From the Cover: Global declines in coral reef calcium carbonate production under ocean acidification and warming

Ocean warming and acidification threaten the future growth of coral reefs. This is because the calcifying coral reef taxa that construct the calcium carbonate frameworks and cement the reef together are highly sensitive to ocean warming and acidification. However, the global-scale effects of ocean warming and acidification on rates of coral reef net carbonate production remain poorly constrained despite a wealth of studies assessing their effects on the calcification of individual organisms. Here, we present global estimates of projected future changes in coral reef net carbonate production under ocean warming and acidification. We apply a meta-analysis of responses of coral reef taxa calcification and bioerosion rates to predicted changes in coral cover driven by climate change to estimate the net carbonate production rates of 183 reefs worldwide by 2050 and 2100. We forecast mean global reef net carbonate production under representative concentration pathways (RCP) 2.6, 4.5, and 8.5 will decline by 76, 149, and 156%, respectively, by 2100. While 63% of reefs are projected to continue to accrete by 2100 under RCP2.6, 94% will be eroding by 2050 under RCP8.5, and no reefs will continue to accrete at rates matching projected sea level rise under RCP4.5 or 8.5 by 2100. Projected reduced coral cover due to bleaching events predominately drives these declines rather than the direct physiological impacts of ocean warming and acidification on calcification or bioerosion. Presently degraded reefs were also more sensitive in our analysis. These findings highlight the low likelihood that the world’s coral reefs will maintain their functional roles without near-term stabilization of atmospheric CO₂ emissions.

Coral reef ecosystems provide a habitat for a vast array of biodiversity (1, 2), yield billions of dollars of global revenue from fisheries and tourism (3, 4), and protect tropical shorelines from hazards such as storms (5). These functions are dependent on the maintenance of the framework structure of the reefs, the accumulation of which requires the net production of calcium carbonate by resident taxa. This net calcium carbonate production is a balance between gross production minus the loss due to physical, chemical, and biological erosion. However, the net calcium carbonate production and related potential vertical accretion of reefs is increasingly threatened by anthropogenic climate change (5). Vertical reef accretion is the product of a number of processes that include 1) biological net calcium carbonate production (gross production by calcifying taxa minus bioerosion), 2) net sediment production (gross production minus endolithic and pore water–driven dissolution), 3) sediment transport (import and export), 4) physical erosion, and 5) cementation rates (Fig. 1). We refer to this potential vertical accretion of reefs simply as “accretion” hereafter, and note that we focus on sediment dissolution and biological net carbonate production (hereafter referred to as “net carbonate production,” the measurement of which is referred to as “carbonate budgets”), perhaps the best quantified and largest contributors to accretion rates on reefs on short timescales.Open in a separate windowFig. 1.Processes involved in net carbonate production and accretion on reefs as well as the associated methods typically employed to measure this. +ve = positive contribution to accretion with solid lines; −ve = negative contribution with dashed lines. Processes in gray are not included in most carbonate budgets or here. Here, we project the effects of ocean acidification and warming on CCA and coral calcification, chemical components of bioerosion, and sediment dissolution. Only chemical components of bioerosion are included in hydrochemical measurements, while direct sediment production by bioeroders is also included here.Climate change will impact both the abundance and calcification rates of reef taxa responsible for producing calcium carbonate, such as corals and coralline algae (2, 6, 7), while simultaneously altering the bioerosion and recycling of this calcium carbonate by resident bioeroders, such as sponges and cyanobacteria (8, 9). Both net carbonate production and accretion are already declining regionally in response to fishing pressure, disease, and marine heatwaves (10–13). Such changes have profound implications for societally relevant ecosystem service provisioning (11), and rapid climate change impacts are projected to further exacerbate these negative trajectories. Specifically, ocean warming and associated marine heatwaves will reduce gross carbonate production rates on coral reefs, as coral cover is reduced by more frequent and severe mass bleaching events (14–16) and as elevated temperatures decrease the calcification rates of coral and coralline algae under more severe warming scenarios (6, 17). Ocean acidification is also projected to reduce the calcification rates of key taxa such as corals and coralline algae that form reef structures and associated sediments (6, 7, 18, 19) while further reducing accretion by increasing the dissolution of carbonate sediments (20) and enhancing rates of bioerosion (8, 9). Furthermore, the combined impacts of ocean warming and acidification are predicted to be amplified under higher CO₂ emission scenarios (6, 19).While the responses of reef-forming taxa to ocean warming and acidification have been the focus of considerable scientific effort in recent decades (2, 6, 7), quantitative predictions of the impacts of climate change on global coral reef net carbonate production and reef accretion are limited. Specifically, existing projections are largely theoretical, limited to specific locations, only include sea level rise and not ocean acidification or warming, or do not include some of the major processes controlling coral reef net carbonate production (5, 10, 20–23). For example, one prominent model provided important data on lagoon sediment dissolution rates (20), although the link between changes in these rates and forereef accretion is unclear. Other global-scale projections do not include the impacts of ocean warming or acidification (5). How the combined effects of changes in the mortality, calcification, and bioerosion rates of individual reef taxa will manifest spatially across different ocean basins due to ocean warming and acidification remains unresolved.Predicting the trajectories of future net carbonate production is complicated by uncertainties around the magnitude of future declines in coral cover, which is likely to be one of the major drivers of future carbonate budgets of coral reefs; yet, estimating future coral cover is difficult. While coral cover is declining globally due to repeated mass coral bleaching (hereafter referred to as “bleaching”) and other local stressors, there is clear temporal and spatial variability of local anthropogenic impacts (16, 24–26). This makes estimating future coral cover a complex and heavily debated process, even on local scales (27–29). The impacts of marine heatwaves on coral mortality, recovery, and subsequent recruitment cannot be captured accurately in short-term laboratory experiments in the way that changes to calcification can, and currently available projections of coral cover into the future are encumbered with uncertainties that do not allow us to predict exact future cover for any specific region (16, 30, 31).Here, we resolve these challenges of applying laboratory results to real coral reef locations by assessing changes in future carbonate budgets of reefs as a function of integrated robust estimates of the responses of major components of the carbonate budget to climate change as well as including estimates of changes in future coral cover. We collate or measure data from 233 locations on 183 distinct reefs globally (49% Atlantic, 39% in the Indian, and 11% in the Pacific Ocean) to quantify the impacts of ocean warming and acidification on coral reef net carbonate production and then use these data to estimate the impacts on net carbonate production and accretion by 2050 and 2100. We incorporate more than 800 empirically measured changes in net calcification rates of the main producers of calcium carbonate on coral reefs (corals and coralline algae), bioerosion rates, and sediment dissolution in response to ocean warming, acidification, and their interaction from 98 studies. We model the size of the effects of ocean acidification, ocean warming, and their interaction under contrasting Intergovernmental Panel on Climate Change emissions scenarios for representative concentration pathways (RCP) 2.6, 4.5, and 8.5 for the year 2050 and 2100. We then apply these estimated effects to reefs with previously measured rates of net carbonate production, where the cover of corals and coralline algae is well defined (SI Appendix, Table S1). Importantly, we account for the impact of reduced coral cover, which, in most locations, will be further diminished by more severe and frequent bleaching events (16, 25), including estimates of its impacts based on currently available information. We calculate region-specific projections of degree heating weeks (DHW), a commonly used metric that accounts for the severity and duration of marine heatwaves on corals (32) and combine them with reductions in coral cover that were measured after exposure to differing DHWs during the 2016 El Niño event (25). These models (Materials and Methods) are then used to explore the effects of ocean warming and acidification independently, and in interaction with each other, under each climatic scenario on rates of reef net carbonate production and accretion.     

Serum Caspase-3 Levels and Early Mortality of Patients with Malignant Middle Cerebral Artery Infarction

Neurocritical Care - Circulating caspase-3 levels at 24 h of ischemic stroke were found to be associated with poorer functional neurological outcome in a previous study. The aim of this...     

High Serum DNA and RNA Oxidative Damage in Non-surviving Patients with Spontaneous Intracerebral Hemorrhage

Neurocritical Care - One study found higher leukocytes 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels in patients with spontaneous intracerebral hemorrhage (ICH) than in healthy subjects due to...     

High serum caspase-3 levels in hepatocellular carcinoma prior to liver transplantation and high mortality risk during the first year after liver transplantation

Background: Higher liver caspase-3 activity has been found in patients with different liver diseases. However, there is no published data about circulating caspase-3 levels in patients with hepatocellular carcinoma (HCC) who underwent liver transplantation (LT). Therefore, our objective in this study was to determine whether an association between circulating caspase-3 levels in HCC patients prior to LT and one-year mortality after LT exists.

Methods: In this observational and retrospective study, we included HCC patients who underwent LT. We measured serum levels of caspase-3 (as the main executor of apoptosis) and caspase-cleaved cytokeratin (CCCK)-18 (to estimate apoptosis degree) before LT.

Results: One-year surviving LT patients (n = 129) showed lower serum levels of caspase-3 (p = 0.004) and CCCK-18 (p = 0.001) than non-surviving LT patients (n = 16). Logistic regression analysis showed that serum caspase-3 levels prior to LT were associated with one-year after LT mortality (Odds Ratio = 2.612; 95% CI = 1.519–4.493; p = 0.001). We found a positive association between serum levels of caspase-3 and CCCK-18 (rho = 0.26; p = 0.002).

Conclusions: Our study is the first one reporting data of circulating caspase-3 levels prior to LT for HCC, and an association between high serum caspase-3 levels previously to LT and survival at first year after LT.     

Low blood caspase-8 levels in survivor patients of traumatic brain injury

Neurological Sciences - High concentrations of caspase-8 (main initiator caspase of the extrinsic pathway of apoptosis) have been found in brain tissue of patients with traumatic brain injury (TBI)...     

Congenital hamartoma of the scalp with meningothelial, sebaceus, muscular, and immature glandular components

A 4-month-old boy presented with a congenital, solitary, yellowish-red, eroded tumor on the scalp, histologically characterized by an ectopic proliferation of vascular and meningothelial elements intimately admixed with mature connective-tissue elements, adipose tissue, and smooth-muscular fibers. In addition, the presence of characteristic histopathological features of a nevus sebaceus and areas with immature glandular differentiation were observed. The diagnosis of a congenital hamartoma of the scalp with meningothelial, sebaceus, immature glandular, and muscular components was established. We review the heterogeneous group of cutaneous lesions with meningothelial elements and their pathogenesis.     

Sustained high serum caspase-3 concentrations and mortality in septic patients

Caspase-3 is the main executor of the apoptotic process. Higher serum caspase-3 concentrations in non-survivor compared to survivor septic patients have been found. The objectives of this work (with the increase of sample size to 308 patients, and the determination of serum caspase-3 concentrations also on days 4 and 8 of diagnosis of severe sepsis) were to know whether an association between serum caspase-3 concentrationss during the first week, degree of apoptosis, sepsis severity, and sepsis mortality exists. We collected serum samples of 308 patients with severe sepsis from eight intensive care units on days 1, 4 and 8 to measure concentrations of caspase-3 and caspase-cleaved cytokeratin (CCCK)-18 (to assess degree of apoptosis). End point was 30-day mortality. We found higher serum concentrations of caspase-3 and CCCK-18 in non-survivors compared to survivors on days 1 (p < 0.001), 4 (p < 0.001), and 8 (p < 0.001). We found an association between serum caspase-3 concentrations on days 1, 4 and 8 of severe sepsis diagnosis and serum CCCK-18 concentrations (p < 0.001), SOFA (p < 0.001), serum acid lactic concentrations (p < 0.001), and 30-day sepsis mortality (p < 0.001). The new findings of this work were that an association between serum caspase-3 concentrations during the first week, apoptosis degree, sepsis severity, and sepsis mortality exists.