Quantum States Localized on Lagrangian Submanifolds

Let X be a symplectic manifold and Aut(L) the automorphism group of a Kostant-Souriau line bundle on X. *Quantum states for X*, as defined by J.-M. Souriau in the 1990s, are certain positive-definite functions on Aut(L) or, less ambitiously, on any “large enough” subgroup G of Aut(L). This definition has two major drawbacks: when G = Aut(L) there are no known examples; and when G is a Lie subgroup the notion is far from selective enough. In this talk I’ll introduce the concept of a quantum state *localized at Y *, where Y is a coadjoint orbit of a subgroup H of G. I’ll explain how such states often exist and are unique when Y has lagrangian preimage in X, and how this can be regarded as a solving, in a number of cases, A. Weinstein’s “fundamental quantization problem” of attaching state vectors to lagrangian submanifolds

Negotiating over Banking Secrecy: The Case of Switzerland and the European Union

Over the period 2002 to 2003,Switzerland and the European Union (EU) were engaged in negotiations regarding banking secrecy. The EU's stated goal was for Switzerland to abolish banking secrecy. Switzerland refused and offered to impose a withholding tax on interest income instead. The two parties eventually agreed on the latter solution. We examine the effect of these negotiations on the share prices of four Swiss banks: UBS, Credit Suisse Group (CSG), Julius Baer (Baer), and Vontobel. Overall, investors believe that bank profitability will not be impacted by the imposition of the withholding tax. The event-by-event response of the share prices differs across banks. Whereas the two universal banks (UBS and CSG) primarily react to the threat of sanctions on their EU-based operations, the private banks (Baer and Vontobel) react strongly to events suggesting that banking secrecy might be abolished.Banking Secrecy; Switzerland; Event Study

Lack of dietary polyunsaturated fatty acids causes synapse dysfunction in the drosophila visual system

Polyunsaturated fatty acids (PUFAs) are essential nutrients for animals and necessary for the normal functioning of the nervous system. A lack of PUFAs can result from the consumption of a deficient diet or genetic factors, which impact PUFA uptake and metabolism. Both can cause synaptic dysfunction, which is associated with numerous disorders. However, there is a knowledge gap linking these neuronal dysfunctions and their underlying molecular mechanisms. Because of its genetic manipulability and its easy, fast, and cheap breeding, Drosophila melanogaster has emerged as an excellent model organism for genetic screens, helping to identify the genetic bases of such events. As a first step towards the understanding of PUFA implications in Drosophila synaptic physiology we designed a breeding medium containing only very low amounts of PUFAs. We then used the fly’s visual system, a well-established model for studying signal transmission and neurological disorders, to measure the effects of a PUFA deficiency on synaptic function. Using both visual performance and eye electrophysiology, we found that PUFA deficiency strongly affected synaptic transmission in the fly’s visual system. These defects were rescued by diets containing omega-3 or omega-6 PUFAs alone or in combination. In summary, manipulating PUFA contents in the fly’s diet was powerful to investigate the role of these nutrients on the fly´s visual synaptic function. This study aims at showing how the first visual synapse of Drosophila can serve as a simple model to study the effects of PUFAs on synapse function. A similar approach could be further used to screen for genetic factors underlying the molecular mechanisms of synaptic dysfunctions associated with altered PUFA levels

On the Geometric Interpretation of the Nonnegative Rank

The nonnegative rank of a nonnegative matrix is the minimum number of nonnegative rank-one factors needed to reconstruct it exactly. The problem of determining this rank and computing the corresponding nonnegative factors is difficult; however it has many potential applications, e.g., in data mining, graph theory and computational geometry. In particular, it can be used to characterize the minimal size of any extended reformulation of a given combinatorial optimization program. In this paper, we introduce and study a related quantity, called the restricted nonnegative rank. We show that computing this quantity is equivalent to a problem in polyhedral combinatorics, and fully characterize its computational complexity. This in turn sheds new light on the nonnegative rank problem, and in particular allows us to provide new improved lower bounds based on its geometric interpretation. We apply these results to slack matrices and linear Euclidean distance matrices and obtain counter-examples to two conjectures of Beasly and Laffey, namely we show that the nonnegative rank of linear Euclidean distance matrices is not necessarily equal to their dimension, and that the rank of a matrix is not always greater than the nonnegative rank of its square

Sodium, renin, aldosterone, catecholamines, and blood pressure in diabetes mellitus

Sodium, renin, aldosterone, catecholamines, and blood pressure in diabetes mellitus. Interrelations among plasma renin activity (PRA), aldosterone and Cortisol levels, blood volume, exchangeable sodium, urinary catecholamines, and blood pressure were studied in 35 normal subjects and 60 age-matched non-azotemic patients with diabetes mellitus (60% with hypertension, 15% with orthostatic hypotension). Basal PRA, plasma aldosterone, cortisol, blood volume, plasma potassium, and urinary electrolytes were comparable in diabetic and normal subjects. Diabetic patients, however, had a 10% increase in body sodium (P < 0.01), and 8% of them showed normal postural PRA responses and subnormal aldosterone responses; 22% had subnormal PRA and normal aldosterone responses, and 17% had subnormal responses of PRA and aldosterone. Non-PRA-related aldosterone responses could not be explained by ACTH or electrolytes. Orthostatic decreases in blood pressure correlated (P < 0.01) with both catecholamine excretion and basal PRA. This suggests that in diabetes mellitus, body sodium is increased. Basal PRA and plasma aldosterone are usually normal, but their postural responses are frequently impaired. Absent aldosterone responses, despite normal PRA responsiveness, may reflect an adrenal abnormality or an ineffective form of renin. Marked postural aldosterone stimulation, unrelated to PRA, ACTH, or electrolytes, points to a potent unknown factor in aldosterone control. Low levels of free peripheral catecholamines and PRA may be complementary factors contributing to postural hypotension.Sodium, rénine, aldostérone, catécholamines et pression artérielle dans le diabèté sucré. Les inter-relations entre l'activité rénine plasmatique (PRA), les concentrations d'aldostérone et de cortisol, le volume sanguin, le sodium échangeable, les catécholamines urinaires et la pression artérielle ont été étudiées chez 35 sujets normaux et 60 malades atteints de diabété, sans insuffisance rénale et dont les âges étaient appariés (60% avaient une hypertension et 15% une hypotension orthostatique). La PRA de base, l'aldostérone et le Cortisol plasmatiques, le volume sanguin, le potassium plasmatique et les électrolytes urinaires étaient comparables chez les diabétiques et les sujets normaux. Les malades diabétiques, cependant, ont une augmentation de 10% de leur sodium corporel (P < 0,01). Huit pour cent d'entre eux ont une réponse posturale de PRA normale et une réponse de l'aldostérone inférieure à la normale, 22% ont une réponse de PRA inférieure à la normale et une reponse de l'aldosterone normale, et 17% ont des réponses de PRA et de l'aldostérone inférieures à la normale. Les réponses de l'aldostérone sans rapport avec PRA ne peuvent pas être expliquées par l'ACTH ou les électrolytes. Les diminutions de la pression artérielle liées à l'orthostatisme sont correlées (P < 0,01) à la fois avec l'excrétion de catécholamines et la PRA de base. Ceci suggére qu'au cours du diabéte le sodium corporel est augmenté. La PRA et l'aldosterone de base sont souvent normales mais leur réponse posturale est souvent modifiée. L'absence de réponse de l'aldosterone malgré une réponse normale de PRA peut traduire une anomalie surrénale ou une forme de rénine inefficace. Une stimulation posturale importante de l'aldostérone non expliquée par la PRA, l'ACTH ou les électrolytes oriente vers un facteur inconnu mais puissant du contrôle de la sécrétion d'aldostérone. Des concentrations basses de catécholamines libres et une PRA basse peuvent être des facteurs complémentaires qui participent à l'hypotension posturale

Sodium, renin, aldosterone, catecholamines, and blood pressure in diabetes mellitus

Sodium, renin, aldosterone, catecholamines, and blood pressure in diabetes mellitus. Interrelations among plasma renin activity (PRA), aldosterone and Cortisol levels, blood volume, exchangeable sodium, urinary catecholamines, and blood pressure were studied in 35 normal subjects and 60 age-matched non-azotemic patients with diabetes mellitus (60% with hypertension, 15% with orthostatic hypotension). Basal PRA, plasma aldosterone, cortisol, blood volume, plasma potassium, and urinary electrolytes were comparable in diabetic and normal subjects. Diabetic patients, however, had a 10% increase in body sodium (P < 0.01), and 8% of them showed normal postural PRA responses and subnormal aldosterone responses; 22% had subnormal PRA and normal aldosterone responses, and 17% had subnormal responses of PRA and aldosterone. Non-PRA-related aldosterone responses could not be explained by ACTH or electrolytes. Orthostatic decreases in blood pressure correlated (P < 0.01) with both catecholamine excretion and basal PRA. This suggests that in diabetes mellitus, body sodium is increased. Basal PRA and plasma aldosterone are usually normal, but their postural responses are frequently impaired. Absent aldosterone responses, despite normal PRA responsiveness, may reflect an adrenal abnormality or an ineffective form of renin. Marked postural aldosterone stimulation, unrelated to PRA, ACTH, or electrolytes, points to a potent unknown factor in aldosterone control. Low levels of free peripheral catecholamines and PRA may be complementary factors contributing to postural hypotension.Sodium, rénine, aldostérone, catécholamines et pression artérielle dans le diabèté sucré. Les inter-relations entre l'activité rénine plasmatique (PRA), les concentrations d'aldostérone et de cortisol, le volume sanguin, le sodium échangeable, les catécholamines urinaires et la pression artérielle ont été étudiées chez 35 sujets normaux et 60 malades atteints de diabété, sans insuffisance rénale et dont les âges étaient appariés (60% avaient une hypertension et 15% une hypotension orthostatique). La PRA de base, l'aldostérone et le Cortisol plasmatiques, le volume sanguin, le potassium plasmatique et les électrolytes urinaires étaient comparables chez les diabétiques et les sujets normaux. Les malades diabétiques, cependant, ont une augmentation de 10% de leur sodium corporel (P < 0,01). Huit pour cent d'entre eux ont une réponse posturale de PRA normale et une réponse de l'aldostérone inférieure à la normale, 22% ont une réponse de PRA inférieure à la normale et une reponse de l'aldosterone normale, et 17% ont des réponses de PRA et de l'aldostérone inférieures à la normale. Les réponses de l'aldostérone sans rapport avec PRA ne peuvent pas être expliquées par l'ACTH ou les électrolytes. Les diminutions de la pression artérielle liées à l'orthostatisme sont correlées (P < 0,01) à la fois avec l'excrétion de catécholamines et la PRA de base. Ceci suggére qu'au cours du diabéte le sodium corporel est augmenté. La PRA et l'aldosterone de base sont souvent normales mais leur réponse posturale est souvent modifiée. L'absence de réponse de l'aldosterone malgré une réponse normale de PRA peut traduire une anomalie surrénale ou une forme de rénine inefficace. Une stimulation posturale importante de l'aldostérone non expliquée par la PRA, l'ACTH ou les électrolytes oriente vers un facteur inconnu mais puissant du contrôle de la sécrétion d'aldostérone. Des concentrations basses de catécholamines libres et une PRA basse peuvent être des facteurs complémentaires qui participent à l'hypotension posturale

Comprehensive exploration of the effects of miRNA SNPs on monocyte gene expression

We aimed to assess whether pri-miRNA SNPs (miSNPs) could influence monocyte gene expression, either through marginal association or by interacting with polymorphisms located in 3'UTR regions (3utrSNPs). We then conducted a genome-wide search for marginal miSNPs effects and pairwise miSNPs × 3utrSNPs interactions in a sample of 1,467 individuals for which genome-wide monocyte expression and genotype data were available. Statistical associations that survived multiple testing correction were tested for replication in an independent sample of 758 individuals with both monocyte gene expression and genotype data. In both studies, the hsa-mir-1279 rs1463335 was found to modulate in cis the expression of LYZ and in trans the expression of CNTN6, CTRC, COPZ2, KRT9, LRRFIP1, NOD1, PCDHA6, ST5 and TRAF3IP2 genes, supporting the role of hsa-mir-1279 as a regulator of several genes in monocytes. In addition, we identified two robust miSNPs × 3utrSNPs interactions, one involving HLA-DPB1 rs1042448 and hsa-mir-219-1 rs107822, the second the H1F0 rs1894644 and hsa-mir-659 rs5750504, modulating the expression of the associated genes. As some of the aforementioned genes have previously been reported to reside at disease-associated loci, our findings provide novel arguments supporting the hypothesis that the genetic variability of miRNAs could also contribute to the susceptibility to human diseases

The Choice of the Filtering Method in Microarrays Affects the Inference Regarding Dosage Compensation of the Active X-Chromosome

The hypothesis of dosage compensation of genes of the X chromosome, supported by previous microarray studies, was recently challenged by RNA-sequencing data. It was suggested that microarray studies were biased toward an over-estimation of X-linked expression levels as a consequence of the filtering of genes below the detection threshold of microarrays.To investigate this hypothesis, we used microarray expression data from circulating monocytes in 1,467 individuals. In total, 25,349 and 1,156 probes were unambiguously assigned to autosomes and the X chromosome, respectively. Globally, there was a clear shift of X-linked expressions toward lower levels than autosomes. We compared the ratio of expression levels of X-linked to autosomal transcripts (X∶AA) using two different filtering methods: 1. gene expressions were filtered out using a detection threshold irrespective of gene chromosomal location (the standard method in microarrays); 2. equal proportions of genes were filtered out separately on the X and on autosomes. For a wide range of filtering proportions, the X∶AA ratio estimated with the first method was not significantly different from 1, the value expected if dosage compensation was achieved, whereas it was significantly lower than 1 with the second method, leading to the rejection of the hypothesis of dosage compensation. We further showed in simulated data that the choice of the most appropriate method was dependent on biological assumptions regarding the proportion of actively expressed genes on the X chromosome comparative to the autosomes and the extent of dosage compensation.This study shows that the method used for filtering out lowly expressed genes in microarrays may have a major impact according to the hypothesis investigated. The hypothesis of dosage compensation of X-linked genes cannot be firmly accepted or rejected using microarray-based data