In layout-to-image (L2I) synthesis, controlled complex scenes are generated from coarse information like bounding boxes. Such a task is exciting to many downstream applications because the input layouts offer strong guidance to the generation process while remaining easily reconfigurable by humans. In this paper, we proposed STyled LAYout Diffusion (STAY Diffusion), a diffusion-based model that produces photo-realistic images and provides fine-grained control of stylized objects in scenes. Our approach learns a global condition for each layout, and a self-supervised semantic map for weight modulation using a novel Edge-Aware Normalization (EA Norm). A new Styled-Mask Attention (SM Attention) is also introduced to cross-condition the global condition and image feature for capturing the objects' relationships. These measures provide consistent guidance through the model, enabling more accurate and controllable image generation. Extensive benchmarking demonstrates that our STAY Diffusion presents high-quality images while surpassing previous state-of-the-art methods in generation diversity, accuracy, and controllability.

Recent deep generative models (DGMs) such as generative adversarial networks (GANs) and diffusion probabilistic models (DPMs) have shown their impressive ability in generating high-fidelity photorealistic images. Although looking appealing to human eyes, training a model on purely synthetic images for downstream image processing tasks like image classification often results in an undesired performance drop compared to training on real data. Previous works have demonstrated that enhancing a real dataset with synthetic images from DGMs can be beneficial. However, the improvements were subjected to certain circumstances and yet were not comparable to adding the same number of real images. In this work, we propose a new taxonomy to describe factors contributing to this commonly observed phenomenon and investigate it on the popular CIFAR-10 dataset. We hypothesize that the Content Gap accounts for a large portion of the performance drop when using synthetic images from DGM and propose strategies to better utilize them in downstream tasks. Extensive experiments on multiple datasets showcase that our method outperforms baselines on downstream classification tasks both in case of training on synthetic only (Synthetic-to-Real) and training on a mix of real and synthetic data (Data Augmentation), particularly in the data-scarce scenario.

The task of few-shot GAN adaptation aims to adapt a pre-trained GAN model to a small dataset with very few training images. While existing methods perform well when the dataset for pre-training is structurally similar to the target dataset, the approaches suffer from training instabilities or memorization issues when the objects in the two domains have a very different structure. To mitigate this limitation, we propose a new smoothness similarity regularization that transfers the inherently learned smoothness of the pre-trained GAN to the few-shot target domain even if the two domains are very different. We evaluate our approach by adapting an unconditional and a class-conditional GAN to diverse few-shot target domains. Our proposed method significantly outperforms prior few-shot GAN adaptation methods in the challenging case of structurally dissimilar source-target domains, while performing on par with the state of the art for similar source-target domains.

The discovery of disease-causing genes is a critical step towards understanding the nature of a disease and determining a possible cure for it. In recent years, many computational methods to identify disease genes have been proposed. However, making full use of disease-related (e.g., symptoms) and gene-related (e.g., gene ontology and protein-protein interactions) information to improve the performance of disease gene prediction is still an issue. Here, we develop a heterogeneous disease-gene-related network (HDGN) embedding representation framework for disease gene prediction (called HerGePred). Based on this framework, a low-dimensional vector representation (LVR) of the nodes in the HDGN can be obtained. Then, we propose two specific algorithms, namely, an LVR-based similarity prediction and a random walk with restart on a reconstructed heterogeneous disease-gene network (RW-RDGN), to predict disease genes with high performance. First, to validate the rationality of the framework, we analyze the similarity-based overlap distribution of disease pairs and design an experiment for disease-gene association recovery, the results of which revealed that the LVR of nodes performs well at preserving the local and global network structure of the HDGN. Then, we apply tenfold cross validation and external validation to compare our methods with other well-known disease gene prediction algorithms. The experimental results show that the RW-RDGN performs better than the state-of-the-art algorithm. The prediction results of disease candidate genes are essential for molecular mechanism investigation and experimental validation. The source codes of HerGePred and experimental data are available at https://github.com/yangkuoone/HerGePred.

Objective: Investigating the molecular mechanisms of symptoms is a vital task in precision medicine to refine disease taxonomy and improve the personalized management of chronic diseases. Although there are abundant experimental studies and computational efforts to obtain the candidate genes of diseases, the identification of symptom genes is rarely addressed. We curated a high-quality benchmark dataset of symptom-gene associations and proposed a heterogeneous network embedding for identifying symptom genes. Methods: We proposed a heterogeneous network embedding representation algorithm, which constructed a heterogeneous symptom-related network that integrated symptom-related associations and applied an embedding representation algorithm to obtain the low-dimensional vector representation of nodes. By measuring the relevance between symptoms and genes via calculating the similarities of their vectors, the candidate genes of given symptoms can be obtained. Results: A benchmark dataset of 18 270 symptom-gene associations between 505 symptoms and 4549 genes was curated. We compared our method to baseline algorithms (FSGER and PRINCE). The experimental results indicated our algorithm achieved a significant improvement over the state-of-the-art method, with precision and recall improved by 66.80% (0.844 vs 0.506) and 53.96% (0.311 vs 0.202), respectively, for TOP@3 and association precision improved by 37.71% (0.723 vs 0.525) over the PRINCE. Conclusions: The experimental validation of the algorithms and the literature validation of typical symptoms indicated our method achieved excellent performance. Hence, we curated a prediction dataset of 17 479 symptom-candidate genes. The benchmark and prediction datasets have the potential to promote investigations of the molecular mechanisms of symptoms and provide candidate genes for validation in experimental settings.