Lead-gen and ecommerce managers: two Google Ads bidding changes landed this summer. Here's what shifts, what doesn't, and which campaigns to audit first.
The post Google Ads Bidding Strategies: Where To Spend Your Time In 2026 appeared first on Search Engine Journal.
Amazon pulled out of U.S. Google Shopping in July 2025 and still hasn't returned. Here's what a year of auction data reveals for retailers.
The post Amazon Left US Google Shopping A Year Ago & Never Came Back appeared first on Search Engine Journal.
Google's August 17 update pushes budget-limited Target CPA and Target ROAS campaigns toward their stated targets, risking higher costs unless advertisers audit and adjust first.
The post Google Ads Adds Target-Based Bidding For Ecommerce Campaigns appeared first on Search Engine Journal.
Neonatal necrotizing enterocolitis (NEC) remains one of pediatricsβ most devastating intestinal disorders, and safer, mechanism-driven therapies are urgently needed. New findings suggest that tiny vesicles naturally present in human breast milkβexosomesβmay offer protection by delivering a specific regulatory microRNA.
Researchers report that exosomes enriched with miR-144-5p can help restore the intestinal tight junction barrier, a key defense line that collapses during NEC. By focusing on miR-144-5p, the team moves beyond earlier observations that breast milk exosomes can reduce NEC severity and instead pinpoints a molecular cargo likely responsible for part of that benefit.
The study centers on how NEC damages epithelial integrity and promotes inflammatory signaling. Tight junction disruption is associated with increased permeability, bacterial translocation, and worsening inflammationβconditions that accelerate disease progression in vulnerable newborns. The investigators therefore examined whether miR-144-5p could counter these barrier failures in NEC contexts.
Mechanistically, the work links miR-144-5p action to the TLR4/NF-ΞΊB pathway, a well-known inflammatory axis. Toll-like receptor 4 (TLR4) senses danger-associated cues and can trigger NF-ΞΊB activation, driving transcription of pro-inflammatory mediators. In NEC, exaggerated signaling through this route contributes to tissue injury and impaired repair.
By modulating this cascade, miR-144-5p appears to dampen downstream inflammatory responses while promoting recovery of junctional structure. The paperβs data indicate that exosomal delivery is central: miRNAs packaged within vesicles can be taken up by recipient cells more efficiently than naked RNA, enabling functional gene regulation in target intestinal compartments.
Together, the results support a model in which breast milk exosomal miR-144-5p alleviates NEC by suppressing TLR4-driven NF-ΞΊB activation, thereby reducing inflammatory injury and enabling tighter regulation of epithelial junctions. If translated, such a cargo-guided approach could complement existing supportive NEC treatments.
While additional work will be required to confirm efficacy across models and to evaluate safety, the study provides a clear mechanistic roadmap: therapeutic exosomes or miRNA mimics that bias TLR4/NF-ΞΊB activity may be a promising strategy for protecting the neonatal gut.
Subject of Research: Neonatal necrotizing enterocolitis (NEC), breast milk-derived exosomes, miR-144-5p, tight junction barrier repair, TLR4/NF-ΞΊB signaling.
Article Title: Human milk exosomal-miR-144-5p alleviates neonatal necrotizing enterocolitis by regulating the TLR4/NF-ΞΊB pathway.
Article References: Chen, Z., Chen, C., Hu, X. et al. Human milk exosomal-miR-144-5p alleviates neonatal necrotizing enterocolitis by regulating the TLR4/NF-ΞΊB pathway. Pediatr Res (2026). https://doi.org/10.1038/s41390-026-05305-9
Image Credits: AI Generated
DOI: 10.1038/s41390-026-05305-9
Keywords:
Login