2,453 research outputs found
Is Mercosur an optimum currency area?
We find that generalized purchasing power parity does not hold for Mercosur, and thus that the South American trade group does not constitute an optimum currency area. We also find that the role of the United States cannot be neglected in the region, and that high short run volatility of real exchange rates is accompanied by slow adjustment processes of between 2 and 16 years (PPP puzzle).generalized purchasing power parity; optimum currency area; Mercosur; PPP puzzle
Is Mercosur an optimum currency area? An assessment using generalized purchasing power parity
We consider the cointegration approach of generalized purchasing power parity to show that a necessary condition for Mercosur to be an optimum currency area is met. Yet there are still large cross-country differences as to cast doubt on the success of either monetary union or official dollarization. The PPP puzzle is also found to occur in Mercosur.
Some Jazz : Fox-Trot
Illustration of men and their shadows playing the saxophone.https://scholarsjunction.msstate.edu/cht-sheet-music/5062/thumbnail.jp
Caracterização morfológica de isolados de rizóbio em feijoeiro (Phaseolus vulgaris L.), no Estado de Santa Catarina.
Line-symmetric motion generators
When a rigid body is axially reflected through a moving line, its image undergoes a so-called line-symmetricmotion. The space comprising all possible line-symmetric motions that share a common initial line is a four-dimensional submanifold, denoted M4, in the special Euclidean group SE(3). Recently, we showed that M4 may be used to characterize motions of a line-symmetric body that are free of self-spin and sliding, thus lending itself to applications such as remote center of motion devices for minimal invasive surgery and haptic interfaces. Aiming at designing robot mechanisms for these applications, we present in this paper a systematic enumeration of line-symmetric motion generators (LSMGs), i.e., robot mechanisms that generate the line-symmetric motion manifold M4, following a procedure based on symmetric space theory. LSMGs present a ubiquitous line symmetry of their joint axes, thus offering a new understanding of the line-symmetric motions
The Neural Correlates of Problem States: Testing fMRI Predictions of a Computational Model of Multitasking
Background: It has been shown that people can only maintain one problem state, or intermediate mental representation, at a time. When more than one problem state is required, for example in multitasking, performance decreases considerably. This effect has been explained in terms of a problem state bottleneck. Methodology: In the current study we use the complimentary methodologies of computational cognitive modeling and neuroimaging to investigate the neural correlates of this problem state bottleneck. In particular, an existing computational cognitive model was used to generate a priori fMRI predictions for a multitasking experiment in which the problem state bottleneck plays a major role. Hemodynamic responses were predicted for five brain regions, corresponding to five cognitive resources in the model. Most importantly, we predicted the intraparietal sulcus to show a strong effect of the problem state manipulations. Conclusions: Some of the predictions were confirmed by a subsequent fMRI experiment, while others were not matched by the data. The experiment supported the hypothesis that the problem state bottleneck is a plausible cause of th
Is Mercosur an optimum currency area?
We find that generalized purchasing power parity does not hold for Mercosur, and thus that the South American trade group does not constitute an optimum currency area. We also find that the role of the United States cannot be neglected in the region, and that high short run volatility of real exchange rates is accompanied by slow adjustment processes of between 2 and 16 years (PPP puzzle)
Endocrine Disrupting Contaminants—Beyond the Dogma
Descriptions of endocrine disruption have largely been associated with wildlife and driven by observations documenting estrogenic, androgenic, antiandrogenic, and antithyroid actions. These actions, in response to exposure to ecologically relevant concentrations of various environmental contaminants, have now been established in numerous vertebrate species. However, many potential mechanisms and endocrine actions have not been studied. For example, the DDT [1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane] metabolite, p,p′-DDE [1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene] is known to disrupt prostaglandin synthesis in the uterus of birds, providing part of the explanation for DDT-induced egg shell thinning. Few studies have examined prostaglandin synthesis as a target for endocrine disruption, yet these hormones are active in reproduction, immune responses, and cardiovascular physiology. Future studies must broaden the basic science approach to endocrine disruption, thereby expanding the mechanisms and endocrine end points examined. This goal should be accomplished even if the primary influence and funding continue to emphasize a narrower approach based on regulatory needs. Without this broader approach, research into endocrine disruption will become dominated by a narrow dogma, focusing on a few end points and mechanisms
Nonclassic lipoid congenital adrenal hyperplasia masquerading as familial glucocorticoid deficiency
Context: Familial glucocorticoid deficiency (FGD) is an autosomal recessive disorder resulting from resistance to the action of ACTH on the adrenal cortex. Affected individuals are deficient in cortisol and, if untreated, are likely to succumb to hypoglycemia and/or overwhelming infection. Mutations of the ACTH receptor (MC2R) and the melanocortin 2 receptor accessory protein (MRAP), FGD types 1 and 2 respectively, account for approximately 45% of cases.
Objective: A locus on chromosome 8 has previously been linked to the disease in three families, but no underlying gene defect has to date been identified.
Design: The study design comprised single-nucleotide polymorphism genotyping and mutation detection.
Setting: The study was conducted at secondary and tertiary referral centers.
Patients: Eighty probands from families referred for investigation of the genetic cause of FGD participated in the study.
Interventions: There were no interventions.
Results: Analysis by single-nucleotide polymorphism array of the genotype of one individual with FGD previously linked to chromosome 8 revealed a large region of homozygosity encompassing the steroidogenic acute regulatory protein gene, STAR. We identified homozygous STAR mutations in this patient and his affected siblings. Screening of our total FGD patient cohort revealed homozygous STAR mutations in a further nine individuals from four other families.
Conclusions: Mutations in STAR usually cause lipoid congenital adrenal hyperplasia, a disorder characterized by both gonadal and adrenal steroid deficiency. Our results demonstrate that certain mutations in STAR (R192C and the previously reported R188C) can present with a phenotype indistinguishable from that seen in FGD
PACSIN2 as a modulator of autophagy and mercaptopurine cytotoxicity: mechanisms in lymphoid and intestinal cells
PACSIN2 variants are associated with gastrointestinal effects of thiopurines and thiopurine methyltransferase activity through an uncharacterized mechanism that is postulated to involve auto-phagy. This study aims to clarify the role of PACSIN2 in autophagy and in thiopurine cytotoxicity in leukemic and intestinal models. Higher autophagy and lower PACSIN2 levels were observed in inflamed compared with non-inflamed colon biopsies of in-flammatory bowel disease pediatric patients at diagnosis. PAC-SIN2 was identified as an inhibitor of autophagy, putatively through inhibition of autophagosome formation by a protein- protein interaction with LC3-II, mediated by a LIR motif. Moreover, PACSIN2 resulted a modulator of mercaptopurine-induced cyto-toxicity in intestinal cells, suggesting that PACSIN2-regulated autophagy levels might influence thiopurine sensitivity. However, PACSIN2 modulates cellular thiopurine methyltransferase activity via mechanisms distinct from its modulation of autophagy
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