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Discours prononcé par Sarmiento en 1865 devant la Société Historique de Rhode-Island, ce texte est d'abord une réflexion sur l'unité des deux Amériques. D'une modernisation impulsée par le génie nord-américain au partage d'une destinée commune, Sarmiento rappelle ce qui rapproche ces deux parts du continent. Ainsi replacé dans une même histoire européenne et américaine, le devenir du continent est relu à la lumière des thèmes chers à l'auteur : le procès de civilisation, le poids des religions, l'éducation et la lutte contre les tyrannies. Texte d'histoire et d'historien, il est aussi un plaidoyer à l'adresse des États-Unis pour soutenir le développement de l'Amérique du Sud et découvrir aussi bien ses richesses que sa civilisation.

Since they were first proposed as nonviral transfection agents for their gene-carrying capacity, magnetic nanoparticles have been studied thoroughly, both in vitro and in vivo. Great effort has been made to manufacture biocompatible magnetic nanoparticles for use in the theragnosis of cancer and other diseases. Here we survey recent advances in the study of magnetic nanoparticles, as well as the polymers and other coating layers currently available for gene therapy, their synthesis, and bioconjugation processes. In addition, we review several gene therapy models based on magnetic nanoparticles. ; Vladimir Mulens holds a predoctoral fellowship from the Fundación La Caixa-CNB program. Some work discussed here was partially supported by grants from the Spanish Ministry of Economy and Competitiveness (SAF-2011-23639 to DFB and MAT2011-23641 and CSD2007-00010 to MPM), the Madrid Regional Government (S009/MAT-1726 to MPM), the Research Network in Inflammation and Rheumatic Diseases (RIER) of the ISCIII-MSPS Cooperative Research Thematic Network program (RD08/0075/0015 to DFB), and the Guerbet Research. ; Peer Reviewed

In the planning of a country's economic policy, exchange rate policy has a major role, especially in less developed countries where industrial policies and foreign trade are mainly based on the exchange rate competitiveness. Therefore, it is not surprising that the exchange rate policy is used by governments and policy makers to assess the country's competitive position in the world trade. In practice, the real exchange rate (RER) is associated with the evaluation of the external position of countries through the price elasticity analysis between exports and imports. However, the assessment of countries competitive position on the basis of price elasticity is a simplified overview for understanding reality. Despite the research efforts made to cast light on the field of concern, a causal relationship between the behavior of the RER and highest competitiveness indicators remain unclear. In fact, this relationship disregards the effects of non-price competitiveness, such as competitive advantages based on the value added like high technologies applied to new products developments and new processes designs. To round up, some authors and policy makers support the assumption that the overvaluation of a currency deteriorates the competitive position of a country and that competitive devaluations facilitate growth through its positive impact on the share of the tradable goods in the economy, especially in the industry. Nevertheless, there is vast empirical evidence supporting that an appreciation of the RER will not always result in a loss of competitiveness and, conversely, RER depreciation will not always imply a higher competitiveness performance. Thus, competitiveness policies strongly based on the RER evolution through time can lead to misleading conclusions. This thesis is focused on the effects of the real exchange rate as an instrument of macroeconomic policy aimed at achieving higher indicators of competitiveness in the business sector. Theoretical and empirical evidence is offered to business decision-makers as useful information.

11 pages, 8 figures.-- PMID: 17998387 [PubMed].-- PMCID: PMC2118532.-- Printed version published Nov 26, 2007. ; Supporting information attached: Information on Western blots, Immunoprecipitation assays, the Rac activation assay, the FACS-based conjugate formation assay, the Actin polymerization assay, and Stimulation with antibody-coated beads and immunofluorescence.-- Also available at: http://jem.rupress.org/cgi/content/full/jem.20070366/DC1 ; Class I phosphoinositide 3–kinases (PI3Ks) constitute a family of enzymes that generates 3-phosphorylated polyphosphoinositides at the cell membrane after stimulation of protein tyrosine (Tyr) kinase–associated receptors or G protein–coupled receptors (GPCRs). The class I PI3Ks are divided into two types: class I(A) p85/p110 heterodimers, which are activated by Tyr kinases, and the class I(B) p110γ isoform, which is activated by GPCR. Although the T cell receptor (TCR) is a protein Tyr kinase–associated receptor, p110γ deletion affects TCR-induced T cell stimulation. We examined whether the TCR activates p110γ, as well as the consequences of interfering with p110γ expression or function for T cell activation. We found that after TCR ligation, p110γ interacts with Gα(q/11), lymphocyte-specific Tyr kinase, and ζ-associated protein. TCR stimulation activates p110γ which affects 3-phosphorylated polyphosphoinositide levels at the immunological synapse. We show that TCR-stimulated p110γ controls RAS-related C3 botulinum substrate 1 activity, F-actin polarization, and the interaction between T cells and antigen-presenting cells, illustrating a crucial role for p110γ in TCR-induced T cell activation. ; I. Alcázar holds a predoctoral fellowship from the Association for International Cancer Research, M. Marqués receives a predoctoral fellowship from the Spanish Ministry of Education and Science University Instructor Training Program, and D.F. Barber held a Ramón y Cajal contract from the Spanish Ministry of Education and Science and a Contract-in-Aid from the Fundación Científica de la Asociación Española Contra el Cancer. This work was supported by grants from the European Union (QLRT2001-02171), the Community of Madrid (8.3/0030/2000), the Ramón Areces Foundation (to D.F. Barber and A.C. Carrera), and the Spanish Dirección General de Ciencia y Desarrollo Tecnológico (SAF2004-00815 and SAF2004-05955- C02-01 to D.F. Barber A.C. Carrera, respectively). The Department of Immunology and Oncology was founded and is supported by the Spanish National Research Council (Consejo Superior de Investigaciones Científicas) and by Pfizer. ; Peer reviewed

Although iron oxide magnetic nanoparticles (MNP) have been proposed for numerous biomedical applications, little is known about their biotransformation and long-term toxicity in the body. Dimercaptosuccinic acid (DMSA)-coated magnetic nanoparticles have been proven efficient for in vivo drug delivery, but these results must nonetheless be sustained by comprehensive studies of long-term distribution, degradation and toxicity. We studied DMSA-coated magnetic nanoparticle effects in vitro on NCTC 1469 non-parenchymal hepatocytes, and analyzed their biodistribution and biotransformation in vivo in C57BL/6 mice. Our results indicate that DMSA-coated magnetic nanoparticles have little effect on cell viability, oxidative stress, cell cycle or apoptosis on NCTC 1469 cells in vitro. In vivo distribution and transformation were studied by alternating current magnetic susceptibility measurements, a technique that permits distinction of MNP from other iron species. Our results show that DMSA-coated MNP accumulate in spleen, liver and lung tissues for extended periods of time, in which nanoparticles undergo a process of conversion from superparamagnetic iron oxide nanoparticles to other non-superparamagnetic iron forms, with no significant signs of toxicity. This work provides the first evidence of DMSA-coated magnetite nanoparticle biotransformation in vivo. ; RM holds a post-doctoral contract supported by EU-FP7 MULTIFUN project (no. 262943), LG holds a Sara Borrell post-doctoral contract (CD09/00030) from the Carlos III Health Institute, Spanish Ministry for Health, Social Services and Equality (MSSSI), and TMZ received a FPU pre-doctoral fellowship from the Spanish Ministry of Economy and Competitiveness (MINECO). This work was partially supported by grants from the MINECO (SAF-2011-23639 to DFB and MAT2011-23641 and CSD2007-00010 to MPM), the Research Network in Inflammation and Rheumatic Diseases (RIER) of the ISCIII-MSSSI Cooperative Research Thematic Network program (RD08/0075/0015 to DFB), the Madrid regional government (S009/MAT-1726 to MPM), and EU-FP7 MULTIFUN project (no. 262943 to DFB and MPM). ; S2009/MAT-1726/Nanobiomagnet ; Peer Reviewed

Atherosclerosis is an inflammatory disease regulated by infiltrating monocytes and T cells, among other cell types. Macrophage recruitment to atherosclerotic lesions is controlled by monocyte infiltration into plaques. Once in the lesion, macrophage proliferation in situ, apoptosis, and differentiation to an inflammatory (M1) or anti-inflammatory phenotype (M2) are involved in progression to advanced atherosclerotic lesions. We studied the role of phosphoinositol-3-kinase (PI3K) p110γ in the regulation of in situ apoptosis, macrophage proliferation and polarization towards M1 or M2 phenotypes in atherosclerotic lesions. We analyzed atherosclerosis development in LDLR(-/-)p110γ(+/-) and LDLR(-/-)p110γ(-/-) mice, and performed expression and functional assays in tissues and primary cells from these and from p110γ(+/-) and p110γ(-/-) mice. Lack of p110γ in LDLR(-/-) mice reduces the atherosclerosis burden. Atherosclerotic lesions in fat-fed LDLR(-/-)p110γ(-/-) mice were smaller than in LDLR(-/-)p110γ(+/-) controls, which coincided with decreased macrophage proliferation in LDLR(-/-)p110γ(-/-) mouse lesions. This proliferation defect was also observed in p110γ(-/-) bone marrow-derived macrophages (BMM) stimulated with macrophage colony-stimulating factor (M-CSF), and was associated with higher intracellular cyclic adenosine monophosphate (cAMP) levels. In contrast, T cell proliferation was unaffected in LDLR(-/-)p110γ(-/-) mice. Moreover, p110γ deficiency did not affect macrophage polarization towards the M1 or M2 phenotypes or apoptosis in atherosclerotic plaques, or polarization in cultured BMM. Our results suggest that higher cAMP levels and the ensuing inhibition of macrophage proliferation contribute to atheroprotection in LDLR(-/-) mice lacking p110γ. Nonetheless, p110γ deletion does not appear to be involved in apoptosis, in macrophage polarization or in T cell proliferation. ; This work was supported by the Spanish Ministry of Science and Innovation (SAF-2007-60498, SAF-2008-00471, SAF-2011-23639 to DFB, SAF201016044 to VA, AP2007-01711 to TMZ, BES-2009-016547 to RS), the Research Network in Inflammation and Rheumatic Diseases (RIER) of the ISCIII-MSPS Cooperative Research Thematic Network program (RD08/0075/0015 to DFB), the Madrid Regional Government (200520M040 to DFB) and the Thematic Research Network in Cardiovascular Diseases (RECAVA; RD06/0014/0021 to VA). ; Sí

The following authors were omitted from the original version of this Data Descriptor: Markus Reichstein and Nicolas Vuichard. Both contributed to the code development and N. Vuichard contributed to the processing of the ERA-Interim data downscaling. Furthermore, the contribution of the co-author Frank Tiedemann was re-evaluated relative to the colleague Corinna Rebmann, both working at the same sites, and based on this re-evaluation a substitution in the co-author list is implemented (with Rebmann replacing Tiedemann). Finally, two affiliations were listed incorrectly and are corrected here (entries 190 and 193). The author list and affiliations have been amended to address these omissions in both the HTML and PDF versions. © 2021, This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply.