Accumulation primitive du capital

Résumé

L’accumulation primitive du capital est une théorie économique selon laquelle la Révolution industrielle a été rendue possible par l'accumulation de capital dans le temps, assurant des capacités d'investissement aux capitalistes. Cette théorie est développée par Karl Marx dans le Capital (chapitres 26 à 33) pour expliquer la révolution industrielle du . Si le concept est d'origine marxiste, il a été traité par la suite par d'autres économistes, qui l'ont affiné ou l'ont contesté, en particulier grâce aux statistiques et recherches historiques postérieures à la mort de Marx.[source?] Pour les marxistes, cette approche est le cœur du matérialisme dialectique, qui analyse l’histoire pour tenter de comprendre l’économie. Les détracteurs y voient au contraire un biais induit par le désir de valider des thèses économiques et sociales. De fait, la thèse de Marx a conservé une forte influence sur les grilles de lecture de la révolution industrielle, bien au-delà des cercles marxistes.

Source officielle

https://fr.wikipedia.org/wiki/Accumulation_primitive_du_capital

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Investigating the Biological Mechanisms underlying the Initiation of Autoimmunity against Beta Cell Antigens in Type 1 Diabetes

Chiara Cianciaruso

Type 1 diabetes (T1D) is an autoimmune disease characterized by circulating autoantibodies, lymphocytic infiltration of pancreatic islets of Langerhans, and cell-specific destruction of beta cells, leading to insulin deficiency and symptomatic hyperglycemia. Some of the major target autoantigens in T1D are intracellular proteins, such as GAD65, IA-2 and proinsulin, whose initial encounter with the immune system is poorly understood. Here we describe a method for culturing monolayers of primary pancreatic islet cells in vitro, which enables detailed observation of proteins and sub-cellular processes in primary human and rat beta cells by super-resolution and live-cell light microscopy. This technical advance is broadly applicable to obtaining novel biological insights as demonstrated by our identification of a mechanism to control proliferation in primary beta cells through growth and disassembly of primary cilia. This protocol also allowed us to identify two novel interrelated mechanisms for how beta cell proteins, such as the antigen GAD65, can become target of autoimmunity and initiate T1D. A triggering factor that these two pathways have in common is represented by endoplasmic reticulum (ER) stress, to which pancreatic islet beta cells are particularly susceptible, and can be induced by inflammatory factors such as Th1 cytokines. In the first mechanism, we show that ER stress in beta cells perturbs the palmitoylation cycle controlling GAD65 endomembrane distribution, resulting in aberrant accumulation of the palmitoylated form in Golgi membranes. The palmitoylated form has heightened immunogenicity, exhibiting increased uptake by antigen presenting cells (APCs) and T cell stimulation compared to the non-palmitoylated form. Similar accumulation of GAD65 in Golgi membranes is observed in human beta cells in pancreatic sections from GAD65 autoantibody positive individuals, who have not yet progressed to clinical onset of T1D, and T1D patients with residual beta cell mass and ongoing T cell infiltration of islets. Thus, aberrant accumulation of immunogenic GAD65 in Golgi membranes facilitates inappropriate presentation to the immune system following release from stressed and/or damaged beta cells, triggering autoimmunity. In the second mechanism, we present that, following a pathway originating from the Golgi, both rat and human pancreatic islets release the intracellular beta cell autoantigens GAD65, IA-2 and proinsulin in a subtype of extracellular vesicles called exosomes. Islet-exosomes are then taken up by and can activate APCs including dendritic cells. Accordingly, anchoring of GAD65 to exosome-mimetic liposomes strongly boosts antigen presentation and T cell activation in the context of the human T1D susceptibility haplotype HLA-DR4. Furthermore, cytokine-induced ER stress enhances exosome secretion by beta cells, induces exosomal release of the immunostimulatory chaperones calreticulin, Gp96 and ORP150 and increases exosomal stimulation of APCs. Therefore, stress-induced exosomal release of intracellular autoantigens and immunostimulatory chaperones may play a role in initiation of autoimmune responses in T1D.

EPFL2017

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Accumulation of spectra is a common approach for improvement of the signal-to-noise ratio (SNR) in mass spectrometry. However, severe degradation of the overall spectrum can occur if some individual mass spectra, affected by peak broadening, are included in the accumulation process. In this contribution, we discuss potential sources and effects of spectral distortions by using examples from mass spectra acquired by our miniature laser ablation/ionisation time-of-flight mass spectrometer. We show how recent developments in acquisition systems enable to identify individual spectra subjected to peak broadening and present a filtering method capable of systematic and reproducible exclusion of such spectra from the accumulation process. We show that the method can be used on a wide range of materials and present a detailed case study performed on a trevorite mineral sample. Using this method, improvements of the isotope accuracy of Si, Ni, and Cr by factors between 1.6 and 7.7 were achieved. Finally, we discuss the limitations of the method and provide complementary analysis of other materials in the supplementary documents provided with this contribution.

WILEY2019

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, , ,

Activation volumes characteristic of room temperature compressive plastic deformation in Au- 45.2 at.% Cu- 1.7 at.% Pt, a near-AuCu alloy that orders to a fully L1(0) structure, are measured using the repeated stress-relaxation method. Four different ordering treatments (540 and 10(5)s at either 250 or 400 degrees C) are conducted on samples prior to deformation, leading to a classical two-variant polytwin structure after ordering at 400 degrees C, or alternatively a three-variant highly twinned structure at 250 degrees C. In both structures, {110} twin boundaries only a few tens of nanometres apart separate variants and constitute the main barriers to dislocation glide. All four ordered nanotwinned microstructures have an initial effective activation volume V-eff of 100-120 b(3); however, the two structures differ strongly as they work harden. The two-variant polytwin structure yields a straight line on a Haasen plot, showing that work hardening is associated with an increase in slip obstacle density, most likely dislocation debris at intervariant boundaries. The three-variant structure on the other hand shows a nearly constant (slightly decreasing) activation volume. This suggests that there is little obstacle accumulation when three variants are present, likely because plastic deformation occurs by slip of superdislocation only. (C) 2011 Elsevier Ltd. All rights reserved.

Elsevier2011

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Investigating the Biological Mechanisms underlying the Initiation of Autoimmunity against Beta Cell Antigens in Type 1 Diabetes

Chiara Cianciaruso

EPFL2017