7 research outputs found

    Autoadaptive motion modelling for MR-based respiratory motion estimation

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    © 2016 The Authors.Respiratory motion poses significant challenges in image-guided interventions. In emerging treatments such as MR-guided HIFU or MR-guided radiotherapy, it may cause significant misalignments between interventional road maps obtained pre-procedure and the anatomy during the treatment, and may affect intra-procedural imaging such as MR-thermometry. Patient specific respiratory motion models provide a solution to this problem. They establish a correspondence between the patient motion and simpler surrogate data which can be acquired easily during the treatment. Patient motion can then be estimated during the treatment by acquiring only the simpler surrogate data.In the majority of classical motion modelling approaches once the correspondence between the surrogate data and the patient motion is established it cannot be changed unless the model is recalibrated. However, breathing patterns are known to significantly change in the time frame of MR-guided interventions. Thus, the classical motion modelling approach may yield inaccurate motion estimations when the relation between the motion and the surrogate data changes over the duration of the treatment and frequent recalibration may not be feasible.We propose a novel methodology for motion modelling which has the ability to automatically adapt to new breathing patterns. This is achieved by choosing the surrogate data in such a way that it can be used to estimate the current motion in 3D as well as to update the motion model. In particular, in this work, we use 2D MR slices from different slice positions to build as well as to apply the motion model. We implemented such an autoadaptive motion model by extending our previous work on manifold alignment.We demonstrate a proof-of-principle of the proposed technique on cardiac gated data of the thorax and evaluate its adaptive behaviour on realistic synthetic data containing two breathing types generated from 6 volunteers, and real data from 4 volunteers. On synthetic data the autoadaptive motion model yielded 21.45% more accurate motion estimations compared to a non-adaptive motion model 10 min after a change in breathing pattern. On real data we demonstrated the methods ability to maintain motion estimation accuracy despite a drift in the respiratory baseline. Due to the cardiac gating of the imaging data, the method is currently limited to one update per heart beat and the calibration requires approximately 12 min of scanning. Furthermore, the method has a prediction latency of 800 ms. These limitations may be overcome in future work by altering the acquisition protocol

    Multi-tasking to Correct: Motion-Compensated MRI via Joint Reconstruction and Registration

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    This work addresses a central topic in Magnetic Resonance Imaging (MRI) which is the motion-correction problem in a joint reconstruction and registration framework. From a set of multiple MR acquisitions corrupted by motion, we aim at - jointly - reconstructing a single motion-free corrected image and retrieving the physiological dynamics through the deformation maps. To this purpose, we propose a novel variational model. First, we introduce an L2L^2 fidelity term, which intertwines reconstruction and registration along with the weighted total variation. Second, we introduce an additional regulariser which is based on the hyperelasticity principles to allow large and smooth deformations. We demonstrate through numerical results that this combination creates synergies in our complex variational approach resulting in higher quality reconstructions and a good estimate of the breathing dynamics. We also show that our joint model outperforms in terms of contrast, detail and blurring artefacts, a sequential approach.Cambridge Cancer Centre, CMIH and CCIMI, University of Cambridge

    Dynamic Cone-beam CT Reconstruction using Spatial and Temporal Implicit Neural Representation Learning (STINR)

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    Objective: Dynamic cone-beam CT (CBCT) imaging is highly desired in image-guided radiation therapy to provide volumetric images with high spatial and temporal resolutions to enable applications including tumor motion tracking/prediction and intra-delivery dose calculation/accumulation. However, the dynamic CBCT reconstruction is a substantially challenging spatiotemporal inverse problem, due to the extremely limited projection sample available for each CBCT reconstruction (one projection for one CBCT volume). Approach: We developed a simultaneous spatial and temporal implicit neural representation (STINR) method for dynamic CBCT reconstruction. STINR mapped the unknown image and the evolution of its motion into spatial and temporal multi-layer perceptrons (MLPs), and iteratively optimized the neuron weighting of the MLPs via acquired projections to represent the dynamic CBCT series. In addition to the MLPs, we also introduced prior knowledge, in form of principal component analysis (PCA)-based patient-specific motion models, to reduce the complexity of the temporal INRs to address the ill-conditioned dynamic CBCT reconstruction problem. We used the extended cardiac torso (XCAT) phantom to simulate different lung motion/anatomy scenarios to evaluate STINR. The scenarios contain motion variations including motion baseline shifts, motion amplitude/frequency variations, and motion non-periodicity. The scenarios also contain inter-scan anatomical variations including tumor shrinkage and tumor position change. Main results: STINR shows consistently higher image reconstruction and motion tracking accuracy than a traditional PCA-based method and a polynomial-fitting based neural representation method. STINR tracks the lung tumor to an averaged center-of-mass error of <2 mm, with corresponding relative errors of reconstructed dynamic CBCTs <10%

    Role of cell-surface receptor LRP1 in the development of lung fibrosis

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    Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease leading to a reduction of lung function, respiratory failure, and death. Around 3 million people are affected by IPF with a median survival after diagnosis of approximately 3 years. Currently there are no effective treatments available partly due to the incomplete understanding of molecular mechanisms that drive fibrosis through excessive accumulation of collagens, the hallmark of IPF. Low-density lipoprotein receptor-related protein 1 (LRP1) is a ubiquitously expressed cell-surface receptor that is involved in many physiological roles. LRP1 mediates clathrin-dependent endocytosis of various molecules (LRP1 ligands) and modulates cellular signalling pathways. The relevance of LRP1 gene to lung function was discovered by a large genome-wide association study. However, little is known about its role in lung health and disease in vitro. In this study, the role of LRP1 in lung tissue in vivo was investigated using conditional Lrp1 knockout (KO) mice models. Since lung tissue consists of a variety of cell types, I first deleted Lrp1 in the whole body. Global deletion of Lrp1 gene in adulthood caused a rapid weight loss (>20%) and gastro-intestinal abnormalities, suggesting a crucial role of LRP1 in the digestion system and difficulty to use this mouse model to investigate the respiratory system. Among various lung cells, fibroblasts play a major role in collagen deposition. I thus specifically deleted Lrp1 in lung fibroblasts and challenged the mice with bleomycin to induce lung fibrosis. I discovered that excess collagen deposition was observed in control mice, whereas almost no collagen accumulation was detected in fibroblast-selective Lrp1 knockout mice. I also found that the inhibition of LRP1-mediated endocytosis induces cell death of various types of cells in vitro, highlighting the cytotoxicity of prolonged presence of LRP1 ligands. Finally, I identified molecules regulated by LRP1 in lung tissue by proteomics analysis. These findings shed light on novel in vivo roles of LRP1 that play a major role in the digestive system. Moreover, fibroblast LRP1 plays a crucial role in excess collagen deposition during the development of lung fibrosis. Identifying molecular mechanisms behind LRP1 function in collagen deposition may uncover new therapeutic approaches for lung fibrosis disease
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