Climate change impacts on mismatches between phytoplankton blooms and fish spawning phenology.

Substantial interannual variability in marine fish recruitment (i.e., the number of young fish entering a fishery each year) has been hypothesized to be related to whether the timing of fish spawning matches that of seasonal plankton blooms. Environmental processes that control the phenology of blooms, such as stratification, may differ from those that influence fish spawning, such as temperature-linked reproductive maturation. These different controlling mechanisms could cause the timing of these events to diverge under climate change with negative consequences for fisheries. We use an earth system model to examine the impact of a high-emissions, climate-warming scenario (RCP8.5) on the future spawning time of two classes of temperate, epipelagic fishes: "geographic spawners" whose spawning grounds are defined by fixed geographic features (e.g., rivers, estuaries, reefs) and "environmental spawners" whose spawning grounds move responding to variations in environmental properties, such as temperature. By the century's end, our results indicate that projections of increased stratification cause spring and summer phytoplankton blooms to start 16 days earlier on average (±0.05 days SE) at latitudes >40°N. The temperature-linked phenology of geographic spawners changes at a rate twice as fast as phytoplankton, causing these fishes to spawn before the bloom starts across >85% of this region. "Extreme events," defined here as seasonal mismatches >30 days that could lead to fish recruitment failure, increase 10-fold for geographic spawners in many areas under the RCP8.5 scenario. Mismatches between environmental spawners and phytoplankton were smaller and less widespread, although sizable mismatches still emerged in some regions. This indicates that range shifts undertaken by environmental spawners may increase the resiliency of fishes to climate change impacts associated with phenological mismatches, potentially buffering against declines in larval fish survival, recruitment, and fisheries. Our model results are supported by empirical evidence from ecosystems with multidecadal observations of both fish and phytoplankton phenology.

Reconciling fisheries catch and ocean productivity.

Photosynthesis fuels marine food webs, yet differences in fish catch across globally distributed marine ecosystems far exceed differences in net primary production (NPP). We consider the hypothesis that ecosystem-level variations in pelagic and benthic energy flows from phytoplankton to fish, trophic transfer efficiencies, and fishing effort can quantitatively reconcile this contrast in an energetically consistent manner. To test this hypothesis, we enlist global fish catch data that include previously neglected contributions from small-scale fisheries, a synthesis of global fishing effort, and plankton food web energy flux estimates from a prototype high-resolution global earth system model (ESM). After removing a small number of lightly fished ecosystems, stark interregional differences in fish catch per unit area can be explained (r = 0.79) with an energy-based model that (i) considers dynamic interregional differences in benthic and pelagic energy pathways connecting phytoplankton and fish, (ii) depresses trophic transfer efficiencies in the tropics and, less critically, (iii) associates elevated trophic transfer efficiencies with benthic-predominant systems. Model catch estimates are generally within a factor of 2 of values spanning two orders of magnitude. Climate change projections show that the same macroecological patterns explaining dramatic regional catch differences in the contemporary ocean amplify catch trends, producing changes that may exceed 50% in some regions by the end of the 21st century under high-emissions scenarios. Models failing to resolve these trophodynamic patterns may significantly underestimate regional fisheries catch trends and hinder adaptation to climate change.

Climate, Anchovy, and Sardine.

Anchovy and sardine populated productive ocean regions over hundreds of thousands of years under a naturally varying climate, and are now subject to climate change of equal or greater magnitude occurring over decades to centuries. We hypothesize that anchovy and sardine populations are limited in size by the supply of nitrogen from outside their habitats originating from upwelling, mixing, and rivers. Projections of the responses of anchovy and sardine to climate change rely on a range of model types and consideration of the effects of climate on lower trophic levels, the effects of fishing on higher trophic levels, and the traits of these two types of fish. Distribution, phenology, nutrient supply, plankton composition and production, habitat compression, fishing, and acclimation and adaptation may be affected by ocean warming, acidification, deoxygenation, and altered hydrology. Observations of populations and evaluation of model skill are essential to resolve the effects of climate change on these fish.

Climate change and decadal shifts in the phenology of larval fishes in the California Current ecosystem.

Climate change has prompted an earlier arrival of spring in numerous ecosystems. It is uncertain whether such changes are occurring in Eastern Boundary Current Upwelling ecosystems, because these regions are subject to natural decadal climate variability, and regional climate models predict seasonal delays in upwelling. To answer this question, the phenology of 43 species of larval fishes was investigated between 1951 and 2008 off southern California. Ordination of the fish community showed earlier phenological progression in more recent years. Thirty-nine percent of seasonal peaks in larval abundance occurred earlier in the year, whereas 18% were delayed. The species whose phenology became earlier were characterized by an offshore, pelagic distribution, whereas species with delayed phenology were more likely to reside in coastal, demersal habitats. Phenological changes were more closely associated with a trend toward earlier warming of surface waters rather than decadal climate cycles, such as the Pacific Decadal Oscillation and North Pacific Gyre Oscillation. Species with long-term advances and delays in phenology reacted similarly to warming at the interannual time scale as demonstrated by responses to the El Niño Southern Oscillation. The trend toward earlier spawning was correlated with changes in sea surface temperature (SST) and mesozooplankton displacement volume, but not coastal upwelling. SST and upwelling were correlated with delays in fish phenology. For species with 20th century advances in phenology, future projections indicate that current trends will continue unabated. The fate of species with delayed phenology is less clear due to differences between Intergovernmental Panel on Climate Change models in projected upwelling trends.

Elevated CO2 enhances otolith growth in young fish.

A large fraction of the carbon dioxide added to the atmosphere by human activity enters the sea, causing ocean acidification. We show that otoliths (aragonite ear bones) of young fish grown under high CO2 (low pH) conditions are larger than normal, contrary to expectation. We hypothesize that CO2 moves freely through the epithelium around the otoliths in young fish, accelerating otolith growth while the local pH is controlled. This is the converse of the effect commonly reported for structural biominerals.

Physician attitudes toward regionalization of adult critical care: a national survey.

OBJECTIVE: Regionalization has been proposed as a method to improve outcomes for patients with critical illness. We sought to determine intensivist physician attitudes and potential barriers to the regionalization of adult critical care. DESIGN: Mail survey. SETTING: United States. SUBJECTS: Actively practicing physicians specializing in adult critical care, emergency medicine, or internal medicine listed in the 2008 American Medical Association Physician Masterfile (n = 1200). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: There were 569 eligible respondents (effective response rate = 53.0%). Respondents were similar to nonrespondents. Fifty-nine percent of respondents thought their hospital would mainly receive patients under a regionalized system, and 30% thought their hospital would mainly send patients. Opinions were split about whether regionalization would improve overall patient survival (52% agreed) and healthcare efficiency (66% agreed). Specialists in anesthesiology and surgery-critical care, academic physicians, and physicians who perceived that they would mainly receive patients were more likely to believe that regionalization would improve outcomes and efficiency (p < 0.001). The most commonly endorsed barriers to regionalization were personal strain on patient's families (66% agreed), current lack of a strong central authority (64% agreed), and the potential to overwhelm capacity at large hospitals (55% agreed). Commonly endorsed strategies to implement regionalization included using objective criteria to determine eligibility for transfer (87% agreed), developing common information technology platforms across hospitals (86% agreed), and demonstrating in a clinical trial that regionalization is beneficial (81% agreed). CONCLUSIONS: Intensivist physicians have mixed opinions about regionalization, with little consensus about whether regionalization will improve outcomes. Most felt that regionalization will improve patient outcomes, but many expressed concerns about unintended adverse consequences. Respondents identified several barriers and potential implementation strategies that can help policymakers design a regionalized system of critical care in the United States.

Perceived barriers to the regionalization of adult critical care in the United States: a qualitative preliminary study.

BACKGROUND: Regionalization of adult critical care services may improve outcomes for critically ill patients. We sought to develop a framework for understanding clinician attitudes toward regionalization and potential barriers to developing a tiered, regionalized system of care in the United States. METHODS: We performed a qualitative study using semi-structured interviews of critical care stakeholders in the United States, including physicians, nurses and hospital administrators. Stakeholders were identified from a stratified-random sample of United States general medical and surgical hospitals. Key barriers and potential solutions were identified by performing content analysis of the interview transcriptions. RESULTS: We interviewed 30 stakeholders from 24 different hospitals, representing a broad range of hospital locations and sizes. Key barriers to regionalization included personal and economic strain on families, loss of autonomy on the part of referring physicians and hospitals, loss of revenue on the part of referring physicians and hospitals, the potential to worsen outcomes at small hospitals by limiting services, and the potential to overwhelm large hospitals. Improving communication between destination and source hospitals, provider education, instituting voluntary objective criteria to become a designated referral center, and mechanisms to feed back patients and revenue to source hospitals were identified as potential solutions to some of these barriers. CONCLUSION: Regionalization efforts will be met with significant conceptual and structural barriers. These data provide a foundation for future research and can be used to inform policy decisions regarding the design and implementation of a regionalized system of critical care.

Enhancement of stress-induced apoptosis in B-lineage cells by caspase-9 inhibitor.

We have established human B-lineage (BLIN) acute lymphoblastic leukemia cell lines that retain a dependency on fibroblast monolayers for survival and proliferation. Eight hours following removal from adherent cell contact BLIN cells undergo a decrease in mitochondrial transmembrane potential and an increase in annexin V binding. Unexpectedly, the caspase-9 inhibitor (C9i) benzyloxycarbonyl-Leu-Glu-His-Asp-fluoromethylketone enhanced the appearance of apoptotic cells within 8 hours following removal of BLIN cells from fibroblast monolayers. C9i enhancement of apoptosis was dose dependent and did not occur with irreversible inhibitors of caspases-2, -3, -6, and -8. C9i also enhanced apoptosis in cord blood-derived CD19(+) B-lineage cells (but not myeloid cells) removed from murine stromal cells. Longer exposure (> 18 hours) to C9i culminated in apoptosis in a panel of B-lineage acute lymphoblastic leukemia (ALL) cell lines in the presence or absence of fibroblast monolayers, as well as in 2 proliferating leukemic cell lines (RAMOS and CEM). BLIN-4L cells made deficient in caspase-9 by RNA interference exhibited no resistance to apoptotic signals and actually showed increased apoptotic sensitivity to staurosporine. These collective results suggest that a 4-amino acid caspase inhibitor of caspase-9 can promote apoptosis and that at least some types of apoptotic pathways in B-lineage ALL do not require caspase-9.