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Exploring the potential active components and mechanisms of Tetrastigma hemsleyanum against ulcerative colitis based on network pharmacology in LPS-induced RAW264.7 cells.

J Ethnopharmacol

January 2025

College of Life Sciences, Key Laboratory of Plant Secondary Metabolism and Regulation of Zhejiang Province, Zhejiang Sci-Tech University, Xuelin Road, Xiasha District, Hangzhou 310018, People's Republic of China. Electronic address:

Ethnopharmacological Relevance: Ulcerative colitis (UC) is a chronic form of inflammatory bowel disease, which current treatments often show limited effectiveness. Ferroptosis, a newly recognized form of programmed cell death has been implicated in UC pathogenesis, suggesting that it may be viable therapeutic target. Tetrastigma hemsleyanum (TH) has shown potential anti-UC effects, though it is unclear whether its therapeutic benefits are mediated by ferroptosis.

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Malate initiates a proton-sensing pathway essential for pH regulation of inflammation.

Signal Transduct Target Ther

December 2024

Department of Orthopedic Surgery/Sports Medicine Center, Southwest Hospital, Army Medical University, Chongqing, 400038, China.

Metabolites can double as a signaling modality that initiates physiological adaptations. Metabolism, a chemical language encoding biological information, has been recognized as a powerful principle directing inflammatory responses. Cytosolic pH is a regulator of inflammatory response in macrophages.

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Postingestive nutrient stimulation conditions food preferences through striatal dopamine and may be associated with blunted brain responses in obesity. In a cross-sectional study, we tested flavor-nutrient conditioning (FNC) with maltodextrin-enriched yogurt, with maltodextrin previously optimized for concentration and dextrose equivalents (n = 57), and to mask texture cues (n = 102). After conditioning, healthy volunteers (n = 52) increased preference for maltodextrin-paired (+102 kcal, CS+), relative to control (+1.

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Regulatory T (T) cells are a suppressive subset of CD4 T cells that maintain immune homeostasis and restrain inflammation. Three decades after their discovery, the promise of strategies to harness T cells for therapy has never been stronger. Multiple clinical trials seeking to enhance endogenous T cells or deliver them as a cell-based therapy have been performed and hint at signs of success, as well as to important limitations and unanswered questions.

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The cyclic GMP-AMP synthase/stimulator of interferon genes (cGAS/STING) pathway is a critical driver of type I interferon (IFN-I) and antitumor CD8+ T cell responses after radiotherapy (RT). In this issue of the JCI, two reports describe mechanisms that restrained STING signaling and abrogated antitumor immunity after RT. Wen, Wang, and colleagues discovered that IFN-I mediated the induction of YTHDF1, an RNA N6-methyladenosine-binding protein, in DCs after RT promoted cathepsin-mediated STING degradation.

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