Modeling the population effects of hypoxia on Atlantic croaker (Micropogonias undulatus) in the northwestern Gulf of Mexico

The northwestern Gulf of Mexico currently experiences a large hypoxic area (“dead zone”) during the summer. While the local effects of hypoxia on organisms have been documented, the population-level effects are largely unknown. I developed a spatially-explicit, individual-based model to analyze how hypoxia effects on Atlantic croaker reproduction, growth, and mortality in the northwestern Gulf of Mexico could lead to population-level responses. The model follows the hourly growth, mortality, reproduction, and movement of individuals on a 300 x 800 spatial grid of 1 km2 cells for 100 years. Chlorophyll-a concentration, water temperature, and dissolved oxygen were specified daily for each grid cell for an average year, which was repeated every year. A bioenergetics model was used to represent growth, mortality was assumed age- and size-dependent, and the movement behavior of juveniles and adults was modeled as an unconditioned response to external cues (kinesis) coupled with a neighborhood search algorithm that emulated hypoxia avoidance. Hypoxia effects were imposed using vitality-repair submodels that convert time-varying exposures to reduced hourly growth, increased hourly mortality, and reduced annual fecundity. Results showed that 80 years of either mild or intermediate hypoxia produced small reductions in population abundance, while severe hypoxia caused a 31% reduction in long-term population abundance. The response to severe hypoxia was added age-1 and age-2 daily mortality (8-9%) and a 5% average reduction in eggs per individual. Relatively few individuals (5%) were exposed each hour but many individuals (20-40%) experienced at least one hour of low DO each year. The effects slowly built up in the model over years; population abundance slowly declined for 40 years before the 31% reduction was realized. Under more realistic hypoxia conditions of mild, intermediate, and severe hypoxia years occurring in proportion to their historical frequency, the model predicted an 18-29% decrease in the long-term population abundance. Sensitivity analysis showed hypoxia effects via reduced growth were small, and aspects of avoidance behavior were important in determining the population response. I discuss the strengths and weaknesses of the modeling, and future plans for refining the analysis based on data from ongoing field and laboratory studies

Modeling the Population Effects of Hypoxia on Atlantic Croaker (Micropogonias undulatus) in the Northwestern Gulf of Mexico: Part 2—Realistic Hypoxia and Eutrophication

Quantifying the population-level effects of hypoxia on coastal fish species has been challenging. In the companion paper (part 1), we described an individual-based population model (IBM) for Atlantic croaker in the northwestern Gulf of Mexico (NWGOM) designed to quantify the long-term population responses to low dissolved oxygen (DO) concentrations during the summer. Here in part 2, we replace the idealized hypoxia conditions with realistic DO concentrations generated from a 3-dimensional water quality model. Three years were used and randomly arranged into a time series based on the historical occurrence of mild, intermediate, and severe hypoxia year types.We also used another water quality model to generate multipliers of the chlorophyll concentrations to reflect that croaker food can be correlated to the severity of hypoxia. Simulations used 100 years under normoxia and hypoxia conditions to examine croaker population responses to the following: (1) hypoxia with food uncoupled and coupled to the severity of hypoxia, (2) hypoxia reducing benthos due to direct mortality, (3) how much hypoxia would need to be reduced to offset decreased croaker food expected under 25 and 50% reduction in nutrient loadings, and (4) key assumptions about avoidance movement. Direct mortality on benthos had no effect on long-term simulated croaker abundance, and the effect of hypoxia (about a 25% reduction in abundance) was consistent whether chlorophyll (food) varied with hypoxia or not. Reductions in hypoxia needed with a 25% reduction in nutrient loadings to result in minimal loss of croaker is feasible, and the croaker population will likely do as well as possible (approach abundance under normoxia) under the 50% reduction in nutrient loadings. We conclude with a discussion of why we consider our simulation-based estimates of hypoxia causing a 25% reduction the long-term population abundance of croaker in the NWGOM to be realistic and robust

Modeling the Population Effects of Hypoxia on Atlantic Croaker (Micropogonias undulatus) in the Northwestern Gulf of Mexico: Part 1—Model Description and Idealized Hypoxia

We developed a spatially explicit, individual-based model to analyze how hypoxia effects on reproduction, growth, and mortality of Atlantic croaker in the northwestern Gulf of Mexico lead to population-level responses. The model follows the hourly growth, mortality, reproduction, and movement of individuals on a 300 × 800 spatial grid of 1-km2 cells for 140 years. Chlorophyll-a concentration, water temperature, and dissolved oxygen (DO) were specified daily for each grid cell and repeated for each year of the simulation. A bioenergetics model was used to represent growth, mortality was assumed stage- and age-dependent, and the movement behavior of juveniles and adults was modeled based on temperature and avoidance of low DO. Hypoxia effects were imposed using exposure effect submodels that converted time-varying exposures to low DO to reduced hourly growth, increased hourly mortality, and reduced annual fecundity. Results showed that 100 years of either mild or intermediate hypoxia produced small reductions in population abundance, while repeated severe hypoxia caused a 19% reduction in long-term population abundance. Relatively few individuals were exposed to low DO each hour, but many individuals experienced some exposure. The response was dominated by a 5% average reduction in annual fecundity of individuals. Under conditions of random sequences of mild, intermediate, and severe hypoxia years occurring in proportion to their historical frequency, the model predicted a 10% decrease in the long-term population abundance of croaker. A companion paper substitutes hourly DO values from a three-dimensional water quality model for the idealized hypoxia and results in a more realistic population reduction of about 25%

Modeling the Population Effects of Hypoxia on Atlantic Croaker (Micropogonias undulatus) in the Northwestern Gulf of Mexico: Part 2—Realistic Hypoxia and Eutrophication

Quantifying the population-level effects of hypoxia on coastal fish species has been challenging. In the companion paper (part 1), we described an individual-based population model (IBM) for Atlantic croaker in the northwestern Gulf of Mexico (NWGOM) designed to quantify the long-term population responses to low dissolved oxygen (DO) concentrations during the summer. Here in part 2, we replace the idealized hypoxia conditions with realistic DO concentrations generated from a 3-dimensional water quality model. Three years were used and randomly arranged into a time series based on the historical occurrence of mild, intermediate, and severe hypoxia year types. We also used another water quality model to generate multipliers of the chlorophyll concentrations to reflect that croaker food can be correlated to the severity of hypoxia. Simulations used 100 years under normoxia and hypoxia conditions to examine croaker population responses to the following: (1) hypoxia with food uncoupled and coupled to the severity of hypoxia, (2) hypoxia reducing benthos due to direct mortality, (3) how much hypoxia would need to be reduced to offset decreased croaker food expected under 25 and 50% reduction in nutrient loadings, and (4) key assumptions about avoidance movement. Direct mortality on benthos had no effect on long-term simulated croaker abundance, and the effect of hypoxia (about a 25% reduction in abundance) was consistent whether chlorophyll (food) varied with hypoxia or not. Reductions in hypoxia needed with a 25% reduction in nutrient loadings to result in minimal loss of croaker is feasible, and the croaker population will likely do as well as possible (approach abundance under normoxia) under the 50% reduction in nutrient loadings. We conclude with a discussion of why we consider our simulation-based estimates of hypoxia causing a 25% reduction the long-term population abundance of croaker in the NWGOM to be realistic and robust

Targeted inhibition of gut bacterial β-glucuronidase activity enhances anticancer drug efficacy

Irinotecan treats a range of solid tumors, but its effectiveness is severely limited by gastrointestinal (GI) tract toxicity caused by gut bacterial β-glucuronidase (GUS) enzymes. Targeted bacterial GUS inhibitors have been shown to partially alleviate irinotecan-induced GI tract damage and resultant diarrhea in mice. Here, we unravel the mechanistic basis for GI protection by gut microbial GUS inhibitors using in vivo models. We use in vitro, in fimo, and in vivo models to determine whether GUS inhibition alters the anticancer efficacy of irinotecan. We demonstrate that a single dose of irinotecan increases GI bacterial GUS activity in 1 d and reduces intestinal epithelial cell proliferation in 5 d, both blocked by a single dose of a GUS inhibitor. In a tumor xenograft model, GUS inhibition prevents intestinal toxicity and maintains the antitumor efficacy of irinotecan. Remarkably, GUS inhibitor also effectively blocks the striking irinotecan-induced bloom of Enterobacteriaceae in immune-deficient mice. In a genetically engineered mouse model of cancer, GUS inhibition alleviates gut damage, improves survival, and does not alter gut microbial composition; however, by allowing dose intensification, it dramatically improves irinotecan's effectiveness, reducing tumors to a fraction of that achieved by irinotecan alone, while simultaneously promoting epithelial regeneration. These results indicate that targeted gut microbial enzyme inhibitors can improve cancer chemotherapeutic outcomes by protecting the gut epithelium from microbial dysbiosis and proliferative crypt damage.</p