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We tackle the problem of estimating correspondences from a general marker, such as a movie poster, to an image that captures such a marker. Conventionally, this problem is addressed by fitting a homography model based on sparse feature matching. However, they are only able to handle plane-like markers and the sparse features do not sufficiently utilize appearance information. In this paper, we propose a novel framework NeuralMarker, training a neural network estimating dense marker correspondences under various challenging conditions, such as marker deformation, harsh lighting, etc. Deep learning has presented an excellent performance in correspondence learning once provided with sufficient training data. However, annotating pixel-wise dense correspondence for training marker correspondence is too expensive. We observe that the challenges of marker correspondence estimation come from two individual aspects: geometry variation and appearance variation. We, therefore, design two components addressing these two challenges in NeuralMarker. First, we create a synthetic dataset FlyingMarkers containing marker-image pairs with ground truth dense correspondences. By training with FlyingMarkers, the neural network is encouraged to capture various marker motions. Second, we propose the novel Symmetric Epipolar Distance (SED) loss, which enables learning dense correspondence from posed images. Learning with the SED loss and the cross-lighting posed images collected by Structure-from-Motion (SfM), NeuralMarker is remarkably robust in harsh lighting environments and avoids synthetic image bias. Besides, we also propose a novel marker correspondence evaluation method circumstancing annotations on real marker-image pairs and create a new benchmark. We show that NeuralMarker significantly outperforms previous methods and enables new interesting applications, including Augmented Reality (AR) and video editing. [ABSTRACT FROM AUTHOR]

ATP-sensitive potassium channels (KATP channels) play pivotal roles in excitable cells and link cellular metabolism with membrane excitability. The action potential converts electricity into dynamics by ion channel-mediated ion exchange to generate systole, involved in every heartbeat. Activation of the KATP channel repolarizes the membrane potential and decreases early afterdepolarization (EAD)-mediated arrhythmias. KATP channels in cardiomyocytes have less function under physiological conditions but they open during severe and prolonged anoxia due to a reduced ATP/ADP ratio, lessening cellular excitability and thus preventing action potential generation and cell contraction. Small active molecules activate and enhance the opening of the KATP channel, which induces the repolarization of the membrane and decreases the occurrence of malignant arrhythmia. Accumulated evidence indicates that mutation of KATP channels deteriorates the regulatory roles in mutation-related diseases. However, patients with mutations in KATP channels still have no efficient treatment. Hence, in this study, we describe the role of KATP channels and subunits in angiocardiopathy, summarize the mutations of the KATP channels and the functional regulation of small active molecules in KATP channels, elucidate the potential mechanisms of mutant KATP channels and provide insight into clinical therapeutic strategies. [ABSTRACT FROM AUTHOR]

Aims: Heart failure (HF) is a chronic heart disease with a high incidence and mortality. Due to the regulatory complexity of gene coexpression networks, the underlying hub genes regulation in HF remain incompletely appreciated. We aimed to explore potential key modules and genes for HF using weighted gene coexpression network analysis (WGCNA). Methods and results: The expression profiles by high throughput sequencing of heart tissues samples from HF and non‐HF samples were obtained from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) between HF and non‐HF samples were firstly identified. Then, a coexpression network was constructed to identify key modules and potential hub genes. The biological functions of potential hub genes were analysed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses. Finally, a protein–protein interaction (PPI) network was constructed using the STRING online tool. A total of 135 DEGs (133 up‐regulated and 2 down‐regulated DEGs) between HF and non‐HF samples were identified in the GSE135055 and GSE123976 datasets. Moreover, a total of 38 modules were screened based on WGCNA in the GSE135055 dataset, and six potential hub genes (UCK2, ASB1, CCNI, CUX1, IRX6, and STX16) were screened from the key module by setting the gene significance over 0.2 and the module membership over 0.8. Furthermore, 78 potential hub genes were obtained by taking the intersection of the 135 DEGs and all genes in the key module, and enrichment analysis revealed that they were mainly involved in the MAPK and PI3K‐AKT signalling pathways. Finally, in a PPI network constructed with the 78 potential hub genes, CUX1 and ASB1 were identified as hub genes in HF because they were also identified as potential hub genes in the WGCNA. Conclusions: To the best of our knowledge, our study is the first to employ WGCNA to identify the key module and hub genes for HF. Our study identified a module and two genes that might play important roles in HF, which may provide potential biomarkers for the diagnosis of HF and improve our knowledge of the molecular mechanisms underlying HF. [ABSTRACT FROM AUTHOR]