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European responses to Asia’s enhanced role as an aid donor

Freitas, Raquel; Mah, Luís
Fonte: CIES-IUL Publicador: CIES-IUL
Tipo: Trabalho em Andamento
Publicado em //2012 Português
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Asia is affirming itself as a newcomer and strong donor of aid to developing countries. China has been in the spotlight, but also countries such as India or South Korea have been stepping up their efforts at international development cooperation. These new actors, albeit with diverse approaches, challenge Europe’s global weight and leadership role and are driving it to rethink its development aid policies. Europe has developed a highly complex system of disbursing aid to developing countries attaching it to criteria of macro-economic performance and good governance. The principle of ownership as set by the Paris Declaration (2005) affirms that “partner countries exercise effective leadership over their development policies, and strategies and co-ordinate development actions”. European countries have promoted it as a cornerstone principle for aid effectiveness, claiming to give aid recipients the capacity to decide their policies autonomously, in contrast to previous policies of conditionality in aid. Yet, the praxis is far from matching the discourse, as Europe seeks to be deeply involved in the policy process of aid recipients. Asian donors, on the other hand, tend to be less concerned with the normative discourse or with the policy process of aid recipients and more focused on mutual economic gains of the relationship. In this scenario ownership takes on a different frame. This paper explores how Europe is reacting to this new context and to what extent it is adjusting its development aid policies.

AID Associates with Single-Stranded DNA with High Affinity and a Long Complex Half-Life in a Sequence-Independent Manner▿

Larijani, Mani; Petrov, Alexander P.; Kolenchenko, Oxana; Berru, Maribel; Krylov, Sergey N.; Martin, Alberto
Fonte: American Society for Microbiology Publicador: American Society for Microbiology
Tipo: Artigo de Revista Científica
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Activation-induced cytidine deaminase (AID) initiates secondary antibody diversification processes by deaminating cytidines on single-stranded DNA. AID preferentially mutates cytidines preceded by W(A/T)R(A/G) dinucleotides, a sequence specificity that is evolutionarily conserved from bony fish to humans. To uncover the biochemical mechanism of AID, we compared the catalytic and binding kinetics of AID on WRC (a hot-spot motif, where W equals A or T and R equals A or G) and non-WRC motifs. We show that although purified AID preferentially deaminates WRC over non-WRC motifs to the same degree observed in vivo, it exhibits similar binding affinities to either motif, indicating that its sequence specificity is not due to preferential binding of WRC motifs. AID preferentially deaminates bubble substrates of five to seven nucleotides rather than larger bubbles and preferentially binds to bubble-type rather than to single-stranded DNA substrates, suggesting that the natural targets of AID are either transcription bubbles or stem-loop structures. Importantly, AID displays remarkably high affinity for single-stranded DNA as indicated by the low dissociation constants and long half-life of complex dissociation that are typical of transcription factors and single-stranded DNA binding protein. These findings suggest that AID may persist on immunoglobulin and other target sequences after deamination...

Viral induction of AID is independent of the interferon and the Toll-like receptor signaling pathways but requires NF-κB

Gourzi, Polyxeni; Leonova, Tatyana; Papavasiliou, F. Nina
Fonte: The Rockefeller University Press Publicador: The Rockefeller University Press
Tipo: Artigo de Revista Científica
Publicado em 19/02/2007 Português
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Activation-induced cytidine deaminase (AID) is expressed in germinal centers of lymphoid organs during immunoglobulin diversification, in bone marrow B cells after infection with Abelson murine leukemia retrovirus (Ab-MLV), and in human B cells after infection by hepatitis C virus. To understand how viruses signal AID induction in the host we asked whether the AID response was abrogated in cells deficient in the interferon pathway or in signaling via the Toll-like receptors. Here we show that AID is not an interferon responsive gene and abrogation of Toll-like receptor signaling does not diminish the AID response. However, we found that NF-κB was required for expression of virally induced AID. Since NF-κB binds and activates the AID promoter, these results mechanistically link viral infection with AID transcription. Thus, induction of AID by viruses could be the result of several signaling pathways that culminate in NF-κB activation, underscoring the versatility of this host defense program.

Expression, purification, and characterization of a structurally disordered and functional C-terminal autoinhibitory domain (AID) of the 70 kDa 40S ribosomal protein S6 kinase-1 (S6K1)

Ragan, Timothy J.; Ross, Duncan B.; Keshwani, Malik M.; Harris, Thomas K.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
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S6K1 is a member of the AGC subfamily of serine-threonine protein kinases, whereby catalytic activation requires dual phosphorylation of critical residues in the conserved T-loop (T229) and hydrophobic motif (HM; T389) peptide regions of its catalytic kinase domain (residues 1-398). In addition to its kinase domain, S6K1 contains a C-terminal autoinhibitory domain (AID; residues 399-502), which prevents T-loop and HM phosphorylation; and autoinhibition is relieved on multi-site Ser-Thr phosphorylation of the AID (S411, S418, T421, and S424). Interestingly, 66 of the 104 C-terminal AID amino acid residues were computer predicted to exist in structurally disordered peptide regions, begetting interest as to how such dynamics could be coupled to autoregulation. To begin addressing this issue, we developed and optimized protocols for efficient AID expression and purification. Consistent with computer predictions, aberrant mobilities in both SDS-PAGE and size-exclusion chromatography, as well as low chemical shift dispersion in 1H-15N HSQC NMR spectra, indicated purified recombinant AID to be largely unfolded. Yet, trans-addition of purified AID effectively inhibited PDK1-catalyzed T-loop phosphorylation of a catalytic kinase domain construct of S6K1. Using an identical purification protocol...

AID expression levels determine the extent of cMyc oncogenic translocations and the incidence of B cell tumor development

Takizawa, Makiko; Tolarová, Helena; Li, Zhiyu; Dubois, Wendy; Lim, Susan; Callen, Elsa; Franco, Sonia; Mosaico, Maria; Feigenbaum, Lionel; Alt, Frederick W.; Nussenzweig, André; Potter, Michael; Casellas, Rafael
Fonte: The Rockefeller University Press Publicador: The Rockefeller University Press
Tipo: Artigo de Revista Científica
Publicado em 01/09/2008 Português
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Immunoglobulin (Ig) isotype switching is a recombination event that changes the constant domain of antibody genes and is catalyzed by activation-induced cytidine deaminase (AID). Upon recruitment to Ig genes, AID deaminates cytidines at switch (S) recombination sites, leading to the formation of DNA breaks. In addition to their role in isotype switching, AID-induced lesions promote Igh-cMyc chromosomal translocations and tumor development. However, cMyc translocations are also present in lymphocytes from healthy humans and mice, and thus, it remains unclear whether AID directly contributes to the dynamics of B cell transformation. Using a plasmacytoma mouse model, we show that AID+/− mice have reduced AID expression levels and display haploinsufficiency both in the context of isotype switching and plasmacytomagenesis. At the Ig loci, AID+/− lymphocytes show impaired intra- and inter-switch recombination, and a substantial decrease in the frequency of S mutations and chromosomal breaks. In AID+/− mice, these defects correlate with a marked decrease in the accumulation of B cell clones carrying Igh-cMyc translocations during tumor latency. These results thus provide a causality link between the extent of AID enzymatic activity...

The Interaction between AID and CIB1 Is Nonessential for Antibody Gene Diversification by Gene Conversion or Class Switch Recombination

Demorest, Zachary L.; MacDuff, Donna A.; Brown, William L.; Morham, Scott G.; Parise, Leslie V.; Harris, Reuben S.
Fonte: Public Library of Science Publicador: Public Library of Science
Tipo: Artigo de Revista Científica
Publicado em 20/07/2010 Português
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Activation-induced deaminase (AID) initiates somatic hypermutation, gene conversion and class switch recombination by deaminating variable and switch region DNA cytidines to uridines. AID is predominantly cytoplasmic and must enter the nuclear compartment to initiate these distinct antibody gene diversification reactions. Nuclear AID is relatively short-lived, as it is efficiently exported by a CRM1-dependent mechanism and it is susceptible to proteasome-dependent degradation. To help shed light on mechanisms of post-translational regulation, a yeast-based screen was performed to identify AID-interacting proteins. The calcium and integrin binding protein CIB1 was identified by sequencing and the interaction was confirmed by immunoprecipitation experiments. The AID/CIB1 resisted DNase and RNase treatment, and it is therefore unlikely to be mediated by nucleic acid. The requirement for CIB1 in AID-mediated antibody gene diversification reactions was assessed in CIB1-deficient DT40 cells and in knockout mice, but immunoglobulin gene conversion and class switch recombination appeared normal. The DT40 system was also used to show that CIB1 over-expression has no effect on gene conversion and that AID-EGFP subcellular localization is normal. These combined data demonstrate that CIB1 is not required for AID to mediate antibody gene diversification processes. It remains possible that CIB1 has an alternative...

Local Sequence Targeting in the AID/APOBEC Family Differentially Impacts Retroviral Restriction and Antibody Diversification*

Kohli, Rahul M.; Maul, Robert W.; Guminski, Amy F.; McClure, Rhonda L.; Gajula, Kiran S.; Saribasak, Huseyin; McMahon, Moira A.; Siliciano, Robert F.; Gearhart, Patricia J.; Stivers, James T.
Fonte: American Society for Biochemistry and Molecular Biology Publicador: American Society for Biochemistry and Molecular Biology
Tipo: Artigo de Revista Científica
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Nucleic acid cytidine deaminases of the activation-induced deaminase (AID)/APOBEC family are critical players in active and innate immune responses, playing roles as target-directed, purposeful mutators. AID specifically deaminates the host immunoglobulin (Ig) locus to evolve antibody specificity, whereas its close relative, APOBEC3G (A3G), lethally mutates the genomes of retroviral pathogens such as HIV. Understanding the basis for the target-specific action of these enzymes is essential, as mistargeting poses significant risks, potentially promoting oncogenesis (AID) or fostering drug resistance (A3G). AID prefers to deaminate cytosine in WRC (W = A/T, R = A/G) motifs, whereas A3G favors deamination of CCC motifs. This specificity is largely dictated by a single, divergent protein loop in the enzyme family that recognizes the DNA sequence. Through grafting of this substrate-recognition loop, we have created enzyme variants of A3G and AID with altered local targeting to directly evaluate the role of sequence specificity on immune function. We find that grafted loops placed in the A3G scaffold all produced efficient restriction of HIV but that foreign loops in the AID scaffold compromised hypermutation and class switch recombination. Local targeting...

The mechanisms regulating the subcellular localization of AID

Patenaude, Anne-Marie; Di Noia, Javier M
Fonte: Landes Bioscience Publicador: Landes Bioscience
Tipo: Artigo de Revista Científica
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Activation induced deaminase (AID) is a unique enzyme that directly introduces mutations in the immunoglobulin genes to generate antibody diversity during the humoral immune response. Since this mutator enzyme poses a measurable risk of off-target mutation, which can be deleterious or transforming for a cell, several regulatory mechanisms exist to control its activity. At least three of these mechanisms affect AID subcellular localization. It was recently found that AID is actively imported into the nucleus, most likely through importin-α/β recognizing a structural nuclear localization signal. However, AID is largely excluded from the nucleus in steady state thanks to two mechanisms. In addition to nuclear export through the exportin CRM1, a mechanism retaining AID in the cytoplasm exists. Cytoplasmic retention hinders the passive diffusion of AID into the nucleus playing an important role in the nuclear exclusion of AID. Subcellular localization of AID also determines its stability. The regulation of the nuclear fraction of AID by these many mechanisms has functional implications for antibody diversification.

Cytoplasmic activation-induced cytidine deaminase (AID) exists in stoichiometric complex with translation elongation factor 1α (eEF1A)

Häsler, Julien; Rada, Cristina; Neuberger, Michael S.
Fonte: National Academy of Sciences Publicador: National Academy of Sciences
Tipo: Artigo de Revista Científica
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Activation-induced cytidine deaminase (AID) is a B lymphocyte-specific DNA deaminase that acts on the Ig loci to trigger antibody gene diversification. Most AID, however, is retained in the cytoplasm and its nuclear abundance is carefully regulated because off-target action of AID leads to cancer. The nature of the cytosolic AID complex and the mechanisms regulating its release from the cytoplasm and import into the nucleus remain unknown. Here, we show that cytosolic AID in DT40 B cells is part of an 11S complex and, using an endogenously tagged AID protein to avoid overexpression artifacts, that it is bound in good stoichiometry to the translation elongation factor 1 alpha (eEF1A). The AID/eEF1A interaction is recapitulated in transfected cells and depends on the C-terminal domain of eEF1A (which is not responsible for GTP or tRNA binding). The eEF1A interaction is destroyed by mutations in AID that affect its cytosolic retention. These results suggest that eEF1A is a cytosolic retention factor for AID and extend on the multiple moonlighting functions of eEF1A.

AID-Initiated Off-Target DNA Breaks are Detected and Resolved During S-Phase

Hasham, Muneer G.; Snow, Kathy J.; Donghia, Nina M.; Branca, Jane A.; Lessard, Mark D.; Stavnezer, Janet; Shopland, Lindsay S.; Mills, Kevin D.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
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Activation-induced cytidine deaminase (AID) initiates DNA double strand breaks (DSBs) in the immunoglobulin heavy chain gene (Igh) to stimulate isotype class switch recombination (CSR), and widespread breaks in non-Igh (off-target) loci throughout the genome. Because the DSBs that initiate class switching occur during the G1 phase of the cell cycle, and are repaired via end joining, CSR is considered a predominantly G1 reaction. By contrast, AID-induced non-Igh DSBs are repaired by homologous recombination. Although little is known about the connection between the cell cycle and either induction or resolution of AID-mediated non-Igh DSBs, their repair by homologous recombination implicates post-G1 phases. Coordination of DNA breakage and repair during the cell cycle is critical to promote normal class switching and prevent genomic instability. To understand how AID-mediated events are regulated through the cell cycle, we have investigated G1-to-S control in AID-dependent genome-wide DSBs. We find that AID-mediated off-target DSBs, like those induced in the Igh locus, are generated during G1. These data suggest that AID-mediated DSBs can evade G1/S checkpoint activation and persist beyond G1, becoming resolved during S-phase. Interestingly...

A role for the RNA pol II–associated PAF complex in AID-induced immune diversification

Willmann, Katharina L.; Milosevic, Sara; Pauklin, Siim; Schmitz, Kerstin-Maike; Rangam, Gopinath; Simon, Maria T.; Maslen, Sarah; Skehel, Mark; Robert, Isabelle; Heyer, Vincent; Schiavo, Ebe; Reina-San-Martin, Bernardo; Petersen-Mahrt, Svend K.
Fonte: The Rockefeller University Press Publicador: The Rockefeller University Press
Tipo: Artigo de Revista Científica
Publicado em 22/10/2012 Português
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Antibody diversification requires the DNA deaminase AID to induce DNA instability at immunoglobulin (Ig) loci upon B cell stimulation. For efficient cytosine deamination, AID requires single-stranded DNA and needs to gain access to Ig loci, with RNA pol II transcription possibly providing both aspects. To understand these mechanisms, we isolated and characterized endogenous AID-containing protein complexes from the chromatin of diversifying B cells. The majority of proteins associated with AID belonged to RNA polymerase II elongation and chromatin modification complexes. Besides the two core polymerase subunits, members of the PAF complex, SUPT5H, SUPT6H, and FACT complex associated with AID. We show that AID associates with RNA polymerase-associated factor 1 (PAF1) through its N-terminal domain, that depletion of PAF complex members inhibits AID-induced immune diversification, and that the PAF complex can serve as a binding platform for AID on chromatin. A model is emerging of how RNA polymerase II elongation and pausing induce and resolve AID lesions.

A systematic literature review on first aid provided by laypeople to trauma victims

Tannvik, T D; Bakke, H K; Wisborg, T
Fonte: Blackwell Publishing Ltd Publicador: Blackwell Publishing Ltd
Tipo: Artigo de Revista Científica
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Death from trauma is a significant and international problem. Outcome for patients suffering out-of-hospital cardiac arrests is significantly improved by early cardiopulmonary resuscitation. The usefulness of first aid given by laypeople in trauma is less well established. The aim of this study was to review the existing literature on first aid provided by laypeople to trauma victims and to establish how often first aid is provided, if it is performed correctly, and its impact on outcome. A systematic review was carried out, according to preferred reporting items for systematic reviews and meta-analysis (PRISMA) guidelines, of all studies involving first aid provided by laypeople to trauma victims. Cochrane, Embase, Medline, Pubmed, and Google Scholar databases were systematically searched. Ten eligible articles were identified involving a total of 5836 victims. Eight studies were related to patient outcome, while two studies were simulation based. The proportion of patients who received first aid ranged from 10.7% to 65%. Incorrect first aid was given in up to 83.7% of cases. Airway handling and haemorrhage control were particular areas of concern. One study from Iraq investigated survival and reported a 5.8% reduction in mortality. Two retrospective autopsy-based studies estimated that correct first aid could have reduced mortality by 1.8–4.5%. There is limited evidence regarding first aid provided by laypeople to trauma victims. Due to great heterogeneity in the studies...

AID and Apobec3G haphazard deamination and mutational diversity

Jaszczur, Malgorzata; Bertram, Jeffrey G.; Pham, Phuong; Scharff, Matthew D.; Goodman, Myron F.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
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Activation-induced deoxycytidine deaminase (AID) and Apobec 3G (Apo3G) cause mutational diversity by initiating mutations on regions of single-stranded (ss) DNA. Expressed in B cells, AID deaminates C → U in actively transcribed immunoglobulin (Ig) variable and switch regions to initiate the somatic hypermutation (SHM) and class switch recombination (CSR) that are essential for antibody diversity. Apo3G expressed in T cells catalyzes C deaminations on reverse transcribed cDNA causing HIV-1 retroviral inactivation. When operating properly, AID- and Apo3G-initiated mutations boost human fitness. Yet, both enzymes are potentially powerful somatic cell “mutators”. Loss of regulated expression and proper genome targeting can cause human cancer. Here, we review well-established biological roles of AID and Apo3G. We provide a synopsis of AID partnering proteins during SHM and CSR, and describe how an Apo2 crystal structure provides “surrogate” insight for AID and Apo3G biochemical behavior. However, large gaps remain in our understanding of how dC deaminases search ssDNA to identify trinucleotide motifs to deaminate. We discuss two recent methods to analyze ssDNA scanning and deamination. Apo3G scanning and deamination is visualized in real-time using single-molecule FRET...

Zebrafish AID is capable of deaminating methylated deoxycytidines

Abdouni, Hala; King, Justin J.; Suliman, Mussa; Quinlan, Matthew; Fifield, Heather; Larijani, Mani
Fonte: Oxford University Press Publicador: Oxford University Press
Tipo: Artigo de Revista Científica
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Activation-induced cytidine deaminase (AID) deaminates deoxycytidine (dC) to deoxyuracil (dU) at immunoglobulin loci in B lymphocytes to mediate secondary antibody diversification. Recently, AID has been proposed to also mediate epigenetic reprogramming by demethylating methylated cytidines (mC) possibly through deamination. AID overexpression in zebrafish embryos was shown to promote genome demethylation through G:T lesions, implicating a deamination-dependent mechanism. We and others have previously shown that mC is a poor substrate for human AID. Here, we examined the ability of bony fish AID to deaminate mC. We report that zebrafish AID was unique among all orthologs in that it efficiently deaminates mC. Analysis of domain-swapped and mutant AID revealed that mC specificity is independent of the overall high-catalytic efficiency of zebrafish AID. Structural modeling with or without bound DNA suggests that efficient deamination of mC by zebrafish AID is likely not due to a larger catalytic pocket allowing for better fit of mC, but rather because of subtle differences in the flexibility of its structure.

Generation and Repair of AID-initiated DNA Lesions in B Lymphocytes

Chen, Zhangguo; Wang, Jing H.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
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Activation-induced deaminase (AID) initiates the secondary antibody diversification process in B lymphocytes. In mammalian B cells, this process includes somatic hypermutation (SHM) and class switch recombination (CSR), both of which require AID. AID induces U:G mismatch lesions in DNA that are subsequently converted into point mutations or DNA double stranded breaks during SHM/CSR. In a physiological context, AID targets immunoglobulin (Ig) loci to mediate SHM/CSR. However, recent studies reveal genome-wide access of AID to numerous non-Ig loci. Thus, AID poses a threat to the genome of B cells if AID-initiated DNA lesions cannot be properly repaired. In this review, we focus on the molecular mechanisms that regulate the specificity of AID targeting and the repair pathways responsible for processing AID-initiated DNA lesions.

Individual Substitution Mutations in the AID C Terminus That Ablate IgH Class Switch Recombination

Kadungure, Tatenda; Ucher, Anna J.; Linehan, Erin K.; Schrader, Carol E.; Stavnezer, Janet
Fonte: Public Library of Science Publicador: Public Library of Science
Tipo: Artigo de Revista Científica
Publicado em 12/08/2015 Português
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Activation-induced cytidine deaminase (AID) is essential for class switch recombination (CSR) and somatic hypermutation (SHM) of Ig genes. The C terminus of AID is required for CSR but not for SHM, but the reason for this is not entirely clear. By retroviral transduction of mutant AID proteins into aid-/- mouse splenic B cells, we show that 4 amino acids within the C terminus of mouse AID, when individually mutated to specific amino acids (R190K, A192K, L196S, F198S), reduce CSR about as much or more than deletion of the entire C terminal 10 amino acids. Similar to ΔAID, the substitutions reduce binding of UNG to Ig Sμ regions and some reduce binding of Msh2, both of which are important for introducing S region DNA breaks. Junctions between the IgH donor switch (S)μ and acceptor Sα regions from cells expressing ΔAID or the L196S mutant show increased microhomology compared to junctions in cells expressing wild-type AID, consistent with problems during CSR and the use of alternative end-joining, rather than non-homologous end-joining (NHEJ). Unlike deletion of the AID C terminus, 3 of the substitution mutants reduce DNA double-strand breaks (DSBs) detected within the Sμ region in splenic B cells undergoing CSR. Cells expressing these 3 substitution mutants also have greatly reduced mutations within unrearranged Sμ regions...

América Latina y el Caribe: ayuda oficial al desarrollo en el punto de inflexión del milenio

Tezanos Vázquez, Sergio; Martínez de la Cueva Astigarraga, Aitor
Fonte: Universidad Nacional Autónoma de México Publicador: Universidad Nacional Autónoma de México
Tipo: info:eu-repo/semantics/article; publishedVersion
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RESUMEN. Los países de América Latina y El Caribe (alc) han sido importantes receptores de aod desde la creación del Comité de Ayuda al Desarrollo de la ocde. No obstante, su participación en el sistema de ayuda se ha visto alterada en los primeros años del siglo xxi como consecuencia de los cambios introducidos en la agenda internacional de desarrollo. La estrategia de los odm concede especial atención a los países que retrasan la consecución universal de los objetivos, lo que motiva la reasignación de la ayuda desde los países de desarrollo intermedio hacia los países más pobres. En este contexto, dado el positivo avance de alc en los odm, el nuevo mapamundi de la ayuda aminora la importancia de la región. Este artículo analiza los flujos de aod desembolsados a alc desde 1990 y ofrece propuestas de reforma para construir un sistema de ayuda más eficiente, que compense la pérdida de volumen con incrementos en calidad.; ABSTRACT. The countries of Latin America and the Caribbean (LAC) have been large recipients of official development aid (ODA) since the creation of the OECD’s Development Aid Committee. Nevertheless, their participation in the aid system has changed in the opening years of the 21st century as a consequence of changes introduced in the international development agenda. The millennium development goals (MDG) strategy concedes special attention to countries that challenge the universal securing of the goals...

The Challenges of Australian Official Development Assistance to Burma

Williams, Megan
Fonte: Universidade Nacional da Austrália Publicador: Universidade Nacional da Austrália
Tipo: Relatório
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On May 2, 2008, millions of people across the Irrawaddy Delta in Burma took shelter as flood waters surged and winds of up to 200km/h carved a path of destruction, destroying villages and flooding agricultural fields throughout the Delta. The worst disaster ever recorded in Burma, Cyclone Nargis killed an estimated 140,000 people and displaced at least 800,000 more. The world watched, stunned, at not only the extent of devastation caused by the cyclone, but by the shockingly inadequate response of the Burmese regime who failed to launch any substantial relief effort and moved to block many private donors and international aid agencies from the worst affected areas. For the international community this brought to the fore the complicated environment within which aid agencies operate in Burma. Poverty in Burma is widespread. More than 30 percent of the population lives in acute poverty with an estimated 90 percent of the country spending three quarters of income, less than 65c, on food. What makes this poverty more intense is the low level of Official Development Assistance (ODA) the country has received despite the obvious need. After a brutal crackdown on pro-democracy protests in 1988 and the ruling regime's refusal to recognise the results of democratic elections in 1990...

Helping Africa Feed Itself Increasing Agricultural Productivity for Poverty Reduction

Silvers, Brooke
Fonte: Universidade Nacional da Austrália Publicador: Universidade Nacional da Austrália
Tipo: Relatório
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This report seeks to identify the role Australian aid can play in promoting agricultural productivity in Africa. Agriculture is central to Africa's development, stability and prosperity. However for many years, it has been neglected by African Governments and the international community alike. As the rest of the world experienced immense agricultural growth, Africa has lagged behind, stunted by the lack of technological advancements, infrastructure, and inadequate irrigation and fertilizer availability. Negative annual crop growth rates and increasing population have contributed to Africa's embedded poverty and severe food insecurity. Furthermore if predictions are correct, not only will Africa fail to meet the Millennium Development Goals by 2015, its the incidence of poverty and food scarcity will also increase. The myriad of literature on Africa's development unanimously draws correlations between increased agricultural productivity and decreased poverty, particularly in rural areas where poverty and deprivation are most severe. Agriculture has the potential to increase employment opportunities for rural and non-rural industries, connect smallholder farmers to market value chains, increase smallholder profitability and sustainability and lower the price of food for those who produce and consume it. Focusing on enhancing agricultural production for Africa's development presents unique opportunities for Australia's aid program. Even though Australia is a relatively small donor in Africa...

Where did all the aid go? an in-depth analysis of increased health aid flows over the past 10 years

Piva,Paolo; Dodd,Rebecca
Fonte: World Health Organization Publicador: World Health Organization
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/12/2009 Português
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OBJECTIVE: To examine how health aid is spent and channelled, including the distribution of resources across countries and between subsectors. Our aim was to complement the many qualitative critiques of health aid with a quantitative review and to provide insights on the level of development assistance available to recipient countries to address their health and health development needs. METHODS: We carried out a quantitative analysis of data from the Aggregate Aid Statistics and Creditor Reporting System databases of the Organisation for Economic Co-operation and Development, which are the most reliable sources of data on official development assistance (ODA) for health from all traditional bilateral and multilateral sources and from partnerships such as the Global Fund to Fight AIDS, Tuberculosis and Malaria. FINDINGS: The analysis shows that while health ODA is rising and capturing a larger share of total ODA, there are significant imbalances in the allocation of health aid which run counter to internationally recognized principles of "effective aid". Countries with comparable levels of poverty and health need receive remarkably different levels of aid. Funding for Millennium Development Goal 6 (combat HIV/AIDS, malaria and other diseases) accounts for much of the recent increase in health ODA...