Institutionen und Wirtschaftswachstum in den OECD-Ländern

Für einzelne Länder ist es von Interesse zu erfahren, ob ihre institutionellen Regelungen diejenigen Eigenschaften aufweisen, mit denen erfahrungsgemäß ein hohes Wachstum des Pro-Kopf-Einkommens erreicht werden kann. Eine solche Einschätzung kann mit dem vom ifo Institut in Zusammenarbeit mit Theo Eicher, University of Washington, Seattle, entwickelten Institutionenindex vorgenommen werden. Er basiert auf einem Verfahren, mit dem solche Institutionen identifiziert werden, die in hohem Maße zum Wachstum des Pro-Kopf-Einkommens beitragen, und gestattet es, das Institutionengefüge von Ländern und seine Veränderungen miteinander zu vergleichen. Die stärkste Verbesserung ihrer institutionellen Wachstumsbedingungen gemessen an der Rangposition konnten Neuseeland, Australien und Finnland erreichen. Die größten Einbußen im Länderranking musste Japan hinnehmen. Lag Japan 1994 noch auf Rang 2, so nahm es 2007 die Rangposition 14 beim Institutionenindex ein. Ein weiteres Land, das relativ zu anderen Ländern verloren hat, ist Norwegen. Es verschlechterte sich von Rang 6 auf Rang 13. Deutschland nimmt bei dem Institutionenindex eine gute Mittellage ein. Im Vergleich mit anderen OECD-Ländern weist das deutsche Institutionengefüge eine relativ gute Qualität auf. Im Jahr 1994 nahm Deutschland die 7. und 2007 die 11. Rangposition ein. Deutschland zeichnet sich insbesondere durch gute institutionelle Rahmenbedingungen aus. Es verfügt über eine ausgezeichnete Verwaltung, die Eigentumsrechte werden geschützt, das Land ist politisch stabil, und es herrscht weitgehend Recht und Ordnung. Andererseits ist Deutschland nicht frei von Korruption und das Vertrauen in die Politik ist vergleichsweise niedrig. Ein weiterer Pluspunkt neben den institutionellen Rahmenbedingungen ist die Offenheit des Landes. Die deutsche Wirtschaft ist dem internationalen Wettbewerb ausgesetzt und nutzt die von der Konkurrenz ausgehenden wachstumsfördernden Impulse

Combined Simulation of a Micro Permanent Magnetic Linear Contactless Displacement Sensor

The permanent magnetic linear contactless displacement (PLCD) sensor is a new type of displacement sensor operating on the magnetic inductive principle. It has many excellent properties and has already been used for many applications. In this article a Micro-PLCD sensor which can be used for microelectromechanical system (MEMS) measurements is designed and simulated with the CST EM STUDIO® software, including building a virtual model, magnetostatic calculations, low frequency calculations, steady current calculations and thermal calculations. The influence of some important parameters such as air gap dimension, working frequency, coil current and eddy currents etc. is studied in depth

Genetic architecture of subcortical brain structures in 38,851 individuals

Subcortical brain structures are integral to motion, consciousness, emotions and learning. We identified common genetic variation related to the volumes of the nucleus accumbens, amygdala, brainstem, caudate nucleus, globus pallidus, putamen and thalamus, using genome-wide association analyses in almost 40,000 individuals from CHARGE, ENIGMA and UK Biobank. We show that variability in subcortical volumes is heritable, and identify 48 significantly associated loci (40 novel at the time of analysis). Annotation of these loci by utilizing gene expression, methylation and neuropathological data identified 199 genes putatively implicated in neurodevelopment, synaptic signaling, axonal transport, apoptosis, inflammation/infection and susceptibility to neurological disorders. This set of genes is significantly enriched for Drosophila orthologs associated with neurodevelopmental phenotypes, suggesting evolutionarily conserved mechanisms. Our findings uncover novel biology and potential drug targets underlying brain development and disease

Genetic architecture of subcortical brain structures in 38,851 individuals

Subcortical brain structures are integral to motion, consciousness, emotions and learning. We identified common genetic variation related to the volumes of the nucleus accumbens, amygdala, brainstem, caudate nucleus, globus pallidus, putamen and thalamus, using genome-wide association analyses in almost 40,000 individuals from CHARGE, ENIGMA and UK Biobank. We show that variability in subcortical volumes is heritable, and identify 48 significantly associated loci (40 novel at the time of analysis). Annotation of these loci by utilizing gene expression, methylation and neuropathological data identified 199 genes putatively implicated in neurodevelopment, synaptic signaling, axonal transport, apoptosis, inflammation/infection and susceptibility to neurological disorders. This set of genes is significantly enriched for Drosophila orthologs associated with neurodevelopmental phenotypes, suggesting evolutionarily conserved mechanisms. Our findings uncover novel biology and potential drug targets underlying brain development and disease

Causal effect of plasminogen activator inhibitor type 1 on coronary heart disease

Background--Plasminogen activator inhibitor type 1 (PAI-1) plays an essential role in the fibrinolysis system and thrombosis. Population studies have reported that blood PAI-1 levels are associated with increased risk of coronary heart disease (CHD). However, it is unclear whether the association reflects a causal influence of PAI-1 on CHD risk. Methods and Results--To evaluate the association between PAI-1 and CHD, we applied a 3-step strategy. First, we investigated the observational association between PAI-1 and CHD incidence using a systematic review based on a literature search for PAI-1 and CHD studies. Second, we explored the causal association between PAI-1 and CHD using a Mendelian randomization approach using summary statistics from large genome-wide association studies. Finally, we explored the causal effect of PAI-1 on cardiovascular risk factors including metabolic and subclinical atherosclerosis measures. In the systematic meta-analysis, the highest quantile of blood PAI-1 level was associated with higher CHD risk comparing with the lowest quantile (odds ratio=2.17; 95% CI: 1.53, 3.07) in an age- and sex-adjusted model. The effect size was reduced in studies using a multivariable-adjusted model (odds ratio=1.46; 95% CI: 1.13, 1.88). The Mendelian randomization analyses suggested a causal effect of increased PAI-1 level on CHD risk (odds ratio=1.22 per unit increase of log-transformed PAI-1; 95% CI: 1.01, 1.47). In addition, we also detected a causal effect of PAI-1 on elevating blood glucose and high-density lipoprotein cholesterol. Conclusions--Our study indicates a causal effect of elevated PAI-1 level on CHD risk, which may be mediated by glucose dysfunction