Modelling Environmental Impacts on Marine Ecosystems and Coral Reefs

Coral reefs are the iconic ecosystem of tropical seas and yet they are under increasing pressure as a result of multiple climatic stressors. This thesis uses observations and models to further understanding of environmental impacts on coral reefs. In particular it examines the impact of rising Sea Surface Temperature (SST) and ocean acidification on coral growth and the frequency of coral bleaching events. UK ocean biogeochemical models are assessed for implementation in the next UK Earth System Model. This analysis finds little evidence that more complex ocean biogeochemical models provide better simulations of large scale biogeochemical features. An established wavelet-based spatial comparison technique is used to analyse the spatial scales that Earth System Models can skillfully simulate patterns of SSTs. It is shown that in coral regions, current models cannot skilfully simulate patterns of historical SST anomalies at sub-regional (<32◦) scales. These findings are used in combination with SST and aragonite saturation state outputs from Earth System Models to show that historical Caribbean coral growth has been influenced by anthropogenic aerosol emissions over the 20th Century. Earth System Model outputs are also used to make projections of global coral bleaching throughout the 21st Century. It is shown that under even the most extreme conventional mitigation scenarios the majority of the world’s coral reefs are projected to experience levels of thermal stress induced bleaching that cause reef degradation throughout the 21st Century. Geoengeering scenarios involving the injection of SO2 into the stratosphere can reduce the projected thermal stress on coral reefs relative to conventional mitigation scenarios but such benefits are shown to be highly dependent on the sensitivity of coral bleaching thresholds to ocean acidification

An iron cycle cascade governs the response of equatorial Pacific ecosystems to climate change

Earth System Models project that global climate change will reduce ocean net primary production (NPP), upper trophic level biota biomass and potential fisheries catches in the future, especially in the eastern equatorial Pacific. However, projections from Earth System Models are undermined by poorly constrained assumptions regarding the biological cycling of iron, which is the main limiting resource for NPP over large parts of the ocean. In this study, we show that the climate change trends in NPP and the biomass of upper trophic levels are strongly affected by modifying assumptions associated with phytoplankton iron uptake. Using a suite of model experiments, we find 21st century climate change impacts on regional NPP range from −12.3% to +2.4% under a high emissions climate change scenario. This wide range arises from variations in the efficiency of iron retention in the upper ocean in the eastern equatorial Pacific across different scenarios of biological iron uptake, which affect the strength of regional iron limitation. Those scenarios where nitrogen limitation replaced iron limitation showed the largest projected NPP declines, while those where iron limitation was more resilient displayed little future change. All model scenarios have similar skill in reproducing past inter‐annual variations in regional ocean NPP, largely due to limited change in the historical period. Ultimately, projections of end of century upper trophic level biomass change are altered by 50%–80% across all plausible scenarios. Overall, we find that uncertainties in the biological iron cycle cascade through open ocean pelagic ecosystems, from plankton to fish, affecting their evolution under climate change. This highlights additional challenges to developing effective conservation and fisheries management policies under climate change

Circulating microRNAs in sera correlate with soluble biomarkers of immune activation but do not predict mortality in ART treated individuals with HIV-1 infection: A case control study

Introduction: The use of anti-retroviral therapy (ART) has dramatically reduced HIV-1 associated morbidity and mortality. However, HIV-1 infected individuals have increased rates of morbidity and mortality compared to the non-HIV-1 infected population and this appears to be related to end-organ diseases collectively referred to as Serious Non-AIDS Events (SNAEs). Circulating miRNAs are reported as promising biomarkers for a number of human disease conditions including those that constitute SNAEs. Our study sought to investigate the potential of selected miRNAs in predicting mortality in HIV-1 infected ART treated individuals. Materials and Methods: A set of miRNAs was chosen based on published associations with human disease conditions that constitute SNAEs. This case: control study compared 126 cases (individuals who died whilst on therapy), and 247 matched controls (individuals who remained alive). Cases and controls were ART treated participants of two pivotal HIV-1 trials. The relative abundance of each miRNA in serum was measured, by RTqPCR. Associations with mortality (all-cause, cardiovascular and malignancy) were assessed by logistic regression analysis. Correlations between miRNAs and CD4+ T cell count, hs-CRP, IL-6 and D-dimer were also assessed. Results: None of the selected miRNAs was associated with all-cause, cardiovascular or malignancy mortality. The levels of three miRNAs (miRs -21, -122 and -200a) correlated with IL-6 while miR-21 also correlated with D-dimer. Additionally, the abundance of miRs -31, -150 and -223, correlated with baseline CD4+ T cell count while the same three miRNAs plus miR- 145 correlated with nadir CD4+ T cell count. Discussion: No associations with mortality were found with any circulating miRNA studied. These results cast doubt onto the effectiveness of circulating miRNA as early predictors of mortality or the major underlying diseases that contribute to mortality in participants treated for HIV-1 infection

Development and Validation of a Risk Score for Chronic Kidney Disease in HIV Infection Using Prospective Cohort Data from the D:A:D Study

Ristola M. on työryhmien DAD Study Grp ; Royal Free Hosp Clin Cohort ; INSIGHT Study Grp ; SMART Study Grp ; ESPRIT Study Grp jäsen.Background Chronic kidney disease (CKD) is a major health issue for HIV-positive individuals, associated with increased morbidity and mortality. Development and implementation of a risk score model for CKD would allow comparison of the risks and benefits of adding potentially nephrotoxic antiretrovirals to a treatment regimen and would identify those at greatest risk of CKD. The aims of this study were to develop a simple, externally validated, and widely applicable long-term risk score model for CKD in HIV-positive individuals that can guide decision making in clinical practice. Methods and Findings A total of 17,954 HIV-positive individuals from the Data Collection on Adverse Events of Anti-HIV Drugs (D:A:D) study with >= 3 estimated glomerular filtration rate (eGFR) values after 1 January 2004 were included. Baseline was defined as the first eGFR > 60 ml/min/1.73 m2 after 1 January 2004; individuals with exposure to tenofovir, atazanavir, atazanavir/ritonavir, lopinavir/ritonavir, other boosted protease inhibitors before baseline were excluded. CKD was defined as confirmed (>3 mo apart) eGFR In the D:A:D study, 641 individuals developed CKD during 103,185 person-years of follow-up (PYFU; incidence 6.2/1,000 PYFU, 95% CI 5.7-6.7; median follow-up 6.1 y, range 0.3-9.1 y). Older age, intravenous drug use, hepatitis C coinfection, lower baseline eGFR, female gender, lower CD4 count nadir, hypertension, diabetes, and cardiovascular disease (CVD) predicted CKD. The adjusted incidence rate ratios of these nine categorical variables were scaled and summed to create the risk score. The median risk score at baseline was -2 (interquartile range -4 to 2). There was a 1: 393 chance of developing CKD in the next 5 y in the low risk group (risk score = 5, 505 events), respectively. Number needed to harm (NNTH) at 5 y when starting unboosted atazanavir or lopinavir/ritonavir among those with a low risk score was 1,702 (95% CI 1,166-3,367); NNTH was 202 (95% CI 159-278) and 21 (95% CI 19-23), respectively, for those with a medium and high risk score. NNTH was 739 (95% CI 506-1462), 88 (95% CI 69-121), and 9 (95% CI 8-10) for those with a low, medium, and high risk score, respectively, starting tenofovir, atazanavir/ritonavir, or another boosted protease inhibitor. The Royal Free Hospital Clinic Cohort included 2,548 individuals, of whom 94 individuals developed CKD (3.7%) during 18,376 PYFU (median follow-up 7.4 y, range 0.3-12.7 y). Of 2,013 individuals included from the SMART/ESPRIT control arms, 32 individuals developed CKD (1.6%) during 8,452 PYFU (median follow-up 4.1 y, range 0.6-8.1 y). External validation showed that the risk score predicted well in these cohorts. Limitations of this study included limited data on race and no information on proteinuria. Conclusions Both traditional and HIV-related risk factors were predictive of CKD. These factors were used to develop a risk score for CKD in HIV infection, externally validated, that has direct clinical relevance for patients and clinicians to weigh the benefits of certain antiretrovirals against the risk of CKD and to identify those at greatest risk of CKD.Peer reviewe

Rocky tidal pools: carbonate chemistry, diurnal variability and calcifying organisms in future high-CO₂ conditions

International audienceUnderstanding the coastal ocean variability and quantifying its significance in the global biogeochemical cycles is crucial to our ability to project future changes. In the shallow coastal waters, the contribution of the biological activity to water chemistry can be high locally, and responsible for seasonal and diurnal variations. These variations are not yet well-understood: they are often under-estimated and the general lack of observations means that they are seldom integrated into global predictive models such as those used by the IPCC. In this presentation, we will present results on the natural carbonate chemistry diurnal variability in tidal rock pools in Brittany (France), during emersion times. We chose tidal rock pools as to represent "mini-coastal seas": realistic small mesocosms that simulate coastal environments with extreme variability. These have the advantage to be closed systems containing a range of calcifying organisms such as coralline encrusting and non-encrusting algae, that influence and are influenced by the carbonate chemistry. We calculated calcification of the pools community by using the alkalinity anomaly method and estimated the community photosynthesis/respiration. We also compared night-time dissolution and day-time calcification. Finally, we manipulated the pools chemistry at emersion by adding CO2 to mimick future acidification changes, and explored the impact of seawater acidification on the calcification of the tidal pools' communities

Ocean acidification enhances primary productivity and nocturnal carbonate dissolution in intertidal rock pools

International audienceHuman CO2 emissions are modifying ocean carbonate chemistry, causing ocean acidification and likely already impacting marine ecosystems. In particular, there is concern that coastal, benthic calcifying organisms will be negatively affected by ocean acidification, a hypothesis largely supported by laboratory studies. The inter-relationships between carbonate chemistry and marine calcifying communities in situ are complex, and natural mesocosms such as tidal pools can provide useful community-level insights. In this study, we manipulated the carbonate chemistry of intertidal pools to investigate the influence of future ocean acidification on net community production (NCP) and calcification (NCC) at emersion. Adding CO2 at the start of the tidal emersion to simulate future acidification (+1500 µatm pCO2, target pH 7.5) modified net production and calcification rates in the pools. By day, pools were fertilized by the increased CO2 (+20 % increase in NCP, from 10 to 12 mmol O2 m−2 h−1), while there was no measurable impact on NCC. During the night, pools experienced net community dissolution (NCC < 0), even under present-day conditions, when waters were supersaturated with regard to aragonite. Adding CO2 to the pools increased nocturnal dissolution rates by 40 % (from −0.7 to −1.0 mmol CaCO3 m−2 h−1) with no consistent impact on nocturnal community respiration. Our results suggest that ocean acidification is likely to alter temperate intertidal community metabolism on sub-daily timescales, enhancing both diurnal community production and nocturnal calcium carbonate dissolution

Consistent trophic amplification of marine biomass declines under climate change

The impact of climate change on the marine food web is highly uncertain. Nonetheless, there is growing consensus that global marine primary production will decline in response to future climate change, largely due to increased stratification reducing the supply of nutrients to the upper ocean. Evidence to date suggests a potential amplification of this response throughout the trophic food web, with more dramatic responses at higher trophic levels. Here we show that trophic amplification of marine biomass declines is a consistent feature of the Coupled Model Intercomparison Project Phase 5 (CMIP5) Earth System Models, across different scenarios of future climate change. Under the business-as-usual Representative Concentration Pathway 8.5 (RCP8.5) global mean phytoplankton biomass is projected to decline by 6.1% +/- 2.5% over the twenty-first century, while zooplankton biomass declines by 13.6% +/- 3.0%. All models project greater relative declines in zooplankton than phytoplankton, with annual zooplankton biomass anomalies 2.24 +/- 1.03 times those of phytoplankton. The low latitude oceans drive the projected trophic amplification of biomass declines, with models exhibiting variable trophic interactions in the mid-to-high latitudes and similar relative changes in phytoplankton and zooplankton biomass. Under the assumption that zooplankton biomass is prey limited, an analytical explanation of the trophic amplification that occurs in the low latitudes can be derived from generic plankton differential equations. Using an ocean biogeochemical model, we show that the inclusion of variable C:N:P phytoplankton stoichiometry can substantially increase the trophic amplification of biomass declines in low latitude regions. This additional trophic amplification is driven by enhanced nutrient limitation decreasing phytoplankton N and P content relative to C, hence reducing zooplankton growth efficiency. Given that most current Earth System Models assume that phytoplankton C:N:P stoichiometry is constant, such models are likely to underestimate the extent of negative trophic amplification under projected climate change