L'hostilité aux OGM survit-elle à des produits attractifs ?

Nous testons ici les dispositions à payer des consommateurs pour des aliments transgéniques de seconde génération, c'est-à-dire ayant des caractéristiques innovantes attractives pour le consommateur par rapport au produit conventionnel. Nous testons également les dispositions à payer de tels produits lorsqu'ils sont obtenus avec des technologies alternatives aux biotechnologies transgéniques. Les résultats indiquent que la disposition à payer positive pour une caractéristique désirable obtenue grâce à un organisme génétiquement modifié compense la perte de disposition à payer qu'entraine, pour le consommateur, l'usage d'une telle technologie. Pour un même produit amélioré pour le consommateur, le recours à la technologie transgénique conduit à une disposition à payer toujours inférieure à celles proposée pour les autres technologies. L'écart est néanmoins d'une ampleur réduite, même si les OGM continuent à subir le coût d'une image négative.aliment génétiquement modifié;, évaluation de préférences individuelles; économie expérimentale

Handbook of remote working for social innovators

Sem resumo disponível.publishe

Memory consolidation in the cerebellar cortex

Several forms of learning, including classical conditioning of the eyeblink, depend upon the cerebellum. In examining mechanisms of eyeblink conditioning in rabbits, reversible inactivations of the control circuitry have begun to dissociate aspects of cerebellar cortical and nuclear function in memory consolidation. It was previously shown that post-training cerebellar cortical, but not nuclear, inactivations with the GABA(A) agonist muscimol prevented consolidation but these findings left open the question as to how final memory storage was partitioned across cortical and nuclear levels. Memory consolidation might be essentially cortical and directly disturbed by actions of the muscimol, or it might be nuclear, and sensitive to the raised excitability of the nuclear neurons following the loss of cortical inhibition. To resolve this question, we simultaneously inactivated cerebellar cortical lobule HVI and the anterior interpositus nucleus of rabbits during the post-training period, so protecting the nuclei from disinhibitory effects of cortical inactivation. Consolidation was impaired by these simultaneous inactivations. Because direct application of muscimol to the nuclei alone has no impact upon consolidation, we can conclude that post-training, consolidation processes and memory storage for eyeblink conditioning have critical cerebellar cortical components. The findings are consistent with a recent model that suggests the distribution of learning-related plasticity across cortical and nuclear levels is task-dependent. There can be transfer to nuclear or brainstem levels for control of high-frequency responses but learning with lower frequency response components, such as in eyeblink conditioning, remains mainly dependent upon cortical memory storage

Handbook of remote working for social innovators

No abstract available.publishe

Skeletal muscle channelopathies: a guide to diagnosis and management.

Skeletal muscle channelopathies are a group of rare episodic genetic disorders comprising the periodic paralyses and the non-dystrophic myotonias. They may cause significant morbidity, limit vocational opportunities, be socially embarrassing, and sometimes are associated with sudden cardiac death. The diagnosis is often hampered by symptoms that patients may find difficult to describe, a normal examination in the absence of symptoms, and the need to interpret numerous tests that may be normal or abnormal. However, the symptoms respond very well to holistic management and pharmacological treatment, with great benefit to quality of life. Here, we review when to suspect a muscle channelopathy, how to investigate a possible case and the options for therapy once a diagnosis is made

Suffering in long-term cancer survivors: An evaluation of the PRISM-R2 in a population-based cohort

The Pictorial Representation of Illness and Self Measure-Revised 2 (PRISM-R2) has been developed as generic measure to assess suffering. The aim of this study was to evaluate the ability of this instrument to identify long-term cancer survivors with high levels of suffering who may need additional support. 1299 cancer survivors completed the PRISM-R2, the Short Form Health Survey (SF-36), and the Quality of Life-Cancer Survivors questionnaire (QoL-CS). The PRISM-R2 distinguishes between the Self-Illness Separation (SIS) and Illness Perception Measure (IPM), both measuring aspects of suffering. 112 (9%) cancer survivors reported high suffering according to IPM. This group had a higher cancer stage at diagnosis, more cancer recurrences, more comorbidities, and were lower educated compared to people reporting less suffering. The PRISM-R2 could explain substantial amounts of variance (10-14%) in the psychological aspects of the SF-36 and QoL-CS. The IPM also discriminated statistically and clinically significant between high- and low-health status. The PRISM-R2 proved to be able to discriminate between individuals with good and deteriorated levels of QoL. Further evaluation of its validity and screening potential is recommended

Methods matter: a meta-regression on the determinants of willingness-to-pay studies on biofortified foods

Following the growing evidence on biofortification as a cost-effective micronutrient strategy, various researchers have elicited consumers’ willingness to pay (WTP) for biofortified crops in an effort to justify and determine their adoption. This review presents a meta-analysis of WTP studies on biofortified foods, either developed through conventional breeding or using genetic modification technology. On the basis of 122 estimates from 23 studies (9507 respondents), consumers are generally willing to pay 21.3% more for biofortified crops. Because WTP estimates are often determined through different valuation methods and procedures, a meta-regression was carried out to examine the role of potential determinants. Aside from contextual factors, such as type of food crop, target nutrient, and region(but not breeding technique), various methodological factors significantly influence premiums, including the type of respondent, nature of the study, study environment, participation fee, and provided information. The findings allow researchers to better anticipate potential methodological biases when examining WTP for (biofortified) foods,while it gives policy makers a broad understanding of the potential demand for different biofortified crops in various settings

The Transcription Factor YY1 Is a Substrate for Polo-Like Kinase 1 at the G2/M Transition of the Cell Cycle

Yin-Yang 1 (YY1) is an essential multifunctional zinc-finger protein. It has been shown over the past two decades to be a critical regulator of a vast array of biological processes, including development, cell proliferation and differentiation, DNA repair, and apoptosis. YY1 exerts its functions primarily as a transcription factor that can activate or repress gene expression, dependent on its spatial and temporal context. YY1 regulates a large number of genes involved in cell cycle transitions, many of which are oncogenes and tumor-suppressor genes. YY1 itself has been classified as an oncogene and was found to be upregulated in many cancer types. Unfortunately, our knowledge of what regulates YY1 is very minimal. Although YY1 has been shown to be a phosphoprotein, no kinase has ever been identified for the phosphorylation of YY1. Polo-like kinase 1 (Plk1) has emerged in the past few years as a major cell cycle regulator, particularly for cell division. Plk1 has been shown to play important roles in the G/M transition into mitosis and for the proper execution of cytokinesis, processes that YY1 has been shown to regulate also. Here, we present evidence that Plk1 directly phosphorylates YY1 in vitro and in vivo at threonine 39 in the activation domain. We show that this phosphorylation is cell cycle regulated and peaks at G2/M. This is the first report identifying a kinase for which YY1 is a substrate