Financial stability in the EU new Member States, acceding and candidate countries.

Rapid credit growth in the EU new Member States, acceding and candidate countries has raised the issue of financial stability in the region. This rapid credit growth has been accompanied by the deterioration in the current account balance and the large-scale distribution of foreign currency loans. In the first part of this study, we analyse the overall stability of the banking sector vis-à-vis the very rapid credit growth. Given the high share of foreign currency loans, we examine the exposure to exchange rate risk. We identify that the main vulnerability for the banking system stems from the open currency position held by fi nal borrowers (households and businesses). These economic agents are generally not hedged against exchange rate risk. In the event of a depreciation in the national currency, the banking system would therefore be exposed to an increase in payment defaults on foreign currency loans. We consider this to be “indirect” credit risk for the banking system. In the second part, we explore the likelihood of a currency crisis. We estimate an econometric model for the link between credit growth and the current account balance showing a significant negative relationship in these countries, i.e. a 1-percentage-point increase in credit flow as a percentage of GDP deteriorates the current account-to-GDP ratio by 0.5 percentage point. Consequently, excessively high credit growth would contribute to deteriorate the current account beyond a sustainable level and would increase the likelihood of a currency crisis. Currently, external vulnerability remains contained in the countries under review, though it has increased in most of them since 2000. Lastly, we implement causality tests to evaluate the nature of credit growth. When the causality detected indicates that credit growth fuels domestic demand, and not the opposite, this could be interpreted as a potential risk for the system insofar as strong credit growth may lead to excessive demand beyond that related to a simple catching-up process. For countries where this test is significant, a causal relationship from credit growth to domestic demand has been detected in Bulgaria, Estonia, Latvia and Poland. The causality detected in Croatia and Romania is heading in the opposite direction.credit growth, new Member States, monetary approach to the balance of payments, currency crisis, banking crisis.

Le rôle international de l’euro depuis 1999 : facteurs et enjeux.

euro, monnaie internationale, moyen de paiement, unité de compte, réserve de valeur.

La croissance des crédits dans les pays d’Europe centrale et orientale est-elle excessive ?

Les taux de croissance du crédit dépassent ou avoisinent 30 à 50 % l’an dans certains pays d’Europe centrale, orientale et du sud-est (pays baltes, Bulgarie, Roumanie, Albanie et Macédoine). Ces taux de croissance élevés sont-ils susceptibles de générer des « excès » de crédit, dommageables à l’économie ? Ou s’agit-il d’un effet normal du rattrapage, pour des pays peu bancarisés au moment de leur transition ?Crédits bancaires, convergence, rattrapage.

Les enjeux de l’euroïsation dans les régions voisines de la zone euro.

L’euroïsation unilatérale, de jure ou de facto, n’est pas exempte de risques potentiels pour la stabilité financière des pays concernés. Elle ne saurait remplacer l’adhésion à la zone euro qui exige le respect des critères d’entrée dans l’Union monétaire.euroïsation/dollarisation, monnaie internationale, stabilité financière.

Two-way interplays between capital buffers, credit and output: evidence from French banks

We assess the extent to which capital buffers (the capital banks hold in excess of the regulatory minimum) exacerbate rather than reduce the cyclical behavior of credit. We empirically study the relationships between output gap, capital buffers and loan growth with firm-level data for French banks over the period 1993—2009. Our findings reveal that bank capital buffers intensify the cyclical credit fluctuations arising from the output gap developments, all the more as better quality capital is considered. Moreover, by performing Granger causality tests at the bank level, we find evidence of a two-way causality between capital buffers and loan growth, pointing to mutually reinforcing mechanisms. Overall, those empirical results lend support to a countercyclical financial regulation that focuses on highest-quality capital and aims at smoothing loan growth.Bank Capital Regulation, Procyclicality, Capital Buffers, Business Cycle Fluctuations, Basel III.

Dissection of the Role of PfEMP1 and ICAM-1 in the Sensing of Plasmodium falciparum-Infected Erythrocytes by Natural Killer Cells

BACKGROUND: Host innate immunity contributes to malaria clinical outcome by providing protective inflammatory cytokines such as interferon-γ, and by shaping the adaptive immune response. Plasmodium falciparum (Pf) is the etiologic agent of the most severe forms of human malaria. Natural Killer (NK) cells are lymphocytes of the innate immune system that are the first effectors to produce interferon-γ in response to Pf. However, the molecular bases of Pf-NK cell recognition events are unknown. Our study focuses on the role of Pf erythrocyte membrane protein 1 (PfEMP1), a major Pf virulence factor. PfEMP1 is expressed on parasitized-erythrocytes and participates to vascular obstruction through the binding to several host receptors. PfEMP1 is also a pivotal target for host antibody response to Pf infection. METHODOLOGY/PRINCIPAL FINDINGS: Using genetically-engineered parasite mutant strains, a human genetic deficiency, and blocking antibodies, we identified two receptor-ligand pairs involved in two uncoupled events occurring during the sensing of Pf infection by NK cells. First, PfEMP1 interaction with one of its host receptor, chondroitin sulfate A, mediates the cytoadhesion of Pf-infected erythrocytes to human NK cell lines, but is not required for primary NK cell activation. Second, intercellular adhesion molecule-1 (ICAM-1), another host receptor for PfEMP1, is mandatory for NK cell interferon-γ response. In this case, ICAM-1 acts via its engagement with its host ligand, LFA-1, and not with PfEMP1, consistent with the obligatory cross-talk of NK cells with macrophages for their production of interferon-γ. CONCLUSION/SIGNIFICANCE: PfEMP1-independent but ICAM-1/LFA-1-dependent events occurring during NK cell activation by Pf highlight the fundamental role of cellular cooperation during innate immune response to malaria

Merozoite release from Plasmodium falciparum-infected erythrocytes involves the transfer of DiIC16 from infected cell membrane to Maurer’s clefts

Merozoite release from infected erythrocytes is a complex process, which is still not fully understood. Such process was characterised at ultra-structural level in this work by labelling erythrocyte membrane with a fluorescent lipid probe and subsequent photo-conversion into an electron-dense precipitate. A lipophilic DiIC16 probe was inserted into the infected erythrocyte surface and the transport of this phospholipid analogue through the erythrocyte membrane was followed up during 48 h of the asexual erythrocyte cycle. The lipid probe was transferred from infected erythrocyte membranes to Maurer’s clefts during merozoite release, thereby indicating that these membranes remained inside host cells after parasite release. Fluorescent structures were never observed inside infected erythrocytes preceding merozoite exit and merozoites released from infected erythrocyte were not fluorescent. However, specific precipitated material was localised bordering the parasitophorous vacuole membrane and tubovesicular membranes when labelled non-infected erythrocytes were invaded by merozoites. It was revealed that lipids were interchangeable from one membrane to another, passing from infected erythrocyte membrane to Maurer’s clefts inside the erythrocyte ghost, even after merozoite release. Maurer’s clefts became photo-converted following merozoite release, suggesting that these structures were in close contact with infected erythrocyte membrane during merozoite exit and possibly played some role in malarial parasite exit from the host cell