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Itaconate restrains acute proinflammatory activation of microglia MG after traumatic brain injury in mice.

Sci Transl Med

March 2025

Clinical Neuroscience Research Center, Department of Neurosurgery and Neurology, Tulane University School of Medicine, New Orleans, LA 70112, USA.

Traumatic brain injury (TBI) rapidly triggers proinflammatory activation of microglia, contributing to secondary brain damage post-TBI. Although the governing role of energy metabolism in shaping the inflammatory phenotype and function of immune cells has been increasingly recognized, the specific alterations in microglial bioenergetics post-TBI remain poorly understood. Itaconate, a metabolite produced by the enzyme aconitate decarboxylase 1 [IRG1; encoded by immune responsive gene 1 ()], is a pivotal metabolic regulator in immune cells, particularly in macrophages.

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Pancreatic cancer (PC) is a highly metastatic malignancy. More than 80% of patients with PC present with advanced-stage disease, preventing potentially curative surgery. The neuropeptide Y (NPY) system, best known for its role in controlling energy homeostasis, has also been shown to promote tumorigenesis in a range of cancer types, but its role in PC has yet to be explored.

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The integration of social robots into family environments raises critical questions about their long-term influence on family interactions. This study explores the potential of social robots as conversational catalysts in human-human dyadic interaction, focusing on enhancing high-quality, reciprocal conversations between parents and children during dialogic coreading activities. With the increasing prevalence of social robots in homes and the recognized importance of parent-child exchanges for children's developmental milestones, this work presents a comprehensive empirical investigation involving more than 70 parent-child dyads over a period of 1 to 2 months.

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Objective: This study aims to investigate and analyze the differentially expressed genes (DEGs) in CD34 + hematopoietic stem cells (HSCs) from patients with myelodysplastic syndromes (MDS) through bioinformatics analysis, with the ultimate goal of uncovering the potential molecular mechanisms underlying pathogenesis of MDS. The findings of this study are expected to provide novel insights into clinical treatment strategies for MDS.

Methods: Initially, we downloaded three datasets, GSE81173, GSE4619, and GSE58831, from the public Gene Expression Omnibus (GEO) database as our training sets, and selected the GSE19429 dataset as the validation set.

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Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation, pannus formation, and progressive joint destruction. The inflammatory milieu in RA drives endothelial cell activation and upregulation of adhesion molecules, thus facilitating leukocyte infiltration into the synovium. Reelin, a circulating glycoprotein previously implicated in endothelial activation and leukocyte recruitment in diseases such as atherosclerosis and multiple sclerosis, has emerged as a potential upstream regulator of these processes.

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