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Potent marine neurotoxins known as brevetoxins are produced by the 'red tide' dinoflagellate Karenia brevis. They kill large numbers of fish and cause illness in humans who ingest toxic filter-feeding shellfish or inhale toxic aerosols. The toxins are also suspected of having been involved in events in which many manatees and dolphins died, but this has usually not been verified owing to limited confirmation of toxin exposure, unexplained intoxication mechanisms and complicating pathologies. Here we show that fish and seagrass can accumulate high concentrations of brevetoxins and that these have acted as toxin vectors during recent deaths of dolphins and manatees, respectively. Our results challenge claims that the deleterious effects of a brevetoxin on fish (ichthyotoxicity) preclude its accumulation in live fish, and they reveal a new vector mechanism for brevetoxin spread through food webs that poses a threat to upper trophic levels.

Between 1993 and 2003, 713 (24%) of 2,940 dead Florida manatees (Trichechus manatus latirostris) recovered from Florida waters and examined were killed by watercraft-induced trauma. It was determined that this mortality was the result of watercraft trauma because the external wound patterns and the internal lesions seen during gross necropsy are recognizable and diagnostic. This study documents the methods used in determining watercraft-related mortality during gross necropsy and explains why these findings are diagnostic. Watercraft can inflict sharp- and blunt-force trauma to manatees, and both types of trauma can lead to mortality. This mortality may be a direct result of the sharp and blunt forces or from the chronic effects resulting from either force. In cases in which death is caused by a chronic wound-related complication, the original incident is usually considered to be the cause of death. Once a cause of death is determined, it is recorded in an extensive database and is used by Federal and state managers in developing strategies for the conservation of the manatee. Common sequelae to watercraft-induced trauma include skin lesions, torn muscles, fractured and luxated bones, lacerated internal organs, hemothorax, pneumothorax, pyothorax, hydrothorax, abdominal hemorrhage and ascites, and pyoperitoneum.

Unexpected brevetoxin vectors may account for deaths long after or remote from an algal bloom. Red alert A string of recent reports have claimed that the deaths of groups of dolphins and manatees off the Florida coast have been caused by red tides (toxic algal blooms). It has been hard to verify the true cause of these deaths. But the discovery that algal toxins accumulate in fish and seagrass, food for dolphins and manatees, respectively, suggests that the red tides are indeed to blame. Potent marine neurotoxins known as brevetoxins are produced by the ‘red tide’ dinoflagellate Karenia brevis . They kill large numbers of fish and cause illness in humans who ingest toxic filter-feeding shellfish or inhale toxic aerosols 1 . The toxins are also suspected of having been involved in events in which many manatees and dolphins died, but this has usually not been verified owing to limited confirmation of toxin exposure, unexplained intoxication mechanisms and complicating pathologies 2 , 3 , 4 . Here we show that fish and seagrass can accumulate high concentrations of brevetoxins and that these have acted as toxin vectors during recent deaths of dolphins and manatees, respectively. Our results challenge claims that the deleterious effects of a brevetoxin on fish (ichthyotoxicity) preclude its accumulation in live fish, and they reveal a new vector mechanism for brevetoxin spread through food webs that poses a threat to upper trophic levels.

Abstract Objective We compared the effects of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) on insulin sensitivity and other important metabolic adaptations in adults with obesity. Methods Thirty-one inactive adults with obesity (age: 31 ± 6 years; body mass index: 33 ± 3 kg/m2) completed 12 weeks (4 sessions/week) of either HIIT (10 × 1-minute at 90%HRmax, 1-minute active recovery; n = 16) or MICT (45 minutes at 70%HRmax; n = 15). To assess the direct effects of exercise independent of weight/fat loss, participants were required to maintain body mass. Results Training increased peak oxygen uptake by ~10% in both HIIT and MICT (P < 0.0001), and body weight/fat mass were unchanged. Peripheral insulin sensitivity (hyperinsulinemic-euglycemic clamp) was ~20% greater the day after the final exercise session compared to pretraining (P < 0.01), with no difference between HIIT and MICT. When trained participants abstained from exercise for 4 days, insulin sensitivity returned to pretraining levels in both groups. HIIT and MICT also induced similar increases in abundance of many skeletal muscle proteins involved in mitochondrial respiration and lipid and carbohydrate metabolism. Training-induced alterations in muscle lipid profile were also similar between groups. Conclusion Despite large differences in training intensity and exercise time, 12 weeks of HIIT and MICT induce similar acute improvements in peripheral insulin sensitivity the day after exercise, and similar longer term metabolic adaptations in skeletal muscle in adults with obesity. These findings support the notion that the insulin-sensitizing effects of both HIIT and MICT are mediated by factors stemming from the most recent exercise session(s) rather than adaptations that accrue with training.

The narrative of biodiversity decline in response to human impacts is overly simplistic because different biodiversity metrics show different trajectories at different spatial scales. It is also debated whether human-caused biodiversity changes lead to subsequent, accelerating change (cascades) in ecological communities, or alternatively build increasingly robust community networks with decreasing extinction rates and reduced invasibility. Mechanistic approaches are needed that simultaneously reconcile different metrics of biodiversity change, and explore the robustness of communities to further change. We develop a trophically-structured, mainland-archipelago metacommunity model of community assembly. Varying the parameters across model simulations shows that local alpha diversity (the number of species per island) and regional gamma diversity (the total number of species in the archipelago) depend on both the rate of extirpation per island and on the rate of dispersal between islands within the archipelago. In particular, local diversity increases with increased dispersal and heterogeneity between islands, but regional diversity declines because the islands become biotically similar and local one-island and few-island species are excluded (homogenisation, or reduced beta diversity). This mirrors changes observed empirically: real islands have gained species (increased local and island-scale community diversity) with increased human-assisted transfers of species, but global diversity has declined with the loss of endemic species. However, biological invasions may be self-limiting. High-dispersal, high local-diversity model communities become resistant to subsequent invasions, generating robust species-community networks unless dispersal is extremely high. A mixed-up world is likely to lose many species, but the resulting ecological communities may nonetheless be relatively robust. Biodiversity is commonly regarded as threatened due to human impacts, but biodiversity metrics at different scales produce contradictory results. A framework is needed that can reproduce and connect these results across scales and address whether biodiversity change will inexorably accelerate following perturbation or become self-limiting as new ecological communities form. We address this challenge by constructing size-structured model communities using a mainland/island paradigm and tracking diversity at different scales. Our simulations reproduce the literature’s discrepancy across scales and provide new insight. Ecological communities (islands) gain species with increasing (human-assisted) dispersal, but global diversity declines with the consequent loss of endemic species. Communities also become less invasible as dispersal increases, suggesting that human-mediated dispersal favours robust communities that resist subsequent change.