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Accurate geometric quantification of the human heart is a key step in the diagnosis of numerous cardiac diseases, and in the management of cardiac patients. Ultrasound imaging is the primary modality for cardiac imaging, however acquisition requires high operator skill, and its interpretation and analysis is difficult due to artifacts. Reconstructing cardiac anatomy in 3D can enable discovery of new biomarkers and make imaging less dependent on operator expertise, however most ultrasound systems only have 2D imaging capabilities. We propose both a simple alteration to the Pix2Vox++ networks for a sizeable reduction in memory usage and computational complexity, and a pipeline to perform reconstruction of 3D anatomy from 2D standard cardiac views, effectively enabling 3D anatomical reconstruction from limited 2D data. We evaluate our pipeline using synthetically generated data achieving accurate 3D whole-heart reconstructions (peak intersection over union score > 0.88) from just two standard anatomical 2D views of the heart. We also show preliminary results using real echo images.
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http://dx.doi.org/10.1007/978-3-031-16902-1_9 | DOI Listing |
Am J Chin Med
September 2025
Shanghai Frontiers Science Center of TCM Chemical Biology, Institute of Interdisciplinary Integrative Medicine Research, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.
Astragaloside IV (ASIV), the main active component of the traditional Chinese medicine HuangQi, exhibits ameliorating effects on myocardial fibrosis through unclear mechanisms. To investigate the effects of ASIV on Endothelial-to-mesenchymal transition (EndMT) in myocardial fibrosis, 10 ng/mL TGF-β1 was used to induce EndMT in human umbilical vein endothelial cells (HUVECs) and a 5 mg/kg/d subcutaneous injection of Isoproterenol (ISO) was used to induce myocardial fibrosis in mice . The drug affinity-responsive target stability (DARTS) was used to identify the target proteins of ASIV in endothelial cells.
View Article and Find Full Text PDFKorean J Physiol Pharmacol
September 2025
Department of Endocrinology, The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan 410007, China.
The progression of renal fibrosis is difficult to reverse, and Poria cocos, one of the main components of Wenyang Zhenshuai Granules, has been shown to be crucial to the development of the epithelial-mesenchymal transition (EMT). This study aimed to examine the molecular mechanism by which Poricoic Acid A (PAA) inhibited the advancement of EMT in renal tubular epithelial (RTE) cells. The protein levels of sprouty RTK signaling antagonist 2 (SPRY2) extracellular regulated protein kinases (ERK), and p-ERK were measured.
View Article and Find Full Text PDFJ Microbiol Immunol Infect
September 2025
Department of Pediatrics, MacKay Children's Hospital and MacKay Memorial Hospital, Taipei, Taiwan.
Background: Respiratory syncytial virus (RSV) is a leading cause of respiratory infections in infants and young children. The COVID-19 pandemic significantly disrupted global RSV epidemiology. This study aimed to investigate the impact of the pandemic on RSV epidemiology in northern Taiwan from 2018 to 2023.
View Article and Find Full Text PDFArch Cardiovasc Dis
August 2025
Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart, Lung and Blood Vessel Diseases, No. 2 Anzhen Road, Chaoyang District, Beijing 100029, China. Electronic address:
Trends Immunol
September 2025
Baker Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia; Department of Cardiometabolic Health, The University of Melbourne, Melbourne, Victoria 3010, Australia. Electronic address:
Neutrophil extracellular trap (NET) formation, or NETosis, is a key innate immune response that contributes to cardiovascular diseases, including vascular inflammation, atherosclerosis, and thrombosis. In the cardiovascular system, neutrophils encounter mechanical cues such as shear stress, matrix stiffness, and cyclic stretch that influence their activation and NET release. This review examines emerging evidence linking altered mechanotransduction to dysregulated NETosis in vascular aging and cardiovascular pathology.
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