Measuring aid flows : a new approach

Debate about the effectiveness of foreign aid has intensified in recent years, as budgetary pressures on aid have increased in donor countries. Whatever the merits of opposing arguments, the question is: do conventional measures of aid (such as OECD's Net ODA), which lump together grants and loans, accurately reflect true aid flows? The authors analyze the methodological shortcomings of conventional measures of aid and propose a new approach, which measures official aid flows as the sum of grants and the grant-equivalents of official loans (in a new aggregate they call"Effective Development Assistance,"or EDA). They show how results using this conceptually superior measure may differ significantly from conventional aggregates, providing a quite different view on major aid trends. They implement their approach empirically using data on some 40,000 official loans from the World Bank's DRS database--virtually all of the official loans to 133 developing countries from 1975 to 1995. The numerical results underscore several points: 1) The conventional approach has led to systematic overestimates of the concessionality of official loans. This overestimate has increased significantly since the mid-1980s. Conventional methods show a rising trend; the new method shows the opposite. 2) Net ODA increasingly overstates the true aid content of official flows, although the divergence between the two approaches is somewhat muted by the rising relative importance of grants over loans in total official flows.Strategic Debt Management,Economic Adjustment and Lending,Banks&Banking Reform,Payment Systems&Infrastructure,Economic Theory&Research,Economic Adjustment and Lending,Banks&Banking Reform,Strategic Debt Management,Economic Theory&Research,Payment Systems&Infrastructure

Inhibiting the Plasmodium eIF2α Kinase PK4 Prevents Artemisinin-Induced Latency

Artemisinin and its derivatives (ARTs) are frontline antimalarial drugs. However, ART monotherapy is associated with a high frequency of recrudescent infection, resulting in treatment failure. A subset of parasites is thought to undergo ART-induced latency, but the mechanisms remain unknown. Here, we report that ART treatment results in phosphorylation of the parasite eukaryotic initiation factor-2α (eIF2α), leading to repression of general translation and latency induction. Enhanced phosphorylated eIF2α correlates with high rates of recrudescence following ART, and inhibiting eIF2α dephosphorylation renders parasites less sensitive to ART treatment. ART-induced eIF2α phosphorylation is mediated by the Plasmodium eIF2α kinase, PK4. Overexpression of a PK4 dominant-negative or pharmacological inhibition of PK4 blocks parasites from entering latency and abolishes recrudescence after ART treatment of infected mice. These results show that translational control underlies ART-induced latency and that interference with this stress response may resolve the clinical problem of recrudescent infection

TECHNIQUES FOR THE STUDY OF THE STRUCTURAL PROPERTIES.

The evolution of our understanding of the behavior of oxide nanostructures depends heavily on the structural information obtained from a wide range of physical methods traditionally used in solid state physics, surface science and inorganic chemistry. In this chapter, we describe several techniques that are useful for the characterization of the structural properties of oxide nanostructures: X-ray diffraction (XRD) and scattering, X-ray absorption fine structure (XAFS), Raman spectroscopy, transmission electron microscopy (TEM), scanning tunneling microscopy (STM) and atomic force microscopy (AFM). The ultimate goal is to obtain information about the spatial arrangement of atoms in the nanostructures with precise interatomic distances and bond angles. This may not be possible for complex systems and one may get only partial information about the local geometry or morphology

Video-Assisted Thoracoscopy For Penetrating Cardiac Box Injury in Stable Patients

Introduction: In high-volume trauma centers, especially in developing countries, penetrating cardiac box injuries are frequent. Although many aspects of penetrating chest injuries have been well established, video-assisted thoracoscopy is still finding its place in cardiac box trauma and algorithmic approaches are still lacking. The purpose of this manuscript is to provide a streamlined recommendation for penetrating cardiac box injury in stable patients. Methods: Literature review was carried out using PubMed/ MEDLINE and Google Scholar databases to identify articles describing the characteristics and concepts of penetrating cardiac box trauma, including the characteristics of tamponade, cardiac ultrasound, indications and techniques of pericardial windows and, especially, the role of video-assisted thoracoscopy in stable patients. Results: Penetrating cardiac box injuries, whether by stab or gunshot wounds, require rapid surgical consultation. Unstable patients require immediate open surgery, however, determining which stable patients should be taken to thoracoscopic surgery is still controversial. Here, the classification of penetrating cardiac box injury used in Colombia is detailed, as well as the algorithmic approach to these types of trauma. Conclusion: Although open surgery is mandatory in unstable patients with penetrating cardiac box injuries, a more conservative and minimally invasive approach may be undertaken in stable patients. As rapid decision-making is critical in the trauma bay, surgeons working in high-volume trauma centers should expose themselves to thoracoscopy and always consider this possibility in the setting of penetrating cardiac box injuries in stable patients, always in the context of an experienced trauma team

Class IB-Phosphatidylinositol 3-Kinase (PI3K) Deficiency Ameliorates IA-PI3K-Induced Systemic Lupus but Not T Cell Invasion

Abstract Class I PI3K catalyzes formation of 3-poly-phosphoinositides. The family is divided into IA isoforms, activated by Tyr kinases and the IB isoform (PI3Kγ), activated by G protein-coupled receptors. Mutations that affect PI3K are implicated in chronic inflammation, although the differential contribution of each isoform to pathology has not been elucidated. Enhanced activation of class IA-PI3K in T cells extends CD4+ memory cell survival, triggering an invasive lymphoproliferative disorder and systemic lupus. As both IA- and IB-PI3K isoforms regulate T cell activation, and activated pathogenic CD4+ memory cells are involved in triggering systemic lupus, we examined whether deletion of IB could reduce the pathological consequences of increased IA-PI3K activity. IB-PI3Kγ deficiency did not abolish invasion or lymphoproliferation, but reduced CD4+ memory cell survival, autoantibody production, glomerulonephritis, and systemic lupus. Deletion of the IB-PI3Kγ isoform thus decreased survival of pathogenic CD4+ memory cells, selectively inhibiting systemic lupus development. These results validate the PI3Kγ isoform as a target for systemic lupus erythematosus treatment

Multilateral Safety Nets for Financial Crises

There is an increasing need for a system of international lending of last resort (ILLR) to provide a safety net in the event of financial crises in vulnerable countries as financial globalization deepens and spreads. Multilateral progress to address liquidity and solvency crises has been patchy and inconsistent, with no clear distinction between the two; in particular, there is still no framework to address sovereign debt restructuring. This paper proposes an integrated system of specialized ILLR facilities to address problems of liquidity, adjustment, and debt restructuring in a focused but robust way as crises evolve and morph, structured in tiers to cater to countries capacity to prequalify for automatic support. It further proposes feasible legal reform to subject creditors to standstills and seniority dilution as in domestic bankruptcy in order to empower ILLR to facilitate orderly workouts in debt restructuring. Multilateral development banks would play important supporting roles

He II lambda-4686 in Eta Carinae: Collapse of the Wind-Wind Collision Region During Periastron Passage

The periodic spectroscopic events in Eta Carinae are now well established and occur near the periastron passage of two massive stars in a very eccentric orbit. Several mechanisms have been proposed to explain the variations of different spectral features, such as an eclipse by the wind-wind collision boundary, a shell ejection from the primary star or accretion of its wind onto the secondary. All of them have problems explaining all the observed phenomena. To better understand the nature of the cyclic events we performed a dense monitoring of Eta Carinae with 5 Southern telescopes during the 2009 low excitation event, resulting in a set of data of unprecedented quality and sampling. The intrinsic luminosity of the He II lambda-4686 emission line (L approx 310 solar L) just before periastron reveals the presence of a very luminous transient source of extreme UV radiation emitted in the wind-wind collision (WWC) region. Clumps in the primary's wind probably explain the flare-like behavior of both the X-ray and He II lambda-4686 light-curves. After a short-lived minimum, He II lambda-4686 emission rises again to a new maximum, when X-rays are still absent or very weak. We interpret this as a collapse of the WWC onto the "surface" of the secondary star, switching off the hard X-ray source and diminishing the WWC shock cone. The recovery from this state is controlled by the momentum balance between the secondary's wind and the clumps in the primary's wind

Plasma levels of phosphorylated tau 181 are associated with cerebral metabolic dysfunction in cognitively impaired and amyloid-positive individuals

Alzheimer’s disease biomarkers are primarily evaluated through MRI, PET and CSF methods in order to diagnose and monitor disease. Recently, advances in the assessment of blood-based biomarkers have shown promise for simple, inexpensive, accessible and minimally invasive tools with diagnostic and prognostic value for Alzheimer’s disease. Most recently, plasma phosphorylated tau181 has shown excellent performance. The relationship between plasma phosphorylated tau181 and cerebral metabolic dysfunction assessed by [18F]fluorodeoxyglucose PET in Alzheimer’s disease is still unknown. This study was performed on 892 older individuals (297 cognitively unimpaired; 595 cognitively impaired) from the Alzheimer’s Disease Neuroimaging Initiative cohort. Plasma phosphorylated tau181 was assessed using single molecular array technology and metabolic dysfunction was indexed by [18F]fluorodeoxyglucose PET. Cross-sectional associations between plasma and CSF phosphorylated tau181 and [18F]fluorodeoxyglucose were assessed using voxelwise linear regression models, with individuals stratified by diagnostic group and by β-amyloid status. Associations between baseline plasma phosphorylated tau181 and longitudinal (24 months) rate of brain metabolic decline were also assessed in 389 individuals with available data using correlations and voxelwise regression models. Plasma phosphorylated tau181 was elevated in β-amyloid positive and cognitively impaired individuals as well as in apolipoprotein E ε4 carriers and was significantly associated with age, worse cognitive performance and CSF phosphorylated tau181. Cross-sectional analyses showed strong associations between plasma phosphorylated tau181 and [18F]fluorodeoxyglucose PET in cognitively impaired and β-amyloid positive individuals. Voxelwise longitudinal analyses showed that baseline plasma phosphorylated tau181 concentrations were significantly associated with annual rates of metabolic decline in cognitively impaired individuals, bilaterally in the medial and lateral temporal lobes. The associations between plasma phosphorylated tau181 and reduced brain metabolism, primarily in cognitively impaired and in β-amyloid positive individuals, supports the use of plasma phosphorylated tau181 as a simple, low-cost, minimally invasive and accessible tool to both assess current and predict future metabolic dysfunction associated with Alzheimer’s disease, comparatively to PET, MRI and CSF methods