Variabilidade de Stemphylium solari, Weber, agente causal de mancha foliar do tomateiro, no estado de São Paulo

O presente trabalho trata do estudo da variabilidade do fungo, Stemphylium solani Weber, agente causal da Mancha Foliar do tomateiro (Lycopersicum esculentun Mill.), "Mancha de Estemfilium" que está se tornando cada vez mais importante em tôda área, onde se cultiva o tomateiro. Os autores isolaram 33 culturas de S. solani, de 12 municípios do Estado de São Paulo e estudaram suas capacidades de esporulação em meio de cultura. O modo de esporulação dos isolamentos variou bastante e reisolamentos e repicagens sucessivas mostraram que todos os isolamentos mantiveramas características culturais originais. Dois isolamentos (T-347 e T-419) comportaram-se de maneira bastante diferente dos demais isolamentos. Assim, êstes esporulavam espontânea e abundantemente em quaisquer meios, e nos testes de patogenicidade em tomateiro da variedade Santa Cruz, mostraram possuir elevada patogenicidade, que também confirmada estatìsticamente. Com base na capacidade de esporular em meios de cultura, patogenicidade em tomateiro suscetível e estabilidade das características culturais, os autores propuseram a classificação de S. solani, em 3 raças fisiológicas e discutem sua importância na interpretação de dados divergentes da literatura. Além disso, chamam a atenção para as culturas patogênicas capazes de esporular espontâneamente no meio de batata-dextroseagar e suas aplicações nos trabalhos de melhoramento do tomateiro.

Glomevella cingulata (Stonem.) spauld. et v. schrenk. F. SP. phaseoli N.F., fase ascógena do agente causal da antracnose do feijoeiro

O presente trabalho versa sobre a obtenção da fase perfeita de Colletotriohum lindemuthianum (Sacc. et Magn.) Scrib., dirimindo duvidas quanto a sua existência, suscitada pelo primeiro relato feito por SHEAR e WOOD (1913). Após ter encontrado duas linhagens heterotálicas que formaram ascosporos em acasalamentos, os autores estudaram alguns fatores ambientais que favorecem a reprodução sexuada, chegando-se as seguintes conclusões: peritecios se formaram sobre varios meios de cultura semi-sintéticos em cuja composição entram glucose, Ca(N0(3))2.4H(2)0(, MgSO4.7H2O e KH2PO4, agar e água; a quantidade de glucose deve ser igual ou maior do que 4g/l, a de Ca(NO3)2.4H2O de 0,15 a 0,60 g/l e a relação C/N deve estar entre 29,8 a 89,6:1; a adição de vitaminas alterou levemente o nível de aproveitamento de Ca(NO3)2.4H2O, nao havendo boa produção de peritécio ao nível de 0,15 g/l mas permitindo-se ate o nível de 1 g/l, mantendo-se as relações C/N mais ou menos no mesmo nivel; a luz, nos estágios final ou inicial ou em períodos alternados acima de 8 horas, inibiu a formação de ascosporos, sendo, portanto, essencial a escuridão contínua; peritécios se formaram sob condições de pH variável de 4,0 a 6,0; peritécios ejetam ascosporos em condições de alta umidade; a temperatura em que foram obtidos os peritécios foi sempre de 209C. Do acasalamento de linhagens conidiais de C.lindemuthianum o autor obteve resultados a priori comparáveis aos de trabalhos genéticos feitos com G.cingulata, chegando-se a conclusão de que as linhagens usadas sao heterotãlicas possivelmente condicionadas por varios fatores genéticos. Isolamentos ascospóricos foram inoculados, sendo todos patogênicos ao feijoeiro, pelo menos para a variedade Michelite. Comparando morfológicamente a fase ascogena de C.lindemuthvanwn com G.cvngulata, o autor propõe o nome de Glomerelia cingulata (Stonem.) Spauld et v. Schrenk f.phaseoli n.f.

Exercice physique et athérosclérose : quels sont les mécanismes physiologiques et moléculaires de l'exercice qui préviennent et protègent de l'athérosclérose? : approche chez un modèle expérimental d'athérosclérose : la souris génétiquement dépourvue en apolipoprotéine E (apoE-/-)

RESUME : L'athérosclérose, pathologie inflammatoire artérielle chronique, est à l'origine de la plupart des maladies cardiovasculaires qui constituent l'une des premières causes de morbidité et mortalité en France. Les études observationnelles et expérimentales montrent que l'exercice physique prévient la mortalité cardiovasculaire. Cependant, les mécanismes précisant les bénéfices cliniques de l'exercice sur l'athérosclérose sont encore largement inconnus. Le but général de ce travail a donc été d'explorer, en utilisant un modèle expérimental d'athérosclérose, la souris hypercholestérolémique génétiquement dépourvue en apolipoprotéine E (apoE-/-), les mécanismes athéroprotecteurs de l'exercice. La dysfonction endothéliale, généralement associée aux facteurs de risque cardiovasculaire, serait l'une des étapes précoces majeures de l'athérogenèse. Elle est caractérisée par une diminution de la biodisponibilité en monoxyde d'azote (NO) avec la perte de ses propriétés vasculo-protectrices, ce qui favorise un climat pro-athérogène (stress oxydatif, adhésion et infiltration des cellules inflammatoires dans la paroi artérielle...) conduisant à la formation de la plaque athéromateuse. L'objectif de notre premier travail a donc été d'explorer les effets de l'exercice d'une part, sur le développement des plaques athéromateuses et d'autre part, sur la fonction endothéliale de la souris apoE-/-. Nos résultats montrent que l'exercice réduit significativement l'extension de l'athérosclérose et prévient la dysfonction endothéliale. L'explication pharmacologique montre que l'exercice stimule la fonction endothéliale via, notamment, une plus grande sensibilité des récepteurs endothéliaux muscariniques, ce qui active les événements signalétiques cellulaires récepteurs-dépendants à l'origine d'une bioactivité accrue de NO. Les complications cliniques graves de l'athérosclérose sont induites par la rupture de la plaque instable provoquant la formation d'un thrombus occlusif et l'ischémie du territoire tissulaire en aval. L'objectif de notre deuxième travail a été d'examiner l'effet de l'exercice sur la qualité/stabilité de la plaque. Nos résultats indiquent que l'exercice de longue durée stabilise la plaque en augmentant le nombre de cellules musculaires lisses et en diminuant le nombre de macrophages intra-plaques. Nos résultats montrent aussi que la phosphorylation de la eNOS (NO Synthase endothéliale) Akt-dépendante n'est pas le mécanisme moléculaire majeur à l'origine de ce bénéfice. Enfin, dans notre troisième travail, nous avons investigué l'effet de l'exercice sur le développement de la plaque vulnérable. Nos résultats montrent, chez un modèle murin de plaque instable (modèle d'hypertension rénovasculaire à rénine et angiotensine II élevés) que l'exercice prévient l'apparition de la plaque vulnérable indépendamment d'un effet hémodynamique. Ce bénéfice serait associé à une diminution de l'expression vasculaire des récepteurs AT1 de l'Angiotensine II. Nos résultats justifient l'importance de l'exercice comme outil préventif des maladies cardiovasculaires. ABSTRACT : Atherosclerosis, a chronic inflammatory disease, is one of the main causes of morbidity and mortality in France. Observational and experimental data indicate that regular physical exercise has a positive impact on cardiovascular mortality. However, the mechanisms by which exercise exerts clinical benefits on atherosclerosis are still unknown. The general aim of this work was to elucidate the anti-atherosclerotic effects of exercise, using a mouse model of atherosclerosis: the apolipoprotein E-deficient mice (apoE-/- mice). Endothelial dysfunction, generally associated with cardiovascular risk factors, has been recognized to be a major and early step in atherogenesis. Endothelial dysfunction is characterized by Nitric Oxide (NO) biodisponibility reduction with loss of NO-mediated vasculoprotective actions. This leads to vascular effects such as increased oxidative stress and increased adhesion of inflammatory cells into arterial wall thus playing a role in atherosclerotic plaque development. Therefore, one of the objective of our study was to explore the effects of exercise on atherosclerotic plaque extension and on endothelial function in apoE-/- mice. Results show that exercise significantly reduces plaque progression and prevents endothelial dysfunction. Pharmacological explanation indicates that exercise stimulates endothelial function by increasing muscarinic receptors sensitivity which in turn activates intracellular signalling receptor-dependent events leading to increased NO bioactivity. The clinical manifestations of atherosclerosis are the consequences of unstable plaque rupture with thrombus formation leading to tissue ischemia. The second aim of our work was to determine the effect of exercise on plaque stability. We demonstrate that long-term exercise stabilizes atherosclerotic plaques as shown by decreased macrophage and increased Smooth Muscle Cells plaque content. Our results also suggest that the Akt-dependent eNOS phosphorylation pathway is not the primary molecular mechanism mediating these beneficial effects. Finally, we assessed a putative beneficial effect of exercise on vulnerable plaque development. In a mouse model of Angiotensine II (Ang II)-mediated vulnerable atherosclerotic plaques, we provide fist evidence that exercise prevents atherosclerosis progression and plaque vulnerability. The beneficial effect of swimming was associated with decreased aortic Ang II AT1 receptor expression independently from any hemodynamic change. These findings suggest clinical benefit of exercise in terms of cardiovascular event protection.

The causal relationship between Individual’s choice behavior and self-reported satisfaction: the case of residential mobility in the EU

One of the most persistent and lasting debates in economic research refers to whether the answers to subjective questions can be used to explain individuals’ economic behavior. Using panel data for twelve EU countries, in the present study we analyze the causal relationship between self-reported housing satisfaction and residential mobility. Our results indicate that: i) households unsatisfied with their current housing situation are more likely to move; ii) housing satisfaction raises after a move, and; iii) housing satisfaction increases with the transition from being a renter to becoming a homeowner. Some interesting cross-country differences are observed. Our findings provide evidence in favor of use of subjective indicators of satisfaction with certain life domains in the analysis of individuals’ economic conduct.

Développement d'indicateurs pour le contrat de prestations 2008 entre le Cipret et le Département de l'économie et de la santé (DES) : élaboration d'une théorie d'action du Cipret Genève selon le Modèle de catégorisation des résultats de Promotion Santé Suisse

[Table des matières] 1. Introduction. 2. Méthode. 3. Théorie d'action et plan de monitorage des résultats des activités du Cipret (Centre d'information et de prévention du tabagisme) : priorités pour l'année 2008: Axe 1: Informer sur les conséquences de la consommation de tabac et sur la promotion de la santé. Axe 2: Contribuer à la cohérence de la politique de santé publique en matière de tabac. Axe 3: Diminuer le nombre de nouveaux fumeurs. Axe 4: Aider au sevrage du tabac. Annexes.

What is the Causal Effect of Information and Learning about a Public Good on Willingness to Pay?

In this study we elicit agents’ prior information set regarding a public good, exogenously give information treatments to survey respondents and subsequently elicit willingness to pay for the good and posterior information sets. The design of this field experiment allows us to perform theoretically motivated hypothesis testing between different updating rules: non-informative updating, Bayesian updating, and incomplete updating. We find causal evidence that agents imperfectly update their information sets. We also field causal evidence that the amount of additional information provided to subjects relative to their pre-existing information levels can affect stated WTP in ways consistent overload from too much learning. This result raises important (though familiar) issues for the use of stated preference methods in policy analysis.

The Causal effect of education on aggregate income

Empirical studies assume that the macro Mincer return on schooling is con- stant across countries. Using a large sample of countries this paper shows that countries with a better quality of education have on average relatively higher macro Mincer coeficients. As rich countries have on average better educational quality, differences in human capital between countries are larger than has been typically assumed in the development accounting literature. Consequently, factor accumulation explains a considerably larger share of income differences across countries than what is usually found.

Rôle de l'activation de c-Jun N-terminal kinase (JNK) dans un modèle de glaucome chez le rat et neuroprotection par inhibition de la voie de JNK

RESUME : Dans ce travail effectué chez le rat adulte, l'excitotoxicité rétinienne est élicitée par injection intravitréenne de NMDA. Les lésions en résultant sont localisées dans la rétine interne. Elles prennent la forme de pycnoses dans la couche des cellules ganglionnaires (corps cellulaires des cellules ganglionnaires et amacrines déplacées) et dans la partie interne de la couche nucléaire interne (cellules amacrines). Cette localisation est liée à la présence de récepteurs au glutamate de type NMDA sur ces cellules. L'activation de ces récepteurs entraîne un influx calcique et l'activation de diverses enzymes (phospholipase A, calpaïnes, calmoduline, synthase d'oxyde nitrique). La signalisation se poursuit en aval en partie par les voies des Mitogen Activated Protein Kinase (MAPK) : ERK, p38, ]NK. Dans les expériences présentées, toutes trois sont activées après l'injection de NMDA. Dans les cascades de signalisation de JNK, trois kinases s'ancrent sur une protéine scaffold. Les MAPKKK phosphorylent MKK4 et MKK7, qui phosphorylent JNK. JNK a de nombreuses cibles nucléaires (dont le facteur de transcription c-Jun) et cytoplasmiques. La voie de JNK est bloquée par l'inhibiteur peptidique D-JNKI-1 en empêchant l'interaction de la kinase avec son substrat. L'inhibiteur est formé de 20 acides aminés du domaine de liaison JBD et de 10 acides aminés de la partie TAT du virus HIV. L'injection intravitréenne de D-JNKI-1 permet une diminution des taux de JNK et c-Jun phosphorylés dans les lysats de rétine. L'effet prépondérant est la restriction importante des altérations histologiques des couches internes de la rétine. L'évaluation par électrorétinogramme met en sus en évidence une sauvegarde de la fonction cellulaire. Ce travail a ainsi permis d'établir la protection morphologique et fonctionnelle des cellules de la rétine interne par inhibition spécifique de la voie de JNK lors d'excitotoxicité. SUMMARY Excitotoxicity in the retina associates with several pathologies like retinal ischemia, traumatic optic neuropathy and glaucoma. In this study, excitotoxicity is elicited by intravitreal NMDA injection in adult rats. Lesions localise in the inner retina. They present as pyknotic cells in the ganglion cell layer (ganglion cells and displaced amacrines) and the inner nuclear layer (amacrine cells). These cells express NMDA glutamate receptors. The receptor activation leads to a calcium flow into the cell and hence enzyme activation (phospholipase, calpains, calmodulin, nitric oxide synthase). The subsequent signaling pathways can involve the Mitogen Activated Protein Kinases (MAPK): ERK, p38 end JNK. These were all activated in our experiments. The signaling cascade organises around several scaffold proteins. The various MAPKKK phosphorylate MKK4 and MKK7, which phosphorylate JNK. JNK targets are of nuclear (c-Jun transcription factor) or cytoplasmic localisation. The peptidic inhibitor D-JNKI-1, 20 amino acids from the JNK binding domain JBD coupled to 10 amino acids of the TAT transporter, disrupts the binding of JNK with its substrate. Intravitreal injection of the inhibitor lowers phosphorylated forms of JNK and c-Jun in retinal extracts. It protects strongly against histological lesions in the inner retina and allows functional rescue.

On making causal claims: A review and recommendations

Social scientists often estimate models from correlational data, where the independent variable has not been exogenously manipulated; they also make implicit or explicit causal claims based on these models. When can these claims be made? We answer this question by first discussing design and estimation conditions under which model estimates can be interpreted, using the randomized experiment as the gold standard. We show how endogeneity--which includes omitted variables, omitted selection, simultaneity, common methods bias, and measurement error--renders estimates causally uninterpretable. Second, we present methods that allow researchers to test causal claims in situations where randomization is not possible or when causal interpretation is confounded, including fixed-effects panel, sample selection, instrumental variable, regression discontinuity, and difference-in-differences models. Third, we take stock of the methodological rigor with which causal claims are being made in a social sciences discipline by reviewing a representative sample of 110 articles on leadership published in the previous 10 years in top-tier journals. Our key finding is that researchers fail to address at least 66 % and up to 90 % of design and estimation conditions that make causal claims invalid. We conclude by offering 10 suggestions on how to improve non-experimental research.

De novo mutation in the KCNQ1 gene causal to Jervell and Lange-Nielsen syndrome.

Jervell and Lange-Nielsen syndrome (JLNS) is an autosomal recessive disorder, clinically characterized by severe cardiac arrhythmias [due to prolonged QTc interval in electrocardiogram (ECG)] and bilateral sensory neural deafness. Molecular defects causal to JLNS are either homozygous or compound heterozygous mutations, predominantly in the KCNQ1 gene and occasionally in the KCNE1 gene. As the molecular defect is bi-allelic, JLNS patients inherit one pathogenic mutation causal to the disorder from each parent. In this report, we show for the first time that such a disorder could also occur due to a spontaneous de novo mutation in the affected individual, not inherited from the parent, which makes this case unique unlike the previously reported JLNS cases.