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In this study, the fused deposition modeling method was used to fabricate 3D-printed polycaprolactone (PCL). This study introduces a cost-effective post-fabrication treatment by using a Solubilized Amniotic Membrane (SAM) extracellular matrix (ECM) as a biological surface modifier. The employment of SAM provides an easy approach to overcoming the current challenges in the way of using fresh, cryopreserved, or dehydrated tissue. Four groups were included in this study, including neat PCL, oxygen plasma-treated PCL, SAM 0.001%w/v (SAM1), and SAM 0.005%w/v (SAM5). According to the SEM images, the diameter of each 3D-printed filament and filament distance were around 573 μm and 372 μm, respectively. The FTIR-ATR spectra confirmed the presence of amide groups in specimen, containing SAM. A higher weight loss rate was obtained for oxygen plasma-treated PCL and SAM-containing samples than neat PCL. The results of in vitro studies revealed that the optimized content of SAM (SAM 5) could promote the osteogenesis potency of Wharton-Jelly Mesenchymal Stem Cells (WJ-MSCs), cultured on the 3D-printed scaffolds in terms of alkaline phosphatase activity, calcium deposition and real-time PCR assessment of alkaline phosphatase, osteocalcin, and osteonectin. Also, in vivo, the collagen content in the control group and SAM 5 was 30.89 ± 1.73 and 44.24 ± 2.91, respectively. According to the Micro-CT assessment, the bone volume fraction was remarkably improved in the presence of SAM5 as it increased from 36.52 ± 1.56% in the control group to 42.66 ± 2.17% in SAM5. The results of the present study provide a promising surface modification approach by employing SAM for the future of bone tissue engineering scaffolds.

Macrophage metabolism is closely linked to their phenotype and function, which is why there is growing interest in studying the metabolic reprogramming of macrophages. Bioactive glass (BG) S53P4 is a bioactive material used especially in bone applications. Additionally, BG S53P4 has been shown to affect macrophages, but the mechanisms through which the possible immunomodulatory effects are conveyed remain unclear. According to the results presented here, the lipopolysaccharide (LPS) induced suppression in oxidative phosphorylation is rescued in macrophages cultured with BG S53P4 before the inflammatory stimulus. Additionally, BG S53P4-exposed macrophages expressed lower mRNA levels of inflammatory cytokines Il6 and Il1b , as well as demonstrated decreased activation of inflammatory interferon regulatory factor (IRF) and NF-κB pathways and nitrogen oxide secretion in response to LPS. These results did not rely on cells being in direct contact with the material as similar effects were observed in the presence of BG S53P4-conditioned medium. Our findings link the immunomodulatory properties of BG S53P4 and macrophage metabolism, which improves our understanding of the mechanisms underlying the clinical efficacy of bioactive glasses. Graphical Abstract

Lactobacilli are the most common probiotic bacteria found in the human gut microbiota, and the presence of acquired antibiotic resistance determinants carried on mobile genetic elements must be screened due to safety concerns. Unnecessary and inappropriate antibiotic therapy, as well as ingested antibiotic resistance bacteria (originating from food or food products), influence the abundance of antibiotic resistance genes in human guts, with serious clinical consequences. The current study looked into the antibiotic resistance of lactobacilli isolated from the guts of sepsis patients on long-term antibiotic therapy. The broth microdilution method was used to investigate the minimum inhibitory concentrations (MICs) of antibiotics such as imipenem, meropenem, erythromycin, tetracycline, cefepime, ciprofloxacin, and gentamycin, and the molecular genetic basis of resistance was studied based on the MIC values. The isolates were phenotypically resistant to tetracycline (20%), fluoroquinolone (20%), and macrolide (5%). Following that, resistance genes for tetracycline [tet(L), tet(O), tet(K), and tet(M)], macrolide [erm(B) and erm(C)], and beta-lactams [bla(CMY)] were investigated. Tetracycline or macrolide resistance genes were not found in the isolates, and only one isolate possessed the bla(CMY) resistance gene. The findings suggested that tetracycline and macrolide resistance may be linked to other resistance genes that were not investigated in this study. Because tetracyclines, fluoroquinolones, and macrolides are commonly used in clinics and animals, there has been concern about the spread of resistance in humans. If acquired antibiotic resistance is passed down through mobile genetic elements, it may serve as a reservoir of resistance for gut pathogens and other microbiome environments.