This review explores the role of Pseudomonas aeruginosa biofilms in cystic fibrosis (CF) pathogenesis. Biofilms, the main bacterial lifestyle in CF lungs, are key in therapy failure, immune evasion, and chronic infection persistence. This review examines biofilm structure, emphasizing extracellular polymeric substances (Psl, Pel, alginate, eDNA) and their roles in structural stability, resistance to antibiotics, and immune modulation. Regulatory mechanisms, including c‐di‐GMP signaling and quorum‐sensing systems, are detailed as key drivers of biofilm formation and maintenance. The review also highlights polymicrobial interactions, particularly with Staphylococcus aureus , Candida spp., and Aspergillus spp., and commensal bacteria, illustrating how interaction dynamics shape microbial behavior, virulence, and treatment outcomes. Methods for studying biofilms in CF‐like conditions, such as advanced in vitro models and transcriptomic analyses, are outlined for their relevance in replicating the complex lung environment. Emerging antibiofilm strategies, including matrix‐disrupting enzymes, quorum‐sensing inhibitors, bacteriophage therapies, and nanomedicine, are discussed as promising tools to combat biofilm resilience. The review underscores the need for innovative therapeutic approaches and a deeper understanding of microbial and host interactions to improve clinical outcomes in CF patients.

Background: Male EBP disorder with neurologic defects (MEND) syndrome is an X‐linked disease caused by hypomorphic mutations in the EBP (emopamil‐binding protein) gene. Modifier genes may explain the clinical variability among individuals who share a primary mutation.Methods: We studied four males (Patient 1 to Patient 4) exhibiting a descending degree of phenotypic severity from a family with MEND syndrome. To identify candidate modifier genes that explain the phenotypic variability, variants of homeostasis cholesterol genes identified by whole‐exome sequencing (WES) were ranked according to the predicted magnitude of their effect through an in‐house scoring system.Results: Twenty‐seven from 105 missense variants found in 45 genes of the four exomes were considered significant (−5 to −9 scores). We found a direct genotype–phenotype association based on the differential accumulation of potentially functional gene variants among males. Patient 1 exhibited 17 variants, both Patients 2 and 3 exhibited nine variants, and Patient 4 exhibited only five variants.Conclusion: We conclude that APOA5 (rs3135506), ABCA1 (rs9282541), and APOB (rs679899 and rs12714225) are the most relevant candidate modifier genes in this family. Relative accumulation of the deficiencies associated with variants of these genes along with other lesser deficiencies in other genes appears to explain the variable expressivity in MEND syndrome.

Gestational diabetes mellitus (GDM) develops silently during early pregnancy, yet its earliest circulating molecular signatures remain poorly defined. In this exploratory biomarker study, we characterized first-trimester circulating microRNA (miRNAs) associated with later GDM using a pool-based small RNA sequencing approach. Using a systematic and unbiased sequencing strategy with locus-level miRNA resolution, we profiled the first-trimester plasma miRNome and prioritized a set of 18 mature miRNAs from among 255 detected species. Set-level functional enrichment analyses based on curated and predicted miRNA–target interactions derived primarily from cellular and tissue-based studies showed annotation-based convergence on pathways related to Ca²⁺ homeostasis, glucagon–insulin regulatory circuits, and PI3K–AKT signaling. Network analysis indicated coordinated associations among these miRNAs and shared target pathways involved in insulin secretion and insulin sensitivity. Key contributors—including miR-29a-3p, miR-29c-3p, miR-146a-5p, let-7a-5p, and miR-182-5p—were linked, through in silico target annotation, to central metabolic regulators such as PTEN, PIK3R1, AKT1, AKT2, and components of Ca²⁺ signaling (ATP2A2, CALM1/3, ITPR1, RYR2). These circulating miRNAs should be interpreted primarily as biomarkers reflecting coordinated metabolic states rather than as direct causal mediators. Most identified miRNAs have not been previously reported in the context of first-trimester GDM, supporting the exploratory and hypothesis-generating nature of this circulating miRNA signature in early gestational metabolic research.