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Wojciech Kulczycki,Benjamin Pfister,Joerg Koenigstorfer 글로벌지식마케팅경영학회 2020 Journal of Global Sport Management Vol.5 No.4
The purpose of this study was to assess the influence of partnership for corporate social responsibility (CSR) in the context of the sponsorship of the 2014 men’s FIFA (F ed eration Internationale de Football Association) World Cup on host city residents’ evaluations of sponsors. One hundred sixty Rio de Janeiro residents participated in the experiment. The results showed that partnerships with FIFA or the Brazilian government, which are both accused of mismanagement and corruption, worsened attitudes toward the sponsor compared to a CSR engagement without a partnership. Thus, adverse effects when partnering for CSR were found. Furthermore, the linkage to FIFA made the sponsor more dependent on the host city residents’ overall evaluation of the sports federation. The dependency on FIFA can be good or bad for sponsor brands: attitude to the sponsor and, hence, behavioral intentions to engage with the sponsor increase (decrease) with better (worse) attitude toward the sports federation.
Mount, Matthew P.,Zhang, Yi,Amini, Mandana,Callaghan, Steve,Kulczycki, Jerzy,Mao, Zixu,Slack, Ruth S.,Anisman, Hymie,Park, David S. American Society for Biochemistry and Molecular Bi 2013 The Journal of biological chemistry Vol.288 No.20
<P>We have earlier reported the critical nature of calpain-CDK5-MEF2 signaling in governing dopaminergic neuronal loss <I>in vivo</I>. CDK5 mediates phosphorylation of the neuronal survival factor myocyte enhancer factor 2 (MEF2) leading to its inactivation and loss. However, the downstream factors that mediate MEF2-regulated survival are unknown. Presently, we define <I>Nur77</I> as one such critical downstream survival effector. Following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment <I>in vivo</I>, <I>Nur77</I> expression in the nigrostriatal region is dramatically reduced. This loss is attenuated by expression of MEF2. Importantly, MEF2 constitutively binds to the <I>Nur77</I> promoter in neurons under basal conditions. This binding is lost following 1-methyl-4-phenylpyridinium treatment. <I>Nur77</I> deficiency results in significant sensitization to dopaminergic loss following 1-methyl-4-phenylpyridinium/MPTP treatment, <I>in vitro</I> and <I>in vivo</I>. Furthermore, <I>Nur77</I>-deficient MPTP-treated mice displayed significantly reduced levels of dopamine and 3,4-Dihydroxyphenylacetic acid in the striatum as well as elevated post synaptic FosB activity, indicative of increased nigrostriatal damage when compared with WT MPTP-treated controls. Importantly, this sensitization in <I>Nur77</I>-deficient mice was rescued with ectopic <I>Nur77</I> expression in the nigrostriatal system. These results indicate that the inactivation of <I>Nur77</I>, induced by loss of MEF2 activity, plays a critical role in nigrostriatal degeneration <I>in vivo</I>.</P>