Development Aid: The Anatomy of a Crisis

Este trabajo presenta un marco interpretativo sobre la crisis de la cooperación al desa­rrollo. Partiendo del análisis de algunos de sus síntomas, se centra en la consideración de las transformaciones que se han operado en las últimas décadas y que han afectado especialmente a la identidad de la cooperación, como son las relativas a la globalización de los procesos económicos y sociales y a la vigencia del paradigma Norte-Sur como modelo interpretativo de los conflictos sobre desarrollo. Finalmente, se discuten algunos aspectos relativos a los objetivos, instrumentos y actores de la cooperación al desarrollo, planteando la influencia de todo ello en el debate sobre una posible readaptación y puesta al día de la misma.The current study presents an interpretive framework on the crisis of development aid. The study begins with the analysis of some of its symptoms, centers on considerations about transformations that have operated during the last decades and have particularly affected the identity of aid (such as those related to the globalization of economic and social processes) and have affected the validity of the North-South paradigm as an interpretive model of conflicts over development. Finally, several aspects are addressed in relation to development aid objectives, instruments, and actors, demonstrating their collective influence in the debate over a possible re-adaptation and updating of development aid

Espainia bidegurutzean: krisi ekonomikoa eta erreforma politikoa 1973-1986

1973ko petrolioaren bat bateko igoera politikoa gertatu zenean, krisiaren atzetik etorri zen beheraldiak Bigarren Mundu Gerra bukatu zenetik zetorren kapitalismoaren Urrezko Aroa deituriko hazkunde garaia bukarazi zuen. Beheraldiak Espainia oso egoera politiko berezian harrapatu zuen: diktadura luze baten heriotzaren bezperako azken hil hatsetan. Beheraldiak bi elementu berezi ekarri zituen: estanflazioa eta langabezia. Estanflazioa ordura arte inoiz gertatu gabeko fenomeno bat izan zen: ekonomiaren uzkurtzearekin batera gertatutako inflazioa. Langabezia ere ezohikoa izan zen krisia lehertu zen arte, frankismoko lan legediak eta hazkunde ekonomikoak langabezia tasa baxu mantendu zuelakoz. Egoerak aldaketa politiko zein ekonomiko sakonak eskatzen zituen, baina eliteak eta biztanleriaren gehiengoak ez zuen haustura erradikalik nahi. Lan honen helburua garai hartako politika ekonomiko batzuen azaleko errepaso bat egitea litzateke. Orduan eratu zuten sistema politikoa monarkia parlamentario konstituzionala izan zen. Eredu ekonomikoari dagokionez, Europako mendebaldeko ekonomia kapitalista sozialetan jarri zuten arreta. Haiei imitatuz, Europako Elkarte Ekonomikoan sartzea jarri zuten helburu. Baina helburua betetzeko neurri gogor eta gatazkatsuak hartu behar izan zituzten. Ezin litezke garai honetan gertatu ziren aldaketa ekonomiko guztiak ulertu, garaiko joan-etorri politikoak aztertu gabe. UCD zein PSOEren gobernu ezberdinen joera nagusia orduan mendebaldean erabiltzen ari ziren kutsu neoliberaleko neurriak ezartzea izan ziren. Hartu ziren neurriek ezkerreko oposizioaren adostasuna behar zuten. Horretarako, ezkerrak frankismoan zituen aldarrikapen iraultzaileei uko egin eta hitzarmen sozialaren alde egin zuen. Orokorrean, jarrera horrek langileen egora kaltetu zuen, baina trukean zenbati onura txiki eta sistema demokratiko eta parlamentario bat lortu zuten. Orduan burututako politika ekonomikoek eta sortu zen sistema akumulatibo berriak gaur arteko egoera ekonomikoa baldintzatu dute. Espainiako imaginario kolektiboan garrantzi handiko garaia izan zen aztergai duguna. Haren inguruan Trantsizoaren Kultura deiturikoa eratu zen eta erregimen berriaren mito sortzailea mundu guztiarentzako eredugarria izan zela aldarrikatu izan da, oso prozesu gatazkatsua izan zela ezkutatuz. Gaur egun, bizi dugun beheraldi ekonomikoak garai hartan eratu zen erregimena ezbaian jarri eta politika ekonomikoen inguruko duda piztu du. Orduan gertatutakoak, bai politikan bai ekonomian, gizartearen intereseko gaiak bihurtu dira, esparru akademiko zein informaletan

Compatibilidad o conflicto entre objetivos sociales y financieros de las microfinanzas: debates teóricos y evidencia empírica

Las microfinanzas representan un sector en crecimiento, que no está exento de cuestionamientos. Los efectos de estas prácticas, así como los posibles conflictos entre los objetivos sociales y financieros, son cuestiones aún debatidas que precisan profundización.El artículo parte de los análisis teóricos y empíricos, que abordan diferentes aspectos sobre las Instituciones Microfinancieras y su operativa. En el sector conviven los enfoques orientados a las necesidades de desarrollo y sociales, junto a otros más cercanos a la economía financiera y a la ampliación de la base del sistema financiero. Las posibles tensiones entre estas visiones, que podrían por ejemplo plantear problemas para trabajar atendiendo a los más pobres de forma sostenible, se sitúan como una preocupación clave.En este marco, partiendo de un profundo análisis teórico y bibliográfico, se realiza un estudio cuantitativo a partir de una amplia base de datos, que abarca más de 1.000 instituciones microfinancieras, tratadas con un Análisis de Componentes Principales. Además de arrojar luz sobre otras cuestiones, el artículo concluye que no existe una contradicción insoslayable entre la búsqueda de una mayor proyección social de las Instituciones Microfinancieras y su propia solvencia financiera, mostrando que, en la práctica, ambas cuestiones pueden ser compatibles y complementarias

Ca2+ activation kinetics of the two aspartate-glutamate mitochondrial carriers, aralar and citrin: Role in the heart malate-aspartate NADH shuttle

Ca2+ regulation of the Ca2+ binding mitochondrial carriers for aspartate/glutamate (AGCs) is provided by their N-terminal extensions, which face the intermembrane space. The two mammalian AGCs, aralar and citrin, are members of the malate-aspartate NADH shuttle. We report that their N-terminal extensions contain up to four pairs of EF-hand motifs plus a single vestigial EF-hand, and have no known homolog. Aralar and citrin contain one fully canonical EF-hand pair and aralar two additional half-pairs, in which a single EF-hand is predicted to bind Ca2+. Shuttle activity in brain or skeletal muscle mitochondria, which contain aralar as the major AGC, is activated by Ca2+ with S0.5 values of 280-350 nM; higher than those obtained in liver mitochondria (100-150 nM) that contain citrin as the major AGC. We have used aralar- and citrin-deficient mice to study the role of the two isoforms in heart, which expresses both AGCs. The S0.5 for Ca 2+ activation of the shuttle in heart mitochondria is about 300 nM, and it remains essentially unchanged in citrin-deficient mice, although it undergoes a drastic reduction to about 100 nM in aralar-deficient mice. Therefore, aralar and citrin, when expressed as single isoforms in heart, confer differences in Ca2+ activation of shuttle activity, probably associated with their structural differences. In addition, the results reveal that the two AGCs fully account for shuttle activity in mouse heart mitochondria and that no other glutamate transporter can replace the AGCs in this pathwayThis work was supported in part by grants from the Ministerio de Educacio´ n y Ciencia (BFU2005-C02-01, GEN2003-20235-C05-03/NAC), Instituto de Salud Carlos III del Ministerio de Sanidad (PI042457), European Union (LSHM-CT-2006-518153) (to J. S.), by Grant SAF2004-06843-C03 from the Ministerio de Educacio´ n y Ciencia (to P. G.-P.), by an institutional grant from the Fundacio´ n Ramo´ n Areces to the CBMSO, and by Grants-in-Aid for Scientific Research (16390100) from the Japan Society for the Promotion of Science (to K. K.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fac

Mitochondrial movement in Aralar/Slc25a12/AGC1 deficient cortical neurons

The elevated energy demands in the brain are fulfilled mainly by glucose catabolism. In highly polarized neurons, about 10–50% of mitochondria are transported along microtubules using mitochondrial-born ATP to locations with high energy requirements. In this report, we have investigated the impact of Aralar deficiency on mitochondrial transport in cultured cortical neurons. Aralar/slc25a12/AGC1 is the neuronal isoform of the aspartate-glutamate mitochondrial carrier, a component of the malate-aspartate shuttle (MAS) which plays an important role in redox balance, which is essential to maintain glycolytic pyruvate supply to neuronal mitochondria. Using live imaging microscopy we observed that the lack of Aralar does not affect the number of moving mitochondria nor the Ca2+-induced stop, the only difference being a 10% increase in mitochondrial velocity in Aralar deficient neurons. Therefore, we evaluated the possible fuels used in each case by studying the relative contribution of oxidative phosphorylation and glycolysis to mitochondrial movement using specific inhibitors. We found that the ATP synthase inhibitor oligomycin caused a smaller inhibition of mitochondrial movement in Aralar-KO than control neurons, whereas the glycolysis inhibitor iodoacetate had similar effects in neurons from both genotypes. In line with these findings, the decrease in cytosolic ATP/ADP ratio caused by oligomycin was more pronounced in control than in Aralar-KO neurons, but no differences were observed with iodoacetate. Oligomycin effect was reverted by aralar re-expression in knock out cultures. As mitochondrial movement is not reduced in Aralar-KO neurons, these results suggest that these neurons may use an additional pathway for mitochondria movement and ATP/ADP ratio maintenanceThis work was supported by grants S2010/BMD-2402, and a grant from Fundación Ramón Areces to JS; SAF2014-56929-R to JS and BP; SAF2017-82560-R to BP and AdA and an institutional grant from Fundación Ramón Areces to the Centro de Biología Molecular Severo Ochoa. LC has been the recipient of a Junta de Ampliación de Estudios Consejo Superior de Investigaciones Científicas and CIBERER postdoctoral contracts. The authors declare no competing financial interest

Role of aralar, the mitochondrial transporter of aspartate-glutamate, in brain N-acetylaspartate formation and Ca2+ signaling in neuronal mitochondria

"This is the peer reviewed version of the following article: Journal of Neuroscience Research 85.15 (2007): 3359-3366, which has been published in final form at https://doi.org/10.1002/jnr.21299. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions"Aralar, the Ca2+-dependent mitochondrial aspartate-glutamate carrier expressed in brain and skeletal muscle, is a member of the malate-aspartate NADH shuttle. Disrupting the gene for aralar, SLC25a12, in mice has enabled the discovery of two new roles of this carrier. On the one hand, it is required for synthesis of brain aspartate and N-acetylaspartate, a neuron-born metabolite that supplies acetate for myelin lipid synthesis; and on the other, it is essential for the transmission of small Ca2+ signals to mitochondria via an increase in mitochondrial NADHMinisterio de Educación y Ciencia; Contract grant numbers: BFU2005-C02-01 and GEN2003-20235-C05-03/NAC; Contract grant sponsor: Instituto de Salud Carlos III del Ministerio de Sanidad; Contract grant numbers: PI042457; Contract grant sponsor: European Union; Contract grant numbers: LSHM-CT-2006-518153 (to J.S.); Contract grant sponsor: Fundación Ramón Areces (institutional grant to Centro de Biología Molecular Severo Ochoa

Regulation of neuronal energy metabolism by calcium: role of MCU and aralar/malate-aspartate shuttle

Calcium is a major regulator of cellular metabolism. Calcium controls mitochondrial respiration, and calcium signaling is used to meet cellular energetic demands through energy production in the organelle. Although it has been widely assumed that Ca2+-actions require its uptake by mitochondrial calcium uniporter (MCU), alternative pathways modulated by cytosolic Ca2+ have been recently proposed. Recent findings have indicated a role for cytosolic Ca2+ signals acting on mitochondrial NADH shuttles in the control of cellular metabolism in neurons using glucose as fuel. It has been demonstrated that AGC1/Aralar, the component of the malate/aspartate shuttle (MAS) regulated by cytosolic Ca2+, participates in the maintenance of basal respiration exerted through Ca2+-fluxes between ER and mitochondria, whereas mitochondrial Ca2+-uptake by MCU does not contribute. Aralar/MAS pathway, activated by small cytosolic Ca2+ signals, provides in fact substrates, redox equivalents and pyruvate, fueling respiration. Upon activation and increases in workload, neurons upregulate OxPhos, cytosolic pyruvate production and glycolysis, together with glucose uptake, in a Ca2+-dependent way, and part of this upregulation is via Ca2+ signaling. Both MCU and Aralar/MAS contribute to OxPhos upregulation, Aralar/MAS playing a major role, especially at small and submaximal workloads. Ca2+ activation of Aralar/MAS, by increasing cytosolic NAD+/NADH provides Ca2+-dependent increases in glycolysis and cytosolic pyruvate production priming respiration as a feed-forward mechanism in response to workload. Thus, except for glucose uptake, these processes are dependent on Aralar/MAS, whereas MCU is the relevant target for Ca2+ signaling when MAS is bypassed, by using pyruvate or β-hydroxybutyrate as substrate

Exogenous aralar/slc25a12 can replace citrin/slc25a13 as malate aspartate shuttle component in liver

The deficiency of CITRIN, the liver mitochondrial aspartate–glutamate carrier (AGC), is the cause of four human clinical phenotypes, neonatal intrahepatic cholestasis caused by CITRIN deficiency (NICCD), silent period, failure to thrive and dyslipidemia caused by CITRIN deficiency (FTTDCD), and citrullinemia type II (CTLN2). Clinical symptoms can be traced back to disruption of the malate-aspartate shuttle due to the lack of citrin. A potential therapy for this condition is the expression of aralar, the AGC present in brain, to replace citrin. To explore this possibility we have first verified that the NADH/NAD+ ratio increases in hepatocytes from citrin(−/−) mice, and then found that exogenous aralar expression reversed the increase in NADH/NAD+ observed in these cells. Liver mitochondria from citrin (−/−) mice expressing liver specific transgenic aralar had a small (~ 4–6 nmoles x mg prot−1 x min−1) but consistent increase in malate aspartate shuttle (MAS) activity over that of citrin(−/−) mice. These results support the functional replacement between AGCs in the liver. To explore the significance of AGC replacement in human therapy we studied the relative levels of citrin and aralar in mouse and human liver through absolute quantification proteomics. We report that mouse liver has relatively high aralar levels (citrin/aralar molar ratio of 7.8), whereas human liver is virtually devoid of aralar (CITRIN/ARALAR ratio of 397). This large difference in endogenous aralar levels partly explains the high residual MAS activity in liver of citrin(−/−) mice and why they fail to recapitulate the human disease, but supports the benefit of increasing aralar expression to improve the redox balance capacity of human liver, as an effective therapy for CITRIN deficienc