Droits à produire transférables

Cet article propose une analyse de l’évolution du système d’accès au foncier conchylicole en France ainsi qu’une étude de son fonctionnement actuel. Il traite la question de la répartition des moyens de production dans un secteur dominé par le modèle de l’exploitation familiale et ayant vocation à maintenir une base sociale créatrice d’emplois dans certaines zones d’activité du littoral. Le régime d’accès au foncier conchylicole s’apparente à un système de droits à produire transférables. Cependant, le développement spontané du marché des concessions conchylicoles dans un contexte de faible intervention de l’administration provoque des effets non désirés dont la manifestation est ici vérifiée empiriquement, sur données quantitatives et qualitatives. La discussion finale porte sur la recherche d’outils de régulation et d’indicateurs économiques pour un meilleur fonctionnement du marché des concessions.This paper sets out an historical analysis of the rights-based system applied to the French shellfish-farming sector and a study of the current operating way of this system. It addresses the issue of the distribution of production means within an industry whose two main characteristics are the familial exploitation model and the specific social objectives like jobs creation in some coastal areas. The shellfish farming rights-based system has evolved toward a transferable production-rights system. However, the spontaneous emergence of a market for production-rights in the context of a weak administrative intervention is likely to generate unintended effects, whose occurrence is tested using quantitative and qualitative data. The final discussion searches for the economic indicators and the regulation tools which could improve the efficiency of the shellfish farming concessions market

Zooming in on VY CMa ejecta

The Atacama Large Millimeter/Submillimeter Array (ALMA), Cagliari, Italy 14–18 October 2019ALMA has allowed us to study the ejecta around evolved stars with unprecedented resolution. This extremely high resolution at the millimeter domain provides a unique tool to study the processes taking place in the innermost regions of these evolved stars. In particular, the processes leading to the mass ejections of the Red Supergiant stars are unknown. The pulsation process responsible for mass ejection in the intermediate mass AGB phase does not work in the high mass evolved stars. Therefore, studying the characteristics of the mass ejections near the photosphere of the massive stars is essential to constrain the processes leading to the observed gas ejection. In this sense, we have obtained interferometric maps in the range 231.7 ¿ 235.3 GHz of the ejecta around the Red Supergiant star VY CMa with an spatial resolution of 0.02>. These maps revealed a level of complexity higher than previously anticipated from previous observations. The complexity seems to be due both to structural and chemical processes. The molecular lines covered within these maps range from upper energies 19 up to 3400 K, tracing different excitation conditions. We will present a global view of the different structures observedThe research leading to these results has received funding from the European Research Council under the European Union’s Seventh Framework Programme (FP/2007-2013) / ERC Grant Agreement n. 610256 (NANOCOSMOS). We would also like to thank the Spanish MINECO for funding support from grants CSD2009-00038, AYA2012-32032, AYA2016-75066-C2-1-P & AYA2016-78994-P. M.A. also thanks for funding support from the Ramón y Cajal programme of Spanish MINECO (RyC-2014- 16277)

Genetic Variants of Alcohol Metabolizing Enzymes and Alcohol-Related Liver Cirrhosis Risk

Alcohol-related liver disease (ARLD) is a major public health issue caused by excessive alcohol consumption. ARLD encompasses a wide range of chronic liver lesions, alcohol-related liver cirrhosis being the most severe and harmful state. Variations in the genes encoding the enzymes, which play an active role in ethanol metabolism, might influence alcohol exposure and hence be considered as risk factors of developing cirrhosis. We conducted a case-control study in which 164 alcohol-related liver cirrhosis patients and 272 healthy controls were genotyped for the following functional single nucleotide variations (SNVs): ADH1B gene, rs1229984, rs1041969, rs6413413, and rs2066702; ADH1C gene, rs35385902, rs283413, rs34195308, rs1693482, and rs35719513; CYP2E1 gene, rs3813867. Furthermore, copy number variations (CNVs) for ADH1A, ADH1B, ADH1C, and CYP2E1 genes were analyzed. A significant protective association with the risk of developing alcohol-related liver cirrhosis was observed between the mutant alleles of SNVs ADH1B rs1229984 (Pc value = 0.037) and ADH1C rs283413 (Pc value = 0.037). We identified CNVs in all genes studied, ADH1A gene deletions being more common in alcohol-related liver cirrhosis patients than in control subjects, although the association lost statistical significance after multivariate analyses. Our findings support that susceptibility to alcohol-related liver cirrhosis is related to variations in alcohol metabolism genes

Detection of C3O in IRC+10216: Oxygen-Carbon chain chemistry in the outer envelope

The oxygen-bearing species C3O has been identified in the circumstellar envelope of the carbon star IRC +10216. The J = 8-->7, 9-->8, 10-->9, 14-->13, and 15-->14 transitions were detected at 2 and 3 mm using the Arizona Radio Observatory’s 12 m telescope. Measurements of the J = 9-->8, 10-->9, and 12-->11 lines were simultaneously conducted at the IRAM 30 m telescope. The line profiles of C3O are roughly U-shaped, indicating an extended shell distribution for this molecule in IRC +10216. The total column density derived for C3O is 1.2x10^12 cm^-2, at least an order of magnitude higher than that predicted by current chemical models. However, a revised model that includes reactions of atomic oxygen with carbon-chain radicals, such as l-C3H and C4, can reproduce the observed abundance. This model also predicts that C3O arises from a shell source with an outer radius near r ∼ 30", consistent with the observations. These results suggest that gas phase neutral-neutral chemistry may be producing the oxygen-bearing molecules present in the outer envelope of IRC +10216.This material is based on work supported by the National Aeronautics and Space Administration through the NASA Astrobiology Institute under Cooperative Agreement CAN-02-OSS-02 issued through the Office of Space Science. We also acknowledge support from Spanish MEC under project AYA2003-2785 and from "Comunidad de Madrid" under PRICIT project S-0505/ESP-0237 (ASTROCAM). E. D. T. thanks NSF for a graduate research fellowship, and M. A. acknowledges Spanish MEC for a predoctoral grant AP2003-4619.Peer reviewe

Detoxifying enzymes at the cross-roads of inflammation, oxidative stress, and drug hypersensitivity: role of glutathione transferase P1-1 and aldose reductase

9 p.-2 figPhase I and II enzymes are involved in the metabolism of endogenous reactive compounds as well as xenobiotics, including toxicants and drugs. Genotyping studies have established several drug metabolizing enzymes as markers for risk of drug hypersensitivity. However, other candidates are emerging that are involved in drug metabolism but also in the generation of danger or costimulatory signals. Enzymes such as aldo-keto reductases (AKR) and glutathione transferases (GST) metabolize prostaglandins and reactive aldehydes with proinflammatory activity, as well as drugs and/or their reactive metabolites. In addition, their metabolic activity can have important consequences for the cellular redox status, and impacts the inflammatory response as well as the balance of inflammatory mediators, which can modulate epigenetic factors and cooperate or interfere with drug-adduct formation. These enzymes are, in turn, targets for covalent modification and regulation by oxidative stress, inflammatory mediators, and drugs. Therefore, they constitute a platform for a complex set of interactions involving drug metabolism, protein haptenation, modulation of the inflammatory response, and/or generation of danger signals with implications in drug hypersensitivity reactions. Moreover, increasing evidence supports their involvement in allergic processes. Here, we will focus on GSTP1-1 and aldose reductase (AKR1B1) and provide a perspective for their involvement in drug hypersensitivityThis work has been supported by grants SAF2012-36519 from MINECO and SAF-2015-68590-R from MINECO/FEDER and ISCIII RETIC RIRAAF RD12/0013/0008 to DP,and RD12/0013/0002 to J A.Peer reviewe

Toward a clinical practice guide in pharmacogenomics testing for functional polymorphisms of drug-metabolizing enzymes. Gene/drug pairs and barriers perceived in Spain

The development of clinica lpractice recommendations or guidelines for the clinical use of biomarkers is an issue of great importance withr regard to adverse drug reactions.The poten-tial of pharmacogenomicbiomarkers has been extensively investigated in recent years.However,several barriers to implementing the use of pharmacogenomics testing exist.We conducted a survey among members of the Spanish Societies of Pharmacology and Clinical Pharmacology to obtain information about the perception of such barriers and to compare the perceptions of participants about the relative importance of majorgene/drug pairs.Of 11 potential barriers,the highest importance was attributed to lack of institutional support for pharmacogenomic stesting,and to the issues related to the lack of guidelines.Of the proposed gene/drug pairs the highest importance was assigned to HLA-B/abacavir, UGT1A1/irinotecan, and CYP2D6/tamoxifen.In this perspective article,we compare the relative importance of 29 gene/drugpairs in the Spanish study with that of the same pairs in the American Society for Clinical Pharmacology and Therapeutic sstudy,and we provide suggestions and areas of focus to develop a guide for clinical practice in pharmacogenomics testingThe work in the author’s laboratory is financed by Grants PS09/00943, PS09/00469, RETICS RIRAAF RD07/0064/0016, and CIBERehd from Instituto de Salud CarlosIII,Madrid, Spain, and by Grants GR10068 from Junta de Extremadura, Spain. Financed in part with FEDER funds from the European Unio

Pharmacogenomics of prostaglandin and leukotriene receptors

Los antecedentes genéticos individuales junto con los efectos ambientales se cree que están detrás de muchas enfermedades complejas. Una serie de variantes genéticas, principalmente los SNPs (single nucleotide polymorphisms), han demostrado estar asociados con diferentes patologías y afecciones inflamatorias, que representan potenciales dianas terapéuticas. Las prostaglandinas (PTGs) y leucotrienos (LTs) son eicosanoides derivados del ácido araquidónico y relacionados con ácidos grasos poliinsaturados participan tanto en la homeostasis normal y en condiciones inflamatorias. Estos mediadores lípidos bioactivos son sintetizados a través de dos grandes vías enzimáticas multipaso: PTGs por la ciclooxigenasa y la lipooxigenasa DE 5 LTS. Los principales efectos fisiológicos de PTGs incluyen vasodilatación y la fuga vascular (PTGE2); la maduración de los mastocitos, eosinófilos, y reacciones alérgicas (PTGD2); vascular y la contracción del músculo liso de las vías respiratorias (PTGF2), e inhibición de la agregación plaquetaria (PTGI2). LTB4 está principalmente involucrado en el reclutamiento de los neutrófilos, fuga vascular y en la función de la barrera epitelial, mientras que cisteinil LTs (CysLTs) (LTC4, LTD4 y LTE4) inducen la broncoconstricción y extravasación de neutrófilos, y también participar en la fuga vascular. PTGs y LTs ejercen sus funciones biológicas mediante su unión a receptores afines, que pertenecen a las siete transmembranas acopladas a proteínas G, la superfamilia de receptores. Los SNPs en genes que codifican estos receptores pueden influir en su funcionalidad, ya que tienen un papel en la susceptibilidad a las enfermedades y la respuesta al tratamiento de los medicamentos. En esta revisión resumimos los SNPs en PTGs y receptores de LTs y su relevancia en enfermedades humanas. También ofrecemos información sobre la expresión génica. Por último, podemos especular sobre la dirección futura de este tema.Individual genetic background together with environmental effects are thought to be behind many human complex diseases. A number of genetic variants, mainly single nucleotide polymorphisms (SNPs), have been shown to be associated with various pathological and inflammatory conditions, representing potential therapeutic targets. Prostaglandins (PTGs) and leukotrienes (LTs) are eicosanoids derived from arachidonic acid and related polyunsaturated fatty acids that participate in both normal homeostasis and inflammatory conditions. These bioactive lipid mediators are synthesized through two major multistep enzymatic pathways: PTGs by cyclooxygenase and LTs by 5-lipoxygenase. The main physiological effects of PTGs include vasodilation and vascular leakage (PTGE2); mast cell maturation, eosinophil recruitment, and allergic responses (PTGD2); vascular and respiratory smooth muscle contraction (PTGF2), and inhibition of platelet aggregation (PTGI2). LTB4 is mainly involved in neutrophil recruitment, vascular leakage, and epithelial barrier function, whereas cysteinyl LTs (CysLTs) (LTC4, LTD4, and LTE4) induce bronchoconstriction and neutrophil extravasation, and also participate in vascular leakage. PTGs and LTs exert their biological functions by binding to cognate receptors, which belong to the seven transmembrane, G protein-coupled receptor superfamily. SNPs in genes encoding these receptors may influence their functionality and have a role in disease susceptibility and drug treatment response. In this review we summarize SNPs in PTGs and LTs receptors and their relevance in human diseases. We also provide information on gene expression. Finally, we speculate on future directions for this topic.Trabajo patrocinado por: Programa Miguel Servet. Ref CP14/00034, para José Antonio Cornejo García Ministerio de Economía y Competitividad y Instituto Nacional de Salud Carlos III y Fondos FEDER. Programa Sara Borrell. Ref. CD14/00242, para James R. Perkins Ministerio de Economía y Competitividad e Instituto Nacional de Salud Carlos III y Fondos FEDER. Becas FISPI12/02247, FISPI13/02598 y FISPI15/00726 Servicio Público de Salud de Andalucía. Beca PI-0279-2012 Junta de Extremadura y Fondos FEDER. Beca GR15026peerReviewe

Pharmacogenetic Factors Affecting Asthma Treatment Response. Potential Implications for Drug Therapy

Asthma is a frequent disease, mainly characterized by airway inflammation, in which drug therapy is crucial in its management. The potential of pharmacogenomics testing in asthma therapy has been, to date, little explored. In this review, we discuss pharmacogenetic factors affecting asthma treatment, both related to drugs used as controller medications for regular maintenance, such as inhaled corticosteroids, anti-leukotriene agents, long-acting beta-agonists, and the new biologic agents used to treat severe persistent asthma. In addition, we discuss current pharmacogenomics knowledge for rescue medications provided to all patients for as-needed relief, such as short-acting beta-agonists. Evidence for genetic variations as a factor related to drugs response has been provided for the following genes and groups of drugs: Inhaled corticosteroids: FCER2; anti-leukotriene agents: ABCC1, and LTC4S; beta-agonists: ADRB2. However, the following genes require further studies confirming or rejecting association with the response to asthma therapy: ADCY9, ALOX5, ARG1, ARG2, CRHR1, CRHR2, CYP3A4, CYP3A5, CYSLTR1, CYSLTR2, GLCCI1, IL4RA, LTA4H, ORMDL3, SLCO2B1, SPATS2L, STIP1, T, TBX21, THRA, THRB, and VEGFA. Although only a minority of these genes are, at present, listed as associated with drugs used in asthma therapy, in the Clinical Pharmacogenomics Implementation Consortium gene-drug pair list, this review reveals that sufficient evidence to start testing the potential of clinical pharmacogenomics in asthma therapy already exists. This evidence supports the inclusion in pilot pharmacogenetics tests of at least four genes. Hopefully these tests, if proven useful, will increase the efficiency and the safety of asthma therapy

The Maser-emitting Structure and Time Variability of the SiS Lines J =14-13 and 15-14 in IRC+10216

2 pags., 1 tab. -- Why Galaxies Care About AGB Stars: A Continuing Challenge through Cosmic Time Proceedings IAU Symposium No. 343, 2019 F. Kerschbaum, M. Groenewegen & H. Olofsson, eds.AGB stars are important contributors of processed matter to the ISM. However, the physical and chemical mechanisms involved in its ejection are still poorly known. This process is expected to have remarkable effects in the innermost envelope, where the dust grains are formed, the gas is accelerated, the chemistry is active, and the radiative excitation becomes important. A good tracer of this region in C-rich stars is SiS, an abundant refractory molecule that can display maser lines, very sensitive to changes in the physical conditions. We present high angular resolution interferometer observations (HPBW â‰30.″.25) of the v = 0 J = 14-13 and 15-14 SiS maser lines towards the archetypal AGB star IRC+10216, carried out with CARMA and ALMA to explore the inner 1> region around the central star. We also present an ambitious monitoring of these lines along one single pulsation period carried out with the IRAM 30 m telescope.The research leading to these results has received funding from the European Research Council under the European Union’s Seventh Framework Programme (FP7/2007-2013)/ ERC grant agreement n◦ 610256: NANOCOSMO

Trends in Qualifying Biomarkers in Drug Safety. Consensus of the 2011 Meeting of the Spanish Society of Clinical Pharmacology

In this paper we discuss the consensus view on the use of qualifying biomarkers in drug safety, raised within the frame of the XXIV meeting of the Spanish Society of Clinical Pharmacology held in Málaga (Spain) in October, 2011. The widespread use of biomarkers as surrogate endpoints is a goal that scientists have long been pursuing. Thirty years ago, when molecular pharmacogenomics evolved, we anticipated that these genetic biomarkers would soon obviate the routine use of drug therapies in a way that patients should adapt to the therapy rather than the opposite. This expected revolution in routine clinical practice never took place as quickly nor with the intensity as initially expected. The concerted action of operating multicenter networks holds great promise for future studies to identify biomarkers related to drug toxicity and to provide better insight into the underlying pathogenesis. Today some pharmacogenomic advances are already widely accepted, but pharmacogenomics still needs further development to elaborate more precise algorithms and many barriers to implementing individualized medicine exist. We briefly discuss our view about these barriers and we provide suggestions and areas of focus to advance in the field