Politique de la théorie et conceptualisation économique dans la méthodologie de Max Weber

Cette recherche s’appuie sur l’article classique de Sheldon Wolin (1981) pour analyser les interventions méthodologiques de Max Weber en tant qu’une politique par laquelle il légitime son activité intellectuelle. Elle interroge la politique wébérienne de la théorie à la lumière de son contexte : les débats dans lesquels était plongée l’École historique allemande d’économie politique au tournant du XXe siècle. Cette étude expose dans un premier temps les critiques formulées par Weber à l’endroit de deux des fondateurs de l’École historique, Wilhelm Roscher et Karl Knies, en s’appuyant sur les trois articles méthodologiques de Weber à leur sujet (1903-1906). J’y montre que Weber légitime dans ces articles sa pratique d’une « science de la réalité » par une critique de l’incompatibilité de la formation « émanatiste » de concepts de Roscher et Knies à l’empirisme qu’ils revendiquent. Elle traite dans un second temps de l’intervention de Weber dans la suite du Methodenstreit, dans lequel se sont opposées les économistes Gustav von Schmoller de l’École historique allemande et Carl Menger de l’École marginaliste autrichienne. J’y propose que la critique épistémologique néo-kantienne du naturalisme développée par Weber dans son remarquable essai sur « L’“objectivité” de la connaissance dans les sciences et politiques sociales » (1904) doive être comprise comme s’adressant autant à l’historisme allemand qu’au marginalisme autrichien. Elle vise par le fait même la légitimation d’une compréhension wébérienne de la science économique aujourd’hui méconnue (la Sozialökonomik), dont le Grundriss der Sozialökonomik (1914) fut l’expression la plus aboutie.This enquiry draws on Sheldon Wolin’s 1981 classic article to analyze Max Weber’s methodological writings as expressing a politics by means of which he legitimizes his intellectual activity. It examines the Weberian politics of theory in light of its context: the debates in which the German Historical School of Political Economy was engaged at the turn of the 20th century. This study first outlines Weber’s criticisms of two of the founders of the Historical School, Wilhelm Roscher and Karl Knies, on the basis of his three methodological articles on the subject (1903–1906). I show that Weber legitimizes his practice of a “science of reality” by criticizing the incompatibility of Roscher and Knies’ “emanationist” concept formation with the empiricism they advocated. It then discusses Weber’s methodological essays in the wake of the Methodenstreit, which opposed economists Gustav von Schmoller of the German Historical School and Carl Menger of the Austri-an Marginalist School. I argue that the neo-Kantian epistemological critique of naturalism that Weber develops in his 1904 authoritative essay on “The ‘objectivity’ of knowledge in social science and social policy” should be understood as addressing both German historism and Austrian marginalism. It thus aims to legitimize a nowadays little-known Weberian understanding of economics (Sozialökonomik), of which the 1914 Grundriss der Sozialökonomik was the most accomplished expression

Model Checking Contest @ Petri Nets, Report on the 2013 edition

This document presents the results of the Model Checking Contest held at Petri Nets 2013 in Milano. This contest aimed at a fair and experimental evaluation of the performances of model checking techniques applied to Petri nets. This is the third edition after two successful editions in 2011 and 2012. The participating tools were compared on several examinations (state space generation and evaluation of several types of formul{\ae} -- reachability, LTL, CTL for various classes of atomic propositions) run on a set of common models (Place/Transition and Symmetric Petri nets). After a short overview of the contest, this paper provides the raw results from the contest, model per model and examination per examination. An HTML version of this report is also provided (http://mcc.lip6.fr).Comment: one main report (422 pages) and two annexes (1386 and 1740 pages

Web Report on the Model Checking Contest @ Petri Net 2013

http://mcc.lip6.f

Strigolactones play an important role in shaping exodermal morphology via a KAI2-dependent pathway

The majority of land plants have two suberized root barriers: the endodermis and the hypodermis (exodermis). Both barriers bear non-suberized passage cells that are thought to regulate water and nutrient exchange between the root and the soil. We learned a lot about endodermal passage cells, whereas our knowledge on hypodermal passage cells (HPCs) is still very scarce. Here we report on factors regulating the HPC number in Petunia roots. Strigolactones exhibit a positive effect, whereas supply of abscisic acid (ABA), ethylene, and auxin result in a strong reduction of the HPC number. Unexpectedly the strigolactone signaling mutant d14/dad2 showed significantly higher HPC numbers than the wild-type. In contrast, its mutant counterpart max2 of the heterodimeric receptor DAD2/MAX2 displayed a significant decrease in HPC number. A mutation in the Petunia karrikin sensor KAI2 exhibits drastically decreased HPC amounts, supporting the hypothesis that the dimeric KAI2/MAX2 receptor is central in determining the HPC number

The Nlrp3 inflammasome regulates acute graft-versus-host disease

The success of allogeneic hematopoietic cell transplantation is limited by acute graft-versus-host disease (GvHD), a severe complication accompanied by high mortality rates. Yet, the molecular mechanisms initiating this disease remain poorly defined. In this study, we show that, after conditioning therapy, intestinal commensal bacteria and the damage-associated molecular pattern uric acid contribute to Nlrp3 inflammasome-mediated IL-1β production and that gastrointestinal decontamination and uric acid depletion reduced GvHD severity. Early blockade of IL-1β or genetic deficiency of the IL-1 receptor in dendritic cells (DCs) and T cells improved survival. The Nlrp3 inflammasome components Nlrp3 and Asc, which are required for pro-IL-1β cleavage, were critical for the full manifestation of GvHD. In transplanted mice, IL-1β originated from multiple intestinal cell compartments and exerted its effects on DCs and T cells, the latter being preferentially skewed toward Th17. Compatible with these mouse data, increased levels of active caspase-1 and IL-1β were found in circulating leukocytes and intestinal GvHD lesions of patients. Thus, the identification of a crucial role for the Nlrp3 inflammasome sheds new light on the pathogenesis of GvHD and opens a potential new avenue for the targeted therapy of this severe complication

Association of the PHACTR1/EDN1 genetic locus with spontaneous coronary artery dissection

Background: Spontaneous coronary artery dissection (SCAD) is an increasingly recognized cause of acute coronary syndromes (ACS) afflicting predominantly younger to middle-aged women. Observational studies have reported a high prevalence of extracoronary vascular anomalies, especially fibromuscular dysplasia (FMD) and a low prevalence of coincidental cases of atherosclerosis. PHACTR1/EDN1 is a genetic risk locus for several vascular diseases, including FMD and coronary artery disease, with the putative causal noncoding variant at the rs9349379 locus acting as a potential enhancer for the endothelin-1 (EDN1) gene. Objectives: This study sought to test the association between the rs9349379 genotype and SCAD. Methods: Results from case control studies from France, United Kingdom, United States, and Australia were analyzed to test the association with SCAD risk, including age at first event, pregnancy-associated SCAD (P-SCAD), and recurrent SCAD. Results: The previously reported risk allele for FMD (rs9349379-A) was associated with a higher risk of SCAD in all studies. In a meta-analysis of 1,055 SCAD patients and 7,190 controls, the odds ratio (OR) was 1.67 (95% confidence interval [CI]: 1.50 to 1.86) per copy of rs9349379-A. In a subset of 491 SCAD patients, the OR estimate was found to be higher for the association with SCAD in patients without FMD (OR: 1.89; 95% CI: 1.53 to 2.33) than in SCAD cases with FMD (OR: 1.60; 95% CI: 1.28 to 1.99). There was no effect of genotype on age at first event, P-SCAD, or recurrence. Conclusions: The first genetic risk factor for SCAD was identified in the largest study conducted to date for this condition. This genetic link may contribute to the clinical overlap between SCAD and FMD

Mortality and pulmonary complications in patients undergoing surgery with perioperative SARS-CoV-2 infection: an international cohort study

Background: The impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on postoperative recovery needs to be understood to inform clinical decision making during and after the COVID-19 pandemic. This study reports 30-day mortality and pulmonary complication rates in patients with perioperative SARS-CoV-2 infection. Methods: This international, multicentre, cohort study at 235 hospitals in 24 countries included all patients undergoing surgery who had SARS-CoV-2 infection confirmed within 7 days before or 30 days after surgery. The primary outcome measure was 30-day postoperative mortality and was assessed in all enrolled patients. The main secondary outcome measure was pulmonary complications, defined as pneumonia, acute respiratory distress syndrome, or unexpected postoperative ventilation. Findings: This analysis includes 1128 patients who had surgery between Jan 1 and March 31, 2020, of whom 835 (74·0%) had emergency surgery and 280 (24·8%) had elective surgery. SARS-CoV-2 infection was confirmed preoperatively in 294 (26·1%) patients. 30-day mortality was 23·8% (268 of 1128). Pulmonary complications occurred in 577 (51·2%) of 1128 patients; 30-day mortality in these patients was 38·0% (219 of 577), accounting for 81·7% (219 of 268) of all deaths. In adjusted analyses, 30-day mortality was associated with male sex (odds ratio 1·75 [95% CI 1·28–2·40], p\textless0·0001), age 70 years or older versus younger than 70 years (2·30 [1·65–3·22], p\textless0·0001), American Society of Anesthesiologists grades 3–5 versus grades 1–2 (2·35 [1·57–3·53], p\textless0·0001), malignant versus benign or obstetric diagnosis (1·55 [1·01–2·39], p=0·046), emergency versus elective surgery (1·67 [1·06–2·63], p=0·026), and major versus minor surgery (1·52 [1·01–2·31], p=0·047). Interpretation: Postoperative pulmonary complications occur in half of patients with perioperative SARS-CoV-2 infection and are associated with high mortality. Thresholds for surgery during the COVID-19 pandemic should be higher than during normal practice, particularly in men aged 70 years and older. Consideration should be given for postponing non-urgent procedures and promoting non-operative treatment to delay or avoid the need for surgery. Funding: National Institute for Health Research (NIHR), Association of Coloproctology of Great Britain and Ireland, Bowel and Cancer Research, Bowel Disease Research Foundation, Association of Upper Gastrointestinal Surgeons, British Association of Surgical Oncology, British Gynaecological Cancer Society, European Society of Coloproctology, NIHR Academy, Sarcoma UK, Vascular Society for Great Britain and Ireland, and Yorkshire Cancer Research

Carbon cycle history through the Jurassic–Cretaceous boundary: A new global δ13C stack

publisher: Elsevier articletitle: Carbon cycle history through the Jurassic–Cretaceous boundary: A new global δ13C stack journaltitle: Palaeogeography, Palaeoclimatology, Palaeoecology articlelink: http://dx.doi.org/10.1016/j.palaeo.2016.03.016 content_type: article copyright: Copyright © 2016 Published by Elsevier B.V

Beta-naphthoflavone inhibits the induction of hepatic oestrogen-dependent proteins by 17alpha-ethynylestradiol in mosquitofish (Gambusia holbrooki)

The interactive effects of an aryl hydrocarbon receptor (AhR) agonist and of a xenoestrogen on biomarker responses were studied in the liver of male mosquitofish (Gambusia holbrooki). Hepatic 7-ethoxyresorufin O-deethylase (EROD) enzymatic activity was measured as a biomarker of exposure to the model AhR agonist beta-naphthoflavone (bNF). Hepatic proteins indicating the exposure of males to the synthetic oestrogen 17alpha-ethynylestradiol (EE2) were monitored by Western blot analysis using immunoserum prepared for this study. After a semi-static exposure only to waterborne EE2, Western blot analysis of liver homogenate revealed the induction of two protein bands (a double band at 205 kDa and a single band at 125 kDa). The interaction between bNF and EE2 was investigated by analysing, on the one hand, EROD activity and, on the other hand, immunoreactivity corresponding to the two oestrogen-dependent protein bands in the liver of fish exposed to different concentrations of bNF for 2 days, then to the same concentrations of bNF plus 0.1 µg l−1 EE2 for 5 days. EE2 changed neither the basal activity of EROD nor its rate of induction with 1.0 and 4.0 µg l−1 bNF. On the other hand, the induction of oestrogen-dependent proteins with 0.1 µg l−1 EE2 was inhibited by exposure to 4.0 µg l−1 bNF. These results together with literature data suggest that field monitoring of xenoestrogen contamination through the analysis of oestrogen-dependent protein in male fish as a biomarker should take into account the possible negative interference of AhR agonists