Mitigation of lampricide toxicity to juvenile lake sturgeon: the importance of water alkalinity and life stage.

The pesticide, 3-trifluoromethyl-4-nitrophenol (TFM), is used to control invasive sea lamprey (Petromyzon marinus) populations in the Laurentian Great Lakes. Applied to infested tributaries, it is most toxic to larval sea lamprey, which have a low capacity to detoxify TFM. However, TFM can be toxic to lake sturgeon (Acipenser fulvescens), whose populations are at risk throughout the basin. They are most vulnerable to TFM in early life stages, with the greatest risk of non-target mortality occurring in waters with high alkalinity. We quantified TFM toxicity and used radio-labelled TFM (14C-TFM) to measure TFM uptake rates in lake sturgeon in waters of different pH and alkalinity. Regardless of pH or alkalinity, TFM uptake was 2-3-fold higher in young-of-the-year (YOY) than in age 1-year-plus (1+) sturgeon, likely due to higher mass-specific metabolic rates in the smaller YOY fish. As expected, TFM uptake was highest at lower (pH 6.5) versus higher (pH 9.0) pH, indicating that it is taken up across the gills by diffusion in its unionized form. Uptake decreased as alkalinity increased from low (~50 mg L-1 as CaCO3) to moderate alkalinity (~150 mg L-1 as CaCO3), before plateauing at high alkalinity (~250 mg L-1 as CaCO3). Toxicity curves revealed that the 12-h LC50 and 12-h LC99.9 of TFM to lake sturgeon were in fact higher (less toxic) than in sea lamprey, regardless of alkalinity. However, in actual treatments, 1.3-1.5 times the minimum lethal TFM concentration (MLC = LC99.9) to lamprey is applied to maximize mortality, disproportionately amplifying TFM toxicity to sturgeon at higher alkalinities. We conclude that limiting TFM treatments to late summer/early fall in waters of moderate-high alkalinity, when lake sturgeon are larger with lower rates of TFM uptake, would mitigate non-target TFM effects and help conserve populations of these ancient, culturally important fishes.

A portable trap with electric lead catches up to 75% of an invasive fish species.

A novel system combining a trap and pulsed direct current electricity was able to catch up to 75% of tagged invasive sea lamprey Petromyzon marinus in free-flowing streams. Non-target mortality was rare and impacts to non-target migration were minimal; likely because pulsed direct current only needed to be activated at night (7 hours of each day). The system was completely portable and the annual cost of the trapping system was low ($4,800 U.S. dollars). Use of the technology is poised to substantially advance integrated control of sea lamprey, which threaten a fishery valued at 7 billion U.S. dollars annually, and help restore sea lamprey populations in Europe where they are native, but imperiled. The system may be broadly applicable to controlling invasive fishes and restoring valued fishes worldwide, thus having far reaching effects on ecosystems and societies.

BCR-ABL1 kinase domain mutation analysis in an Irish cohort of chronic myeloid leukemia patients.

While tyrosine kinase inhibitor (TKI) therapy is the mainstay of modern management of chronic myeloid leukemia (CML), a significant proportion of CML patients may be refractory or lose their initial response to TKI therapy through a number of cellular and molecular mechanisms of which acquired mutations in the BCR-ABL1 kinase domain (KD) are the most common. BCR-ABL1 KD mutations were prospectively identified in order to inform clinical decisions on subsequent therapy. Direct sequencing of the BCR-ABL1 KD was performed in 85 CML patients that were either TKI refractory or displayed increasing BCR-ABL1 transcript levels by serial monitoring after an initial molecular response. Twenty-three BCR-ABL1 KD mutations were detected in 21 CML patients and were detected across the KD. Mutations were associated with specific TKI resistance, indicating change and enabling rational selection of subsequent therapy. Serial molecular monitoring of BCR-ABL1 transcripts in CML patients allows appropriate selection of CML patients for BCR-ABL1 KD mutation analysis associated with acquired TKI resistance. Identification of these KD mutations is essential in order to direct alternative treatment strategies in such CML patients.