L’organisation communautaire au temps de l’exclusion et de l’économie sociale

Dans cet article, les auteurs définissent d’abord l’exclusion à partir de ses deux aspects fondamentaux, soit l’exclusion du travail et la rupture des liens sociaux. Ils présentent ensuite l’économie sociale, sa place dans l’économie globale, ses liens avec l’insertion sociale et le travail. Le troisième point porte sur l’organisation communautaire où les auteurs proposent d’investir leur énergie non pas seulement dans l’économie sociale mais aussi dans le domaine relationnel.First, the authors define the sociological concept of exclusion according to its fundamental characteristics, such as the exclusion from the labor market and the rupture of social bond. Then, they present what is called the social economy, its place within the global economy, its links with social insertion and work. Third, they propose that community organizers should pay attention not only to building a social economy but also to reconstructing social bond

The E-NTPDase Family of Ectonucleotidases: Structure Function Relationships and Pathophysiological Significance

Ectonucleotidases are ectoenzymes that hydrolyze extracellular nucleotides to the respective nucleosides. Within the past decade, ectonucleotidases belonging to several enzyme families have been discovered, cloned and characterized. In this article, we specifically address the cell surface-located members of the ecto-nucleoside triphosphate diphosphohydrolase (E-NTPDase/CD39) family (NTPDase1,2,3, and 8). The molecular identification of individual NTPDase subtypes, genetic engineering, mutational analyses, and the generation of subtype-specific antibodies have resulted in considerable insights into enzyme structure and function. These advances also allow definition of physiological and patho-physiological implications of NTPDases in a considerable variety of tissues. Biological actions of NTPDases are a consequence (at least in part) of the regulated phosphohydrolytic activity on extracellular nucleotides and consequent effects on P2-receptor signaling. It further appears that the spatial and temporal expression of NTPDases by various cell types within the vasculature, the nervous tissues and other tissues impacts on several patho-physiological processes. Examples include acute effects on cellular metabolism, adhesion, activation and migration with other protracted impacts upon developmental responses, inclusive of cellular proliferation, differentiation and apoptosis, as seen with atherosclerosis, degenerative neurological diseases and immune rejection of transplanted organs and cells. Future clinical applications are expected to involve the development of new therapeutic strategies for transplantation and various inflammatory cardiovascular, gastrointestinal and neurological diseases

Purinergic Signalling in Immune System Regulation in Health and Disease

The concept of a purinergic signalling system was first proposed by Professor Geoffrey Burnstock over 30 years ago. This includes the cellular responses to purine nucleotides, such as ATP, and nucleosides, such as adenosine, that act as extracellular messengers playing a role through specific nucleotide and adenosine receptors in all systems. Indeed, in addition to their role in cellular metabolism, nucleotides as well as nucleosides are extracellular mediators that activate biological responses in all cells. Cells subjected to activation or shear or mechanical stress release nucleotides such as ATP, ADP, UTP, and UDP in large amounts. All cells can release nucleotides in a controlled fashion [1]. The mechanisms of nucleotide release have been the focus of intense research activities but are still not fully understood. While activated platelets and neurons release nucleotides by exocytosis, neutrophils, and T lymphocytes use pannexin-1 hemichannels for nucleotide efflux, some cells also constitutively release nucleotides

Connectivité entre les populations du fjord du Saguenay et celles du golfe du Saint-Laurent

L’analyse des marqueurs microsatellites et d’allozymes chez différentes espèces de poissons de fond (morue, flétan du Groenland et sébaste) et de crustacés (crabe des neiges et crevette nordique) montre que les organismes du Saguenay et du Saint-Laurent appartiennent aux mêmes populations. La seule différenciation génétique est observée au locus Pan I chez la morue. Cette différenciation pourrait toutefois être causée par la sélection, qui agirait dans le fjord du Saguenay, plutôt que par l’isolement génétique de la population. Les données complémentaires disponibles pour les poissons de fond (composition élémentaire des otolithes, morphométrie et faune parasitaire) montrent que les individus capturés dans le Saguenay diffèrent de ceux du Saint-Laurent. Ces différences suggèrent que les individus du Saguenay et du Saint-Laurent passent la majeure partie de leur cycle vital dans des environnements différents. Considérant la très faible survie larvaire observée dans le fjord, cette revue suggère que les populations de poissons de fond du Saguenay constituent des populations puits, dont le recrutement dépend de l’apport de juvéniles depuis le Saint-Laurent. Une fois les individus installés dans le Saguenay, ils y passent la majorité de leur vie. Même si nous ne possédons pas de données complémentaires pour les crustacés, il est possible que le même mécanisme opère chez ces espèces.Microsatellite and allozyme analyses on various species of bottom fishes (cod, Greenland halibut and redfish) and crustaceans (snow crab, northern shrimp) show that individuals from the Saguenay Fjord and from the St. Lawrence belong to the same populations. The only genetic difference observed is at the Pan I locus of cod. This differentiation may be caused by selection that would act in the Saguenay Fjord, rather than due to the genetic isolation of the population. Complementary data available for bottom fish (elemental composition of otoliths, body morphometry, and parasite fauna) show clear differences between the Saguenay and the St. Lawrence. These differences suggest residence of individuals in the Saguenay and the St. Lawrence for a large proportion of their life cycle. Considering the low larval survival observed in the fjord, this review suggests that the bottom fish populations from the Saguenay represent sink populations whose recruitment depends largely or solely on migration of juveniles from the St. Lawrence. Although there are no complementary data for crustacean species, it is possible that migration and residence are processes operating for those species as well

Induction of NTPDase1/CD39 by Reactive Microglia and Macrophages Is Associated With the Functional State During EAE

Purinergic signaling is critically involved in neuroinflammation associated with multiple sclerosis (MS) and its major inflammatory animal model, experimental autoimmune encephalomyelitis (EAE). Herein, we explored the expression of ectonucleoside triphosphate diphosphohydrolase1 (NTPDase1/CD39) in the spinal cord, at the onset (Eo), peak (Ep), and end (Ee) of EAE. Several-fold increase in mRNA and in NTPDase1 protein levels were observed at Eo and Ep. In situ hybridization combined with fluorescent immunohistochemistry showed that reactive microglia and infiltrated mononuclear cells mostly accounted for the observed increase. Colocalization analysis revealed that up to 80% of Iba1 immunoreactivity and ∼50% of CD68 immunoreactivity was colocalized with NTPDase1, while flow cytometric analysis revealed that ∼70% of mononuclear infiltrates were NTPDase1+ at Ep. Given the main role of NTPDase1 to degrade proinflammatory ATP, we hypothesized that the observed up-regulation of NTPDase1 may be associated with the transition between proinflammatory M1-like to neuroprotective M2-like phenotype of microglia/macrophages during EAE. Functional phenotype of reactive microglia/macrophages that overexpress NTPDase1 was assessed by multi-image colocalization analysis using iNOS and Arg1 as selective markers for M1 and M2 reactive states, respectively. At the peak of EAE NTPDase1 immunoreactivity showed much higher co-occurrence with Arg1 immunoreactivity in microglia and macrophages, compared to iNOS, implying its stronger association with M2-like reactive phenotype. Additionally, in ∼80% of CD68 positive cells NTPDase1 was coexpressed with Arg1 compared to negligible fraction coexpresing iNOS and ∼15% coexpresing both markers, additionally indicating prevalent association of NTPDase1 with M2-like microglial/macrophages phenotype at Ep. Together, our data suggest an association between NTPDase1 up-regulation by reactive microglia and infiltrated macrophages and their transition toward antiinflammatory phenotype in EAE

Histamine Induces ATP Release from Human Subcutaneous Fibroblasts, via Pannexin-1 Hemichannels, Leading to Ca2+Mobilization and Cell Proliferation

Changes in the regulation of connective tissue ATP-mediated mechano-transduction and remodeling may be an important link to the pathogenesis of chronic pain. It has been demonstrated that mast cell-derived histamine plays an important role in painful fibrotic diseases. Here we analyzed the involvement of ATP in the response of human subcutaneous fibroblasts to histamine. Acute histamine application caused a rise in intracellular Ca(2+) ([Ca(2+)]i) and ATP release from human subcutaneous fibroblasts via H1 receptor activation. Histamine-induced [Ca(2+)]i rise was partially attenuated by apyrase, an enzyme that inactivates extracellular ATP, and by blocking P2 purinoceptors with pyridoxal phosphate-6-azo(benzene-2,4-disulfonic acid) tetrasodium salt and reactive blue 2. [Ca(2+)]i accumulation caused by histamine was also reduced upon blocking pannexin-1 hemichannels with (10)Panx, probenecid, or carbenoxolone but not when connexin hemichannels were inhibited with mefloquine or 2-octanol. Brefeldin A, an inhibitor of vesicular exocytosis, also did not block histamine-induced [Ca(2+)]i mobilization. Prolonged exposure of human subcutaneous fibroblast cultures to histamine favored cell growth and type I collagen synthesis via the activation of H1 receptor. This effect was mimicked by ATP and its metabolite, ADP, whereas the selective P2Y1 receptor antagonist, MRS2179, partially attenuated histamine-induced cell growth and type I collagen production. Expression of pannexin-1 and ADP-sensitive P2Y1 receptor on human subcutaneous fibroblasts was confirmed by immunofluorescence confocal microscopy and Western blot analysis. In conclusion, histamine induces ATP release from human subcutaneous fibroblasts, via pannexin-1 hemichannels, leading to [Ca(2+)]i mobilization and cell growth through the cooperation of H1 and P2 (probably P2Y1) receptors.info:eu-repo/semantics/publishedVersio