Propriétés spectroscopiques de U4+ dans ThBr4

L'indexation de raies à zéro phonon du spectre d'absorption de ThBr4 : U4+ est discutée, compte tenu du spectre de vibration de la matrice et des spectres d'émission de ces monocristaux excites par laser

Molecular solids of actinide hexacyanoferrate: Structure and bonding

The hexacyanometallate family is well known in transition metal chemistry because the remarkable electronic delocalization along the metal-cyano-metal bond can be tuned in order to design systems that undergo a reversible and controlled change of their physical properties. We have been working for few years on the description of the molecular and electronic structure of materials formed with [Fe(CN)6]n- building blocks and actinide ions (An = Th, U, Np, Pu, Am) and have compared these new materials to those obtained with lanthanide cations at oxidation state +III. In order to evaluate the influence of the actinide coordination polyhedron on the three- dimensional molecular structure, both atomic number and formal oxidation state have been varied : oxidation states +III, +IV. EXAFS at both iron K edge and actinide LIII edge is the dedicated structural probe to obtain structural information on these systems. Data at both edges have been combined to obtain a three-dimensional model. In addition, qualitative electronic information has been gathered with two spectroscopic tools : UV-Near IR spectrophotometry and low energy XANES data that can probe each atom of the structural unit : Fe, C, N and An. Coupling these spectroscopic tools to theoretical calculations will lead in the future to a better description of bonding in these molecular solids. Of primary interest is the actinide cation ability to form ionic – covalent bonding as 5f orbitals are being filled by modification of oxidation state and/or atomic number

Aid to conflict-affected countries : lessons for donors

The first section looks at the implications of conflict for aid effectiveness and selectivity. We argue that, while aid is generally effective in promoting growth and by implication reducing poverty, it is more effective in promoting growth in post-conflict countries. We then consider the implications of these findings for donor selectivity models and for assessment of donor performance in allocating development aid among recipient countries. We argue that, while further research on aid effectiveness in post-conflict scenarios is needed, existing selectivity models should be augmented with, inter alia, post-conflict variables, and donors should be evaluated on the basis, inter alia, of the share of their aid budgets allocated to countries experiencing post-conflict episodes. We also argue for aid delivered in the form of projects to countries with weak institutions in early post-conflict years. The second section focuses on policies for donors operating in conflict-affected countries. We set out five of the most important principles: (1) focus on broad-based recovery from war; (2) to achieve a broad-based recovery, get involved before the conflict ends; (3) focus on poverty, but avoid &lsquo;wish lists&rsquo;; (4) help to reduce insecurity so aid can contribute more effectively to growth and poverty reduction; and (5) in economic reform, focus on improving public expenditure management and revenue mobilisation. The third section concludes by emphasising the fact that there is no hard or fast dividing line between &lsquo;war&rsquo; and &lsquo;peace&rsquo; and that it may take many years for a society to become truly &lsquo;post&rsquo;-conflict&rsquo;. Donors, therefore, need to prepare for the long haul.<br /

The impact of foreign direct investment, foreign aid and trade on poverty reduction : evidence from Sub-Saharan African countries

Abstract:Despite postulations on the effects of foreign direct investment (FDI), foreign aid, and trade on growth, empirical evidence from extant research has been mixed. The focus of recent research has shifted from the growth effects of these international flows to their poverty reduction effects. However, results have also been mixed. Most studies have examined the empirical evidence of these flows separately and have mostly conducted single country studies. In this study, we use data from twenty-nine countries in Sub-Saharan Africa between the period 1990–2017 to analyze the effects of FDI, trade, and foreign aid on poverty reduction in a single model using the Feasible Generalized Least Square (FGLS) technique. Our results show that FDI and foreign aid have a negative effect on poverty reduction in the countries studied. These results suggest that the level of FDI required to alleviate poverty has not been reached, and foreign aid have not been properly channeled. However, the results show that trade has a positive and significant impact on poverty reduction, especially in low-income countries. We conclude with policy recommendations

Cardiac Alpha-Myosin (MYH6) Is the Predominant Sarcomeric Disease Gene for Familial Atrial Septal Defects

Secundum-type atrial septal defects (ASDII) account for approximately 10% of all congenital heart defects (CHD) and are associated with a familial risk. Mutations in transcription factors represent a genetic source for ASDII. Yet, little is known about the role of mutations in sarcomeric genes in ASDII etiology. To assess the role of sarcomeric genes in patients with inherited ASDII, we analyzed 13 sarcomeric genes (MYH7, MYBPC3, TNNT2, TCAP, TNNI3, MYH6, TPM1, MYL2, CSRP3, ACTC1, MYL3, TNNC1, and TTN kinase region) in 31 patients with familial ASDII using array-based resequencing. Genotyping of family relatives and control subjects as well as structural and homology analyses were used to evaluate the pathogenic impact of novel non-synonymous gene variants. Three novel missense mutations were found in the MYH6 gene encoding alpha-myosin heavy chain (R17H, C539R, and K543R). These mutations co-segregated with CHD in the families and were absent in 370 control alleles. Interestingly, all three MYH6 mutations are located in a highly conserved region of the alpha-myosin motor domain, which is involved in myosin-actin interaction. In addition, the cardiomyopathy related MYH6-A1004S and the MYBPC3-A833T mutations were also found in one and two unrelated subjects with ASDII, respectively. No mutations were found in the 11 other sarcomeric genes analyzed. The study indicates that sarcomeric gene mutations may represent a so far underestimated genetic source for familial recurrence of ASDII. In particular, perturbations in the MYH6 head domain seem to play a major role in the genetic origin of familial ASDII