Analyse exploratoire trimestrielle du marché canadien sur la valeur marginale que place l'investisseur à l'ajout d'1$ d'encaisse (trésorerie)

Cette recherche a pour objectif de mesurer la valeur marginale estimée par les investisseurs canadiens à la suite de l’ajout de 1 dollar d’encaisse, pour la période trimestrielle s’étalant de 2001 à 2013. Autrement dit, nous tentons d’évaluer si l’investisseur déprécie, estime à sa juste valeur nominale ou apprécie la valeur de 1 dollar de trésorerie, et ce à travers son impact sur la valeur marchande de l’équité. Parallèlement, nous tentons d’analyser l’influence des variables liées à la rentabilité, le financement, la croissance et le risque sur la valeur que place l’investisseur à l’ajout de 1 dollar d’encaisse. L’effet sectoriel sera notamment exploré sur l’ensemble de ces périodes. Des études passées ont démontré qu’il existe une asymétrie entre la valeur nominale de 1 dollar d’encaisse et celle estimée par les investisseurs. Plus précisément que l’ajout de 1 dollar de liquidité est évalué à prime. Somme toute, ces analyses affinent leurs résultats en tenant compte de l’influence des autres variables telles que mentionnées plus haut, afin de déterminer celles qui entraînent une appréciation de l’encaisse de celles qui conduisent à sa dépréciation. Nous avons conclu qu’en moyenne la valeur marginale de 1 dollar de liquidité est évaluée à 2,13$ par les investisseurs. Nous avons également pu prouver que les anticipations des investisseurs et le risque total influencent significativement cette estimation. Pour tenter de mesurer la valeur que place l’investisseur à l’ajout de 1 dollar d’encaisse, nous avons utilisé la méthodologie de Pinkowitz et Williamson (2002). Ce faisant, nous avons dans un premier temps mesuré l’impact net de l’encaisse sur la valeur marchande de l’équité en élimant du modèle les variables tenant compte des variations trimestrielles t-2 et t+2. L’hypothèse à vérifier en ce qui concerne l’impact net de l’encaisse est qu’il existe une asymétrie significative entre la valeur de 1 dollar et celle estimée par l’investisseur qui n’est pas uniquement provoquée par l’influence des variations passées et futures de l’encaisse. Les résultats obtenus nous ont permis de prouver que la valeur de 1 dollar d’encaisse est appréciée par l’investisseur, et ce malgré la suppression ou la présence des variables tenant compte des variations. Dans la même ligné, nous avons pu démontrer que, conjointement à l’encaisse au temps t, seules les variations liées aux anticipations des investisseurs impactaient significativement la valeur marchande de l’équité. En ce qui concerne le risque dont l’analyse s’est effectuée en dissociant le risque systématique du risque systémique. L’hypothèse à vérifier est qu’une augmentation du risque systématique entraîne une augmentation de la valeur de l’encaisse estimée par l’investisseur. Les résultats obtenus viennent appuyer cette affirmation. Quant au risque systémique, l’hypothèse à vérifier tente à affirmer qu’en période de crise l’encaisse est sous-estimée par l’investisseur et son impact sur la VME non significatif. Nos résultats nous conduisent à démontrer que pour la crise financière de 2006, cette hypothèse est justifiée, mais nous ne permettent pas de la vérifier pour chaque crise. Finalement, nous tenions à vérifier que dépendamment du secteur étudié, l’encaisse pouvait être plus appréciée par les investisseurs. Or, nos résultats ont montré qu’en présence de la liquidité aucun secteur ne se distingue significativement de ses pairs

Detection of deviations origins in a heat treatment process using Proper Orthogonal Decomposition (POD) basis

International audienceIt is well know that the heat treatment step of gearbox cogwheel induces distortions of the parts. In addition, some deviations of this deformation are often observed, due to unknown changes of process parameters. These deviations, and more precisely the detection of their origin, are the subject of this paper. We propose here a methodology based on the projection of measurements after heat treatment on a POD (Proper Orthogonal Decomposition) basis, extracted from FEM computations. This information about deviation origin can help correct incriminated process parameters

EL ANTAGONISMO INTERCULTURAL ENTRE ESPAÑA Y ESTADOS UNIDOS: LA MASCULINIDAD EN TRES NOVELAS DE ANTONIO MUÑOZ MOLINA

Antonio Muñoz Molina’s narrative repeatedly shows an antagonism between Spain and the United States that relates to ‘masculinity’, one of the fundamental concepts of Hofstede’s intercultural model. In three of his novels, the author particularly elaborates the different positions both countries take towards the binomial ‘masculinity/femininity’ by means of some of the imagologic strategies outlined by Pageaux. More specifically, lexical opposition, hierarchy of characters and stereotyping at the scenario level put forward the protagonists’ ambivalent attitude towards masculinity, this way illustrating the synergy between empirical intercultural studies and a constructivist imagologic viewpoint as formulated by Leerssen.En la narrativa de Antonio Muñoz Molina a menudo se perfila un antagonismo entre España y Estados Unidos que atañe a ‘la masculinidad’, uno de los conceptos fundamentales en el modelo intercultural de Hofstede. En tres de sus novelas, el autor elabora las diferentes posiciones que ambos países ocupan frente al binomio ‘masculinidad/feminidad’, valiéndose de algunas de las estrategias imagológicas descritas por Pageaux. Así, el contraste léxico, la jerarquía de los personajes y la estereotipia en el nivel del guion ponen de relieve la actitud ambivalente de los protagonistas con respecto a la masculinidad, ilustrando así la sinergia entre los estudios interculturales empíricos y una perspectiva imagológica constructivista como la de Leerssen

Protein synthesis persists during necrotic cell death

Cell death is an intrinsic part of metazoan development and mammalian immune regulation. Whereas the molecular events orchestrating apoptosis have been characterized extensively, little is known about the biochemistry of necrotic cell death. Here, we show that, in contrast to apoptosis, the induction of necrosis does not lead to the shut down of protein synthesis. The rapid drop in protein synthesis observed in apoptosis correlates with caspase-dependent breakdown of eukaryotic translation initiation factor (eIF) 4G, activation of the double-stranded RNA-activated protein kinase PKR, and phosphorylation of its substrate eIF2-α. In necrosis induced by tumor necrosis factor, double-stranded RNA, or viral infection, de novo protein synthesis persists and 28S ribosomal RNA fragmentation, eIF2-α phosphorylation, and proteolytic activation of PKR are absent. Collectively, these results show that, in contrast to apoptotic cells, necrotic dying cells retain the opportunity to synthesize proteins

The effect of hypoxia on Daphnia magna performance and its associated microbial and bacterioplankton community: A scope for phenotypic plasticity and microbiome community interactions upon environmental stress?

The depletion of oxygen as a result of increased stratification and decreased oxygen solubility is one of the most significant chemical changes occurring in aquatic ecosystems as a result of global environmental change. Hence, more aquatic organisms will be exposed to hypoxic conditions over time. Deciphering the effects of hypoxia on strong ecological interactors in this ecosystem’s food web is critical for predicting how aquatic communities can respond to such an environmental disturbance. Here (sub-)lethal effects of hypoxia and whether these are genotype specific in Daphnia, a keystone species of freshwater ecosystems, are studied. This is especially relevant upon studying genetic responses with respect to phenotypic switches upon environmental stress. Further, we investigated the effect of hypoxia on the Daphnia microbial community to test if the microbiome plays a role in the phenotypic switch and tolerance to hypoxia. For this, two Daphnia genotypes were exposed for two weeks to either hypoxia or normoxia and host performance was monitored together with changes in the host associated and free-living microbial community after this period. We detected phenotypic plasticity for some of the tested Daphnia performance traits. The microbial community of the bacterioplankton and Daphnia associated microbial community responded via changes in species richness and community composition and structure. The latter response was different for the two genotypes suggesting that the microbiome plays an important role in phenotypic plasticity with respect to hypoxia tolerance in Daphnia, but further testing (e.g., through microbiome transplants) is needed to confirm this

Endoplasmic reticulum Ca2+-homeostasis is altered in small and non-small cell lung cancer cell lines

<p>Abstract</p> <p>Background</p> <p>Knowledge of differences in the cellular physiology of malignant and non-malignant cells is a prerequisite for the development of cancer treatments that effectively kill cancer without damaging normal cells. Calcium is a ubiquitous signal molecule that is involved in the control of proliferation and apoptosis. We aimed to investigate if the endoplasmic reticulum (ER) Ca²⁺-homeostasis is different in lung cancer and normal human bronchial epithelial (NHBE) cells.</p> <p>Methods</p> <p>The intracellular Ca²⁺-signaling was investigated using fluorescence microscopy and the expression of Ca²⁺-regulating proteins was assessed using Western Blot analysis.</p> <p>Results</p> <p>In a Small Cell Lung Cancer (H1339) and an Adeno Carcinoma Lung Cancer (HCC) cell line but not in a Squamous Cell Lung Cancer (EPLC) and a Large Cell Lung Cancer (LCLC) cell line the ER Ca²⁺-content was reduced compared to NHBE. The reduced Ca²⁺-content correlated with a reduced expression of SERCA 2 pumping calcium into the ER, an increased expression of IP₃R releasing calcium from the ER, and a reduced expression of calreticulin buffering calcium within the ER. Lowering the ER Ca²⁺-content with CPA led to increased proliferation NHBE and lung cancer cells.</p> <p>Conclusion</p> <p>The significant differences in Ca²⁺-homeostasis between lung cancer and NHBE cells could represent a new target for cancer treatments.</p

Orai1 contributes to the establishment of an apoptosis-resistant phenotype in prostate cancer cells

The molecular nature of calcium (Ca2+)-dependent mechanisms and the ion channels having a major role in the apoptosis of cancer cells remain a subject of debate. Here, we show that the recently identified Orai1 protein represents the major molecular component of endogenous store-operated Ca2+ entry (SOCE) in human prostate cancer (PCa) cells, and constitutes the principal source of Ca2+ influx used by the cell to trigger apoptosis. The downregulation of Orai1, and consequently SOCE, protects the cells from diverse apoptosis-inducing pathways, such as those induced by thapsigargin (Tg), tumor necrosis factor α, and cisplatin/oxaliplatin. The transfection of functional Orai1 mutants, such as R91W, a selectivity mutant, and L273S, a coiled-coil mutant, into the cells significantly decreased both SOCE and the rate of Tg-induced apoptosis. This suggests that the functional coupling of STIM1 to Orai1, as well as Orai1 Ca2+-selectivity as a channel, is required for its pro-apoptotic effects. We have also shown that the apoptosis resistance of androgen-independent PCa cells is associated with the downregulation of Orai1 expression as well as SOCE. Orai1 rescue, following Orai1 transfection of steroid-deprived cells, re-established the store-operated channel current and restored the normal rate of apoptosis. Thus, Orai1 has a pivotal role in the triggering of apoptosis, irrespective of apoptosis-inducing stimuli, and in the establishment of an apoptosis-resistant phenotype in PCa cells

Identification of a Polycystin-1 Cleavage Product, P100, That Regulates Store Operated Ca2+ Entry through Interactions with STIM1

Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a genetic disorder resulting in large kidney cysts and eventual kidney failure. Mutations in either the PKD1 or PKD2/TRPP2 genes and their respective protein products, polycystin-1 (PC1) and polycystin-2 (PC2) result in ADPKD. PC2 is known to function as a non-selective cation channel, but PC1's function and the function of PC1 cleavage products are not well understood. Here we identify an endogenous PC1 cleavage product, P100, a 100 kDa fragment found in both wild type and epitope tagged PKD1 knock-in mice. Expression of full length human PC1 (FL PC1) and the resulting P100 and C-Terminal Fragment (CTF) cleavage products in both MDCK and CHO cells significantly reduces the store operated Ca2+ entry (SOCE) resulting from thapsigargin induced store depletion. Exploration into the roles of P100 and CTF in SOCE inhibition reveal that P100, when expressed in Xenopus laevis oocytes, directly inhibits the SOCE currents but CTF does not, nor does P100 when containing the disease causing R4227X mutation. Interestingly, we also found that in PC1 expressing MDCK cells, translocation of the ER Ca2+ sensor protein STIM1 to the cell periphery was significantly altered. In addition, P100 Co-immunoprecipitates with STIM1 but CTF does not. The expression of P100 in CHO cells recapitulates the STIM1 translocation inhibition seen with FL PC1. These data describe a novel polycystin-1 cleavage product, P100, which functions to reduce SOCE via direct inhibition of STIM1 translocation; a function with consequences for ADPKD

Flavonoids in prevention of diseases with respect to modulation of Ca-pump function

Flavonoids, natural phenolic compounds, are known as agents with strong antioxidant properties. In many diseases associated with oxidative/nitrosative stress and aging they provide multiple biological health benefits. Ca2+-ATPases belong to the main calcium regulating proteins involved in the balance of calcium homeostasis, which is impaired in oxidative/nitrosative stress and related diseases or aging. The mechanisms of Ca2+-ATPases dysfunction are discussed, focusing on cystein oxidation and tyrosine nitration. Flavonoids act not only as antioxidants but are also able to bind directly to Ca2+-ATPases, thus changing their conformation, which results in modulation of enzyme activity