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Phage display is widely used in biomedical research. One of the great advantages of phage display is the specificity of the connection of a foreign peptide exposed outside the capsid to the intended target. Secondary detection systems, which are often laborious and costly, are required to identify and quantify the peptide/target interaction. In this study, we generated a novel dual-display phage to facilitate the detection and quantification of the peptide/target interaction. First, we generated a biotin-tagged phage by adding a small biotin-accepting peptide (sBT) to gene-3 of the M13K07 helper phage. Subsequently, we enhanced the M13K07 biotin-tagged phage by incorporating a selective peptide on gene-8, which is then exposed to the phage capsid. The exposed peptide acts as a probe to bind to a selective molecular target, whose interaction can be readily visualized thanks to the biotinylated phage. Our versatile dual-display phage exhibits high flexibility; by swapping the displayed peptide/probe, one can change the phage target while retaining the sBT gene in-frame with the pIII. We expect the generated biotin-tagged dual phages to be used as a multifunctional probe to couple with several streptavidin-biotin-based systems. [ABSTRACT FROM AUTHOR]

Objectives: This study investigates the impact of nutrient availability on the growth, adhesion, and biofilm formation of Pseudomonas aeruginosa ATCC 27853 under static conditions. Methods: Bacterial behaviour was evaluated in nutrient-rich Luria–Bertani (LB) broth and nutrient-limited M9 media, specifically lacking carbon (M9-C), nitrogen (M9-N), or phosphorus (M9-P). Bacterial adhesion was analysed microscopically during the transition from reversible to irreversible attachment (up to 120 min) and during biofilm production/maturation stages (up to 72 h). Results: Results demonstrated that LB and M9 media supported bacterial growth, whereas nutrient-starved conditions halted growth, with M9-C and M9-N inducing stationary phases and M9-P leading to cell death. Fractal analysis was employed to characterise the spatial distribution and complexity of bacterial adhesion patterns, revealing that nutrient-limited conditions affected both adhesion density and biofilm architecture, particularly in M9-C. In addition, live/dead staining confirmed a higher proportion of dead cells in M9-P over time (at 48 and 72 h). Conclusions: This study highlights how nutrient starvation influences biofilm formation and bacterial dispersion, offering insights into the survival strategies of P. aeruginosa in resource-limited environments. These findings should contribute to a better understanding of biofilm dynamics, with implications for managing biofilm-related infections and industrial biofouling. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a devastating neurodegenerative disorder characterized by progressive cognitive decline and memory loss, imposing a significant burden on affected individuals and their families. Despite the recent promising progress in therapeutic approaches, more needs to be done to understand the intricate molecular mechanisms underlying the development and progression of AD. Growing evidence points to epigenetic changes as playing a pivotal role in the pathogenesis of the disease. The dynamic interplay between genetic and environmental factors influences the epigenetic landscape in AD, altering gene expression patterns associated with key pathological events associated with disease pathogenesis. To this end, epigenetic alterations not only impact the expression of genes implicated in AD pathogenesis but also contribute to the dysregulation of crucial cellular processes, including synaptic plasticity, neuroinflammation, and oxidative stress. Understanding the complex epigenetic mechanisms in AD provides new avenues for therapeutic interventions. This review comprehensively examines the role of DNA methylation and histone modifications in the context of AD. It aims to contribute to a deeper understanding of AD pathogenesis and facilitate the development of targeted therapeutic strategies. [ABSTRACT FROM AUTHOR]