Factors Controlling Calanoid Copepod Biomass and Distribution in the Upper San Francisco Estuary and Implications for Managing the Imperiled Delta Smelt (Hypomesus transpacificus).

Delta smelt struggle to persist in a dramatically altered estuarine environment. Complex and incompletely understood relationships between food availability, environmental stressors, other components of the species' habitat, and the abundance of delta smelt impede the effective management and recovery of the species. The empirical modeling presented in this study quantitatively describes spatial-temporal biomass values of calanoid copepods, a key prey item for delta smelt, in relation to multiple potential controlling factors. The results underscore the role that river flows through the estuary have in determining prey availability, and demonstrate contributions of water temperature, salinity, and macronutrients in determining copepod biomass. The analysis also shows the importance of non-native, invasive bivalves in determining copepod biomass. Importantly, the analysis describes spatial-temporal shifts in the relative importance of modeled covariates across sampling locations in the Delta. Model results indicate that increasing flows in the fall of wetter years adversely affected copepod biomass, while increases in flows in the spring of drier years provided regional increases in biomass. The results of this analysis can inform resource management decisions and contribute to a comprehensive model that can meaningfully guide efforts to recover the imperiled delta smelt.

Anthropogenic tracers, endocrine disrupting chemicals, and endocrine disruption in Minnesota lakes.

Concentrations of endocrine disrupting chemicals and endocrine disruption in fish were determined in 11 lakes across Minnesota that represent a range of trophic conditions and land uses (urban, agricultural, residential, and forested) and in which wastewater treatment plant discharges were absent. Water, sediment, and passive polar organic integrative samplers (POCIS) were analyzed for steroidal hormones, alkylphenols, bisphenol A, and other organic and inorganic molecular tracers to evaluate potential non-point source inputs into the lakes. Resident fish from the lakes were collected, and caged male fathead minnows were deployed to evaluate endocrine disruption, as indicated by the biological endpoints of plasma vitellogenin and gonadal histology. Endocrine disrupting chemicals, including bisphenol A, 17ß-estradiol, estrone, and 4-nonylphenol were detected in 90% of the lakes at part per trillion concentrations. Endocrine disruption was observed in caged fathead minnows and resident fish in 90% of the lakes. The widespread but variable occurrence of anthropogenic chemicals in the lakes and endocrine disruption in fish indicates that potential sources are diverse, not limited to wastewater treatment plant discharges, and not entirely predictable based on trophic status and land use.

The anti-leukemic Bruton's tyrosine kinase inhibitor alpha-cyano-beta-hydroxy-beta-methyl-N-(2,5-dibromophenyl) propenamide (LFM-A13) prevents fatal thromboembolism.

The leflunomide metabolite analog alpha-cyano-beta-hydroxy-beta-methyl-N-(2,5-dibromophenyl)-propenamide (LFM-A13) is a rationally-designed specific inhibitor of the TEC family protein tyrosine kinase, Bruton's tyrosine kinase (BTK) which plays an important role in platelet physiology by regulating the glycoprotein GPVI-FcRgamma-coupled collagen receptor signaling pathway. At low micromolar concentrations, LFM-A13 inhibited collagen-induced ultrastructural changes indicative of activation. LFM-A13 inhibited collagen (but not thrombin, TRAP-6, or ADP)-induced platelet aggregation in a concentration-dependent fashion with an IC50 value of 2.8 microM. LFM-A13 was not toxic to mice when administered systemically at dose levels ranging from 1 to 100 mg/kg. At nontoxic dose levels, LFM-A13 prolonged the tail bleeding times of mice and improved event-free survival in two mouse models of agonist-induced invariably fatal pulmonary thromboembolism. To our knowledge, LFM-A13 is the first anti-thrombotic agent which prevents platelet aggregation by inhibiting BTK.