CLDN1 (Claudin 1)

In pregnant mice, maternal DHA supplementation mitigated LPS-induced FGR by suppressing NF-κB-mediated inflammatory signaling, modulating gut microbiota composition, and supporting intestinal barrier function, highlighting a potential nutritional strategy to alleviate inflammation-associated adverse pregnancy outcomes.

SPIOCA gavage fortified intestinal barrier integrity-evidenced by elevated ZO-1, ZO-2, Occludin and Claudin-1 expression-and potentiated antitumor immune-cell infiltration, specifically by CD8+ T cells and dendritic cells, into the tumor microenvironment. We therefore preliminarily conclude that SPIOCAs restore gut microbiota homeostasis in lung cancer, thereby enhancing intestinal barrier integrity and converting the tumor immune microenvironment from an immune desert to an immune-inflamed phenotype, ultimately improving lung cancer immunotherapy efficacy.

Drug-gene mapping revealed candidates spanning already in clinical trials for HNC (e.g. Afatinib, Cabozantinib, Dasatinib, Brigatinib, Lenvatinib, Capivasertib, Erdafitinib) and emerging or repurposing candidates (Amuvatinib, XL765 (Voxtalisib), Golotimod, Artenimol, Quercetin, and Acetylsalicylic Acid), offering opportunities for precision repurposing...These included targeted therapies such as Fostamatinib, Nintedanib, Brigatinib, Regorafenib, and Lenvatinib, as well as emerging compounds like Artenimol, Quercetin, and Acetylsalicylic Acid (Aspirin). Through a combination of genomic analysis, network expansion, and literature validation, the GARD pipeline offers a powerful way to accelerate personalized cancer treatments while reducing cost and development time.

B. breve SHMB 8001 represents a potential probiotic strain for alleviating colitis via normalizing intestinal homeostasis.

Additionally, jejunal expression of G-protein coupled receptor 41 (GPR41) and Claudin 1 was markedly higher in the weaned piglets of NaB group than those in control group (P < 0.05). Collectively, these findings suggest that NaB supplementation during mid-to-late gestation could improve placental function in sows, which is associated with enhanced antioxidant capacity, attenuated inflammation, and improved intestinal development in the offspring.

To sum up, our results suggest that the dietary RPB supplementation could affect the ileal SCFA concentration by modulating the microbial community and regulating metabolism, thereby contributing to ileal development and barrier function. This study offers new evidence supporting the use of RPB as a potential application for Tibetan sheep.

Mechanistically, these protective effects were mediated through inhibition of the TLR4/NF-κB signaling pathway. Overall, Zn glycine emerges as a promising nutritional strategy for preventing inflammation-driven bone loss via modulation of the gut-bone axis.

Our findings demonstrate that GN ameliorates AD through a gut-to-brain pathway, mediated by reshaping the microbiota-metabolite axis and repairing the BBB. Thus, GN may represent a promising intervention candidate for AD.

Transcriptomic and network analyses showed that early weaning activated Cytokine-cytokine receptor, NF-κB, TNF and Th17 pathways, whereas probiotics suppressed a weaning-responsive inflammatory gene module, downregulated key hub genes, and enhanced peroxisome proliferator-activated receptor (PPAR) signaling. These results show that supplementing early-weaned lambs with a mixed probiotic generated from sheep is an efficient nutritional strategy to reduce intestinal oxidative and inflammatory damage associated with weaning and to enhance their health and performance.

In contrast, the expression of CD4, CD8, CD31, and CD34 was significantly reduced in PDX0 and PDX1 tumors compared with PTT. OSCC PDX tumors may exhibit instability in the degree of differentiation compared with the donor tumors across passages, as well as alterations in certain components of the TME, including cancer-associated fibroblasts, epithelial-mesenchymal transition-related features, and cellular proliferation characteristics.

P4HB promoted migration, invasion, and EMT of bladder cancer cells by activating the Claudin-1/AMPK/TGF-β1-related pathway.

In LPS-treated cells, HDAC7 knockdown reduced TNF-α, IL-1β, IL-6 levels, and apoptosis, and increased cell viability, which also reversed by Nur77 knockdown. HDAC7 may inhibit Nur77 to exacerbate ARDS by upregulating Igkv14-126, IGLC2, Prss3b, and downregulating Ccdc50 and Chchd7, offering new targets for ARDS treatment.