Prymnesium parvum blooms result in fish kills around the world and are devastating to fish hatcheries, where few management tools are available. Current control strategies include algaecides, nutrient management, and flocculation, which are moderately effective at best and can be toxic to nontarget organisms. A relatively new type of medium, registered by the U.S. Environmental Protection Agency for the control of fecal coliforms in storm water runoff, was evaluated as a possible P. parvum control tool. The medium, called Smart Sponge, was designed to absorb petroleum hydrocarbons; a variant, Smart Sponge Plus, is enhanced with antimicrobial properties. It is these antimicrobial properties that we investigated for possible use in algal bloom management. Our objective was to evaluate the efficacy of this type of medium on the eradication of P. parvum and its associated toxins, with a view toward advancing toxic algae control strategies. Prymnesium parvum was passed through columns of the filter medium. Algal cell counts and visual observations were used to assess mortality; fish bioassays were conducted to assess toxicity. Smart Sponge Plus successfully killed the algae, although toxins were released during filtration. After filtration, 87–100% algal removal was achieved, with the variability potentially being related to cell density at the initiation of the test. Smart Sponge was also successful in reducing associated the toxicity of P. parvum, as was a charcoal medium. Smart Sponge Plus shows promise for use in the management of golden algal blooms by reducing cell density and should be further evaluated in hatchery and field settings.
Adult neural stem cells (NSCs) are neural progenitor cells that differentiate into neurons and glial cells in the brain throughout an organism’s life. The sub ventricular zone(SVZ) in mammals holds a niche of NSCs that are involved in neurologic plasticity, brain damage repair, behavioral response to stimuli, and learning and memory formation. Cultured SVZ-derived NSCs offer an accessible model for investigating the cellular and molecular mechanisms in brain function.Manganese causes neuronal dysfunction, but its cellular mechanisms are unknown. While exposure to manganese results in a neurodegenerative condition known as manganism that mimics symptoms of idiopathic Parkinson’s Disease, people living in mining and industry communities are chronically exposed to manganese through drinking water or inhalation at levels below EPA limits. We are investigating the effects of such low-level manganese on cellular functions of neural cells. The investigation is directed towards examining changes in intracellular signaling pathways and cellular mechanisms in adult NSCs exposed to manganese of adult neurogenesis. We found that MnCl2 impairs normal development and proliferation of neural stem cell behavior. Cultured adult NSCs from the SVZ displayed abnormal morphology when exposed to 500uM and 800uM concentrations of MnCl2 for 24 hours. However, the manganese concentrations causing morphology impairment do not undergo apoptosis. Excess manganese exposure is a concern for West Virginia due to the abundance of welding, mining, and metal manufacturing industries in the area. This research recognizes the unique vulnerability of the brain to manganese and could be used for regulation of manganese exposure limits.
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