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Aspartate Metabolism-Driven Gut Microbiota Dynamics and RIP-Dependent Mitochondrial Function Counteract Oxidative Stress.

Adv Sci (Weinh)

January 2025

Hunan Provincial Key Laboratory of Animal Intestinal Function and Regulation, Hunan international joint laboratory of Animal Intestinal Ecology and Health, Laboratory of Animal Nutrition and Human Health, College of Life Sciences, Hunan Normal University, Changsha, 410081, China.

Aspartate (Asp) metabolism-mediated antioxidant functions have important implications for neonatal growth and intestinal health; however, the antioxidant mechanisms through which Asp regulates the gut microbiota and influences RIP activation remain elusive. This study reports that chronic oxidative stress disrupts gut microbiota and metabolite balance and that such imbalance is intricately tied to the perturbation of Asp metabolism. Under normal conditions, in vivo and in vitro studies reveal that exogenous Asp improves intestinal health by regulating epithelial cell proliferation, nutrient uptake, and apoptosis.

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Aim: To assess hard as well as soft peri-implant tissues within cases having two lost adjacent anterior teeth treated through placing either two implants with two separate crowns or only an implant along with a crown with a cantilever, and evaluating the effect of polyetheretherketone (PEEK) restoration on cantilever design up to 18 months after functional loading.

Materials And Methods: Twenty-seven participants (15 males and 12 females; mean age, 38.6 years; range 20-50 years) with missing two adjacent anterior teeth were treated with implant system (Flotecno implant system, Italy).

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Background/purpose: -2,3,5,4'-tetrahydroxystilbene-2-O-β-D-glucoside (THSG) is a bioactive component in the Chinese herb Polygonum multiflorum, recognized for its anti-inflammatory and lipid-lowering properties. Human dental pulp stem cells (hDPSCs) have excellent capabilities in tooth regeneration, wound healing, and neural repair. The exosomes (Exo) released by hDPSCs contain bioactive molecules that influence cell proliferation, differentiation, and immune responses.

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Phytic acid-based nanomedicine against mTOR represses lipogenesis and immune response for metabolic dysfunction-associated steatohepatitis therapy.

Life Metab

December 2024

State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers and Xijing Hospital of Digestive Diseases, Air Force Medical University, Xi'an, Shaanxi 710032, China.

Metabolic dysfunction-associated steatohepatitis (MASH) is one of the most common chronic liver diseases and is mainly caused by metabolic disorders and systemic inflammatory responses. Recent studies have indicated that the activation of the mammalian (or mechanistic) target of rapamycin (mTOR) signaling participates in MASH progression by facilitating lipogenesis and regulating the immune microenvironment. Although several molecular medicines have been demonstrated to inhibit the phosphorylation or activation of mTOR, their poor specificity and side effects limit their clinical application in MASH treatment.

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Background: Cholestasis plays a critical role in sepsis-associated liver injury (SALI). Intestine-derived fibroblast growth factor 19 (FGF19) is a key regulator for bile acid homeostasis. However, the roles and underlying mechanisms of FGF19 in SALI are still unclear.

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