Occupational Neurotoxicology
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Occupational Neurotoxicology, Volume Seven covers neurotoxicants and exposures to a variety of hazards in the workplace and how they can affect nervous functions in different ways. Metals and organic compounds, both at high level acute exposure and long-term low-level exposure can affect motor functions, cognition, behavior and neurosensory functions. Sections cover Oil leakage in aircraft, aerotoxic syndrome, Organic solvents, WTC neurotoxicities, Environmental intolerance, Pesticides, Carbon monoxide, Mercury Neurotoxicity in Gold Miners, and the Current evolution of neurobehavioral methods.…mehr

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Produktbeschreibung
Occupational Neurotoxicology, Volume Seven covers neurotoxicants and exposures to a variety of hazards in the workplace and how they can affect nervous functions in different ways. Metals and organic compounds, both at high level acute exposure and long-term low-level exposure can affect motor functions, cognition, behavior and neurosensory functions. Sections cover Oil leakage in aircraft, aerotoxic syndrome, Organic solvents, WTC neurotoxicities, Environmental intolerance, Pesticides, Carbon monoxide, Mercury Neurotoxicity in Gold Miners, and the Current evolution of neurobehavioral methods.
Autorenporträt
Dr. Aschner serves as the Harold and Muriel Block Chair in Molecular Pharmacology at Albert Einstein College of Medicine. He served on numerous toxicology panels (Institute of Medicine, US Environmental Protection Agency, Center for Disease Control), and is a member of the Neurotoxicology and Alcohol study section (NIH). Research in our lab focuses on the following topics: (1) Modulation of C. elegans genes (aat, skn-1, daf-16) that are homologous to mammalian regulators of MeHg uptake and cellular resistance will modify dopaminergic neurodegeneration in response to MeHg exposure. (2) Under conditions of MeHg-induced oxidative stress, Nrf2 (a master regulator of antioxidant responses) coordinates the upregulation of cytoprotective genes that combat MeHg-induced oxidative injury, and that genetic and biochemical changes that negatively impact upon Nrf2 function increase MeHg's neurotoxicity. (3) PARK2, a strong PD genetic risk factor, alters neuronal vulnerability to modifiers of

cellular Mn status, particularly at the level of mitochondrial dysfunction and oxidative stress. Our studies are designed to (1) shed novel mechanistic insight into metal-induced neurodegeneration; (2) identify targets for genetic or pharmacologic modulation of neurodegenerative disorders; (3) increase knowledge of the pathway involved in oxidative stress; (4) develop improved research models for human disease using knowledge of environmental sciences.