26 research outputs found

    The Grizzly, April 11, 1986

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    Collegeville Water: Poison • Toombs Speaks on Real Estate • The Time has Come • Wismer, be Realistic! • Letter: Administration Housing Plans are Unfair • Former U.C. Graduate Plays Important Role in Recovery of Challenger Debris • Hair Sneak Preview • Take C and C and See the Progress of Humanity • Greeks Flail Booze Curtail • Looking for Alternatives to the Joys of Alcohol • Women\u27s Lacrosse Wins Five in a Row • Linksters Off to a Great Start • Bears Drop to 4-8 • Women\u27s Track • Profile: Marc Dervishian • Women\u27s Softball Season Heats Up • Women\u27s Tennis Falls to 1-4 • Profile: Leigh Garrison • Gung Ho for Howard • Music: It gets the Irish in me Goinghttps://digitalcommons.ursinus.edu/grizzlynews/1163/thumbnail.jp

    Pass a Law, Any Law, Fast! State Legislative Responses to the Kelo Backlash

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    The Supreme Court in Kelo v. City of New London left protection of property against takings for economic development to the states. Since Kelo, thirty-seven states have enacted legislation to update their eminent domain laws. This paper is the first to theoretically and empirically analyze the factors that influence whether, in what manner, and how quickly states change their laws through new legislation. Fourteen of the thirty-seven new laws offer only weak protections against development takings. The legislative response to Kelo was responsive to measures of the backlash but only in the binary decision whether to pass any new law. The decision to enact a meaningful restriction was more a function of relevant political economy measures. States with more economic freedom, greater value of new housing construction, and less racial and income inequality are more likely to have enacted stronger restrictions, and sooner. Of the thirteen states that have not updated, Arkansas, Oklahoma and Mississippi are highly likely to do so in the future. Hawaii, Massachusetts and New York are unlikely to update ever if at all

    Neurotoxin-induced degeneration of dopamine neurons in Caenorhabditis elegans

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    Parkinson's disease is a complex neurodegenerative disorder characterized by the death of brain dopamine neurons. In mammals, dopamine neuronal degeneration can be triggered through exposure to neurotoxins accumulated by the presynaptic dopamine transporter (DAT), including 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridinium. We have established a system for the pharmacological and genetic evaluation of neurotoxin-induced dopamine neuronal death in Caenorhabditis elegans. Brief (1 h) exposure of green fluorescent protein-tagged, living worms to 6-OHDA causes selective degeneration of dopamine neurons. We demonstrate that agents that interfere with DAT function protect against 6-OHDA toxicity. 6-OHDA-triggered neural degeneration does not require the CED-3/CED-4 cell death pathway, but is abolished by the genetic disruption of the C. elegans DAT

    Next-generation sequencing of AAV.CAP-Mac from Chuapoco et al. (2023) Nature Nanotechnology

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    Dataset of next-generation sequencing of enrichment of AAV.CAP-Mac in various tissues from the publication: Chuapoco, M.R., Flytzanis, N.C., Goeden, N. et al. Adeno-associated viral vectors for functional intravenous gene transfer throughout the non-human primate brain. Nat. Nanotechnol. (2023). https://doi.org/10.1038/s41565-023-01419-xThis work was funded by grants from the National Institutes of Health (NIH): NIH Pioneer DP1NS111369 (to V.G.); P51OD011107 (to the California National Primate Research Center), R01HD091325 (to L.T.); U19NS123719 (to L.T.); UG3MH120095 (to J.T.T. and B.P.L.); P51OD010425 (to the Washington National Primate Research Center); U42OD011123 (to the Washington National Primate Research Center); BRAIN Armamentarium UF1MH128336 (to V.G., T.F.S., L.T. and A.S.F.), and in part by Aligning Science Across Parkinson's (ASAP-020495 to V.G., A.S.F. and L.T.) through the Michael J. Fox Foundation for Parkinson's Research (MJFF)
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