Light transmission through fiber post: the effect on adhesion, elastic modulus and hardness of dual-cure resin cement

OBJECTIVES: The aim of this study was to investigate the effect of fiber post light transmitting ability to the continuity of resin cement-root dentin (C-RD) and resin cement-fiber post (C-FP) interface, elastic modulus and hardness of a dual-cure resin cement. METHODS: Spectrophotometric measurements were applied for the determination of light transmission at coronal, middle and apical level as well as at the apical tip through Tech 21 X-OP (TECH) and DT Light Post (DT). Posts were cemented using dual-cured resin cement (Calibra). Roots were sectioned longitudinally through the post. Epoxy resin replicas were made and used to evaluate C-RD and C-FP interface under SEM. Modulus of elasticity (E) and Vicker's hardness (VH) of the cement layer were assessed. RESULTS: No light transmission was detected through TECH. Light transmission through DT decreased from coronal to apical and rose at the apical tip. TECH presented a significantly lower percentage of continuous C-RD and C-FP interface in comparison to DT. Coronal third of C-RD interface in TECH specimens had a significantly higher percentage of continuity than apical third. No regional differences in continuity of C-RD interface were found in DT specimens. E and VH were significantly lower when TECH was used, and decreased from coronal to apical for both posts. SIGNIFICANCE: Cementation of fiber post with no light transmitting ability using a dual-cured resin cement resulted in lower E and VH of the cement layer, and lower percentage of continuous C-RD and C-FP interface in comparison to cementation of light transmitting fiber post

NK/ILC1 cells mediate neuroinflammation and brain pathology following congenital CMV infection

Congenital human cytomegalovirus (cHCMV) infection of the brain is associated with a wide range of neurocognitive sequelae. Using infection of newborn mice with mouse cytomegalovirus (MCMV) as a reliable model that recapitulates many aspects of cHCMV infection, including disseminated infection, CNS infection, altered neurodevelopment, and sensorineural hearing loss, we have previously shown that mitigation of inflammation prevented alterations in cerebellar development, suggesting that host inflammatory factors are key drivers of neurodevelopmental defects. Here, we show that MCMV infection causes a dramatic increase in the expression of the microglia-derived chemokines CXCL9/CXCL10, which recruit NK and ILC1 cells into the brain in a CXCR3-dependent manner. Surprisingly, brain-infiltrating innate immune cells not only were unable to control virus infection in the brain but also orchestrated pathological inflammatory responses, which lead to delays in cerebellar morphogenesis. Our results identify NK and ILC1 cells as the major mediators of immunopathology in response to virus infection in the developing CNS, which can be prevented by anti-IFN-γ antibodies

Human serum from SARS-CoV-2-vaccinated and COVID-19 patients shows reduced binding to the RBD of SARS-CoV-2 Omicron variant

Background: The COVID-19 pandemic is caused by the betacoronavirus SARS-CoV-2. In November 2021, the Omicron variant was discovered and immediately classified as a variant of concern (VOC), since it shows substantially more mutations in the spike protein than any previous variant, especially in the receptor-binding domain (RBD). We analyzed the binding of the Omicron RBD to the human angiotensin-converting enzyme-2 receptor (ACE2) and the ability of human sera from COVID-19 patients or vaccinees in comparison to Wuhan, Beta, or Delta RBD variants. Methods: All RBDs were produced in insect cells. RBD binding to ACE2 was analyzed by ELISA and microscale thermophoresis (MST). Similarly, sera from 27 COVID-19 patients, 81 vaccinated individuals, and 34 booster recipients were titrated by ELISA on RBDs from the original Wuhan strain, Beta, Delta, and Omicron VOCs. In addition, the neutralization efficacy of authentic SARS-CoV-2 wild type (D614G), Delta, and Omicron by sera from 2× or 3× BNT162b2-vaccinated persons was analyzed. Results: Surprisingly, the Omicron RBD showed a somewhat weaker binding to ACE2 compared to Beta and Delta, arguing that improved ACE2 binding is not a likely driver of Omicron evolution. Serum antibody titers were significantly lower against Omicron RBD compared to the original Wuhan strain. A 2.6× reduction in Omicron RBD binding was observed for serum of 2× BNT162b2-vaccinated persons. Neutralization of Omicron SARS-CoV-2 was completely diminished in our setup. Conclusion: These results indicate an immune escape focused on neutralizing antibodies. Nevertheless, a boost vaccination increased the level of anti-RBD antibodies against Omicron, and neutralization of authentic Omicron SARS-CoV-2 was at least partially restored. This study adds evidence that current vaccination protocols may be less efficient against the Omicron variant