Chile's Free Trade Deals with the EU and the US: A Big Deal?

Chile put into place broad free trade agreements (FTAs) with its two major trading partners: the EU (effective 2003) and the US (effective 2004). This paper quanti- fies their economic effects for the Chilean economy, stemming from the conventional trade components (lower tariffs and higher market access) and other aspects of the lat- ter broad FTAs, including improved intellectual property rights, factor productivity gains, and their fiscal consequences. The paper also considers that the country risk premium may decline and aggregate investment may rise in response to the institutional stability and policy credibility enhanced by the FTAs. Simulation results are reported for steady states and dynamic transition paths, based on a three-sector dynamic general equilibrium model for an open economy inhabited by infinitely-lived representative agents. The model is calibrated to the Chilean economy and the actual features of both trade agreements. The reported effects of FTAs on resource allocations, relative prices, expenditure composition, output, and welfare are generally small due to Chile's high initial trade openness; aggregate output and consumption do not exceed 1% in any given period. On impact, the largest gains come from a lower risk premium that leads to a tem- porary consumption and investment boom, which is reverted in the long run as a result of larger net foreign liabilities. In steady state, the gains from improved factor productivity dominate all other effectsChile, Free Trade Agreements

Spinal cord stimulation alleviates motor deficits in a primate model of Parkinson disease.

Although deep brain electrical stimulation can alleviate the motor symptoms of Parkinson disease (PD), just a small fraction of patients with PD can take advantage of this procedure due to its invasive nature. A significantly less invasive method-epidural spinal cord stimulation (SCS)-has been suggested as an alternative approach for symptomatic treatment of PD. However, the mechanisms underlying motor improvements through SCS are unknown. Here, we show that SCS reproducibly alleviates motor deficits in a primate model of PD. Simultaneous neuronal recordings from multiple structures of the cortico-basal ganglia-thalamic loop in parkinsonian monkeys revealed abnormal highly synchronized neuronal activity within each of these structures and excessive functional coupling among them. SCS disrupted this pathological circuit behavior in a manner that mimics the effects caused by pharmacological dopamine replacement therapy or deep brain stimulation. These results suggest that SCS should be considered as an additional treatment option for patients with PD

Restoration of locomotive function in Parkinson's disease by spinal cord stimulation: mechanistic approach

Specific motor symptoms of Parkinson's disease (PD) can be treated effectively with direct electrical stimulation of deep nuclei in the brain. However, this is an invasive procedure, and the fraction of eligible patients is rather low according to currently used criteria. Spinal cord stimulation (SCS), a minimally invasive method, has more recently been proposed as a therapeutic approach to alleviate PD akinesia, in light of its proven ability to rescue locomotion in rodent models of PD. The mechanisms accounting for this effect are unknown but, from accumulated experience with the use of SCS in the management of chronic pain, it is known that the pathways most probably activated by SCS are the superficial fibers of the dorsal columns. We suggest that the prokinetic effect of SCS results from direct activation of ascending pathways reaching thalamic nuclei and the cerebral cortex. The afferent stimulation may, in addition, activate brainstem nuclei, contributing to the initiation of locomotion. On the basis of the striking change in the corticostriatal oscillatory mode of neuronal activity induced by SCS, we propose that, through activation of lemniscal and brainstem pathways, the locomotive increase is achieved by disruption of antikinetic low-frequency (< 30 Hz) oscillatory synchronization in the corticobasal ganglia circuits

Spinal cord stimulation improves forelimb use in an alpha-synuclein animal model of Parkinson’s disease

Copyright © 2016 Informa UK Limited, trading as Taylor & Francis Group.Neuromodulation by spinal cord stimulation has been proposed as a symptomatic treatment for Parkinson’s disease. We tested the chronic effects of spinal cord stimulation in a progressive model of Parkinson’s based on overexpression of alpha-synuclein in the substantia nigra. Adult Sprague Dawley rats received unilateral injections of adeno-associated virus serotype 6 (AAV6) in the substantia nigra to express alpha-synuclein. Locomotion and forepaw use of the rats were evaluated during the next 10 weeks. Starting on week 6, a group of AAV6-injected rats received spinal cord stimulation once a week. At the end of the experiment, tyrosine hydroxylase and alpha-synuclein immunostaining were performed. Rats with unilateral alpha-synuclein expression showed a significant decrease in the use of the contralateral forepaw, which was mildly but significantly reverted by spinal cord stimulation applied once a week from the 6t

Chronic in vivo multi-circuit neurophysiological recordings in mice.

a b s t r a c t While genetically modified mice have become a widely accepted tool for modeling the influence of gene function on the manifestation of neurological and psychiatric endophenotypes, only modest headway has been made in characterizing the functional circuit changes that underlie the disruption of complex behavioral processes in various models. This challenge partially arises from the fact that even simple behaviors require the coordination of many neural circuits vastly distributed across multiple brain areas. As such, many independent neurophysiological alterations are likely to yield overlapping circuit disruptions and ultimately lead to the manifestation of similar behavioral deficits. Here we describe the expansion of our neurophysiological recording approach in an effort to quantify neurophysiological activity across many large scale brain circuits simultaneously in freely behaving genetically modified mice. Using this expanded approach we were able to isolate up to 70 single neurons and record local field potential (LFP) activity simultaneously across 11 brain areas. Moreover, we found that these neurophysiological signals remained viable up to 16 months after implantation. Thus, our approach provides a powerful tool that will aid in dissecting the central brain network changes that underlie the complex behavioral deficits displayed by various genetically modified mice