Formulae relating the Bernstein and Iwahori-Matsumoto presentations of an affine Hecke algebra

We give explicit formulae for certain elements occurring in the Bernstein presentation of an affine Hecke algebra, in terms of the usual Iwahori- Matsumoto generators. We utilize certain minimal expressions for said elements and we give a sheaf-theoretic interpretation for the existence of these minimal expressions.Comment: To appear, J. of Algebr

Global Commodity Markets - Price Volatility and Financialisation

A significant increase in the level and volatility of many commodity prices over the past decade has led to a debate about what has driven these developments. A particular focus has been on the extent to which they have been driven by increased financial investment in commodity derivatives markets. This article examines the factors behind the increase in the level and volatility of commodity prices. The available evidence suggests that while financial investors can affect the short-run price dynamics for some commodities, the level and volatility of commodity prices appear to be primarily determined by fundamental factors.Commodity; Commodities; Commodity prices; Commodity price; volatility; Speculation; Oil prices; Financialisation; Financialization; G-20; G20; CRB; Derivatives

Gastric Adenocarcinoma Presenting as Chronic Back Pain: A Case Report

Introduction: Early stage gastric cancer is usually asymptomatic. It is not until later stages of the disease, usually with metastasis, that patients typically develop symptoms that would prompt further evaluation.Case Report: We present a case of a patient with chronic back pain who was found to have a gastric antral mass as the etiology of her pain. The patient proceeded to have a partial gastrectomy with complete surgical excision of her early-stage gastric cancer, after which her chronic back pain resolved.Conclusion: This case demonstrates the importance of considering significant pathology in patients presenting with chronic complaints to the emergency department

Distinguishing cause from effect - many deficits associated with developmental dyslexia may be a consequence of reduced and suboptimal reading experience

The cause of developmental dyslexia is still unknown despite decades of intense research. Many causal explanations have been proposed, based on the range of impairments displayed by affected individuals. Here we draw attention to the fact that many of these impairments are also shown by illiterate individuals who have not received any or very little reading instruction. We suggest that this fact may not be coincidental and that the performance differences of both illiterates and individuals with dyslexia compared to literate controls are, to a substantial extent, secondary consequences of either reduced or suboptimal reading experience or a combination of both. The search for the primary causes of reading impairments will make progress if the consequences of quantitative and qualitative differences in reading experience are better taken into account and not mistaken for the causes of reading disorders. We close by providing four recommendations for future research

The Medial Prefrontal Cortex To Dorsal Raphe Circuit In The Antidepressant Action Of Ketamine

Major depressive disorder is a common and debilitating illness for which there is a notable lack of efficient, effective treatment. While currently available pharmacotherapies typically take eight weeks to take effect and fail to do so at all for about a third of patients, the N-methyl-D-aspartate (NMDA) receptor antagonist ketamine has shown a much more favorable effectiveness profile, including improvements in symptoms within hours of administration, even for many patients who do not respond to typical antidepressants. Ketamine, as a modulator of glutamate signaling in the brain, has a distinct mechanism of action from the serotonin and norepinephrine modulators that are currently the mainstay of depression treatment. This dissertation seeks to contribute to the understanding of this unique mechanism, and particularly the brain circuits affected. Rodent studies have shown that ketamine induces a burst of glutamatergic activity in the medial prefrontal cortex (mPFC), which is necessary to produce its antidepressant effect. The downstream targets of this glutamatergic activity that are relevant to the ketamine antidepressant effect are unclear, but recent research has suggested a role for the dorsal raphe nucleus (DRN), which contains most of the brain’s serotonin-producing cells. In this thesis, I first provide a synthesis of the literature on the mechanism of ketamine’s antidepressant effect and the neural circuits that might underlie it. I then investigate the projection from the mPFC to the DRN using optogenetic stimulation of mPFC-originating axon terminals in the DRN, finding that activation of this pathway produces an antidepressant effect on the forced-swim test (FST), which measures “behavioral despair” induced by a stressful environment, but not on other measures of depression-like behavior. I also perform immunohistochemical studies of the DRN, which indicate that both serotonergic and non-serotonergic cells are activated by this stimulation. I then find additional support for this behavioral selectivity using a pharmacological approach: by inhibiting serotonin release during ketamine administration, I find that DRN activity is needed for the antidepressant effect of ketamine on the FST but not on other behavioral tests. Finally, I interrogate the projection from the mPFC to the nucleus accumbens using the same optogenetic approach as before. These experiments show that activation of the mPFC-to-DRN pathway produces an antidepressant effect on a particular subset of depression-like behavior and supports a role for serotonin signaling in the behavior measured by the FST

Linkage between increased nociception and olfaction via a SCN9A haplotype

Background and Aims: Mutations reducing the function of Nav1.7 sodium channels entail diminished pain perception and olfactory acuity, suggesting a link between nociception and olfaction at ion channel level. We hypothesized that if such link exists, it should work in both directions and gain-of-function Nav1.7 mutations known to be associated with increased pain perception should also increase olfactory acuity. Methods: SCN9A variants were assessed known to enhance pain perception and found more frequently in the average population. Specifically, carriers of SCN9A variants rs41268673C>A (P610T; n = 14) or rs6746030C>T (R1150W; n = 21) were compared with non-carriers (n = 40). Olfactory function was quantified by assessing odor threshold, odor discrimination and odor identification using an established olfactory test. Nociception was assessed by measuring pain thresholds to experimental nociceptive stimuli (punctate and blunt mechanical pressure, heat and electrical stimuli). Results: The number of carried alleles of the non-mutated SCN9A haplotype rs41268673C/rs6746030C was significantly associated with the comparatively highest olfactory threshold (0 alleles: threshold at phenylethylethanol dilution step 12 of 16 (n = 1), 1 allele: 10.6±2.6 (n = 34), 2 alleles: 9.5±2.1 (n = 40)). The same SCN9A haplotype determined the pain threshold to blunt pressure stimuli (0 alleles: 21.1 N/m2, 1 allele: 29.8±10.4 N/m2, 2 alleles: 33.5±10.2 N/m2). Conclusions: The findings established a working link between nociception and olfaction via Nav1.7 in the gain-of-function direction. Hence, together with the known reduced olfaction and pain in loss-of-function mutations, a bidirectional genetic functional association between nociception and olfaction exists at Nav1.7 level

Mechanistic-empirical equivalent single axle loads for urban pavements

The deregulation of the trucking industry in the mid-1980’s resulted in the growth of commercial vehicles not only in number, but also in weight, size and dimension. As a result, road agencies are finding their road networks being subjected to commercial vehicle load spectra greater than those initially projected. The augmented load spectra, combined with the aged state of many in-service roads, are resulting in the accelerated deterioration of our roadway infrastructure. Although much empirical evidence exists regarding the performance of rural pavements subjected to various types of loading, there is a lack of knowledge regarding the operation of commercial vehicles within the urban environment and their ensuing effects on urban roads. Urban municipalities are therefore beginning to realize the importance of identifying and quantifying the effects of commercial vehicle operations (CVO) on urban road assets, traffic congestion and motorist safety. Due to the limitations of conventional Equivalent Single Axle Loads (ESALs) when applied to urban pavements, this research aimed to investigate commercial vehicle load equivalencies for various classes of urban roadway in the City of Saskatoon. Urban load equivalencies were created by combining a traffic load spectra from a typical freeway in the City of Saskatoon with structural deformation and damage responses measured across several urban roadways. This established a framework for calculating the responses incurred from commercial vehicle loading across different types of urban roads. Based on the results of the mechanistic-empirical urban load equivalency analysis performed in this research, urban ESAL factors (ESALFs) for local-industrial roadways were found to range from 50 percent less than to 250 percent greater than conventional load equivalencies. Urban arterial ESALFs ranged from 20 percent to 260 percent greater than conventional load equivalencies. The primary response-based ESALFs for urban local and collector roadways ranged from 150 to 700 percent greater than conventional load equivalencies. The large range in mechanistic-empirical ESALFs across urban road classes indicated that typical urban roadways are much more sensitive to heavy vehicle loads than their rural highway counterparts. In a test urban traffic application, it was calculated that a typical low floor transit vehicle was capable of producing loads ranging from a minimum of nine ESALs on urban local-industrial roadways to a maximum of 140 ESALs on urban local and collector roadways