Accurate brain tumor segmentation plays an important role in clinical diagnosis, treatment planning, and therapeutic response monitoring. Multi-modal MRI provides complementary structural and functional information, but existing methods remain limited by their inadequate exploitation of cross-modal complementarity and their inability to effectively handle modality-specific disparities and redundant information. To address these challenges, this paper proposes a novel hierarchical teacher-student learning framework with adaptive cross-modal fusion. MRI modalities are grouped into teacher modalities (Flair and T1c) and student modalities (T2 and T1) based on their intrinsic tumor-related characteristics. Central to this framework is the Modality Guidance Module (MGM), which consists of two key components designed to achieve multi-modal feature distillation. Within MGM, the Modality Enhancement Module (MEM) extracts highly discriminative features from teacher modalities. While the Modality Fusion Module (MFM) leverages these features to guide and refine the learning of student modalities. To further capture inter-modal dependencies, a Cross-Modal Fusion Module (CMFM) is introduced to adaptively integrate complementary information across all modalities. Extensive experiments on the BraTS 2018, 2019 and 2020 datasets demonstrate that the proposed method achieves superior performance compared with state-of-the-art approaches. Beyond brain tumor segmentation, the hierarchical teacher-student paradigm and adaptive fusion strategy also hold potential for broader multi-modal image analysis tasks.

Abstract This study presents a new machine learning algorithm, named Chemical Environment Graph Neural Network (ChemGNN), designed to accelerate materials property prediction and advance new materials discovery. Graphitic carbon nitride (g-C3N4) and its doped variants have gained significant interest for their potential as optical materials. Accurate prediction of their band gaps is crucial for practical applications; however, traditional quantum simulation methods are computationally expensive and challenging to explore the vast space of possible doped molecular structures. The proposed ChemGNN leverages the learning ability of current graph neural networks (GNNs) to satisfactorily capture the characteristics of atoms' chemical environment underlying complex molecular structures. Our experimental results demonstrate more than 100% improvement in band gap prediction accuracy over existing GNNs on g-C3N4. Furthermore, the general ChemGNN model can precisely foresee band gaps of various doped g-C3N4 structures, making it a valuable tool for performing high-throughput prediction in materials design and development.

Emerging researchindicates that the degenerative biomarkers associated with Alzheimer's disease (AD) exhibit a non-random distribution within the cerebral cortex, instead following the structural brain network. The alterations in brain networks occur much earlier than the onset of clinical symptoms, thereby affecting the progression of brain disease. In this context, the utilization of computational methods to ascertain the propagation patterns of neuropathological events would contribute to the comprehension of the pathophysiological mechanism involved in the evolution of AD. Despite the encouraging findings achieved by existing graph-based deep learning approaches in analyzing irregular graph data, their applications in identifying the spreading pathway of neuropathology are limited due to two disadvantages. They include (1) lack of a common brain network as an unbiased reference basis for group comparison, and (2) lack of an appropriate mechanism for the identification of propagation patterns. To this end, we propose a proof-of-concept harmonic wavelet neural network (HWNN) to predict the early stage of AD and localize disease-related significant wavelets, which can be used to characterize the spreading pathways of neuropathological events across the brain network. The extensive experiments constructed on both synthetic and real datasets demonstrate that our proposed method achieves superior performance in classification accuracy and statistical power of identifying propagation patterns, compared with other representative approaches.

Mounting evidence has revealed that functional brain networks are intrinsically dynamic, undergoing changes over time, even in the resting-state environment. Notably, recent studies have highlighted the existence of a small number of critical brain regions within each functional brain network that exhibit a flexible role in adapting the geometric pattern of brain connectivity over time, referred to as "temporal hub" regions. Therefore, the identification of these temporal hubs becomes pivotal for comprehending the mechanisms that underlie the dynamic evolution of brain connectivity. However, existing spatio-temporal hub identification methods rely on static network-based approaches, wherein each temporal hub region is independently inferred from individual time-segmented networks without considering their temporal consistency and consequently fails to align the evolution of hubs with the dynamic changes in brain states. To address this limitation, we propose a novel spatio-temporal hub identification method that fully leverages dynamic graph embedding to distinguish temporal hubs from peripheral nodes, in which dynamic graph embeddings are learned from both spatial and temporal dimensions. Specifically, to preserve the temporal consistency of evolving networks, we model the dynamic graph embedding as a physical model of time, where the network-to-network transition is mathematically expressed as a total variation of dynamic graph embedding with respect to time. Furthermore, a Grassmannian manifold optimization scheme is introduced to enhance graph embedding learning and capture the time-varying topology of brain networks. Experimental results on both synthetic and real fMRI data demonstrate superior temporal consistency in hub identification, surpassing conventional approaches.

Abstract The article presents a comprehensive summary of Intelligent Ship Marine Object Detection (ISMOD) based on the RGB Camera. Marine object detection plays a pivotal role in enabling intelligent ships to acquire crucial data and security assurances for autonomous navigation. Among the various detection sensors, the RGB Camera is an informative and cost‐effective tool with a wide range of civil applications. In the beginning, the ISMOD metrics based on the RGB camera is analyzed from three significant aspects, namely accuracy, speed, and robustness. Subsequently, the latest research status and comparative overview are presented, encompassing three mainstream detection methods: traditional detection, deep learning detection, and sensor fusion detection. Finally, the existing challenges of ISMOD are discussed and future development trends are recommended. The results demonstrate that forthcoming development will predominantly concentrate on deep learning approaches, complemented by other techniques. It is imperative to advance detection performance in domains such as deep fusion, multi‐feature extraction, multi‐fusion technology, and lightweight detection architecture.

Abstract This paper introduces an enhanced object detection algorithm tailored for indoor shopping applications, a critical component of smart cities and smart shopping ecosystems. The proposed method builds on the YOLOv8n algorithm by integrating a ParNetAttention module into the backbone's C2f module, creating the novel C2f‐ParNet structure. This innovation enhances feature extraction, crucial for detecting intricate details in complex indoor environments. Additionally, the channel‐wise attention‐recurrent feature extraction (CARAFE) module is incorporated into the neck network, improving target feature fusion and focus on objects of interest, thereby boosting detection accuracy. To optimize training efficiency, the model employs the Wise Intersection over Union (WIoUv3) as its regression loss function, accelerating data convergence and improving performance. Experimental results demonstrate the enhanced YOLOv8n achieves a mean average precision (mAP) at 50% threshold (mAP@50) of 61.2%, a 1.2 percentage point improvement over the baseline. The fully optimized algorithm achieves an mAP@50 of 65.9% and an F1 score of 63.5%, outperforming both the original YOLOv8n and existing algorithms. Furthermore, with a frame rate of 106.5 FPS and computational complexity of just 12.9 GFLOPs (Giga Floating‐Point Operations per Second), this approach balances high performance with lightweight efficiency, making it ideal for real‐time applications in smart retail environments.

Alzheimer's disease (AD) is the most common neurodegenerative disease, and it consumes considerable medical resources with increasing number of patients every year. Mounting evidence show that the regulatory disruptions altering the intrinsic activity of genes in brain cells contribute to AD pathogenesis. To gain insights into the underlying gene regulation in AD, we proposed a graph learning method, Single-Cell based Regulatory Network (SCRN), to identify the regulatory mechanisms based on single-cell data. SCRN implements the γ-decaying heuristic link prediction based on graph neural networks and can identify reliable gene regulatory networks using locally closed subgraphs. In this work, we first performed UMAP dimension reduction analysis on single-cell RNA sequencing (scRNA-seq) data of AD and normal samples. Then we used SCRN to construct the gene regulatory network based on three well-recognized AD genes (APOE, CX3CR1, and P2RY12). Enrichment analysis of the regulatory network revealed significant pathways including NGF signaling, ERBB2 signaling, and hemostasis. These findings demonstrate the feasibility of using SCRN to uncover potential biomarkers and therapeutic targets related to AD.

Recently, the fast development of single-cell RNA-seq (scRNA-seq) techniques has enabled high-resolution transcriptomic statistical analysis of individual cells in heterogeneous tissues, which can help researchers to explore the relationship between genes and human diseases. The emerging scRNA-seq data results in new analysis methods aiming to identify cell-level clustering and annotations. However, there are few methods developed to gain insights into the gene-level clusters with biological significance. This study proposes a new deep learning-based framework, scENT (single cell gENe clusTer), to identify significant gene clusters from single-cell RNA-seq data. We started with clustering the scRNA-seq data into multiple optimal groups, followed by a gene set enrichment analysis to identify classes of over-represented genes. Considering high-dimensional data with extensive zeros and dropout issues, scENT integrates perturbation in the learning process of clustering scRNA-seq data to improve its robustness and performance. Experimental results show that scENT outperformed other benchmarking methods on simulation data. To validate the biological insights of scENT, we applied it to the public experimental scRNA-seq data profiled from patients with Alzheimer's disease and brain metastasis. scENT successfully identified novel functional gene clusters and associated functions, facilitating the discovery of prospective mechanisms and the understanding of related diseases.

Since brain network organization is essentially governed by the harmonic waves derived from the Eigen-system of the underlying Laplacian matrix, discovering the harmonic-based alterations provides a new window to understand the pathogenic mechanism of Alzheimer's disease (AD) in a unified reference space. However, current reference (common harmonic waves) estimation studies over the individual harmonic waves are often sensitive to outliers, which are obtained by averaging the heterogenous individual brain networks. To address this challenge, we propose a novel manifold learning approach to identify a set of outlier-immunized common harmonic waves. The backbone of our framework is calculating the geometric median of all individual harmonic waves on the Stiefel manifold, instead of Fréchet mean, thus improving the robustness of learned common harmonic waves to the outliers. A manifold optimization scheme with theoretically guaranteed convergence is tailored to solve our method. The experimental results on synthetic data and real data demonstrate that the common harmonic waves learned by our approach are not only more robust to the outliers than the state-of-the-art methods, but also provide a putative imaging biomarker to predict the early stage of AD.

Adjuvant and salvage radiotherapy after radical prostatectomy requires precise delineations of prostate bed (PB), i.e., the clinical target volume, and surrounding organs at risk (OARs) to optimize radiotherapy planning. Segmenting PB is particularly challenging even for clinicians, e.g., from the planning computed tomography (CT) images, as it is an invisible/virtual target after the operative removal of the cancerous prostate gland. Very recently, a few deep learning-based methods have been proposed to automatically contour non-contrast PB by leveraging its spatial reliance on adjacent OARs (i.e., the bladder and rectum) with much more clear boundaries, mimicking the clinical workflow of experienced clinicians. Although achieving state-of-the-art results from both the clinical and technical aspects, these existing methods improperly ignore the gap between the hierarchical feature representations needed for segmenting those fundamentally different clinical targets (i.e., PB and OARs), which in turn limits their delineation accuracy. This paper proposes an asymmetric multi-task network integrating dynamic cross-task representation adaptation (i.e., DyAdapt) for accurate and efficient co-segmentation of PB and OARs in one-pass from CT images. In the learning-to-learn framework, the DyAdapt modules adaptively transfer the hierarchical feature representations from the source task of OARs segmentation to match up with the target (and more challenging) task of PB segmentation, conditioned on the dynamic inter-task associations learned from the learning states of the feed-forward path. On a real-patient dataset, our method led to state-of-the-art results of PB and OARs co-segmentation. Code is available at https://github.com/ladderlab-xjtu/DyAdapt.

Human brain is a complex yet economically organized system, where a small portion of critical hub regions support the majority of brain functions. The identification of common hub nodes in a population of networks is often simplified as a voting procedure on the set of identified hub nodes across individual brain networks, which ignores the intrinsic data geometry and partially lacks the reproducible findings in neuroscience. Hence, we propose a first-ever group-wise hub identification method to identify hub nodes that are common across a population of individual brain networks. Specifically, the backbone of our method is to learn common graph embedding that can represent the majority of local topological profiles. By requiring orthogonality among the graph embedding vectors, each graph embedding as a data element is residing on the Grassmannian manifold. We present a novel Grassmannian manifold optimization scheme that allows us to find the common graph embeddings, which not only identify the most reliable hub nodes in each network but also yield a population-based common hub node map. Results of the accuracy and replicability on both synthetic and real network data show that the proposed manifold learning approach outperforms all hub identification methods employed in this evaluation.

Chronic obstructive pulmonary disease (COPD) is a prevalent chronic disease with high morbidity and mortality. The early diagnosis of COPD is vital for clinical treatment, which helps patients to have a better quality of life. Because COPD can be ascribed to chronic bronchitis and emphysema, lesions in a computed tomography (CT) image can present anywhere inside the lung with different types, shapes and sizes. Multiple instance learning (MIL) is an effective tool for solving COPD discrimination. In this study, a novel graph convolutional MIL with the adaptive additive margin loss (GCMIL-AAMS) approach is proposed to diagnose COPD by CT. Specifically, for those early stage patients, the selected instance-level features can be more discriminative if they were learned by our proposed graph convolution and pooling with self-attention mechanism. The AAMS loss can utilize the information of COPD severity on a hypersphere manifold by adaptively setting the angular margins to improve the performance, as the severity can be quantified as four grades by pulmonary function test. The results show that our proposed GCMIL-AAMS method provides superior discrimination and generalization abilities in COPD discrimination, with areas under a receiver operating characteristic curve (AUCs) of 0.960 ± 0.014 and 0.862 ± 0.010 in the test set and external testing set, respectively, in 5-fold stratified cross validation; moreover, it demonstrates that graph learning is applicable to MIL and suggests that MIL may be adaptable to graph learning.

Converging evidence shows that disease-relevant brain alterations do not appear in random brain locations, instead, their spatial patterns follow large-scale brain networks. In this context, a powerful network analysis approach with a mathematical foundation is indispensable to understand the mechanisms of neuropathological events as they spread through the brain. Indeed, the topology of each brain network is governed by its native harmonic waves, which are a set of orthogonal bases derived from the Eigen-system of the underlying Laplacian matrix. To that end, we propose a novel connectome harmonic analysis framework that provides enhanced mathematical insights by detecting frequency-based alterations relevant to brain disorders. The backbone of our framework is a novel manifold algebra appropriate for inference across harmonic waves. This algebra overcomes the limitations of using classic Euclidean operations on irregular data structures. The individual harmonic differences are measured by a set of common harmonic waves learned from a population of individual Eigen-systems, where each native Eigen-system is regarded as a sample drawn from the Stiefel manifold. Specifically, a manifold optimization scheme is tailored to find the common harmonic waves, which reside at the center of the Stiefel manifold. To that end, the common harmonic waves constitute a new set of neurobiological bases to understand disease progression. Each harmonic wave exhibits a unique propagation pattern of neuropathological burden spreading across brain networks. The statistical power of our novel connectome harmonic analysis approach is evaluated by identifying frequency-based alterations relevant to Alzheimer's disease, where our learning-based manifold approach discovers more significant and reproducible network dysfunction patterns than Euclidean methods.

Currently, many studies of Alzheimer's disease (AD) are investigating the neurobiological factors behind the acquisition of beta-amyloid (A), pathologic tau (T), and neurodegeneration ([N]) biomarkers from neuroimages. However, a system-level mechanism of how these neuropathological burdens promote neurodegeneration and why AD exhibits characteristic progression is largely elusive. In this study, we combined the power of systems biology and network neuroscience to understand the dynamic interaction and diffusion process of AT[N] biomarkers from an unprecedented amount of longitudinal Amyloid PET scan, MRI imaging, and DTI data. Specifically, we developed a network-guided biochemical model to jointly (1) model the interaction of AT[N] biomarkers at each brain region and (2) characterize their propagation pattern across the fiber pathways in the structural brain network, where the brain resilience is also considered as a moderator of cognitive decline. Our biochemical model offers a greater mathematical insight to understand the physiopathological mechanism of AD progression by studying the system dynamics and stability. Thus, an in-depth system-level analysis allows us to gain a new understanding of how AT[N] biomarkers spread throughout the brain, capture the early sign of cognitive decline, and predict the AD progression from the preclinical stage.