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JMJD8 regulates adipocyte hypertrophy through the interaction with Perilipin 2.

Diabetes

January 2025

Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, US.

Adipocyte hypertrophy significantly contributes to insulin resistance and metabolic dysfunction. Our previous research established JMJD8 as a mediator of insulin resistance, noting its role in promoting adipocyte hypertrophy within an autonomous adipocyte context. Nevertheless, the precise mechanisms underlying this phenomenon remained elusive.

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We consider a discrete-time Markovian random walk with resets on a connected undirected network. The resets, in which the walker is relocated to randomly chosen nodes, are governed by an independent discrete-time renewal process. Some nodes of the network are target nodes, and we focus on the statistics of first hitting of these nodes.

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Introduction: Pulmonary fibrosis (PF) is a chronic and irreversible interstitial lung disease characterized by a lack of effective therapies. Mesenchymal stem cells (MSCs) have garnered significant interest in the realm of lung regeneration due to their abundant availability, ease of isolation, and capacity for expansion. The objective of our study was to investigate the potential therapeutic role of umbilical cord-derived MSCs (UC-MSCs) in the management of PF, with a focus on the alterations in the gut microbiota and its metabolites during the use of UC-MSCs for the treatment of pulmonary fibrosis, as well as the possible mechanisms involved.

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The tendency to automatically imitate others' behavior is well documented. Successful interactions with others require some control of automatic imitation, but the nature of these control mechanisms remains unclear. The present study investigated whether the regulation of automatic imitation involves domain-specific versus domain-general control processes.

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Introduction: Osteoarthritis (OA) is a chronic degenerative joint disorder characterized by an imbalance in chondrocyte metabolism. Ferroptosis has been implicated in the pathogenesis of OA. The role of Sirt1, a deacetylase, in mediating deacetylation during ferroptosis in OA chondrocytes remains underexplored.

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