DNA中早期神经管发育标记“视黄酸”的反应元件之间的序列同源性,以及(2)ZIKV-小头畸形和视黄酸胚胎病的脑缺陷细节之间的全面相似性。视黄酸被认为是通过视黄酸依赖性基因启动子区的视黄酸反应元件(RARE)共有序列(5'-AGGTCA-3')调节神经管前后轴和发育中脑结构定位的最早因子。我们筛选了已经报道的毒力ZIKV毒株(包括与小头畸形相关的毒株)和美国国立卫生研究院遗传序列数据库(GenBank)中的其他病毒的RARE共有重复序列,并获得了有力支持我们的假设的结果,即与小头畸形相关的ZIKV毒株可以通过在发育中的脑细胞基因组中引入额外的RARE共有序列重复序列来沉淀视黄酸依赖性基因调控异常。对我们假设的其他支持来自我们的发现,即筛选其他病毒的RARE共有序列重复仅对那些已知表现出神经嗜性并导致胎儿脑缺陷(可能需要在发育阶段进行母胎传播)的病毒是阳性的。RARE序列重复的数量似乎与筛选的阳性病毒的毒力相匹配。虽然,生物信息学证据和胚胎学特征支持我们的假设,包括动物模型在内的其他研究需要验证我们的主张.此类研究可能会揭示ZIKV-小头畸形的关联,并可能有助于设计与之对抗的方法。
    Owing to the reports of microcephaly as a consistent outcome in the fetuses of pregnant women infected with ZIKV in Brazil, Zika virus (ZIKV)-microcephaly etiomechanistic relationship has recently been implicated. Researchers, however, are still struggling to establish an embryological basis for this interesting causal handcuff. The present study reveals robust evidence in favor of a plausible ZIKV-microcephaly cause-effect liaison. The rationale is based on: (1) sequence homology between ZIKV genome and the response element of an early neural tube developmental marker \"retinoic acid\" in human DNA and (2) comprehensive similarities between the details of brain defects in ZIKV-microcephaly and retinoic acid embryopathy. Retinoic acid is considered as the earliest factor for regulating anteroposterior axis of neural tube and positioning of structures in developing brain through retinoic acid response elements (RARE) consensus sequence (5\'-AGGTCA-3\') in promoter regions of retinoic acid-dependent genes. We screened genomic sequences of already reported virulent ZIKV strains (including those linked to microcephaly) and other viruses available in National Institute of Health genetic sequence database (GenBank) for the RARE consensus repeats and obtained results strongly bolstering our hypothesis that ZIKV strains associated with microcephaly may act through precipitation of dysregulation in retinoic acid-dependent genes by introducing extra stretches of RARE consensus sequence repeats in the genome of developing brain cells. Additional support to our hypothesis comes from our findings that screening of other viruses for RARE consensus sequence repeats is positive only for those known to display neurotropism and cause fetal brain defects (for which maternal-fetal transmission during developing stage may be required). The numbers of RARE sequence repeats appeared to match with the virulence of screened positive viruses. Although, bioinformatic evidence and embryological features are in favor of our hypothesis, additional studies including animal models are warranted to validate our proposition. Such studies are likely to unfold ZIKV-microcephaly association and may help in devising methods to combat it.
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