Perspectives en matière de croissance de la productivité et du PIB potentiel.

Compte rendu d’une conférence internationale, organisée en avril 2006 par la Banque de France et la Banque du Canada, visant à comparer les quantifications et diagnostics concernant les écarts de croissance de la productivité et du PIB potentiel des pays industrialisés.Croissance, croissance potentielle, productivité, institutions, réformes.

A Dutch book coherence condition for conditional completely alternating Choquet expectations

Stemming from de Finetti’s coherence for finitely additive (conditional) probabilities, the paradigm of coherence has been extended to other uncertainty calculi. We study the notion of coherence for conditional completely alternating Choquet expectations, providing an avoiding Dutch book like condition

The CONEstrip algorithm

Uncertainty models such as sets of desirable gambles and (conditional) lower previsions can be represented as convex cones. Checking the consistency of and drawing inferences from such models requires solving feasibility and optimization problems. We consider finitely generated such models. For closed cones, we can use linear programming; for conditional lower prevision-based cones, there is an efficient algorithm using an iteration of linear programs. We present an efficient algorithm for general cones that also uses an iteration of linear programs

Editorial: Myokines, Adipokines, Cytokines in Muscle Pathophysiology.

[No abstract available

Editorial: myokines, adipokines, cytokines in muscle pathophysiology

Individual striated muscle fibers communicate in both a paracrine and endocrine fashion and are also involved in the crosstalk with other tissues and organs such as the adipose tissue, immune system, liver, pancreas, bones, and brain (Delezie andHandschin, 2018). The striatedmuscle, which accounts for 40% of bodymass, presents high biosynthetic activity, and extensive vascularization, features that endorse current thinking that muscle is the largest endocrine system of the body (Benatti and Pedersen, 2015). There are hundreds of muscle secretory products, collectively known as myokines, including proteins, miRNA, and exosomes (Barone et al., 2016). Muscle secretion is significantly affected by muscle contraction (Son et al., 2018) due to the activation of mechanotransduction pathways (Coletti et al., 2016a). It has been suggested that the adipose tissue is also an endocrine organ, producing adipokines- leptin, and other hormones, in addition to cytokines (Galic et al., 2010). The inflammatory infiltrate in fat depots affects the course of several diseases, including cancer (Batista et al., 2012; Sawicka and Krasowska, 2016; Neto et al., 2018; Opatrilova et al., 2018), and an extensive review on the role of adipokines in disease has been published elsewhere (Orzechowski et al., 2014). Myokines, adipokines, and cytokines are major therapeutic targets in both muscular and non-muscular diseases (Lindegaard et al., 2013;Manole et al., 2018), and understanding of their role in tissue crosstalk represents a subject of great interest in current biology.We have therefore chosen to address this paradigm within this Frontiers special issue on “Myokines, Adipokines, Cytokines in Muscle Pathophysiology.

Insects collected from an alpine-subalpine region in SE British Columbia

Insects were caught in a subalpine area of southeastern British Columbia. The list consists of 23 spp. and 37 genera, in families of five orders. The insects were collected during July and August, 1975 as part of a larger study of the ecology of mountain caribou in the Poplar Creek area, north of Nelson, B.C

Vimentin as a target for the treatment of COVID-19

We and others propose vimentin as a possible cellular target for the treatment of COVID-19. This innovative idea is so recent that it requires further attention and debate. The significant role played by vimentin in virus-induced infection however is well established: (1) vimentin has been reported as a co-receptor and/or attachment site for SARS-CoV; (2) vimentin is involved in viral replication in cells; (3) vimentin plays a fundamental role in both the viral infection and the consequent explosive immune-inflammatory response and (4) a lower vimentin expression is associated with the inhibition of epithelial to mesenchymal transition and fibrosis. Moreover, the absence of vimentin in mice makes them resistant to lung injury. Since vimentin has a twofold role in the disease, not only being involved in the viral infection but also in the associated life-threatening lung inflammation, the use of vimentin-targeted drugs may offer a synergistic advantage as compared with other treatments not targeting vimentin. Consequently, we speculate here that drugs which decrease the expression of vimentin can be used for the treatment of patients with COVID-19 and advise that several Food and Drug Administration-approved drugs be immediately tested in clinical trials against SARS-CoV-2, thus broadening therapeutic options for this type of viral infection

Targeting RAGE prevents muscle wasting and prolongs survival in cancer cachexia

Background: Cachexia, a multifactorial syndrome affecting more than 50% of patients with advanced cancer and responsible for ~20% of cancer-associated deaths, is still a poorly understood process without a standard cure available. Skeletal muscle atrophy caused by systemic inflammation is a major clinical feature of cachexia, leading to weight loss, dampening patients' quality of life, and reducing patients' response to anticancer therapy. RAGE (receptor for advanced glycation end-products) is a multiligand receptor of the immunoglobulin superfamily and a mediator of muscle regeneration, inflammation, and cancer. Methods: By using murine models consisting in the injection of colon 26 murine adenocarcinoma (C26-ADK) or Lewis lung carcinoma (LLC) cells in BALB/c and C57BL/6 or Ager−/− (RAGE-null) mice, respectively, we investigated the involvement of RAGE signalling in the main features of cancer cachexia, including the inflammatory state. In vitro experiments were performed using myotubes derived from C2C12 myoblasts or primary myoblasts isolated from C57BL/6 wild type and Ager−/− mice treated with the RAGE ligand, S100B (S100 calcium-binding protein B), TNF (tumor necrosis factor)α±IFN (interferon) γ, and tumour cell- or masses-conditioned media to analyse hallmarks of muscle atrophy. Finally, muscles of wild type and Ager−/− mice were injected with TNFα/IFNγ or S100B in a tumour-free environment. Results: We demonstrate that RAGE is determinant to activate signalling pathways leading to muscle protein degradation in the presence of proinflammatory cytokines and/or tumour-derived cachexia-inducing factors. We identify the RAGE ligand, S100B, as a novel factor able to induce muscle atrophy per se via a p38 MAPK (p38 mitogen-activated protein kinase)/myogenin axis and STAT3 (signal transducer and activator of transcription 3)-dependent MyoD (myoblast determination protein 1) degradation. Lastly, we found that in cancer conditions, an increase in serum levels of tumour-derived S100B and HMGB1 (high mobility group box 1) occurs leading to chronic activation/overexpression of RAGE, which induces hallmarks of cancer cachexia (i.e. muscle wasting, systemic inflammation, and release of tumour-derived pro-cachectic factors). Absence of RAGE in mice translates into reduced serum levels of cachexia-inducing factors, delayed loss of muscle mass and strength, reduced tumour progression, and increased survival. Conclusions: RAGE is a molecular determinant in inducing the hallmarks of cancer cachexia, and molecular targeting of RAGE might represent a therapeutic strategy to prevent or counteract the cachectic syndrome

Tumor microenvironment autophagic processes and cachexia: the missing link?

Cachexia is a syndrome that affects the entire organism and presents a variable plethora of symptoms in patients, always associated with continuous and involuntary degradation of skeletal muscle mass and function loss. In cancer, this syndrome occurs in 50% of all patients, while prevalence increases to 80% as the disease worsens, reducing quality of life, treatment tolerance, therapeutic response, and survival. Both chronic systemic inflammation and immunosuppression, paradoxically, correspond to important features in cachexia patients. Systemic inflammation in cachexia is fueled by the interaction between tumor and peripheral tissues with significant involvement of infiltrating immune cells, both in the peripheral tissues and in the tumor itself. Autophagy, as a process of regulating cellular metabolism and homeostasis, can interfere with the metabolic profile in the tumor microenvironment. Under a scenario of balanced autophagy in the tumor microenvironment, the infiltrating immune cells control cytokine production and secretion. On the other hand, when autophagy is unbalanced or dysfunctional within the tumor microenvironment, there is an impairment in the regulation of immune cell’s inflammatory phenotype. The inflammatory phenotype upregulates metabolic consumption and cytokine production, not only in the tumor microenvironment but also in other tissues and organs of the host. We propose that cachexia-related chronic inflammation can be, at least, partly associated with the failure of autophagic processes in tumor cells. Autophagy endangers tumor cell viability by producing immunogenic tumor antigens, thus eliciting the immune response necessary to counteract tumor progression, while preventing the establishment of inflammation, a hallmark of cachexia. Comprehensive understanding of this complex functional dichotomy may enhance cancer treatment response and prevent/mitigate cancer cachexia. This review summarizes the recent available literature regarding the role of autophagy within the tumor microenvironment and the consequences eliciting the development of cancer cachexia