The viroses and virus-like diseases of the grapevine

A bibliographic report, 1979-198

Etat actuel des connaissances sur les maladies à virus de la vigne

L'existence de plusieurs virus capables d'infecter la vigne revêt une grande importance pour la viticulture. Ces virus sont certainement beaucoup plus répandus qu'on ne pourrait le penser en considérant seulement les cas graves où l'infection provoque le dépérissement rapide des ceps atteints. Tout ce que l'on sait des autres virus, en particulier ceux des arbres fruitiers, nous permet de supposer que les virus de la vigne sont capables de donner, par mutations, de nombreuses souches caractérisées par des degrés divers de virulence.Les viroses graves attirent l'attention, mais elles ne sont pas nécessairement la cause des plus grandes pertes de rendement pour l'ensemble du vignoble. Plus insidieuses sont les infections qui, sans détruire le cep atteint, provoquent presque chaque année le millerandage ou la coulure des grappes, ou un abaissement de la qualité du raisin.Nous avons déjà des raisons de penser que lesTendements faibles de certaines variétés résultent en bonne partie de l'infection par les virus de la dégénérescence infectieuse, conséquence d'une sélection insuffisante ou d'une sensibilité élevée. Les recherches faites en Allemagne (57) et en Californie (23, 25, 26, 27) sur la maladie de l'enroulement montrent en outre que la qualité du raisin peut, elle aussi, être influencée par la présence de virus. Or, SCHEU (57) estime que certaines variétés sont à tel point atteintes d'enroulement que la description même du cépage est basée sur l'aspect des plantes malades. Les essais de transmission par greffe effectués par les auteurs américains (27) confirment les observations de SCHEU, et montrent que ce virus infecte de nombreux cépages et porte-greffe.Une longue étude est donc encore nécessaire, pour laquelle il faut non seulement la collaboration de tous les spécialistes intéressés à ce sujet, mais aussi l'appui de tous ceux qui ont le souci de la prospérité de la viticulture

Les Viroses de la Vigne

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The Use of Pattern Differentiation in WHO-Registered Traditional Chinese Medicine Trials – a systematic review

Introduction: Pattern differentiation is a critical component for traditional Chinese medicine (TCM) diagnosis and treatment. However, the issue of whether pattern differentiation is appropriately applied in TCM Interventional trials, including Chinese herbal medicine (CHM) interventions and non-herbal TCM interventions, is unclear. The aim of this study was to i) systematically review the current status of pattern differentiation used in WHO-registered clinical trials for different types of TCM interventions; and ii) provide suggestions for improving the use of pattern differentiation in future clinical trial design. Methods: The World Health Organization (WHO) International Clinical Trials Registry Platform (ICTRP) database was searched for all TCM interventional trials registered up to 31 December 2017. In this systematic review trials with a TCM pattern differentiation in their design were included. Descriptive statistics were collated to demonstrate the characteristics of pattern differentiation applied for different TCM interventional trials. Results: Among 2,955 TCM interventional trials registered during 1999-2017, 376 (12.7%) trials included pattern differentiation. Of 376 trials, the use of pattern differentiation was identified in –title (30.6%), objective (50.5%), participants inclusion 4 (100%), outcomes (43.6%) and study background (12.5%). Further, 85.4% reported the specific name of the TCM intervention, 10.6% provided the intervention’s targeted pattern, 83.8% reported the specific name of the TCM pattern, 7.2% presented diagnostic criteria for the pattern studied, and 19.1% adopted a pattern-related outcome as primary outcome for evaluation. Conclusion: The reporting and application of pattern differentiation in TCM trials were inadequate and confusing, which was mainly due to lack of clarity regarding study design, objectives, diagnostic criteria and outcomes

Possibilités et limites de la sélection visuelle dans la lutte contre les viroses de la vigne: une expérience avec quelques cépages rouges en Suisse romande

Un travail de sélection portant sur 8 cépages rouges, entrepris en 1954 à la Station Fédérale d'Essars Agricoles de Lausanne (Suisse) et basé sur le seul examen visuel des symptômes a donné des résultats très satisfaisants. Les auteurs soulignent l'intérêt que cette méthode simple et peu coûteuse de sélection présente encore, malgré l'existence de techniques plus raffinées, telles que l'indexage, la sérologie 2t la thermothérapie. Ils décrivent les conditions dans lesquelles elle est susceptible de donner les meilleuns résultats et montrent ses limites: bien qu'elle ne suffise en général pas pour éliminer tous les virus, elle permet d'obtenir à peu de frais une amélioration très sensible du rendement des cépages sélectionnés

Inflammatory Activity of Epithelial Stem Cell Variants from Cystic Fibrosis Lungs Is Not Resolved by CFTR Modulators

Rationale CFTR (cystic fibrosis transmembrane conductance regulator) modulator drugs restore function to mutant channels in patients with cystic fibrosis (CF) and lead to improvements in body mass index and lung function. Although it is anticipated that early childhood treatment with CFTR modulators will significantly delay or even prevent the onset of advanced lung disease, lung neutrophils and inflammatory cytokines remain high in patients with CF with established lung disease despite modulator therapy, underscoring the need to identify and ultimately target the sources of this inflammation in CF lungs. Objectives To determine whether CF lungs, like chronic obstructive pulmonary disease (COPD) lungs, harbor potentially pathogenic stem cell “variants” distinct from the normal p63/Krt5 lung stem cells devoted to alveolar fates, to identify specific variants that might contribute to the inflammatory state of CF lungs, and to assess the impact of CFTR genetic complementation or CFTR modulators on the inflammatory variants identified herein. Methods Stem cell cloning technology developed to resolve pathogenic stem cell heterogeneity in COPD and idiopathic pulmonary fibrosis lungs was applied to end-stage lungs of patients with CF (three homozygous CFTR:F508D, one CFTR F508D/L1254X; FEV1, 14–30%) undergoing therapeutic lung transplantation. Single-cell–derived clones corresponding to the six stem cell clusters resolved by single-cell RNA sequencing of these libraries were assessed by RNA sequencing and xenografting to monitor inflammation, fibrosis, and mucin secretion. The impact of CFTR activity on these variants after CFTR gene complementation or exposure to CFTR modulators was assessed by molecular and functional studies. Measurements and Main Results End-stage CF lungs display a stem cell heterogeneity marked by five predominant variants in addition to the normal lung stem cell, of which three are proinflammatory both at the level of gene expression and their ability to drive neutrophilic inflammation in xenografts in immunodeficient mice. The proinflammatory functions of these three variants were unallayed by genetic or pharmacological restoration of CFTR activity. Conclusions The emergence of three proinflammatory stem cell variants in CF lungs may contribute to the persistence of lung inflammation in patients with CF with advanced disease undergoing CFTR modulator therapy

Endothelin-receptor antagonists are proapoptotic and antiproliferative in human colon cancer cells

Endothelin (ET)-1 can act as an autocrine/paracrine growth factor or an antiapoptotic factor in human cancers. To study the role of ET-1 in human colon cancer, proliferation and apoptosis of colon carcinoma cells was investigated using human HT-29 and SW480 colon carcinoma cells. ET-1 was secreted by these cells. Treatment of cells with bosentan, a dual ET(A/B)-receptor antagonist, decreased cell number. Inhibition of DNA synthesis by bosentan was observed only in the presence of serum. Exogenously added ET-1 did not increase DNA synthesis in serum-deprived cells. SW480 cells were sensitive and HT-29 cells were resistant to FasL-induced apoptosis. Bosentan sensitised resistant HT-29 cells to FasL-induced, caspase-mediated apoptosis, but not to TNF-alpha-induced apoptosis. Bosentan and/or FasLigand (FasL) did not modulate the expression of caspase-8 or FLIP. Bosentan sensitisation to apoptosis was reversed by low concentrations (10(-13)-10(-10) M), but not by high concentrations (10(-9)-10(-7) M) of ET-1. These results suggest that the binding of ET-1 to high-affinity sites inhibits FasL-induced apoptosis, while the binding of either ET-1 or receptor antagonists to low-affinity sites promotes FasL-induced apoptosis. In conclusion, endothelin signalling pathways do not induce human colon cancer cell proliferation, but are survival signals controling resistance to apoptosis