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Objective: Comparative evaluation of antibacterial and anti-adherent properties of surface-modified stainless steel (SS) orthodontic brackets against Streptococcus mutans(S. mutans).Materials and Methods: The study was conducted on 120 SS orthodontic McLaughlin, Bennett, Trevisi (MBT) 0.022″ slot by Leone, Italy. Orthodontic brackets that constituted the sample size were divided into 6 groups, consisting of 20 samples each in two control (non-surface coated) and four experimental groups. The experimental group’s surface coatings were photocatalytic zinc oxide (ZnO) and photocatalytic titanium oxide (TiO2), which were carried out by radiofrequency (RF) magnetron sputtering method for surface modification. Brackets were subjected to microbiological tests against S. mutans. For anti-adherence, weight change, pre- and postexposure, was evaluated to gauge the adherence of bacteria and colony-forming units/milliliter (CFU/mL) count measuring the survival rate of bacterial cells for antibacterial activity.Results: The TiO2-coated group showed statistically significant anti-adherence (P-value < .05) against S. mutansthan control and ZnO groups. The CFU count of TiO2group was lower than control as well as ZnO group.Conclusion: TiO2is superior to ZnO and should be continued to be considered for surface modification of orthodontic brackets against White Spot Lesions (WSLs) and gingivitis.

To elucidate the molecular mechanisms that manifest lung abnormalities during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, we performed whole-transcriptome sequencing of lung autopsies from 31 patients with severe COVID-19 and ten uninfected controls. Using metatranscriptomics, we identified the existence of two distinct molecular signatures of lethal COVID-19. The dominant ‘classical’ signature (n=23) showed upregulation of the unfolded protein response, steroid biosynthesis and complement activation, supported by massive metabolic reprogramming leading to characteristic lung damage. The rarer signature (n=8) that potentially represents ‘cytokine release syndrome’ (CRS) showed upregulation of cytokines such as IL1 and CCL19, but absence of complement activation. We found that a majority of patients cleared SARS-CoV-2 infection, but they suffered from acute dysbiosis with characteristic enrichment of opportunistic pathogens such as Staphylococcus cohnii in ‘classical’ patients and Pasteurella multocida in CRS patients. Our results suggest two distinct models of lung pathology in severe COVID-19 patients, which can be identified through complement activation, presence of specific cytokines and characteristic microbiome. These findings can be used to design personalized therapy using in silico identified drug molecules or in mitigating specific secondary infections.