107 research outputs found

    Los efectos sociales de la política del F. M. I. en la República Dominicana

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    José Serulle Ramia (biografía): Es doctor en economía de la Universidad de París. Ha sido profesor de Economía en la Universidad Autónoma de Santo Domingo, de la cual llegó a ser vicerrector administrativo. Para noviembre de 2016 era embajador de la República Dominicana en Trinidad y Tobago.Serulle Ramia analiza los efectos sociales negativos que tuvo la política de austeridad impuesta al país por el FMI durante la que habría de ser llamada "década perdida de América Latina". El conjunto de medidas tendentes a equilibrar el gasto con los ingresos nacionales a partir de la reducción del gasto público corriente, la inversión pública y el consumo privado empezó a aplicarse en agosto de 1982. Se estructuró a través del Acuerdo de Facilidad Ampliada (enero de 1983), el Acuerdo Puente o Sombra (1984) y el Acuerdo Stand By (1985), pero continuó desarrollándose bajo la iniciativa y el mandato del Dr. Joaquín Balaguer. Aparte de la disminución del gasto público, sus otros componentes consistieron en la restricción del crédito, el aumento de los impuestos indirectos (ITBI, Ad-valorem), la liberalización del mercado de divisas y el impulso a los esquemas productivos orientados a la exportación. A juicio del autor, sus efectos más perniciosos fueron: 1) La disminución de la producción y el decrecimiento de la economía, de modo que sectores como el agrícola llegaron a alcanzar, para 1986, una tasa de crecimiento de -3.1%. 2) La agudización de la crisis en el campo, que en ese entonces aglutinaba el 48% de la población y que se vio afectado por un aumento de la concentración del capital y de la producción en detrimento de los pequeños productores campesinos. 3) El incremento del desempleo, que llegó a alcanzar un 28% de la población económicamente activa. 4) La disminución del salario real de los trabajadores, algo que se ejemplifica con el salario mínimo real, que de 1979 a 1987 disminuyó un 44.6%. 5) La reducción de la inversión en los fundamentales servicios públicos, que se vieron afectados en cuanto a su capacidad de cobertura y calidad: solo el sector educativo registró una reducción del 16.5% en su presupuesto entre 1980 y 1985

    TRANSPORTATION RESILIENCE ARCHITECTURE: A FREMEWORK FOR ANALYSIS OF INFRASTRUCTURE, AGENCY AND USERS

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    How do some countries, or sectors of it, overcome potentially disastrous events while others fail at it? The answer lies on the concept of resilience, and its importance grows as our environment’s deterioration escalates, limiting the access to economic, social, and natural resources. This study evaluates resilience from a transportation perspective and defines it as “the ability for the system to maintain its demonstrated level of service or to restore itself to that level of service in a specified timeframe” (Heaslip, Louisell, & Collura, 2009). The literature shows that previous evaluation approaches usually do not directly integrate all perspectives of a transportation system. In this manner, this study introduces the concept of Transportation Resilience Architecture (TRA) as a framework for evaluating resilience of a transportation system through the cumulative effect of a system’s Infrastructure, Agency and User layer. This research introduces three quantitative methodologies as a way to evaluate resilience through TRA. For Infrastructure, a practical tool for measuring the level of accessibility to “safe zones” is presented, which takes advantage of the logsum measure resulting from Statewide Transportation Models. Results from the two locations analyzed (Frederick, MD and Anacostia, D.C.) suggest a positive correlation between income and accessibility. For Agency, metrics collected through a thorough literature review where combined with survey data to develop an evaluation framework based on Fuzzy Algorithms that yields to an index. The end product highlights the importance of interoperability as a disaster preparedness and response enhancing practice. Finally, for User, a dynamic discrete choice model was adapted to evaluate evacuation behavior, taking into account the disaster’s characteristics and the population’s expectations of them—a first from an evacuation perspective. The proposed framework is estimated using SP evacuation data collected on Louisiana residents. The result indicates that the dynamic discrete choice model excels in incorporating demographic information of respondents, a key input in policy evaluation, and yields significantly more accurate evacuation percentages per forecast

    Quantifying the Increase in Radiation Exposure Associated with SPECT/CT Compared to SPECT Alone for Routine Nuclear Medicine Examinations

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    Purpose. We quantify the additional radiation exposure in terms of effective dose incurred by patients in the CT portion of SPECT/CT examinations. Methods. The effective dose from a variety of common nuclear medicine procedures is calculated and summarized. The extra exposure from the CT portion of the examination is summarized by examination and body part. Two hundred forty-eight scans from 221 patients are included in this study. The effective dose from the CT examination is also compared to average background radiation. Results. We found that the extra effective dose is not sufficient to cause deterministic effects. However, the stochastic effects may be significant, especially in patients undergoing numerous follow-up studies. The cumulative effect might increase the radiation exposure compared to patient management with SPECT alone. Conclusions. While the relative increase in radiation exposure associated with SPECT/CT is generally considered acceptable when compared with the benefits to the patient, physicians should make every effort to minimize this effect by using proper technical procedures and educating patients about the exposure they will receive

    A role for cGMP-dependent protein kinase II in AMPA receptor trafficking and synaptic plasticity

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    Background: Trafficking of AMPA receptors (AMPARs) underlies the activity-dependent modification of synaptic strength and is regulated by specific interactions of AMPAR subunits with other proteins. We have reported (Serulle et al., 2007) 1 that the AMPAR subunit GluR1 binds the cGMP-dependent kinase type II (cGKII) adjacent to the kinase catalytic site, and that this interaction is increased by cGMP. In this complex, cGKII phosphorylates GluR1 at serine 845 (S845) leading to an increase of GluR1 on the plasma membrane. In neurons, cGMP is produced by soluble guanylate cyclase (sGC), which is activated by nitric oxide (NO), which is produced by nNOS under the control of the NMDA receptor. Results: To distinguish the mechanism, we have measured the rate of exogenous GluR1 endocytosis in cultured primary neurons, either the wild type or the S845A or S845D mutants (Figure 1). We find that the S845A mutant (which cannot be phosphorylated) is endocytosed at rate of the wild type, while S845D (phosphomimetic) is endocytosed at a lower rate. Also, cGMP treatment, which elevates the endogenous GluR1 plasma membrane levels (Figure 2A), reduced the rate of of GluR1 endocytosis (Figure 2B). Figure 1 Endocytosis of HAGluR1 is time dependent and is inhibited by the phosphomimetic mutation, S845D Endocytosis of HAGluR1 is time dependent and is inhibited by the phosphomimetic mutation, S845D. Figure 2 Elevation of surface GluR1 and reduction of GluR1 endocytosis by cGMP Elevation of surface GluR1 and reduction of GluR1 endocytosis by cGMP. A. cGMP, elevates surface GluR1. B. cGMP decreases endocytosis of GluR1. Conclusion: These data suggest that S845 phosphorylation increases the plasma membrane levels of GluR1 by reducing the rate of endocytosis

    Fusiform superior cerebellar artery aneurysm treated with flow diversion: A case report

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    © 2020 Published by Scientific Scholar on behalf of Surgical Neurology International. Background: Fusiform aneurysms of the distal superior cerebellar artery are rare and challenging to treat. Due to the rarity of these lesions, there is little consensus regarding their management. Treatment options have traditionally included parent artery sacrifice with either an endovascular approach or microsurgical clipping. Given the small diameter of the superior cerebellar artery, flow diversion has not been typically considered as a viable treatment option for these aneurysms. Case Description: A 67-year-old female presented complaining of severe sudden onset headache. Noncontrast head CT demonstrated no intracranial hemorrhage. Head CT angiogram demonstrated a 4.2 mm fusiform aneurysm in the distal right superior cerebellar artery. The patient underwent treatment with the Pipeline embolization device which was deployed in the right superior cerebellar artery covering the aneurysm. Six-month posttreatment follow-up angiogram demonstrated resolution of the aneurysm with patency of the parent vessel. Conclusion: To the best of our knowledge, this is the first report of a distal superior cerebellar artery aneurysm treated with the Pipeline embolization device. The use of a Pipeline stent to create flow diversion should be considered in a case of a fusiform aneurysm of the right superior cerebellar artery. Treatment with flow diversion may allow for the treatment of the aneurysm while preserving patency of the parent vessel

    Dopamine D1 receptor-mediated enhancement of NMDA receptor trafficking requires rapid PKC-dependent synaptic insertion in the prefrontal neurons

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    Understanding the interaction between dopamine and glutamate, particularly the interaction of dopamine and NMDA receptors, may enable a more rational approach to the treatment of schizophrenia, drug addiction, and other psychiatric disorders. We show that, in prefrontal cortical neurons, dopamine D1-induced enhancement of NMDA receptor function depends on rapid insertion of new NMDA receptor 2B subunits on the synaptic surface. Protein kinase A (PKA) inhibitor, but not protein kinase C (PKC) inhibitor, completely blocked dopamine D1 agonist SKF-81297-induced increase of the total expression of NMDA receptors. Furthermore, SKF-81297 failed to alter the surface expression and synaptic insertion of NMDA receptors in the presence of PKA inhibitor, phospholipase C inhibitor, PKC inhibitor, or Src family kinase inhibitor. Our data suggest that D1-mediated enhancement of NMDA current depends on the NMDA receptor trafficking through rapid synaptic insertion and both PKA and PKC signaling pathways play important roles in the regulatory process. Although both PKA and PKC mediate the D1-induced enhancement of NMDA receptors, the phospholipase C-PKC-Src pathway is only required for surface expression and new synaptic insertion of NMDA receptors

    The cGMP-Dependent Protein Kinase II Is an Inhibitory Modulator of the Hyperpolarization-Activated HCN2 Channel

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    Opening of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels is facilitated by direct binding of cyclic nucleotides to a cyclic nucleotide-binding domain (CNBD) in the C-terminus. Here, we show for the first time that in the HCN2 channel cGMP can also exert an inhibitory effect on gating via cGMP-dependent protein kinase II (cGKII)-mediated phosphorylation. Using coimmunoprecipitation and immunohistochemistry we demonstrate that cGKII and HCN2 interact and colocalize with each other upon heterologous expression as well as in native mouse brain. We identify the proximal C-terminus of HCN2 as binding region of cGKII and show that cGKII phosphorylates HCN2 at a specific serine residue (S641) in the C-terminal end of the CNBD. The cGKII shifts the voltage-dependence of HCN2 activation to 2–5 mV more negative voltages and, hence, counteracts the stimulatory effect of cGMP on gating. The inhibitory cGMP effect can be either abolished by mutation of the phosphorylation site in HCN2 or by impairing the catalytic domain of cGKII. By contrast, the inhibitory effect is preserved in a HCN2 mutant carrying a CNBD deficient for cGMP binding. Our data suggest that bidirectional regulation of HCN2 gating by cGMP contributes to cellular fine-tuning of HCN channel activity

    The Nitric Oxide-Cyclic GMP Pathway Regulates FoxO and Alters Dopaminergic Neuron Survival in Drosophila

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    Activation of the forkhead box transcription factor FoxO is suggested to be involved in dopaminergic (DA) neurodegeneration in a Drosophila model of Parkinson's disease (PD), in which a PD gene product LRRK2 activates FoxO through phosphorylation. In the current study that combines Drosophila genetics and biochemical analysis, we show that cyclic guanosine monophosphate (cGMP)-dependent kinase II (cGKII) also phosphorylates FoxO at the same residue as LRRK2, and Drosophila orthologues of cGKII and LRRK2, DG2/For and dLRRK, respectively, enhance the neurotoxic activity of FoxO in an additive manner. Biochemical assays using mammalian cGKII and FoxO1 reveal that cGKII enhances the transcriptional activity of FoxO1 through phosphorylation of the FoxO1 S319 site in the same manner as LRRK2. A Drosophila FoxO mutant resistant to phosphorylation by DG2 and dLRRK (dFoxO S259A corresponding to human FoxO1 S319A) suppressed the neurotoxicity and improved motor dysfunction caused by co-expression of FoxO and DG2. Nitric oxide synthase (NOS) and soluble guanylyl cyclase (sGC) also increased FoxO's activity, whereas the administration of a NOS inhibitor L-NAME suppressed the loss of DA neurons in aged flies co-expressing FoxO and DG2. These results strongly suggest that the NO-FoxO axis contributes to DA neurodegeneration in LRRK2-linked PD
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