Compositional gossip: a conceptual architecture for designing gossip-based applications

Most proposed gossip-based systems use an ad-hoc design. We observe a low degree of reutilization among this proposals. We present how this limits both the systematic development of gossip-based applications and the number of applications that can benefit from gossip-based construction. We posit that these reinvent-the-wheel approaches poses a significant barrier to the spread and usability of gossip protocols. This paper advocates a conceptual design framework based upon aggregating basic and predefined building blocks BD 2. We show how to compose building blocks within our framework to construct more complex blocks to be used in gossip-based applications. The concept is further depicted with two gossip-based applications described using our building blocks.(undefined

Slicing as a distributed systems primitive

Large-scale distributed systems appear as the major in- frastructures for supporting planet-scale services. These systems call for appropriate management mechanisms and protocols. Slicing is an example of an autonomous, fully decentral- ized protocol suitable for large-scale environments. It aims at organizing the system into groups of nodes, called slices, according to an application-specific criteria where the size of each slice is relative to the size of the full system. This al- lows assigning a certain fraction of nodes to different task, according to their capabilities. Although useful, current slicing techniques lack some features of considerable practical importance. This pa- per proposes a slicing protocol, that builds on existing so- lutions, and addresses some of their frailties. We present novel solutions to deal with non-uniform slices and to per- form online and dynamic slices schema reconfiguration. Moreover, we describe how to provision a slice-local Peer Sampling Service for upper protocol layers and how to en- hance slicing protocols with the capability of slicing over more than one attribute. Slicing is presented as a complete, dependable and inte- grated distributed systems primitive for large-scale systems.(undefined

Brisa: combining efficiency and reliability in epidemic data dissemination

There is an increasing demand for efficient and robust systems able to cope with today's global needs for intensive data dissemination, e.g., media content or news feeds. Unfortunately, traditional approaches tend to focus on one end of the efficiency/robustness design spectrum, by either leveraging rigid structures such as trees to achieve efficient distribution, or using loosely-coupled epidemic protocols to obtain robustness. In this paper we present BRISA, a hybrid approach combining the robustness of epidemic-based dissemination with the effi- ciency of tree-based structured approaches. This is achieved by having dissemination structures such as trees implicitly emerge from an underlying epidemic substrate by a judicious selection of links. These links are chosen with local knowledge only and in such a way that the completeness of data dissemination is not compromised, i.e., the resulting structure covers all nodes. Failures are treated as an integral part of the system as the dissemination structures can be promptly compensated and repaired thanks to the underlying epidemic substrate. Besides presenting the protocol design, we conduct an extensive evaluation in a real environment, analyzing the effectiveness of the structure creation mechanism and its robustness under faults and churn. Results confirm BRISA as an efficient and robust approach to data dissemination in the large scale.This work was supported in part by the Swiss National Foundation under agreement number 200021-127271/1 and by the Portuguese Science Foundation (FCT) grants SFRH/BD/62380/2009 and PTDC/EIA-CCO/115570/200

Scaling up publish/subscribe overlays using interest correlation for link sharing

Topic-based publish/subscribe is at the core of many distributed systems, ranging from application integration middleware to news dissemination. Therefore, much research was dedicated to publish/subscribe architectures and protocols, and in particular to the design of overlay networks for decentralized topic-based routing and efficient message dissemination. Nonetheless, existing systems fail to take full advantage of shared interests when disseminating information, hence suffering from high maintenance and traffic costs, or construct overlays that cope poorly with the scale and dynamism of large networks. In this paper we present StaN, a decentralized protocol that optimizes the properties of gossip-based overlay networks for topicbased publish/subscribe by sharing a large number of physical connections without disrupting its logical properties. StaN relies only on local knowledge and operates by leveraging common interests among participants to improve global resource usage and promote topic and event scalability. The experimental evaluation under two real workloads, both via a real deployment and through simulation shows that StaN provides an attractive infrastructure for scalable topic-based publish/subscribe

Implication de la protéine Bcl-xL dans la mégacaryopoïèse humaine normale et dans le purpura thrombopénique immunologique chronique

The Bcl-xL protein is a member of Bcl-2 anti-apoptotic proteins. It has been shown in mouse that this protein had a major role in platelet production (megakaryopoiesis). Bcl-xL deregulation could lead to megakaryopoiesis impairement and explain some human diseases such as chronic thrombocytopenias. One cause of chronic thrombocytopenia is immune thrombocytopenia (ITP) that associates 2 pathophysiological mechanisms: an immune-mediated platelet destruction and an insufficient production from the bone marrow cells. ITP is a diagnosis of exclusion when all known causes of thrombocytopenia have been ruled out by diagnosis work-up. In ITP cohort of patients followed in our internal medicine department, we have identified some patients with a haematological profile of their disease, ie absence of overt features of auto-immunity, and absence of response to immunomudulatory treatments, or no indication to such treatment because of sufficient platelet count. We demonstrate in this study that Bcl-xL is necessary for megakaryocyte survival during all megakaryopoiesis, contrary to what was found in mouse. Moreover, some patients have an intrinsically impaired proplatelet formation, and some of them also have a decrease of Bcl-xL mRNA and protein in their platelets. These novel observations suggest that a deregulation of Bcl-xL is a possible cause of their disease and lead the way to the identification of a potentially new cause of chronic thrombocytopenia in humanLa protéine Bcl-xL fait partie de la famille des protéines anti-apoptotiques Bcl-2. Il a été montré que cette protéine avait un rôle majeur dans la formation des plaquettes chez la souris (mégacaryopoïèse). Une dérégulation de cette protéine pourrait aboutir à une altération de la mégacaryopoïèse et donner des pathologies humaines comme des thrombopénies chroniques. Une des causes de thrombopénies chroniques est le purpura thrombopénique immunologique (ou PTI), qui associe deux mécanismes physiopathologiques : une destruction auto-immune des plaquettes et une insuffisance de leur production par la moelle osseuse. Le PTI est un diagnostic d’exclusion par élimination de toutes les causes connues de thrombopénie. Au sein de notre cohorte de patients suivis en médecine interne pour cette maladie, nous avons identifié certains patients qui présentaient un profil non-immunologique, c’est-à-dire l’absence d’auto-immunité et une non réponse à tous les traitements immunomodulateurs, ou pas d’indication à un traitement compte tenu d’un taux de plaquettes suffisant. Nous montrons dans ce travail de thèse que Bcl-xL est nécessaire pour la survie du mégacaryocyte humain pendant toute la mégacaryopoïèse, à la différence de la souris. Par ailleurs, certains patients ont une altération intrinsèque de la formation des proplaquettes, et certains d’entre eux ont également une diminution de l’ARN messager et de la protéine Bcl-xL dans leurs plaquettes. Ces observations nouvelles suggèrent l’implication de Bcl-xL dans la physiopathologie de leur maladie et ouvrent la voie à l’identification d’une potentielle nouvelle cause de thrombopénie chronique

Involvement of Bcl-xL in human normal megakaryopoiesis and in chronic immune thrombocytopenia

La protéine Bcl-xL fait partie de la famille des protéines anti-apoptotiques Bcl-2. Il a été montré que cette protéine avait un rôle majeur dans la formation des plaquettes chez la souris (mégacaryopoïèse). Une dérégulation de cette protéine pourrait aboutir à une altération de la mégacaryopoïèse et donner des pathologies humaines comme des thrombopénies chroniques. Une des causes de thrombopénies chroniques est le purpura thrombopénique immunologique (ou PTI), qui associe deux mécanismes physiopathologiques : une destruction auto-immune des plaquettes et une insuffisance de leur production par la moelle osseuse. Le PTI est un diagnostic d’exclusion par élimination de toutes les causes connues de thrombopénie. Au sein de notre cohorte de patients suivis en médecine interne pour cette maladie, nous avons identifié certains patients qui présentaient un profil non-immunologique, c’est-à-dire l’absence d’auto-immunité et une non réponse à tous les traitements immunomodulateurs, ou pas d’indication à un traitement compte tenu d’un taux de plaquettes suffisant. Nous montrons dans ce travail de thèse que Bcl-xL est nécessaire pour la survie du mégacaryocyte humain pendant toute la mégacaryopoïèse, à la différence de la souris. Par ailleurs, certains patients ont une altération intrinsèque de la formation des proplaquettes, et certains d’entre eux ont également une diminution de l’ARN messager et de la protéine Bcl-xL dans leurs plaquettes. Ces observations nouvelles suggèrent l’implication de Bcl-xL dans la physiopathologie de leur maladie et ouvrent la voie à l’identification d’une potentielle nouvelle cause de thrombopénie chronique.The Bcl-xL protein is a member of Bcl-2 anti-apoptotic proteins. It has been shown in mouse that this protein had a major role in platelet production (megakaryopoiesis). Bcl-xL deregulation could lead to megakaryopoiesis impairement and explain some human diseases such as chronic thrombocytopenias. One cause of chronic thrombocytopenia is immune thrombocytopenia (ITP) that associates 2 pathophysiological mechanisms: an immune-mediated platelet destruction and an insufficient production from the bone marrow cells. ITP is a diagnosis of exclusion when all known causes of thrombocytopenia have been ruled out by diagnosis work-up. In ITP cohort of patients followed in our internal medicine department, we have identified some patients with a haematological profile of their disease, ie absence of overt features of auto-immunity, and absence of response to immunomudulatory treatments, or no indication to such treatment because of sufficient platelet count. We demonstrate in this study that Bcl-xL is necessary for megakaryocyte survival during all megakaryopoiesis, contrary to what was found in mouse. Moreover, some patients have an intrinsically impaired proplatelet formation, and some of them also have a decrease of Bcl-xL mRNA and protein in their platelets. These novel observations suggest that a deregulation of Bcl-xL is a possible cause of their disease and lead the way to the identification of a potentially new cause of chronic thrombocytopenia in huma

Construction universelle d'objets partagés sans connaissance des participants

International audienceUne construction universelle est un algorithme permettant à un ensemble de processus concurrents d'accéder à un objet partagé en ayant l'illusion que celui-ci est disponible localement. Dans cet article, nous présentons un algorithme permettant la mise en oeuvre d'une telle construction dans un système à mémoire partagée. Notre construction est sans verrou, et contrairement aux approches proposées précédemment, ne nécessite pas que les processus accédant à l'objet partagé soient connus. De plus, elle est adaptative : en notant n le nombre total de processus dans le système et k <= n le nombre de processus qui utilisent l'objet partagé, tout processus effectue Θ(k) pas de calcul en l'absence de contention