Adversarial feature hybrid framework for steganography with shifted window local loss.

Image steganography is a long-standing image security problem that aims at hiding information in cover images. In recent years, the application of deep learning to steganography has the tendency to outperform traditional methods. However, the vigorous development of CNN-based steganalyzers still have a serious threat to steganography methods. To address this gap, we present an end-to-end adversarial steganography framework based on CNN and Transformer learned by shifted window local loss, called StegoFormer, which contains Encoder, Decoder, and Discriminator. Encoder is a hybrid model based on U-shaped network and Transformer block, which effectively integrates high-resolution spatial features and global self-attention features. In particular, Shuffle Linear layer is suggested, which can enhance the linear layer's competence to extract local features. Given the substantial error in the central patch of the stego image, we propose shifted window local loss learning to assist Encoder in generating accurate stego images via weighted local loss. Furthermore, Gaussian mask augmentation method is designed to augment data for Discriminator, which helps to improve the security of Encoder through adversarial training. Controlled experiments show that StegoFormer is superior to the existing advanced steganography methods in terms of anti-steganalysis ability, steganography effectiveness, and information restoration.

Role of ionizing radiation activated NRF2 in lung cancer radioresistance.

Radiotherapies are commonly used to target remaining tumor niches after surgery of solid tumors but are restricted due to therapeutic resistance. Several pathways of radioresistance have been reported in various cancers. This study investigates the pivotal role of Nuclear factor-erythroid 2-related factor 2 (NRF2) in the activation of DNA damage repair in lung cancer cells after x-rays exposure. To explore the NRF2 activation after ionizing irradiations, this study uses a knockdown of NRF2, which shows potential DNA damage after x-rays irradiation in lung cancers. This work further shows that NRF2 knockdown disrupts damaged DNA repair by inhibiting DNA-dependent protein kinase catalytic subunit. At the same time, NRF2 knockdown by shRNA considerably disparate homologous recombination by interfering with Rad51 expression. Further investigation of the associated pathway reveals that NRF2 activation mediates DNA damage response via the mitogen-activated protein kinase (MAPK) pathway as the knockout of NRF2 directly enhances intracellular MAPK phosphorylation. Similarly, both N-acetylcysteineand constitutive knockout of NRF2 disrupt DNA-dependent protein kinase catalytic subunit, while NRF2 knockout failed to upregulate Rad51 expression after irradiation in-vivo. Taken together, these findings advocate NRF2 plays a critical role in the development of radioresistance by upregulating DNA damage response via the MAPK pathway, which can be of great significance.