19 research outputs found

    Not your father's pension plan: the rise of 401K and other defined contribution plans

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    The number of workers with a 401(k) plan grew from 7.1 million in 1983 to 38.9 million by 1993. The rapid diffusion of 401(k) and other portable defined contribution plans and the decline in defined benefit pensions represent a major change in pension structure. Old-style defined benefit pensions were designed to give a fixed income after retirement, but only for workers who stayed in a job for 20 or 30 years; workers who left early ended up with little or nothing. Resulting changes in portability, access to pension wealth, and riskiness are altering incentives for job tenure and worker mobility, retirement, and saving both before and after retirement.Pensions ; Retirement

    D2R signaling in striatal spiny neurons modulates L-DOPA induced dyskinesia

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    Degeneration of dopaminergic neurons leads to Parkinson's disease (PD), characterized by reduced levels of striatal dopamine (DA) and impaired voluntary movements. DA replacement is achieved by levodopa treatment which in long-term causes involuntary movements or dyskinesia. Dyskinesia is linked to the pulsatile activation of D1 receptors of the striatal medium spiny neurons (MSNs) forming the direct output pathway (dMSNs). The contribution of DA stimulation of D2R in MSNs of the indirect pathway (iMSNs) is less clear. Using the 6-hydroxydopamine model of PD, here we show that loss of DA-mediated inhibition of these neurons intensifies levodopa-induced dyskinesia (LID) leading to reprogramming of striatal gene expression. We propose that the motor impairments characteristic of PD and of its therapy are critically dependent on D2R-mediated iMSNs activity. D2R signaling not only filters inputs to the striatum but also indirectly regulates dMSNs mediated responses

    D2R signaling in striatal spiny neurons modulates L-DOPA induced dyskinesia

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    Degeneration of dopaminergic neurons leads to Parkinson's disease (PD), characterized by reduced levels of striatal dopamine (DA) and impaired voluntary movements. DA replacement is achieved by levodopa treatment which in long-term causes involuntary movements or dyskinesia. Dyskinesia is linked to the pulsatile activation of D1 receptors of the striatal medium spiny neurons (MSNs) forming the direct output pathway (dMSNs). The contribution of DA stimulation of D2R in MSNs of the indirect pathway (iMSNs) is less clear. Using the 6-hydroxydopamine model of PD, here we show that loss of DA-mediated inhibition of these neurons intensifies levodopa-induced dyskinesia (LID) leading to reprogramming of striatal gene expression. We propose that the motor impairments characteristic of PD and of its therapy are critically dependent on D2R-mediated iMSNs activity. D2R signaling not only filters inputs to the striatum but also indirectly regulates dMSNs mediated responses

    Heteroleptic Nickel Complexes for the Markovnikov-Selective Hydroboration of Styrenes

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    First-row transition metal catalysis offers a cheaper, more environmentally sustainable alternative to second- and third-row transition metal catalysts. Nickel has shown great promise as a tool for the borylation of unsaturated compounds to yield boronic esters, but Markovnikov-selective hydroborations of simple styrenes have not been well-explored. Herein, we report the synthesis of benzyl boronic esters via nickel-catalyzed hydroboration of styrenes using a heteroleptic N-heterocyclic carbene (NHC)–phosphine nickel complex, IMes­(Cy<sub>3</sub>P)­NiCl<sub>2</sub>. The IMes­(Cy<sub>3</sub>P)­NiCl<sub>2</sub> complex displays a broad substrate scope and maintains the integrity of yield and regioselectivity when challenged with substrates bearing increased steric hindrance. The heteroleptic complexes also tolerate both electron-withdrawing and -donating groups, in contrast to traditional bis-phosphine and Ni(0) complexes
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