Shahid Beheshti University

The aim of this study is to synthesize and characterize novel electrospun nanofibers composed of biochar, polyvinyl alcohol (PVA), sodium alginate (ALG), and glyoxal (GO). Biochar, known for its exceptional adsorption capacity, was integrated into the polymer matrix to enhance pollutant removal efficiency. Glyoxal was added to improve the nanofibers' electrical conductivity and mechanical strength. The electrospinning process was optimized to produce uniform, bead-free nanofibers by maintaining a 15 cm needle-to-collector distance, a 20 kV voltage, and a 0.8 mL/h feed rate. Characterization techniques such as FESEM, FTIR, XRD, and BET were employed to analyze the morphology, chemical composition, and surface properties of the nanofibers. The results confirmed the successful incorporation of biochar into the polymer matrix, revealing unique structural and morphological properties in the composite material. The research describes a comprehensive method for synthesizing biochar-loaded nanofibers and reports useful characterization information that could inform future research to optimize nanofiber composition for particular environmental applications.•Biochar enhances pollutant adsorption capacity, while glyoxal improves electrical conductivity and mechanical strength. Sodium alginate (ALG) and polyvinyl alcohol (PVA) contribute to biocompatibility and processability, resulting in versatile composite materials.•Nanofiber mats were fabricated using varying concentrations of biochar, ALG, and PVA, with an ALG/PVA ratio of 20:80 % and biochar concentrations of 1 % (w/w).•Optimal electrospinning conditions included a 15 cm needle-to-collector distance, a 20 kV applied voltage, and a feed rate of 0.8 ml/h, ensuring the production of high-quality nanofibers.Method name: Electrospinning.

The burden of Helicobacter pylori infection is exacerbated by rising antibiotic resistance. Probiotics, especially Lactobacillus species, have shown potential as adjunctive therapies for H. pylori infection. This study aimed to isolate a Lactobacillus strain from the gastric microbiome of healthy individuals and assess its probiotic properties against H. pylori.

Gastric biopsies were obtained from a cohort of 10 subjects, and used for bacterial isolation. The Lactobacillus strain was identified to species level using PCR and sequencing, followed by safety assessments. MTT assay was employed to measure AGS cell viability after exposure to various concentrations of H. pylori, as well as live and pasteurized Lactobacillus. Anti-inflammatory properties of the probiotic strain were assessed in AGS cells using RT-qPCR and ELISA. Additionally, the strain's potential to inhibit H. pylori adhesion and invasion was examined. Probiotic Lacticaseibacillus casei strain RIGLD MG-1 was isolated and characterized as non-pathogenic and found to be tolerant to acidic and bile-rich environments, and susceptible to several antibiotics. Live and pasteurized L. casei downregulated the expression of NF-κB, IL-8, TNF-α, and β-catenin, meanwhile upregulated the expression of IL-10 in H. pylori-treated cells. They also alleviated H. pylori-induced proinflammatory response by lowering IL-8 and TNF-α, and boosting IL-10 production. Additionally, both probiotic forms inhibited H. pylori adhesion and invasion in AGS cells.

Our results show that L. casei strain RIGLD MG-1 is safe and demonstrates significant immunomodulatory and anti-adhesion effects, making it a potential probiotic for use as adjunctive therapy to mitigate H. pylori-induced inflammation.

Patients with multiple sclerosis (MS) face a heightened risk of developing chronic obstructive pulmonary disease (COPD). Despite this widely reported association, the pathogenic contributors and processes that may favor the development of COPD in MS patients have yet to be identified. Recent studies have suggested peripheral blood leukocytes as a potential link between COPD and autoimmune disorders. Therefore, this study aimed to unveil shared molecular signatures between MS and COPD using blood transcriptomes. To this end, gene expression datasets obtained from MS and COPD blood specimens were retrieved from the Gene Expression Omnibus (GEO) database. By integrating datasets belonging to each disorder, differentially expressed genes (DEGs) were determined for each disease. Then, the protein-protein interaction (PPI) network was constructed for shared DEGs between MS and COPD. Subsequently, the network was analyzed to identify hub genes and key regulatory miRNAs. The integrated data for MS encompassed 51 samples (28 from MS patients and 23 from controls), and the integrated data for COPD included 450 samples (275 from COPD patients and 175 from controls). A total of 246 genes were found to exhibit identical directions of expression in both MS and COPD. By applying a high confidence threshold (0.7), a PPI network with 74 nodes was constructed. TP53, H4C6, SNRPE, and RPS11 were identified as hub genes according to the degree measure. In addition, 8 miRNAs were identified as key regulators, each interacting with 6 mRNAs. Among these miRNAs, miR-218-5p and miR-142-5p have been previously reported to contribute to the pathogenesis of these diseases, and here they were identified as key regulators of the shared PPI network, suggesting a potential epigenetic link between MS and COPD. In conclusion, the results highlighted the potential role of peripheral blood leucocytes as a bridge between MS and COPD. These findings broaden our understanding of pathogenic contributors linking MS and COPD. While this transcriptomics study identified multiple key players, such as TP53, miR-218-5p, and miR-142-5p, the assessment of their therapeutic efficacy demands further experimental studies.