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Zinc oxide nanoparticles (ZnONPs) are widely utilized across various industries, raising concerns about their potential toxicity, especially in the respiratory system. This study explores the role of autophagy, regulated by microtubule-associated protein 1A/1B-light chain 3B (LC3B), in ZnONPs-induced toxicity using both in vivo (LC3B knockout mice) and in vitro (BEAS-2B cells) models. Our findings demonstrate that LC3B-regulated autophagy mitigates ZnONPs-induced epithelial cell dysfunction and acute lung injury. In the absence of LC3B, oxidative stress, inflammation, and intracellular zinc accumulation are exacerbated, resulting in mitochondrial dysfunction and epithelial cell death. In vitro, LC3B knockdown disrupted zinc ion transporter expression and impaired mitophagic flux in BEAS-2B cells. Treatment with zinc ion chelators alleviated these toxic effects, confirming that free zinc ions play a critical role in driving ZnONPs toxicity. These findings highlight that targeting autophagy and maintaining zinc homeostasis could offer therapeutic strategies to reduce ZnONPs-induced lung damage. [ABSTRACT FROM AUTHOR]

Aim Methodology Results Conclusion Regenerative endodontic procedures (REPs) are tissue engineering‐based treatments aimed at regenerating the pulp‐dentin complex. However, these procedures are not widely practiced or well‐known among dentists due to a lack of training. This study aims to develop a practical hands‐on training model for REPs to enhance students' theoretical knowledge and practical skills.A cost‐effective, easy‐to‐operate, and reusable training model for preclinical training of REPs was developed. A total of 125 undergraduates were divided into an experimental group (REPs model) and a control group (traditional teaching). The students' theoretical knowledge and operational skills were assessed through examinations and practical assessments. Student perceptions were assessed by questionnaires.The experimental group achieved higher scores in theoretical knowledge and operational skills compared to the control group (p < .001). The process evaluation of the experimental group demonstrated a high level of proficiency in executing root canal disinfection steps, with pass rates ranging from 93.5% to 95.2%. Students in both groups perceived the model as valuable for improving critical thinking, stimulating interest, and enhancing their confidence and proficiency.The developed REPs training model is a practical and effective tool for teaching and training regenerative endodontics. It bridges the gap between preclinical and clinical education, enhancing students' confidence and clinical competence. [ABSTRACT FROM AUTHOR]

Bacterial dysbiosis accompanies carcinogenesis in malignancies such as colon and liver cancer, and has recently been implicated in the pathogenesis of pancreatic ductal adenocarcinoma (PDA).sup.1. However, the mycobiome has not been clearly implicated in tumorigenesis. Here we show that fungi migrate from the gut lumen to the pancreas, and that this is implicated in the pathogenesis of PDA. PDA tumours in humans and mouse models of this cancer displayed an increase in fungi of about 3,000-fold compared to normal pancreatic tissue. The composition of the mycobiome of PDA tumours was distinct from that of the gut or normal pancreas on the basis of alpha- and beta-diversity indices. Specifically, the fungal community that infiltrated PDA tumours was markedly enriched for Malassezia spp. in both mice and humans. Ablation of the mycobiome was protective against tumour growth in slowly progressive and invasive models of PDA, and repopulation with a Malassezia species--but not species in the genera Candida, Saccharomyces or Aspergillus--accelerated oncogenesis. We also discovered that ligation of mannose-binding lectin (MBL), which binds to glycans of the fungal wall to activate the complement cascade, was required for oncogenic progression, whereas deletion of MBL or C3 in the extratumoral compartment--or knockdown of C3aR in tumour cells--were both protective against tumour growth. In addition, reprogramming of the mycobiome did not alter the progression of PDA in Mbl- (also known as Mbl2) or C3-deficient mice. Collectively, our work shows that pathogenic fungi promote PDA by driving the complement cascade through the activation of MBL. In humans and mouse models, the mycobiome of pancreatic ductal adenocarcinoma tumours is markedly enriched in Malassezia species compared to that of normal pancreas, which implicates these pathogenic fungi in oncogenesis., Author(s): Berk Aykut [sup.1] , Smruti Pushalkar [sup.2] , Ruonan Chen [sup.1] , Qianhao Li [sup.2] , Raquel Abengozar [sup.1] , Jacqueline I. Kim [sup.1] , Sorin A. Shadaloey [sup.1] [...]

The gut microbiome shapes local and systemic immunity. The liver is presumed to be a protected sterile site. As such, a hepatic microbiome has not been examined. Here, we showed a liver microbiome in mice and humans that is distinct from that of the gut and is enriched in Proteobacteria. It undergoes dynamic alterations with age and is influenced by the environment and host physiology. Fecal microbial transfer experiments revealed that the liver microbiome is populated from the gut in a highly selective manner. Hepatic immunity is dependent on the microbiome, specifically the bacteroidetes species. Targeting bacteroidetes with oral antibiotics reduced hepatic immune cells by approximately 90%, prevented antigen-presenting cell (APC) maturation, and mitigated adaptive immunity. Mechanistically, our findings are consistent with presentation of bacteroidetes-derived glycosphingolipids to NKT cells promoting CCL5 signaling, which drives hepatic leukocyte expansion and activation, among other possible host-microbe interactions. Collectively, we reveal a microbial/glycosphingolipid/NKT/CCL5 axis that underlies hepatic immunity., Introduction Gut microbiota represent the most abundant and diverse collection of commensal organisms in the body (1). The intestinal microbiome plays a fundamental role in shaping the host immune system [...]