Coral composition and bottom-wave metrics improve understanding of the patchiness of cyclone damage on reefs.

Coral reefs are likely to be exposed to more intense cyclones under climate change. Cyclone impacts are spatially highly variable given complex hydrodynamics, and coral-specific sensitivity to wave impacts. Predicting reef vulnerability to cyclones is critical to management but requires high resolution environmental data that are difficult to obtain over broad spatial scales. Using 30m-resolution wave modelling, we tested cyclonic and non-cyclonic wave metrics as predictors of coral damage on 22 reefs after severe cyclone Ita impacted the northern Great Barrier Reef, Australia in 2014. Analyses of coral cover change accounting for the type of coral along a gradient of vulnerability to wave damage (e.g., massive, branching, Acroporids) excluded cyclone-generated surface wave metrics (derived from wave height) as important predictors. Increased bottom stress wave environment (near-bed wave orbital velocity) due to Ita (Ita-Ub) explained spatial patterns of 17% to 46% total coral cover loss only when the initial abundance of Acroporids was accounted for, and only when exceeding 35% cover. Greater coral losses occurred closer to the cyclone path irrespective of coral type. Massive and encrusting corals, however, had losses exacerbated in higher non-cyclonic bottom-wave energy environments (nc-Ub). The effect of community composition on structural vulnerability to wave damage was more important predicting damage that the magnitude of the cyclone-generated waves, especially when reefs are surveyed well beyond where damaging waves are expected to occur. Exposure to Ita-Ub was greater in typically high nc-Ub environments with relatively low cover of the most fragile morphologies explaining why these were the least affected overall. We reveal that the common surface-wave metrics of cyclone intensity may not always be able to predict spatial impacts and conclude that reef vulnerability assessments need to account for chronic wave patterns and differences in community composition in order to provide predictive tools for future conservation and restoration.

Local and Plasma Biomarker Profiles in Localized Aggressive Periodontitis.

Localized aggressive periodontitis (LAP) patients possess a systemic hyperinflammatory response after lipopolysaccharide stimulation. However, the levels of inflammatory and bone biomarkers in plasma, as well as possible associations between local and plasma biomarkers, are unknown in LAP. This cross-sectional study aimed to characterize gingival crevicular fluid (GCF) and plasma biomarker profiles in LAP patients, their healthy siblings (HS), and healthy unrelated controls (HC). Fifty-eight LAP subjects, 33 HS, and 49 HC (African Americans, aged 5 to 25 y) were included. Following collection of clinical parameters with GCF and plasma samples, levels of 16 inflammatory and bone resorption biomarkers were determined with Milliplex. Univariate and correlation analyses were performed among all clinical and laboratorial parameters. Discriminant analyses were used to investigate groups of biomarkers discriminating LAP from HS and HC in GCF and plasma. GCF levels of multiple cytokines and chemokines and RANKL:OPG ratio (receptor activator of nuclear factor kappa-B ligand:osteoprotegerin) were higher in LAP disease, most of which positively correlated with probing depth and attachment loss of sampled sites. A group of IL-12p40, IL-6, IL-12p70, IL-2, and MIP-1α discriminated LAP diseased sites from twheir healthy sites, as well as from HS and HC healthy sites. In plasma, only RANKL levels were increased in LAP versus controls, which positively correlated with the percentage of affected sites and deep/bleeding sites. A plasma inflammatory profile including MIP-1α, IL-8, IL-10, and INF-γ could significantly discriminate LAP patients from HS and HC. No correlations were found between GCF and plasma levels of biomarkers. In conclusion, an inflammatory profile including groups of specific biomarkers in GCF and plasma may significantly discriminate LAP from healthy individuals. The hyperinflammatory response previously found in the peripheral blood of LAP patients is dependent on lipopolysaccharide stimulation, apparently resulting mostly in local tissue destruction and changes in biomarker profile, with a slight influence in the systemic inflammatory profile (ClinicalTrials.gov NCT01330719). Knowledge Transfer Statement: The results of this study can be possibly used by clinicians in the future as diagnostic tools for localized aggressive periodontitis. Thus, in the future, with proper consideration of cost, patient preference, chair-side feasibility and ultimately further studies validating the role of GCF markers for disease progression and response to treatment, this information could lead to more appropriate therapeutic decisions and the development of preventive approaches for susceptible patients.