The Survival Assumption in Intertemporal Economies

In an economy with a non-convex production sector, we provide an assumption on each individual producer, which implies that the survival assumption holds true at the aggregate level for general pricing rules. For the marginal pricing rule, we derive this assumption from the bounded marginal productivity of inputs. We apply this approach to intertemporal economies and we show how our assumption fits well with the time structure leading to a tractable existence result of equilibria, which could be apply to discrete dynamical growth models.General equilibrium theory ; increasing returns ; survival assumption ; marginal pricing ; general pricing rules

L'histoire que nous faisons. Contre les théories de la manipulation

Dans un monde de plus en plus interdépendant, il nous arrive de nous sentir manipulés par les acteurs dominants que sont les institutions économiques internationales, les entreprises mondialisées, les grands médias ou les principaux responsables politiques. Pour autant, l’homme ordinaire d’aujourd’hui n’est-il vraiment qu’une marionnette comme le prétend toute une partie de la critique de gauche ? Ne sommes-nous pas davantage acteurs qu’on nous le prétend et n’avons-nous pas mieux à faire que de voir partout des manipulations et des « agendas cachés » ? C’est à cette réflexion que nous invitent les auteurs

Equilibria with increasing returns: sufficient conditions on bounded production allocations

URL des Cahiers : https://halshs.archives-ouvertes.fr/CAHIERS-MSEVoir aussi l'article basé sur ce document de travail paru dans "Journal of Public Economic Theory", 10, 6, 2008, pp.1033-1068Cahiers de la MSE 2005.45 - Série Bleue - ISSN : 1624-0340This paper deals with the existence of marginal pricing equilibria or equilibria with general pricing rules in an economy with increasing returns to scale or more general types of non convexities in production. Its main contribution is to posit the bounded loss and survival assumptions on a bounded subset of production allocations. Furthermore, the free-disposal assumption is weaken, which allows to consider non positive prices. Finally, we also provide an existence result for a quasi-equilibria, when the survival assumption is weaken on the attainable allocations.Cet article traite du problème de l'existence de l'équilibre de tarification à pertes bornées et de l'équilibre de tarification marginale dans des économies au secteur productif non convexe. La principale contribution est la limitation des hypothèses de pertes bornées et de survivance à des ensembles bornés d'allocations de production. En outre, l'hypothèse de libre disposition est affaiblie, ce qui permet de prendre en compte d'éventuels prix négatifs. Enfin, nous montrons qu'il existe un quasi-équilibre lorsque l'hypothèse de survivance n'est plus valide pour les allocations de production réalisables

The Survival Assumption in Intertemporal Economies

URL des Documents de travail : http://ces.univ-paris1.fr/cesdp/CESFramDP2009.htmDocuments de travail du Centre d'Economie de la Sorbonne 2009.76 - ISSN : 1955-611XIn an economy with a non-convex production sector, we provide an assumption on each individual producer, which implies that the survival assumption holds true at the aggregate level for general pricing rules. For the marginal pricing rule, we derive this assumption from the bounded marginal productivity of inputs. We apply this approach to intertemporal economies and we show how our assumption fits well with the time structure leading to a tractable existence result of equilibria, which could be apply to discrete dynamical growth models.Dans une économie avec un secteur de production non convexe, nous proposons une hypothèse sur chaque producteur qui implique de l'hypothèse de survivance est satisfaite au niveau agrégé pour des règles de tarification générales. Pour la tarification marginale, nous déduisons cette hypothèse du fait que la productivité marginale des facteurs de production est bornée. Nous appliquons ce résultat à des économies intertemporelles et nous montrons que notre hypothèse s'accorde bien avec la structure temporelle et conduit donc à un résultat d'existence maniable qui peut s'appliquer au modèles de croissance en temps discret

Études de la parenté

Emmanuel Désveaux, maître de conférences Critique de la raison parentaire Nous avons poursuivi le travail entamé les années précédentes d’une critique radicale de la raison parentaire, entendue comme l’ensemble du dispositif intellectuel qui s’est construit progressivement au cœur du discours anthropologique autour du thème de l’organisation de la famille et de l’appellation des parents entre eux. L’un des objectifs du séminaire était de repérer, afin de bien souligner combien elles s’oppose..

Orthoparamyxovirinae C Proteins Have a Common Origin and a Common Structural Organization

The protein C is a small viral protein encoded in an overlapping frame of the P gene in the subfamily Orthoparamyxovirinae. This protein, expressed by alternative translation initiation, is a virulence factor that regulates viral transcription, replication, and production of defective interfering RNA, interferes with the host-cell innate immunity systems and supports the assembly of viral particles and budding. We expressed and purified full-length and an N-terminally truncated C protein from Tupaia paramyxovirus (TupV) C protein (genus Narmovirus). We solved the crystal structure of the C-terminal part of TupV C protein at a resolution of 2.4 Å and found that it is structurally similar to Sendai virus C protein, suggesting that despite undetectable sequence conservation, these proteins are homologous. We characterized both truncated and full-length proteins by SEC-MALLS and SEC-SAXS and described their solution structures by ensemble models. We established a mini-replicon assay for the related Nipah virus (NiV) and showed that TupV C inhibited the expression of NiV minigenome in a concentration-dependent manner as efficiently as the NiV C protein. A previous study found that the Orthoparamyxovirinae C proteins form two clusters without detectable sequence similarity, raising the question of whether they were homologous or instead had originated independently. Since TupV C and SeV C are representatives of these two clusters, our discovery that they have a similar structure indicates that all Orthoparamyxovirine C proteins are homologous. Our results also imply that, strikingly, a STAT1-binding site is encoded by exactly the same RNA region of the P/C gene across Paramyxovirinae, but in different reading frames (P or C), depending on which cluster they belong to.French Agence Nationale de la RechercheFond de la Recherche Médicale (FRM)Grenoble Instruct-ERIC centerFRISBIUniversity Grenoble Alpes graduate school (Ecoles Universitaires de Recherche)Peer Reviewe

Structure and functional relevance of the Slit2 homodimerization domain

Slit proteins are secreted ligands that interact with the Roundabout (Robo) receptors to provide important guidance cues in neuronal and vascular development. Slit–Robo signalling is mediated by an interaction between the second Slit domain and the first Robo domain, as well as being dependent on heparan sulphate. In an effort to understand the role of the other Slit domains in signalling, we determined the crystal structure of the fourth Slit2 domain (D4) and examined the effects of various Slit2 constructs on chick retinal ganglion cell axons. Slit2 D4 forms a homodimer using the conserved residues on its concave face, and can also bind to heparan sulphate. We observed that Slit2 D4 frequently results in growth cones with collapsed lamellipodia and that this effect can be inhibited by exogenously added heparan sulphate. Our results show that Slit2 D4–heparan sulphate binding contributes to a Slit–Robo signalling mechanism more intricate than previously thought

Adjuvant Chemotherapy With Sequential or Concurrent Anthracycline and Docetaxel: Breast International Group 02-98 Randomized Trial

Background Docetaxel is more effective than doxorubicin for patients with advanced breast cancer. The Breast International Group 02-98 randomized trial tested the effect of incorporating docetaxel into anthracycline-based adjuvant chemotherapy and compared sequential vs concurrent administration of doxorubicin and docetaxel. Methods Patients with lymph node-positive breast cancer (n = 2887) were randomly assigned to one of four treatments: 1) sequential control (four cycles of doxorubicin at 75 mg/m2, followed by three cycles of cyclophosphamide, methotrexate, and 5-fluorouracil [CMF]); 2) concurrent control (four cycles of doxorubicin at 60 mg/m2 plus cyclophosphamide at 600 mg/m2, followed by three cycles of CMF); 3) sequential docetaxel (three cycles of doxorubicin at 75 mg/m2, followed by three cycles of docetaxel at 100 mg/m2, followed by three cycles of CMF); 4) concurrent docetaxel (four cycles of doxorubicin at 50 mg/m2 plus docetaxel at 75 mg/m2, followed by three cycles of CMF). The primary comparison evaluated the efficacy of including docetaxel regardless of schedule and was planned after 1215 disease-free survival (DFS) events (ie, relapse, second primary cancer, or death from any cause). Docetaxel and control treatment groups were compared by log-rank tests, and hazard ratios (HR) of DFS events were calculated by Cox modeling. All statistical tests were two-sided. Results Due to a lower-than-anticipated rate of relapse, this analysis was performed after 5 years with 732 events. Patients in control arms had a 5-year DFS of 73% (95% confidence interval [CI] = 70% to 75%). Docetaxel treatment resulted in an improvement in DFS of borderline statistical significance compared with control treatment (HR = 0.86, 95% CI = 0.74 to 1.00; P = .05). However, DFS in the sequential docetaxel arm was better than that in the concurrent docetaxel arm (HR = 0.83, 95% CI = 0.69 to 1.00) and in the sequential control arm (HR = 0.79, 95% CI = 0.64 to 0.98). Conclusions Incorporating docetaxel into anthracycline-based therapy resulted in an improvement in DFS that was of borderline statistical significance. However, important differences may be related to doxorubicin and docetaxel scheduling, with sequential but not concurrent administration, appearing to produce better DFS than anthracycline-based chemotherap

Acyltransferase activities of the high-molecular-mass essential penicillin-binding proteins

The high-molecular-mass penicillin-binding proteins (HMM-PBPs), present in the cytoplasmic membranes of all eubacteria, are involved in important physiological events such as cell elongation, septation or shape determination. Up to now it has, however, been very difficult or impossible to study the catalytic properties of the HMM-PBPs in vitro. With simple substrates, we could demonstrate that several of these proteins could catalyse the hydrolysis of some thioesters or the transfer of their acyl moiety on the amino group of a suitable acceptor nucleophile. Many of the acyl-donor substrates were hippuric acid or benzoyl-D-alanine derivatives, and their spectroscopic properties enabled a direct monitoring of the enzymic reaction. In their presence, the binding of radioactive penicillin to the PBPs was also inhibited

Structure of the Vesicular Stomatitis Virus N0-P Complex

Replication of non-segmented negative-strand RNA viruses requires the continuous supply of the nucleoprotein (N) in the form of a complex with the phosphoprotein (P). Here, we present the structural characterization of a soluble, heterodimeric complex between a variant of vesicular stomatitis virus N lacking its 21 N-terminal residues (NΔ21) and a peptide of 60 amino acids (P60) encompassing the molecular recognition element (MoRE) of P that binds RNA-free N (N0). The complex crystallized in a decameric circular form, which was solved at 3.0 Å resolution, reveals how the MoRE folds upon binding to N and competes with RNA binding and N polymerization. Small-angle X-ray scattering experiment and NMR spectroscopy on the soluble complex confirms the binding of the MoRE and indicates that its flanking regions remain flexible in the complex. The structure of this complex also suggests a mechanism for the initiation of viral RNA synthesis