Neural networks-based regularization for large-scale medical image reconstruction

In this paper we present a generalized Deep Learning-based approach for solving ill-posed large-scale inverse problems occuring in medical image reconstruction. Recently, Deep Learning methods using iterative neural networks (NNs) and cascaded NNs have been reported to achieve state-of-the-art results with respect to various quantitative quality measures as PSNR, NRMSE and SSIM across different imaging modalities. However, the fact that these approaches employ the application of the forward and adjoint operators repeatedly in the network architecture requires the network to process the whole images or volumes at once, which for some applications is computationally infeasible. In this work, we follow a different reconstruction strategy by strictly separating the application of the NN, the regularization of the solution and the consistency with the measured data. The regularization is given in the form of an image prior obtained by the output of a previously trained NN which is used in a Tikhonov regularization framework. By doing so, more complex and sophisticated network architectures can be used for the removal of the artefacts or noise than it is usually the case in iterative NNs. Due to the large scale of the considered problems and the resulting computational complexity of the employed networks, the priors are obtained by processing the images or volumes as patches or slices. We evaluated the method for the cases of 3D cone-beam low dose CT and undersampled 2D radial cine MRI and compared it to a total variation-minimization-based reconstruction algorithm as well as to a method with regularization based on learned overcomplete dictionaries. The proposed method outperformed all the reported methods with respect to all chosen quantitative measures and further accelerates the regularization step in the reconstruction by several orders of magnitude

Unrolled three-operator splitting for parameter-map learning in Low Dose X-ray CT reconstruction

We propose a method for fast and automatic estimation of spatially dependent regularization maps for total variation-based (TV) tomography reconstruction. The estimation is based on two distinct sub-networks, with the first sub-network estimating the regularization parameter-map from the input data while the second one unrolling T iterations of the Primal-Dual Three-Operator Splitting (PD3O) algorithm. The latter approximately solves the corresponding TV-minimization problem incorporating the previously estimated regularization parameter-map. The overall network is then trained end-to-end in a supervised learning fashion using pairs of clean-corrupted data but crucially without the need of having access to labels for the optimal regularization parameter-maps

Learning Regularization Parameter-Maps for Variational Image Reconstruction Using Deep Neural Networks and Algorithm Unrolling

We introduce a method for the fast estimation of data-adapted, spatially and temporally dependent regularization parameter-maps for variational image reconstruction, focusing on total variation (TV) minimization. The proposed approach is inspired by recent developments in algorithm unrolling using deep neural networks (NNs) and relies on two distinct subnetworks. The first subnetwork estimates the regularization parameter-map from the input data. The second subnetwork unrolls iterations of an iterative algorithm which approximately solves the corresponding TV-minimization problem incorporating the previously estimated regularization parameter-map. The overall network is then trained end-to-end in a supervised learning fashion using pairs of clean and corrupted data but crucially without the need for access to labels for the optimal regularization parameter-maps. We first prove consistency of the unrolled scheme by showing that the unrolled minimizing energy functional used for the supervised learning -converges, as tends to infinity, to the corresponding functional that incorporates the exact solution map of the TV-minimization problem. Then, we apply and evaluate the proposed method on a variety of large-scale and dynamic imaging problems with retrospectively simulated measurement data for which the automatic computation of such regularization parameters has been so far challenging using the state-of-the-art methods: a 2D dynamic cardiac magnetic resonance imaging (MRI) reconstruction problem, a quantitative brain MRI reconstruction problem, a low-dose computed tomography problem, and a dynamic image denoising problem. The proposed method consistently improves the TV reconstructions using scalar regularization parameters, and the obtained regularization parameter-maps adapt well to imaging problems and data by leading to the preservation of detailed features. Although the choice of the regularization parameter-maps is data-driven and based on NNs, the subsequent reconstruction algorithm is interpretable since it inherits the properties (e.g., convergence guarantees) of the iterative reconstruction method from which the network is implicitly defined

The p53 binding protein PDCD5 is not rate-limiting in DNA damage induced cell death

The tumour suppressor p53 is an important mediator of cell cycle arrest and apoptosis in response to DNA damage, acting mainly by transcriptional regulation of specific target genes. The exact details how p53 modulates this decision on a molecular basis is still incompletely understood. One mechanism of regulation is acetylation of p53 on lysine K120 by the histone-acetyltransferase Tip60, resulting in preferential transcription of proapoptotic target genes. PDCD5, a protein with reported pro-apoptotic function, has recently been identified as regulator of Tip60-dependent p53-acetylation. In an effort to clarify the role of PDCD5 upon DNA damage, we generated cell lines in which PDCD5 expression was conditionally ablated by shRNAs and investigated their response to genotoxic stress. Surprisingly, we failed to note a rate-limiting role of PDCD5 in the DNA damage response. PDCD5 was dispensable for DNA damage induced apoptosis and cell cycle arrest and we observed no significant changes in p53 target gene transcription. While we were able to confirm interaction of PDCD5 with p53, we failed to do so for Tip60. Altogether, our results suggest a role of PDCD5 in the regulation of p53 function but unrelated to cell cycle arrest or apoptosis, at least in the cell types investigated.FP06 RTN ‘ApopTrain’Tyrolean Science FundKrebshilfe-Tyro