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DBPnet: Damper Characteristics-Based Bayesian Physics-Informed Neural Network for Wheel Load Estimation
GL-LFGNN:A Global-Local Dual-branch Causal Graph Neural Network Based on Liang-Kleeman Information Flow for EEG Emotion Recognition
Decoding ML Decision: An Agentic Reasoning Framework for Large-Scale Ranking System
SEA-Eval: A Benchmark for Evaluating Self-Evolving Agents Beyond Episodic Assessment
High-salt diet in macrophage-associated metabolic disorders: Mechanisms and therapeutic implications
Chin Med J (Engl). 2026 May 19. doi: 10.1097/CM9.0000000000004098. Online ahead of print.
ABSTRACT
High-salt diet (HSD) has emerged as a prevalent environmental factor that exacerbates chronic inflammation and insulin resistance in obesity-associated type 2 diabetes (T2D) by modulating macrophage polarization, metabolic reprogramming, and epigenetic imprinting. Current evidence demonstrates that HSD activates p38/mitogen-activated protein kinase (MAPK), nuclear factor kappa-B (NF-κB), and NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome signaling pathways, by which it drives macrophage polarization toward a proinflammatory M1 phenotype while inducing a glycolysis-dominant metabolic shift, thereby establishing a persistent "metabolic memory". Moreover, HSD orchestrates metabolic memory in macrophages through coordinated epigenetic machinery, including histone modifications (Trimethylation of histone H3 at lysine 4 [H3K4me3] and Acetylation of histone H3 at lysine 27 [H3K27ac]), DNA methylation, and noncoding RNAs (e.g., long non-coding RNA MALAT1 and miR-155), leading to sustained inflammatory phenotypes. In multiple metabolic organs (e.g., adipose tissue, liver, pancreas, and gut), the HSD-macrophage axis aggravates systemic insulin resistance through shared proinflammatory signaling and other tissue-specific mechanisms. Most importantly, therapeutic strategies targeting the NLRP3 inflammasome, metabolic pathways, and epigenetic alterations offer novel approaches for managing metabolic inflammation. Future investigations are encouraged to leverage lineage tracing, single-cell sequencing, and spatial multi-omics technologies to advance the development of precision medicine for macrophage-associated metabolic disorders.
PMID:42156155 | DOI:10.1097/CM9.0000000000004098
NAT10 promotes cisplatin resistance and immune escape by increasing the expression of DUSP1 and PD-L1 in gastric cancer
Cell Death Discovery, Published online: 10 April 2026; doi:10.1038/s41420-026-03107-w
NAT10 promotes cisplatin resistance and immune escape by increasing the expression of DUSP1 and PD-L1 in gastric cancerUnified modeling of 3D molecular generation via atomic interactions with PocketXMol
Efficient and Scalable Granular-ball Graph Coarsening Method for Large-scale Graph Node Classification
From Efficiency to Adaptivity: A Deeper Look at Adaptive Reasoning in Large Language Models
The 1000 Chinese Pangenome empowers medical and population genetics
Nature, Published online: 01 April 2026; doi:10.1038/s41586-026-10315-y
Development of the pangenome-informed genome assembly (PIGA) workflow enabled the generation of 1,116 diploid genome assemblies (55 de novo and 1,061 pangenome-informed), representing an extensive resource of medically relevant genic variations.Electric dipole moment drives the dynamics of the TNFR1 complex I signalosome
Nature, Published online: 01 April 2026; doi:10.1038/s41586-026-10304-1
Long-range interactions mediated by protein electric dipole moments have a role in driving the assembly and disassembly of super-signalling complex I for promoting NF-κB signalling.Three Creates All: You Only Sample 3 Steps
Genomic atlas of Bifidobacterium infantis and B. longum informs infant probiotic design
SkillsBench: Benchmarking How Well Agent Skills Work Across Diverse Tasks
CircRNA-encoded RIPK1-98 protein drives lung adenocarcinoma progression
Dev Cell. 2026 Mar 12:S1534-5807(26)00079-1. doi: 10.1016/j.devcel.2026.02.014. Online ahead of print.
ABSTRACT
Unexplored biological matter-including uncharacterized genetic elements, molecular entities, and microbial components-remains poorly understood. Here, we use integrated multi-omics approaches to identify and characterize previously unrecognized protein products encoded by circular RNAs (circRNAs) in human tissue specimens and to delineate their roles in the progression of lung adenocarcinoma (LUAD). The transcription of precursor mRNA by RNA polymerase Ⅱ subunit A (RPB1) is crucial for the biogenesis of these potential circRNA-encoded proteins. Functional and translational analyses link their expression to distinct pathological stages of LUAD in patients. The protein RIPK1-98, encoded by circRIPK1, was identified as functionally distinct from its parental gene product, receptor-interacting serine/threonine kinase 1 (RIPK1). RIPK1-98 modulates cyclin-dependent kinase 2 (CDK2)-dependent cell-cycle regulation, thereby facilitating tumor proliferation in cellular and animal models. Together, these findings suggest that RIPK1-98 serves as a biomarker for cell-cycle progression in LUAD and highlight its potential as a therapeutic target to counteract resistance to first-line treatments, such as osimertinib.
PMID:41825439 | DOI:10.1016/j.devcel.2026.02.014
CircRNA-encoded RIPK1-98 protein drives lung adenocarcinoma progression
Dev Cell. 2026 Mar 12:S1534-5807(26)00079-1. doi: 10.1016/j.devcel.2026.02.014. Online ahead of print.
ABSTRACT
Unexplored biological matter-including uncharacterized genetic elements, molecular entities, and microbial components-remains poorly understood. Here, we use integrated multi-omics approaches to identify and characterize previously unrecognized protein products encoded by circular RNAs (circRNAs) in human tissue specimens and to delineate their roles in the progression of lung adenocarcinoma (LUAD). The transcription of precursor mRNA by RNA polymerase Ⅱ subunit A (RPB1) is crucial for the biogenesis of these potential circRNA-encoded proteins. Functional and translational analyses link their expression to distinct pathological stages of LUAD in patients. The protein RIPK1-98, encoded by circRIPK1, was identified as functionally distinct from its parental gene product, receptor-interacting serine/threonine kinase 1 (RIPK1). RIPK1-98 modulates cyclin-dependent kinase 2 (CDK2)-dependent cell-cycle regulation, thereby facilitating tumor proliferation in cellular and animal models. Together, these findings suggest that RIPK1-98 serves as a biomarker for cell-cycle progression in LUAD and highlight its potential as a therapeutic target to counteract resistance to first-line treatments, such as osimertinib.
PMID:41825439 | DOI:10.1016/j.devcel.2026.02.014