Organization as A Multi-dimensional Network of Actants Mediated by An Organized and Organizing Network of Cultural Rules

Programme du colloque : www.groupelog.umontreal.ca/anglais/LOGConferenceProgram.pdfThis paper aims to provide a complementary perspective to the Montreal School's conceptual framework on the organizing properties of communication. The network metaphor is used to address two issues of this theory: how to link entities with variable ontologies together and how to explain that entities are objects (inherent ontology) and mediators (relational ontology) at the same time? Networks are considered both as material structures (directed graphs seen as topological objects) and as abstracted ones (matrixes). Complex networks display structural properties when they emerge as structures. However, the emergence of structure is only considered as a realization of one of the virtual states and possible patterns of a meta-network made up of at least three networks on several dimensions: a material network of actants, a cognitive network and a cultural network of rules. The latter network is linked to human entities only. Cultural rules are seen as habitus, i.e. kinds of force fields that guide but do not determine action. Human agency is constrained by cultural rules so that human beings are able to reproduce social systems. Agency is also seen as continuous modification and displacement. It modifies the structure of the network of actants and that of the network of rules. The network of actants makes the network of rules evolve through feedback loops. The network of rules generates calculations in the cognitive network. Sensemaking results from the continuous process of reproduction-modification of the cognitive structure.Pas de résumé en françai

Étude des voies de signalisation impliquées lors de la prolifération et l'apoptose des cellules du cancer du sein en réponse aux acides gras

Thèse numérisée par la Direction des bibliothèques de l'Université de Montréal

Étude du rôle de l'action des acides gras dans la prolifération et l'apoptose des cellules du cancer du sein

Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal

L’ontologie variable des actants : pour une épistémologie renouvelée dans les recherches sur les réseaux

Cet article discute un modèle original qui permet de dépasser les antagonismes des différentes écoles de pensée qui s’intéressent à la modélisation des réseaux sociaux. Nous faisons ici le pari qu’un dialogue est possible entre les approches TIC et les approches SHS car les réseaux sont à la fois sociaux et techniques pour relier les utilisateurs entre eux. Les réseaux sont des formes d’organisations complexes ontologiquement hétérogènes.This paper presents an original model that can overcome the antagonisms of different schools of thought with regard to the modeling of social networks.We make here the bet that a dialogue is possible between the approaches ICTS and the human sciences because networks are at the same time social and technical to connect the users between them. Networks are forms of complex and heterogeneous organizations

Increased Susceptibility to Dextran Sulfate Sodium Induced Colitis in the T Cell Protein Tyrosine Phosphatase Heterozygous Mouse

T cell protein tyrosine phosphatase (TC-PTP / PTPN2) is an enzyme that is essential for the proper functioning of the immune system and that participates in the control of cell proliferation, and inflammation. We previously observed that TC-PTP−/− mice display various immunodeficiencies, hypersensitivity to LPS and die within three weeks of birth due to anemia and widespread inflammation. A recent analysis of the Wellcome Trust Case Control Consortium (WTCC) genome wide scan data, reported in 2007, indicated a potential role for TC-PTP in inflammatory bowel disease (IBD). To further investigate the potential role of TC-PTP in IBD, we studied heterozygous TC-PTP mutant mice challenged with dextran sulfate sodium (DSS) in their drinking water. In comparison to control animals, we observed significant changes in the colon mucosa of DSS-treated TC-PTP+/− mice, in the ratio of colon to body weight, as well as an up-regulation of mRNA transcripts for IL-6, IL-23, 1L-12β, IFN-γ, TNF-α. Moreover, up-regulation of serum IL-6 levels in DSS-treated TC-PTP+/− mice confirms that mice with a single copy of the TC-PTP gene display increased susceptibility to systemic inflammation due to bowel epithelial erosion resulting from DSS challenge. Our findings support the lack of modulation of Janus kinases 1 and 3 (Jak1, Jak3), and the downstream signal transducer and activator of transcription 1,3 and 5 (Stat1, Stat3, Stat 5) by PTPN2 in the development of IBD like condition. Pathological and molecular analysis reveal that the deficiency of TC-PTP results in pro-inflammatory condition in the bowel of heterozygous TC-PTP+/− mice. These novel findings in TC-PTP hemi-deficiency support the hypothesis that TC-PTP is an important regulator of inflammatory cytokine signaling and that it may be implicated in the pathophysiology of IBD

Efficient quantum key distribution secure against no-signalling eavesdroppers

By carrying out measurements on entangled states, two parties can generate a secret key which is secure not only against an eavesdropper bound by the laws of quantum mechanics, but also against a hypothetical "post-quantum" eavesdroppers limited by the no-signalling principle only. We introduce a family of quantum key distribution protocols of this type, which are more efficient than previous ones, both in terms of key rate and noise resistance. Interestingly, the best protocols involve large number of measurements. We show that in the absence of noise, these protocols can yield one secret bit per entanglement bit, implying that the key rates in the no-signalling post-quantum scenario are comparable to the key rates in usual quantum key distribution.Comment: 11 pages, 2 color figures. v2: minor modifications, added references, added note on the relation to quant-ph/060604

Ptbp1 and Exosc9 knockdowns trigger skin stability defects through different pathways

AbstractIn humans, genetic diseases affecting skin integrity (genodermatoses) are generally caused by mutations in a small number of genes that encode structural components of the dermal–epidermal junctions. In this article, we first show that inactivation of both exosc9, which encodes a component of the RNA exosome, and ptbp1, which encodes an RNA-binding protein abundant in Xenopus embryonic skin, impairs embryonic Xenopus skin development, with the appearance of dorsal blisters along the anterior part of the fin. However, histological and electron microscopy analyses revealed that the two phenotypes are distinct. Exosc9 morphants are characterized by an increase in the apical surface of the goblet cells, loss of adhesion between the sensorial and peridermal layers, and a decrease in the number of ciliated cells within the blisters. Ptbp1 morphants are characterized by an altered goblet cell morphology. Gene expression profiling by deep RNA sequencing showed that the expression of epidermal and genodermatosis-related genes is also differentially affected in the two morphants, indicating that alterations in post-transcriptional regulations can lead to skin developmental defects through different routes. Therefore, the developing larval epidermis of Xenopus will prove to be a useful model for dissecting the post-transcriptional regulatory network involved in skin development and stability with significant implications for human diseases

DiSSCo Prepare WP7 –D7.3 Assessment tools and direction map to the implementation of common DiSSCo policies

The Distributed System for Scientific Collections (DiSSCo) Research Infrastructure will operate a number of e-services, all of which will have policy requirements for participating institutions. These policies include those related to digital and physical access to specimens, digital image and specimen metadata, and FAIR / Open Data. Previous projects have shown that the policy landscape is complex, and Task 7.3 has developed a policy self-assessment tool that will allow DiSSCo to assess policy alignment across the consortium. This deliverable describes the development of the policy self-assessment tool and provides a walkthrough of the key features. The same technical framework was used to create a digital maturity tool, which was initially proposed by Task 3.1, and this is also described within this document. A set of recommendations are included that outline the future direction for the development of the policy tool.The Distributed System for Scientific Collections (DiSSCo) Research Infrastructure will operate a number´of e-services, all of which will have policy requirements for participating institutions. These policies include those related to digital and physical access to specimens, digital image and specimen metadata, and FAIR / Open Data. Previous projects have shown that the policy landscape is complex, and Task 7.3 has developed a policy self-assessment tool that will allow DiSSCo to assess policy alignment across the consortium. This deliverable describes the development of the policy self-assessment tool and provides a walkthrough of the key features. The same technical framework was used to create a digital maturity tool, which was initially proposed by Task 3.1, and this is also described within this document. A set of recommendations are included that outline the future direction for the development of the policy tool

MICROSCOPE mission analysis, requirements and expected performance

The MICROSCOPE mission aimed to test the Weak Equivalence Principle (WEP) to a precision of $10^{-15}$. The WEP states that two bodies fall at the same rate on a gravitational field independently of their mass or composition. In MICROSCOPE, two masses of different compositions (titanium and platinum alloys) are placed on a quasi-circular trajectory around the Earth. They are the test-masses of a double accelerometer. The measurement of their accelerations is used to extract a potential WEP violation that would occur at a frequency defined by the motion and attitude of the satellite around the Earth. This paper details the major drivers of the mission leading to the specification of the major subsystems (satellite, ground segment, instrument, orbit...). Building upon the measurement equation, we derive the objective of the test in statistical and systematic error allocation and provide the mission's expected error budget.Comment: References update

Magnesium-sensitive upstream ORF controls PRL phosphatase expression to mediate energy metabolism

The phosphatases of regenerative liver (PRL) have been shown to interact with the CNNM magnesium transport regulators. Through this protein complex, PRL controls the levels of intracellular magnesium. Our study uncovers a remarkable posttranscriptional feedback mechanism by which magnesium controls PRL expression in mammalian cells. Here we show that regulation of PRL mRNA translation by magnesium depends on a 5'UTR-located upstream ORF, which is conserved among all vertebrates, proposing an evolutionary molecular mechanism of action by a divalent ion. This magnesium-sensing mechanism, which also involves the key metabolic sensor AMPK, is thus central to maintain cellular homeostasis in mammalian cells.Phosphatases of regenerating liver (PRL-1, PRL-2, and PRL-3, also known as PTP4A1, PTP4A2, and PTP4A3) control magnesium homeostasis through an association with the CNNM magnesium transport regulators. Although high PRL levels have been linked to cancer progression, regulation of their expression is poorly understood. Here we show that modulating intracellular magnesium levels correlates with a rapid change of PRL expression by a mechanism involving its 5'UTR mRNA region. Mutations or CRISPR-Cas9 targeting of the conserved upstream ORF present in the mRNA leader derepress PRL protein synthesis and attenuate the translational response to magnesium levels. Mechanistically, magnesium depletion reduces intracellular ATP but up-regulates PRL protein expression via activation of the AMPK/mTORC2 pathway, which controls cellular energy status. Hence, altered PRL-2 expression leads to metabolic reprogramming of the cells. These findings uncover a magnesium-sensitive mechanism controlling PRL expression, which plays a role in cellular bioenergetics