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Age-related macular degeneration (AMD) is a vision threatening disease in older adults. Anti-VEGF treatment is effective for the majority of neovascular AMD (nAMD) patients, although approximately 30% of nAMD patients have an incomplete response for unknown reasons. Here we assessed the contribution of single nucleotide polymorphisms (SNPs) in key angioinflammatory regulatory genes in nAMD patients with an incomplete response compared to those responsive to anti-VEGF treatment. A total of 25 responsive and 30 nAMD patients with an incomplete response to anti-vascular endothelial growth factor (anti-VEGF) treatment were examined for known SNPs that impact the structure and function of thromobospondin-1 (TSP1), Bcl-2-interacting mediator of cell death (BIM) and complement factor H (CFH). Plasma levels of C-C motif chemokine ligand 2 (CCL2/MCP1), TSP1 and VEGF were assessed by ELISA. Patients responsive to anti-VEGF treatment showed a significant increase in the TSP1 rs2228262 AA allele and a trend for the BIM (rs724710) CT allele. Consistent with previous reports, 42% of the patients responsive to anti-VEGF expressed the CC allele for CFH rs1061170. Although the CFH TT allele had similarly low prevalence in both groups, the TC allele tended to be more prevalent in patients with an incomplete response. Patients with an incomplete response also had increased plasma CCL2/MCP1 levels, consistent with the role increased inflammation has in the pathogenesis of nAMD. Our studies point to new tools to assess the potential responsiveness of nAMD patients to anti-VEGF treatment and suggest the potential use of anti-CCL2 for treatment of nAMD patients with an incomplete response to anti-VEGF. [ABSTRACT FROM AUTHOR]

Viruses have evolved sophisticated mechanisms to manipulate host cell processes and utilize intracellular organelles to facilitate their replication. These complex interactions between viruses and cellular organelles allow them to hijack the cellular machinery and impair homeostasis. Moreover, viral infection alters the cell membrane's structure and composition and induces vesicle formation to facilitate intracellular trafficking of viral components. However, the research focus has predominantly been on the immune response elicited by viruses, often overlooking the significant alterations that viruses induce in cellular organelles. Gaining a deeper understanding of these virus-induced cellular changes is crucial for elucidating the full life cycle of viruses and developing potent antiviral therapies. Exploring virus-induced cellular changes could substantially improve our understanding of viral infection mechanisms. [ABSTRACT FROM AUTHOR]

This study examined whether or not various mouthwashes have significant effects on the viability or morphology of mouse osteoblast-like cells. Mouse calvarial preosteoblast cells were cultured and prepared, then treated with a 0.12% chlorhexidine digluconate solution containing essential oils with or without alcohol, and a cetylpyridinium chloride solution, and sodium fluoride, respectively. Each well was treated with one of six mouthwashes for either 30 sec, 1.5 min, or 4.5 min. The viability of the treated cells was quantitatively analyzed by a Cell Counting Kit-8. The viability of osteogenic progenitor cells decreased significantly irrespectively of the types of mouthwashes. The changes of cell morphology were seen in all groups of mouthwashes; however, they were more noticeable on the chlorhexidine digluconate-treated group. A progressive increase in treatment time over 30 sec did not seem to deteriorate cellular viability. There was no significant difference in viability or morphological change between different formulations of the same brand. Although various mouthwashes without alcohol as an ingredient are available, nonalcoholic mouthwashes were not likely to be less harmful to the cells. Collectively, commercially available mouthwashes could inhibit cell viability and alter the morphology of osteoblastic precursor cells irrespectively of brands, treatment time, or alcohol content.