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Using the local correlation of carrier images to embed secret data in MSBs is a popular scheme for reversible data hiding in encrypted images (RDHEI). However, most existing methods based on this scheme face challenges in achieving complete compression while ensuring security. In this study, an RDHEI method that uses a two-dimensional chaotic system and full bit-plane search (FBPS) is proposed. Specifically, the content owner provides cover images and employs a chaotic system to generate chaotic sequences for inter-block non-symmetrical permutation and intra-block diffusion. The special encryption method, combined with chaos, not only preserves the correlation of pixels within a block but also ensures an extremely high level of security. The FBPS technique is applied to detect all smooth bit planes, not limited to continuous MSBs. For data embedding, ‘0’ and ‘1’ are used to record all smooth and rough bit planes to achieve thorough compression. The results of the experiment show that our proposed method provides a high level of security and achieves 2.142 bit/pixel and 2.339 bit/pixel on the typical datasets BOSSbase (Break Our Steganographic System) and BOWS-2 (Break Our Watermarking System 2nd). Compared with the state-of-the-art methods, the embedding capacity has also been significantly improved.

Peptidylarginine deiminases (PADs) are a family of calcium-dependent enzymes that are involved in a variety of human disorders, including cancer and autoimmune diseases. Although targeting PAD4 has shown no benefit in sepsis, the role of PAD2 remains unknown. Here, we report that PAD2 is engaged in sepsis and sepsis-induced acute lung injury in both human patients and mice. Pad2–/– or selective inhibition of PAD2 by a small molecule inhibitor increased survival and improved overall outcomes in mouse models of sepsis. Pad2 deficiency decreased neutrophil extracellular trap (NET) formation. Importantly, Pad2 deficiency inhibited Caspase-11–dependent pyroptosis in vivo and in vitro. Suppression of PAD2 expression reduced inflammation and increased macrophage bactericidal activity. In contrast to Pad2–/–, Pad4 deficiency enhanced activation of Caspase-11–dependent pyroptosis in BM-derived macrophages and displayed no survival improvement in a mouse sepsis model. Collectively, our findings highlight the potential of PAD2 as an indicative marker and therapeutic target for sepsis.

Sepsis results in millions of deaths every year, with acute lung injury (ALI) being one of the leading causes of mortality in septic patients. As neutrophil extracellular traps (NETs) are abundant in sepsis, neutralizing components of NETs may be a useful strategy to improve outcomes of sepsis. Citrullinated histone H3 (CitH3) has been recently shown to be involved in the NET formation. In this study, we demonstrate that CitH3 damages human umbilical vein endothelial cells (HUVECs) and potentiates NET formation through a positive feedback mechanism. We developed a novel CitH3 monoclonal antibody to target peptidylarginine deiminase (PAD) 2 and PAD 4 generated CitH3. In a mouse model of lethal lipopolysaccharide (LPS) induced shock, neutralizing CitH3 with the newly developed anti-CitH3 monoclonal antibody attenuates inflammatory responses, ameliorates ALI, and improves survival. Our study suggests that effectively blocking circulating CitH3 might be a potential therapeutic method for the treatment of endotoxemia.