101 research outputs found

    When Statutory Regimes Collide:Will Wisconsin Right to Life and Citizens United Invalidate Federal Tax Regulation of Campaign Activity?

    Get PDF
    In Federal Election Commission v. Wisconsin Right to Life (2007) and Citizens United v. Federal Elections Commission (2010), the United States Supreme Court dramatically reduced the ability of Congress to regulate campaign finance activities of corporations and others active in elections. Many of the same activities are still subject to restrictions by the Internal Revenue Code, which regulates the type and amount of political campaign activities that certain nonprofits exempt under federal tax law can engage in. In the wake of the campaign finance decisions, the constitutionality of the tax law’s restrictions on campaign activity is now being challenged in the lower courts. This Article analyzes the two recent campaign finance decisions and campaign finance precedents more broadly to determine how, if at all, the Roberts’ Court’s campaign finance jurisprudence is likely to alter existing tax law jurisprudence in the area of campaign activity. It finds that, for the most part, tax law constitutional doctrines have developed independently of other areas of First Amendment free speech law. Based upon an analysis of the distinctive tax law doctrines, the Article concludes that the tax law provision prohibiting section 501(c)(3) charities from engaging in campaigns is likely to withstand challenges arguing that the provision prevents these nonprofits from engaging in protected political speech. However, there is some likelihood that the tax law prohibition is vulnerable to constitutional attack under traditional doctrines of vagueness or overbreadth due to the lack of precision of the terms of the political prohibition, as these have been elaborated by the IRS and the courts to date

    Neurocalcin Delta Suppression Protects against Spinal Muscular Atrophy in Humans and across Species by Restoring Impaired Endocytosis

    Get PDF
    This document is the Accepted Manuscript version of the following article: Riessland et al., 'Neurocalcin Delta Suppression Protects against Spinal Muscular Atrophy in Humans and across Species by Restoring Impaired Endocytosis', The American Journal of Human Genetics, Vol. 100 (2): 297-315, first published online 26 January 2017. The final, published version is available online at doi: http://dx.doi.org/10.1016/j.ajhg.2017.01.005 © 2017 American Society of Human Genetics.Homozygous SMN1 loss causes spinal muscular atrophy (SMA), the most common lethal genetic childhood motor neuron disease. SMN1 encodes SMN, a ubiquitous housekeeping protein, which makes the primarily motor neuron-specific phenotype rather unexpected. SMA-affected individuals harbor low SMN expression from one to six SMN2 copies, which is insufficient to functionally compensate for SMN1 loss. However, rarely individuals with homozygous absence of SMN1 and only three to four SMN2 copies are fully asymptomatic, suggesting protection through genetic modifier(s). Previously, we identified plastin 3 (PLS3) overexpression as an SMA protective modifier in humans and showed that SMN deficit impairs endocytosis, which is rescued by elevated PLS3 levels. Here, we identify reduction of the neuronal calcium sensor Neurocalcin delta (NCALD) as a protective SMA modifier in five asymptomatic SMN1-deleted individuals carrying only four SMN2 copies. We demonstrate that NCALD is a Ca(2+)-dependent negative regulator of endocytosis, as NCALD knockdown improves endocytosis in SMA models and ameliorates pharmacologically induced endocytosis defects in zebrafish. Importantly, NCALD knockdown effectively ameliorates SMA-associated pathological defects across species, including worm, zebrafish, and mouse. In conclusion, our study identifies a previously unknown protective SMA modifier in humans, demonstrates modifier impact in three different SMA animal models, and suggests a potential combinatorial therapeutic strategy to efficiently treat SMA. Since both protective modifiers restore endocytosis, our results confirm that endocytosis is a major cellular mechanism perturbed in SMA and emphasize the power of protective modifiers for understanding disease mechanism and developing therapies.Peer reviewedFinal Accepted Versio

    A revision of the descriptions of ectomycorrhizas published since 1961

    Full text link

    The Puzzle of Alfarabi's Parallel Works

    No full text
    • …
    corecore