Permeability, Roughness And Topography Of Enamel After Bleaching: Tracking Channels Of Penetration With Silver Nitrate

Aim: This study evaluated the surface roughness, topography and permeability of bovine enamel by profilometry and scanning electron microscopy (SEM) with and without silver nitrate solution, after exposure to different bleaching agents. Methods: Fifty-two enamel samples were randomly divided into four groups (n=13): CP16% -16% carbamide peroxide - Whiteness Perfect; HP6% - 6% hydrogen peroxide - White Class; HP35% - 35% hydrogen peroxide Whiteness HP Maxx; and Control - not bleached and kept in artificial saliva. For roughness analysis, average surface roughness (Ra) and flatness coefficient (Rku) parameters were used. The topography and permeability were examined by SEM. For permeability evaluation, the samples were immersed in a 50% silver nitrate solution and analyzed using a backscattered electron and secondary electron mode. Results: For the roughness (Ra) evaluation, Kruskal-Wallis and Wilcoxon Signed Ranks Test were used, showing an increase on the surface roughness in all bleached groups. The Rku parameter suggested changes on enamel integrity. The SEM micrographs indicated changes on enamel topography and different levels of silver nitrate penetration in the samples of the bleached groups. In the overall analysis, the bleaching agents promoted surface changes and higher silver nitrate penetration when compared to the control group. Conclusions: It may be concluded that different bleaching agents might alter the topography and roughness of enamel surface. Moreover, the higher infiltration of silver nitrate suggests an easier penetration path for the oxygen molecules into the dentin substrate.10116Nathoo, S.A., The chemistry and mechanisms of extrinsic and intrinsic discoloration (1997) J Am Dent Assoc, 128 (SUPPL.), pp. 6S-10SMcEvoy, S.A., Chemical agents for removing intrinsic stains from vital teeth. 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Neuronal pentraxin 2 : a synapse-derived CSF biomarker in genetic frontotemporal dementia

Introduction: Synapse dysfunction is emerging as an early pathological event in frontotemporal dementia (FTD), however biomarkers are lacking. We aimed to investigate the value of cerebrospinal fluid (CSF) neuronal pentraxins (NPTXs), a family of proteins involved in homeostatic synapse plasticity, as novel biomarkers in genetic FTD. Methods: We included 106 presymptomatic and 54 symptomatic carriers of a pathogenic mutation in GRN, C9orf72 or MAPT, and 70 healthy non-carriers participating in the Genetic Frontotemporal dementia Initiative (GENFI), all of whom had at least one CSF sample. We measured CSF concentrations of NPTX2 using an in-house ELISA, and NPTX1 and NPTX receptor (NPTXR) by Western blot. We correlated NPTX2 with corresponding clinical and neuroimaging datasets as well as with CSF neurofilament light chain (NfL) using linear regression analyses. Results: Symptomatic mutation carriers had lower NPTX2 concentrations (median 643 pg/mL, IQR (301-872)) than presymptomatic carriers (1003 pg/mL (624-1358), p<0.001) and non-carriers (990 pg/mL (597-1373), p<0.001) (corrected for age). Similar results were found for NPTX1 and NPTXR. Among mutation carriers, NPTX2 concentration correlated with several clinical disease severity measures, NfL and grey matter volume of the frontal, temporal and parietal lobes, insula and whole brain. NPTX2 predicted subsequent decline in phonemic verbal fluency and Clinical Dementia Rating scale plus FTD modules. In longitudinal CSF samples, available in 13 subjects, NPTX2 decreased around symptom onset and in the symptomatic stage. Discussion: We conclude that NPTX2 is a promising synapse-derived disease progression biomarker in genetic FTD

Age at symptom onset and death and disease duration in genetic frontotemporal dementia : an international retrospective cohort study

Background: Frontotemporal dementia is a heterogenous neurodegenerative disorder, with about a third of cases being genetic. Most of this genetic component is accounted for by mutations in GRN, MAPT, and C9orf72. In this study, we aimed to complement previous phenotypic studies by doing an international study of age at symptom onset, age at death, and disease duration in individuals with mutations in GRN, MAPT, and C9orf72. Methods: In this international, retrospective cohort study, we collected data on age at symptom onset, age at death, and disease duration for patients with pathogenic mutations in the GRN and MAPT genes and pathological expansions in the C9orf72 gene through the Frontotemporal Dementia Prevention Initiative and from published papers. We used mixed effects models to explore differences in age at onset, age at death, and disease duration between genetic groups and individual mutations. We also assessed correlations between the age at onset and at death of each individual and the age at onset and at death of their parents and the mean age at onset and at death of their family members. Lastly, we used mixed effects models to investigate the extent to which variability in age at onset and at death could be accounted for by family membership and the specific mutation carried. Findings: Data were available from 3403 individuals from 1492 families: 1433 with C9orf72 expansions (755 families), 1179 with GRN mutations (483 families, 130 different mutations), and 791 with MAPT mutations (254 families, 67 different mutations). Mean age at symptom onset and at death was 49\ub75 years (SD 10\ub70; onset) and 58\ub75 years (11\ub73; death) in the MAPT group, 58\ub72 years (9\ub78; onset) and 65\ub73 years (10\ub79; death) in the C9orf72 group, and 61\ub73 years (8\ub78; onset) and 68\ub78 years (9\ub77; death) in the GRN group. Mean disease duration was 6\ub74 years (SD 4\ub79) in the C9orf72 group, 7\ub71 years (3\ub79) in the GRN group, and 9\ub73 years (6\ub74) in the MAPT group. Individual age at onset and at death was significantly correlated with both parental age at onset and at death and with mean family age at onset and at death in all three groups, with a stronger correlation observed in the MAPT group (r=0\ub745 between individual and parental age at onset, r=0\ub763 between individual and mean family age at onset, r=0\ub758 between individual and parental age at death, and r=0\ub769 between individual and mean family age at death) than in either the C9orf72 group (r=0\ub732 individual and parental age at onset, r=0\ub736 individual and mean family age at onset, r=0\ub738 individual and parental age at death, and r=0\ub740 individual and mean family age at death) or the GRN group (r=0\ub722 individual and parental age at onset, r=0\ub718 individual and mean family age at onset, r=0\ub722 individual and parental age at death, and r=0\ub732 individual and mean family age at death). Modelling showed that the variability in age at onset and at death in the MAPT group was explained partly by the specific mutation (48%, 95% CI 35\u201362, for age at onset; 61%, 47\u201373, for age at death), and even more by family membership (66%, 56\u201375, for age at onset; 74%, 65\u201382, for age at death). In the GRN group, only 2% (0\u201310) of the variability of age at onset and 9% (3\u201321) of that of age of death was explained by the specific mutation, whereas 14% (9\u201322) of the variability of age at onset and 20% (12\u201330) of that of age at death was explained by family membership. In the C9orf72 group, family membership explained 17% (11\u201326) of the variability of age at onset and 19% (12\u201329) of that of age at death. Interpretation: Our study showed that age at symptom onset and at death of people with genetic frontotemporal dementia is influenced by genetic group and, particularly for MAPT mutations, by the specific mutation carried and by family membership. Although estimation of age at onset will be an important factor in future pre-symptomatic therapeutic trials for all three genetic groups, our study suggests that data from other members of the family will be particularly helpful only for individuals with MAPT mutations. Further work in identifying both genetic and environmental factors that modify phenotype in all groups will be important to improve such estimates. Funding: UK Medical Research Council, National Institute for Health Research, and Alzheimer's Society

Clinical value of cerebrospinal fluid neurofilament light chain in semantic dementia

Background Semantic dementia (SD) is a neurodegenerative disorder characterised by progressive language problems falling within the clinicopathological spectrum of frontotemporal lobar degeneration (FTLD). The development of disease-modifying agents may be facilitated by the relative clinical and pathological homogeneity of SD, but we need robust monitoring biomarkers to measure their efficacy. In different FTLD subtypes, neurofilament light chain (NfL) is a promising marker, therefore we investigated the utility of cerebrospinal fluid (CSF) NfL in SD. Methods This large retrospective multicentre study compared cross-sectional CSF NfL levels of 162 patients with SD with 65 controls. CSF NfL levels of patients were correlated with clinical parameters (including survival), neuropsychological test scores and regional grey matter atrophy (including longitudinal data in a subset). Results CSF NfL levels were significantly higher in patients with SD (median: 2326\u2009pg/mL, IQR: 1628\u20133593) than in controls (577 (446\u2013766), p<0.001). Higher CSF NfL levels were moderately associated with naming impairment as measured by the Boston Naming Test (rs = 120.32, p=0.002) and with smaller grey matter volume of the parahippocampal gyri (rs = 120.31, p=0.004). However, cross-sectional CSF NfL levels were not associated with progression of grey matter atrophy and did not predict survival. Conclusion CSF NfL is a promising biomarker in the diagnostic process of SD, although it has limited cross-sectional monitoring or prognostic abilities

Transport of a genetically modified Pseudomonas fluorescens and its parent strain through undisturbed tropical soil cores

The transport of a genetically modified strain of Pseudomonas fluorescens, BR12, and its parent, BR5, was studied after irrigation of undisturbed clayey and sandy soil cores, simulating heavy tropical rainfall (56.6 mm/h). Vertical transport of both inoculant strains was detected in all soil cores. Transport was negatively affected by the organic matter content of soil, whereas soil texture did not affect the degree of transport. Both factors influenced the survival of the introduced bacteria, in particular that of the modified strain. The initial moisture and structural status of the clayey soil, which was related to seasonal influences, also influenced the degree of bacterial translocation. In cores with two clay soil types, the genetically modified strain was transported to a greater extent than its parent. However, the modified strain showed similar or lower survival rates than its parent in topsoil layers of the different clay soil type and the sandy soil cores. Counts of culturable cells of both inoculant strains in the percolation water remained roughly stable or decreased during the experiment, and the inoculant survival was clearly affected by the soil from which the percolation water was obtained. Both strains showed good survival in the percolation water from microcosms-containing clay soil enriched with manure to about 6% organic matter, whereas their population sizes declined in percolation water from non-manured clay or sandy soil cores. The results suggested that the release of derivatives of P. fluorescens strain BR5 into soils in tropical climates should be carefully planned and monitored in order to guarantee their efficacy as biocontrol agents and to assess the potential contamination of ground and surface waters