Variation in Size and Growth of the Great Scallop Pecten maximus along a Latitudinal Gradient

Understanding the relationship between growth and temperature will aid in the evaluation of thermal stress and threats to ectotherms in the context of anticipated climate changes. Most Pecten maximus scallops living at high latitudes in the northern hemisphere have a larger maximum body size than individuals further south, a common pattern among many ectotherms. We investigated differences in daily shell growth among scallop populations along the Northeast Atlantic coast from Spain to Norway. This study design allowed us to address precisely whether the asymptotic size observed along a latitudinal gradient, mainly defined by a temperature gradient, results from differences in annual or daily growth rates, or a difference in the length of the growing season. We found that low annual growth rates in northern populations are not due to low daily growth values, but to the smaller number of days available each year to achieve growth compared to the south. We documented a decrease in the annual number of growth days with age regardless of latitude. However, despite initially lower annual growth performances in terms of growing season length and growth rate, differences in asymptotic size as a function of latitude resulted from persistent annual growth performances in the north and sharp declines in the south. Our measurements of daily growth rates throughout life in a long-lived ectothermic species provide new insight into spatio-temporal variations in growth dynamics and growing season length that cannot be accounted for by classical growth models that only address asymptotic size and annual growth rate

Gauvain Soleil Noyé

The stature of the character of Gauvain in the novels of Chrétien de Troyes aroused number of studies which conclude in a degradation of the image of the hero the status of which seemed inviolable. It is not that with the Cart that a collection parallel to that of Lancelot, hero of the novel, is committed by Gauvain who fails straightaway in the Bridge under the water where he is close to the drowning and makes sorry figure. The appeal to a functional analysis of the structure of the novel leads to identify Gauvain as the false hero of the wonderful tales which had analyzed Propp. This analysis heuristics clarifies the intuitions of the previous critics which saw in Gauvain an anti-hero. The "sun of the chivalry" flooded in the water of the Bridge "Évage" made so by the tale of the Cart the origin wanted by Christian of this Gauvain's downgrading among the heroes as he makes act. The Cart is the novel-key of the evolution of the sense to be given to the chivalrous exploit as well as to worldly courtesy in the continuity of the work of the novelist champenois. Sense of Lancelot's adventures in the Cart is the proDrôme of the spiritual orientations of Perceval which relegate in the background the "ground" chivalries which illustrated Gauvain

Savoir lire

Teaching to read. — Elaboration of a teaching method for reading for the first elementary year after an investigation conducted in several schools of Nancy- Metz Academy : perspectives in theoretical area, educational choices, advantages of this learning for further teaching of spelling and written language.Elaboration d'une méthode de lecture au cours préparatoire (lre année d'étude), à la suite d'une recherche entreprise dans divers établissements de l'académie de Nancy-Metz : les orientations théoriques, les choix pédagogiques, les avantages de cet apprentissage pour l'enseignement ultérieur de l'orthographe et de la langue écrite.Saber leer. — Elaboración de un método de lectura en el curso preparatorio (1er ario de estudios), a continuación de una investigación intentada en diversos establecimientos de la Academia de Nancy-Metz : las orientaciones teoricas, las opciones pedagógicas, las ventajas de tal aprendizaje para la enseñanza ulterior de la ortografía y de la lengua escrita.Demarolle Pierre, Kooijman Jacques. Savoir lire. In: Revue française de pédagogie, volume 37, 1976. pp. 13-24

Modulation of Cytokine-Induced Astrocytic Endothelin-1 Production as a Possible New Approach to the Treatment of Multiple Sclerosis

Background: In the human central nervous system (CN), resting astrocytes do not visually show endothelin-1 (ET-1)-like immunoreactivity. In patients with multiple sclerosis (MS), an inflammatory disorder of the CNS, high levels of ET-1 are found in reactive astrocytes in demyelinated plaques. ET-1 may contribute to the pathology of MS by interrupting the blood-brain-barrier, enhancing inflammatory responses, excitotoxicity and reducing cerebral blood flow. Methods: We used the human astrocytoma cell line 1321N1 to investigate the role of inflammatory cytokines involved in MS lesions (IL-1 beta, TNF-alpha, IFN-gamma, LPS, IL-10, TGF-beta) on astrocytic ET-1 upregulation. Prucalopride, rolipram, fenofibrate, fluoxetine, simvastatin, daglutril, and resveratrol were investigated as potential candidate drugs to suppress cytokine-induced astrocytic ET-1 production. Effects on ET-1 production were measured using both ELISA and RT-qPCR. Results and Conclusions: ET-1 secretion by astrocytoma cells was only stimulated by the pro-inflammatory cytokines IL-1 beta and TNF-alpha. Fluoxetine, simvastatin, and resveratrol significantly inhibited this IL-1 beta- and TNF-alpha-induced ET-1 production. Simvastatin and resveratrol significantly reduced ET-1 mRNA levels, indicating an effect at the level of transcription. Fluoxetine significantly reduced endothelin converting enzyme-1 mRNA levels, suggesting and effect at the level of protein-processing. The required concentrations of simvastatin (>0.1 mu M) and resveratrol (>10 mu M) cannot be achieved in humans using pharmacologically accepted doses. Fluoxetine exerted a significant inhibitory effect on ET-1 secretion at a concentration of 5 mu M, which is pharmacologically achievable in human brain, but the effect was modest

The pathophysiological role of astrocytic endothelin-1

In the normal central nervous system, endothelin-1 (ET-1) is found in some types of neurons, epithelial cells of the choroid plexus, and endothelial cells of microvessels, but it is usually not detectable in glial cells. However, in different pathological conditions, astrocytes adapting a reactive phenotype express high levels of ET-1 and its receptors, mainly the ETB receptor. ET-1 released by reactive astrocytes appears mainly to have neurodeleterious effects by mechanisms that include constriction of cerebral arterioles leading to impairment of the cerebral microcirculation, increase of blood brain barrier permeability, inflammation, excitotoxicity, impairment of fast axonal transport, and astrogliosis. A few studies in rodents found that ET-1 increased the astrocytic expression of brain-derived neurotrophic factor, glial cell-line derived neurotrophic factor and neurotropin-3, and the production of endocannabinoids. However, whether this occurs in physiological or pathological conditions is unclear. This review summarizes current knowledge about the role of the astrocytic ET-1 system in acute and chronic neurological conditions, including multiple sclerosis, ischemic stroke and hypoxic/ischemic brain injury, traumatic brain injury, subarachnoid hemorrhage, Alzheimer's disease, Binswanger's disease and post stroke dementia, amyotrophic lateral sclerosis, and CNS infections. Counteracting the harmful effects of astrocytic ET-1 may represent a promising therapeutic target for mitigating secondary brain damage in a variety of neurological diseases. We also briefly address the role of astrocytic ET-1 in astrocytic tumors and pain. (C) 2016 Elsevier Ltd. All rights reserved

Astrocyte loss and astrogliosis in neuroinflammatory disorders

Neuroinflammation can lead to either damage of astrocytes or astrogliosis. Astrocyte loss may be caused by cytotoxic T cells as seen in Rasmussen encephalitis, auto-antibodies such as in neuromyelitis optica (aquaporin-4 antibodies), or cytokines such as TNF-alpha in major depressive disorder. Interleukins-1 and -6 appear to be important molecular mediators of astrogliosis. Chronic focal lesions in multiple sclerosis are characterized by a very dense astrogliosis. Other mechanisms, such as astrocytic beta(2) adrenergic receptor deficiency, upregulation of endothelin-1 and tissue transglutaminase, may contribute to astroglial scarring in multiple sclerosis. (C) 2013 Elsevier Ireland Ltd. All rights reserved

Astrocyte loss and astrogliosis in neuroinflammatory disorders

Neuroinflammation can lead to either damage of astrocytes or astrogliosis. Astrocyte loss may be caused by cytotoxic T cells as seen in Rasmussen encephalitis, auto-antibodies such as in neuromyelitis optica (aquaporin-4 antibodies), or cytokines such as TNF-alpha in major depressive disorder. Interleukins-1 and -6 appear to be important molecular mediators of astrogliosis. Chronic focal lesions in multiple sclerosis are characterized by a very dense astrogliosis. Other mechanisms, such as astrocytic beta(2) adrenergic receptor deficiency, upregulation of endothelin-1 and tissue transglutaminase, may contribute to astroglial scarring in multiple sclerosis. (C) 2013 Elsevier Ireland Ltd. All rights reserved

Combination of therapeutic hypothermia and insulin-like growth factor-1 in ischemic stroke rats : effect on infarct size and neurological outcome

COMBINATION OF THERAPEUTIC HYPOTHERMIA AND INSULIN-LIKE GROWTH FACTOR-1 IN ISCHEMIC STROKE RATS: EFFECT ON INFARCT SIZE AND NEUROLOGICAL OUTCOME Arnaud Potvin1, Pieter Olivier1, Joline Goossens1,2,3, Ron Kooijman3, Jacques De Keyser3, Said Hachimi-Idrissi1,2,3 1. Faculty of Medicine and Health Sciences, Ghent University 2. Department of Emergency Medicine, Ghent University Hospital 3. Center for Neurosciences, Free University Brussels Introduction – Intravenous (IV) administration of rt-PA within 4.5 h is the only approved therapeutic measure after stroke onset (IS) [1]. Only a few patients are eligible for this treatment because of presentation delay. Other alternative treatments such as therapeutic hypothermia (TH) and insulin-like growth factor-1 (IGF-1) have shown promising results in animal studies. Subcutaneous (SC) administration of IGF-1 in an animal model was neuroprotective only when administered within 30 min, and not after 2 and 4 hours after stroke onset [2]. We wonder if TH can synergistically be used with IGF-1 and if this combination could broaden the therapeutic window of IGF-1 in a rat model of focal cerebral ischemia [3]. Methods – Male Wistar rats (n=27) weighing 275-300 g were randomly divided into 9 experimental groups: a sham operated group, a normothermic (NT; 37.0±0.5 °C) and hypothermic (HT; 33.0±0.3 °C) control group, three normothermic IGF-1 treated groups and three hypothermic IGF-1 treated groups. SC IGF-1 administration occurred at either 30 min, 2 h or 4 h after ischemia onset. TH was induced within 10 min and maintained for 2 h with a delay of 20 min after the insult. Focal ischemia was induced by a local intracerebral injection of the potent vasoconstrictor endothelin-1 (Et-1). A non-blinded assessor evaluated functional outcome at 3, 6 and 24 h after the insult using the neurological deficit score (NDS), whereupon the animals were sacrificed and their brains were collected for histological examination. After staining with Cresyl Violet, digital images of the 50 μm slices were analyzed using Image J software. Three blinded assessors performed infarct size measurement independently. Results – Although a trend towards higher NDS with TH and later administration of IGF-1, was seen, no significant differences could be observed at either time point (Figure 1). In NT groups, there was a trend towards smaller infarcts with later administration of IGF-1 compared to the NT control group. This was not the case for the HT groups, as the HT control group had the smallest infarct sizes. All NT groups displayed larger infarct sizes than the HT counterparts, except for the NT group with IGF-1 administration at 4 h after stroke onset (Figure 2). Conclusions – Nor IGF-1 administration at any time point nor TH nor the combination of both treatments significantly improved the NDS at 3, 6 or 24 h and infarct size at 24 h. The hypothesis that TH could broaden the therapeutic window of opportunity for subcutaneously injected IGF-1 could not be confirmed. Further research is needed to evaluate whether larger experimental groups or alterations to the treatment protocol might be more effective. [1] Wahlgren et al. (2008). Lancet; 372(9646):1303-9. [2] De Geyter et al. (2013). Neuroscience; 250:253-62. [3] Kollmar et al. (2009). Journal of neurotrauma; 26(3):377-86

Post-stroke treatment with 17β-estradiol exerts neuroprotective effects in both normotensive and hypertensive rats

Although ischemic stroke is a major cause of death worldwide and the predominant cause of acquired disability, the only effective drug therapy that has been developed thus far is reperfusion by tissue plasminogen activator. Since most patients do not qualify for this treatment, new methods have to be developed. It is well known that estradiol (E-2) exerts neuroprotective effects in different models of cerebral ischemia, but post-stroke treatment after an acute stroke has hardly been investigated. As many patients with an acute ischemic stroke have arterial hypertension, it is also of interest to evaluate the influence of this co-morbidity on the treatment efficacy of E-2. The effects of E-2 administered 30 min after a transient middle cerebral artery occlusion (tMCAO) induced by an intracerebral injection of endothelin-1 were assessed in male normotensive Wistar Kyoto (WKY) rats and spontaneously hypertensive rats (SHRs). Treatment with E-2 reduced infarct size in both WKY and SHRs and decreased the number of degenerating neurons, indicating that acute treatment with E-2 is indeed neuroprotective. To address the role of glia in neuroprotection, the effects of E-2 on the activation of microglia and astrocytes was determined. It appeared that E-2 had no effect on microglial activation, but reduced the activation of astrocytes in SHRs but not in the normotensive controls. We conclude that post-stroke E-2 treatment in both normotensive and hypertensive rats is neuroprotective. Although the presence of hypertension changed the astrocytic response to E2, did not affect treatment efficacy. (C) 2017 IBRO. Published by Elsevier Ltd. All rights reserved