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Pulmonary Nodule Detection Using Hybrid Two-Stage 3D CNNs.

使用混合两阶段 3D CNNs 检测肺结节。

  • 影响因子:2.94
  • DOI:10.1002/mp.14161
  • 作者列表:"Tan M","Wu F","Yang B","Ma J","Kong D","Chen Z","Long D
  • 发表时间:2020-04-02

PURPOSE:Early detection of pulmonary nodules is an effective way to improve patients' chances of survival. In this work, we propose a novel and efficient way to build a computer-aided detection (CAD) system for pulmonary nodules based on computed 16 tomography (CT) scans. METHODS:The system can be roughly divided into two steps: nodule candidate detection and false positive reduction. Considering the three-dimensional (3D) nature of nodules, the CAD system adopts 3D convolutional neural networks (CNNs) in both stages. Specifically, in the first stage, a segmentation-based 3D CNN with a hybrid loss is designed to segment nodules. According to the probability maps produced by the segmentation network, a threshold method and connected component analysis are applied to generate nodule candidates. In the second stage, we employ three classification-based 3D CNNs with different types of inputs to reduce false positives. In addition to simple raw data input, we also introduce hybrid inputs to make better use of the output of the previous segmentation network. In experiments, we use data augmentation and batch normalization to avoid overfitting. RESULTS:We evaluate the system on 888 CT scans from the publicly available LIDCIDRI dataset, and our method achieves the best performance by comparing with the state-of-the-art methods, which has a high detection sensitivity of 97.5% with an average of only 1 false positive per scan. An additional evaluation on 115 CT scans from local hospitals is also performed. CONCLUSIONS:Experimental results demonstrate that our method is highly suited for the detection of pulmonary nodules.


目的: 早期发现肺结节是提高患者生存机会的有效方法。在这项工作中,我们提出了一种新颖高效的方法来构建基于计算机 16 断层扫描 (CT) 扫描的肺结节计算机辅助检测 (CAD) 系统。 方法: 该系统大致可分为两个步骤: 结节候选检测和假阳性还原。考虑到结节的三维 (3D) 性质,CAD 系统在两个阶段都采用了 3D 卷积神经网络 (CNNs)。具体来说,在第一阶段,设计了一个基于分割的混合损失的 3D CNN 来分割结节。根据分割网络产生的概率图,应用阈值法和连通分量分析生成结节候选。在第二阶段,我们采用三种基于分类的 3D cnn,具有不同类型的输入,以减少假阳性。除了简单的原始数据输入,我们还引入了混合输入,以更好地利用以前分割网络的输出。在实验中,我们使用数据增强和批量归一化来避免过拟合。 结果: 我们在公开可用的 lididri 数据集的 888 次 ct扫描上评估了该系统,通过与最先进的方法进行比较,我们的方法获得了最佳性能。其检测灵敏度高达 97.5%,平均每次扫描只有 1 个假阳性。还对当地医院的 115 次 ct扫描进行了额外评估。 结论: 实验结果表明,我们的方法非常适合于肺结节的检测。



作者列表:["De Cunto G","Brancaleone V","Riemma MA","Cerqua I","Vellecco V","Spaziano G","Cavarra E","Bartalesi B","D'Agostino B","Lungarella G","Cirino G","Lucattelli M","Roviezzo F"]

METHODS:BACKGROUND AND PURPOSE:A critical role for sphingosine kinase/sphingosine-1-phosphate (S1P) pathway in the control of airway function has been demonstrated in respiratory diseases. Here, we address S1P contribution in a mouse model of mild chronic obstructive pulmonary disease (COPD). EXPERIMENTAL APPROACH:C57BL/6J mice have been exposed to room air or cigarette smoke up to 11 months and killed at different time points. Functional and molecular studies have been performed. KEY RESULTS:Cigarette smoke caused emphysematous changes throughout the lung parenchyma coupled to a progressive collagen deposition in both peribronchiolar and peribronchial areas. The high and low airways showed an increased reactivity to cholinergic stimulation and α-smooth muscle actin overexpression. Similarly, an increase in airway reactivity and lung resistances following S1P challenge occurred in smoking mice. A high expression of S1P, Sph-K2 , and S1P receptors (S1P2 and S1P3 ) has been detected in the lung of smoking mice. Sphingosine kinases inhibition reversed the increased cholinergic response in airways of smoking mice. CONCLUSIONS AND IMPLICATIONS:S1P signalling up-regulation follows the disease progression in smoking mice and is involved in the development of airway hyperresponsiveness. Our study defines a therapeutic potential for S1P inhibitors in management of airways hyperresponsiveness associated to emphysema in smokers with both asthma and COPD.

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作者列表:["Bernstein DM","Toth B","Rogers RA","Kling DE","Kunzendorf P","Phillips JI","Ernst H"]

METHODS::The interim results from this 90-day multi-dose, inhalation toxicology study with life-time post-exposure observation has shown an important fundamental difference in persistence and pathological response in the lung between brake dust derived from brake-pads manufactured with chrysotile, TiO2 or chrysotile alone in comparison to the amphiboles, crocidolite and amosite asbestos. In the brake dust exposure groups no significant pathological response was observed at any time. Slight macrophage accumulation of particles was noted. Wagner-scores, were from 1 to 2 (1 = air-control group) and were similar to the TiO2 group. Chrysotile being biodegradable, shows a weakening of its matrix and breaking into short fibers & particles that can be cleared by alveolar macrophages and continued dissolution. In the chrysotile exposure groups, particle laden macrophage accumulation was noted leading to a slight interstitial inflammatory response (Wagner-score 1-3). There was no peribronchiolar inflammation and occasional very slight interstitial fibrosis. The histopathology and the confocal analyses clearly differentiate the pathological response from amphibole asbestos, crocidolite and amosite, compared to that from the brake dust and chrysotile. Both crocidolite and amosite induced persistent inflammation, microgranulomas, and fibrosis (Wagner-scores 4), which persisted through the post exposure period. The confocal microscopy of the lung and snap-frozen chestwalls quantified the extensive inflammatory response and collagen development in the lung and on the visceral and parietal surfaces. The interim results reported here, provide a clear basis for differentiating the effects from brake dust exposure from those following amphibole asbestos exposure. The subsequent results through life-time post-exposure will follow.

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作者列表:["Zaragosi LE","Deprez M","Barbry P"]

METHODS::The respiratory tract is lined by a pseudo-stratified epithelium from the nose to terminal bronchioles. This first line of defense of the lung against external stress includes five main cell types: basal, suprabasal, club, goblet and multiciliated cells, as well as rare cells such as ionocytes, neuroendocrine and tuft/brush cells. At homeostasis, this epithelium self-renews at low rate but is able of fast regeneration upon damage. Airway epithelial cell lineages during regeneration have been investigated in the mouse by genetic labeling, mainly after injuring the epithelium with noxious agents. From these approaches, basal cells have been identified as progenitors of club, goblet and multiciliated cells, but also of ionocytes and neuroendocrine cells. Single-cell RNA sequencing, coupled to lineage inference algorithms, has independently allowed the establishment of comprehensive pictures of cell lineage relationships in both mouse and human. In line with genetic tracing experiments in mouse trachea, studies using single-cell RNA sequencing (RNAseq) have shown that basal cells first differentiate into club cells, which in turn mature into goblet cells or differentiate into multiciliated cells. In the human airway epithelium, single-cell RNAseq has identified novel intermediate populations such as deuterosomal cells, 'hybrid' mucous-multiciliated cells and progenitors of rare cells. Novel differentiation dynamics, such as a transition from goblet to multiciliated cells have also been discovered. The future of cell lineage relationships in the respiratory tract now resides in the combination of genetic labeling approaches with single-cell RNAseq to establish, in a definitive manner, the hallmarks of cellular lineages in normal and pathological situations.

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