When countries do not do what they say: Systematic discrepancies between exchange rate regime announcements and de facto policies

We study the apparent disconnect between what countries announce to be their exchange rate regime and what they de facto implement. Even though discrepancies between announcements and de facto polices are frequent, there is a lack of understanding of actual patterns and underlying reasons. We contribute to the literature by identifying a number of robust stylized facts by means of an in-depth analysis of a large cross-country dataset. A key insight is that countries that operate under intermediate de facto regimes tend to announce fixed or flexible exchange rate regimes. The exact nature of deviations is related to country characteristics such as trade structure, financial development, and financial openness. Furthermore, regime discrepancies have followed secular trends, which are most likely related to financial globalization and changes in monetary policy design

When countries do not do what they say: Systematic discrepancies between exchange rate regime announcements and de facto policies

We study the apparent disconnect between what countries announce to be their exchange rate regime and what they de facto implement. Even though discrepancies between announcements and de facto polices are frequent, there is a lack of understanding of actual patterns and underlying reasons. We contribute to the literature by identifying a number of robust stylized facts by means of an in-depth analysis of a large cross-country dataset. A key insight is that countries that operate under intermediate de facto regimes tend to announce fixed or flexible exchange rate regimes. The exact nature of deviations is related to country characteristics such as trade structure, financial development, and financial openness. Furthermore, regime discrepancies have followed secular trends, which are most likely related to financial globalization and changes in monetary policy design.Exchange rate regimes; de facto versus de jure; exchange rate policy

AK-Modell mit Staatsverschuldung und fester Defizitquote

Die Auswirkungen einer staatlichen Verschuldung auf das Wirtschaftswachstum werden im Rahmen eines erweiterten neoklassischen Wachstumsmodells mit AK-Technologie analysiert. Der Staat verfolgt das Ziel einer festen Defizitquote und einer langfristig konstanten Schuldenquote. In diesem Fall gibt es eine kritische Defizitquote, bei dessen Unterschreitung ein eindeutiger, stabiler Steady State existiert. Wird hingegen der kritische Wert überschritten, so existiert kein Wachstumsgleichgewicht. -- The effects of public debt on economic growth are analyzed in an augmented neoclassical growth model with AK-technology. The objective of the government is a fixed deficit ratio and in the long run a constant debt ratio. Then there is a critical deficit ratio and if the deficit ratio falls below it, a unique, stable steady state exists. If the critical value is exceeded, there is no steady state.AK-Modell,Wachstum,Staatsverschuldung,feste Defizitquote,AK-model,growth,public debt,fixed deficit ratio

Mongolia

This paper compares the output gap estimates for Mongolia based on a number of different methods. Special attention is paid to the substantial role of mining in the Mongolian economy. We find that a Blanchard and Quah-type joint model of output and inflation provides a more robust estimate of the output gap for Mongolia than the traditional statistical decompositions.Economic growth;Economic models;External shocks;Inflation rates;Production;monetary fund, inflation, aggregate demand, inflation data, inflation rate, monetary policy, monetary economics, macroeconomic stability

Dysferlin mediates membrane tubulation and links T-tubule biogenesis to muscular dystrophy

The multi-C2 domain protein dysferlin localizes to the plasma membrane and the T-tubule system in skeletal muscle; however, its physiological mode of action is unknown. Mutations in the DYSF gene lead to autosomal recessive limb-girdle muscular dystrophy type 2B and Miyoshi myopathy. Here, we show that dysferlin has membrane tubulating capacity and that it shapes the T-tubule system. Dysferlin tubulates liposomes, generates a T-tubule-like membrane system in non-muscle cells, and links the recruitment of phosphatidylinositol 4,5-bisphosphate to the biogenesis of the T-tubule system. Pathogenic mutant forms interfere with all of these functions, indicating that muscular wasting and dystrophy are caused by the dysferlin mutants' inability to form a functional T-tubule membrane system

Dysferlin links excitation–contraction coupling to structure and maintenance of the cardiac transverse–axial tubule system

Aims The multi-C2 domain protein dysferlin localizes to the T-Tubule system of skeletal and heart muscles. In skeletal muscle, dysferlin is known to play a role in membrane repair and in T-tubule biogenesis and maintenance. Dysferlin deficiency manifests as muscular dystrophy of proximal and distal muscles. Cardiomyopathies have been also reported, and some dysferlinopathy mouse models develop cardiac dysfunction under stress. Generally, the role and functional relevance of dysferlin in the heart is not clear. The aim of this study was to analyse the effect of dysferlin deficiency on the transverse-axial tubule system (TATS) structure and on Ca2+ homeostasis in the heart. Methods and results We studied dysferlin localization in rat and mouse cardiomyocytes by immunofluorescence microscopy. In dysferlin-deficient ventricular mouse cardiomyocytes, we analysed the TATS by live staining and assessed Ca2+ handling by patch-clamp experiments and measurement of Ca2+ transients and Ca2+ sparks. We found increasing co-localization of dysferlin with the L-type Ca2+-channel during TATS development and show that dysferlin deficiency leads to pathological loss of transversal and increase in longitudinal elements (axialization). We detected reduced L-type Ca2+-current (I-Ca,I-L) in cardiomyocytes from dysferlin-deficient mice and increased frequency of spontaneous sarcoplasmic reticulum Ca2+ release events resulting in pro-arrhythmic contractions. Moreover, cardiomyocytes from dysferlin-deficient mice showed an impaired response to beta-adrenergic receptor stimulation. Conclusions Dysferlin is required for TATS biogenesis and maintenance in the heart by controlling the ratio of transversal and axial membrane elements. Absence of dysferlin leads to defects in Ca2+ homeostasis which may contribute to contractile heart dysfunction in dysferlinopathy patients