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Attribute reduction is a crucial research area within concept lattices. However, the existing works are mostly limited to either increment or decrement algorithms, rather than considering both. Therefore, dealing with large-scale streaming attributes in both cases may be inefficient. Convolution calculation in deep learning involves a dynamic data processing method in the form of sliding windows. Inspired by this, we adopt slide-in and slide-out windows in convolution calculation to update attribute reduction. Specifically, we study the attribute changing mechanism in the sliding window mode of convolution and investigate five attribute variation cases. These cases consider the respective intersection of slide-in and slide-out attributes, i.e., equal to, disjoint with, partially joint with, containing, and contained by. Then, we propose an updated solution of the reduction set for simultaneous sliding in and out of attributes. Meanwhile, we propose the CLARA-DC algorithm, which aims to solve the problem of inefficient attribute reduction for large-scale streaming data. Finally, through the experimental comparison on four UCI datasets, CLARA-DC achieves higher efficiency and scalability in dealing with large-scale datasets. It can adapt to varying types and sizes of datasets, boosting efficiency by an average of 25%.

Abstract Chromatin modifications, such as histone acetylation, ubiquitination, and methylation, play fundamental roles in maintaining chromatin architecture and regulating gene transcription. Although their crosstalk in chromatin remodeling has been gradually uncovered, the functional relationship between histone ubiquitination and methylation in regulating immunity and inflammation remains unclear. Here, it is reported that USP38 is a novel histone deubiquitinase that works together with the histone H3K4 modifier KDM5B to orchestrate inflammatory responses. USP38 specifically removes the monoubiquitin on H2B at lysine 120, which functions as a prerequisite for the subsequent recruitment of demethylase KDM5B to the promoters of proinflammatory cytokines Il6 and Il23a during LPS stimulation. KDM5B in turn inhibits the binding of NF‐κB transcription factors to the Il6 and Il23a promoters by reducing H3K4 trimethylation. Furthermore, USP38 can bind to KDM5B and prevent it from proteasomal degradation, which further enhances the function of KDM5B in the regulation of inflammation‐related genes. Loss of Usp38 in mice markedly enhances susceptibility to endotoxin shock and acute colitis, and these mice display a more severe inflammatory phenotype compared to wild‐type mice. The studies identify USP38‐KDM5B as a distinct chromatin modification complex that restrains inflammatory responses through manipulating the crosstalk of histone ubiquitination and methylation.

NLRP11 is a primate-specific NOD-like receptor with unclear function. Here the authors show NLRP11 is an inhibitory protein that targets TRAF6 for K48 ubiquitination-mediated proteasomal degradation to limit inflammatory responses.