Die Akademien der Wissenschaften in Zentraleuropa im Kalten Krieg

During the Cold War, the systemic rivalry between East and West was also carried out in the field of scholarship. This volume examines the Academies of Sciences in Central Europe on either side of the Iron Curtain in the early stages of the Cold War (and in some cases beyond). These include academies in the Socialist states (the Slovenian Academy of Sciences and Arts, the Romanian People’s Republic Academy, the Hungarian Academy of Sciences, the Polish Academy of Sciences, the Czechoslovakian Academy of Sciences, and the Slovakian Academy of Sciences), academies in divided Germany (the German Academy of Sciences at Berlin [Academy of Sciences of the GDR], the Saxon Academy of Sciences, the Academy of Agricultural Sciences of the GDR, the Bavarian Academy of Sciences and Humanities, the Heidelberg Academy of Sciences and Humanities, and finally the Leopoldina in Halle/Saale as the all-German Academy of Sciences), and the Austrian Academy of Sciences.Der vorliegende Band ermöglicht erstmals einen vergleichenden Blick auf Akademien der Wissenschaften in Zentraleuropa im Kalten Krieg.Im Kalten Krieg wurde die Systemkonkurrenz zwischen Ost und West auch im Feld der Wissenschaften ausgetragen. Der vorliegende Band thematisiert Akademien der Wissenschaften in Zentraleuropa diesseits und jenseits des Eisernen Vorhangs in der Zeit des frühen Kalten Krieges (und fallweise darüber hinaus). Vertreten sind Akademien in den sozialistischen Staaten (die Slowenische Akademie der Wissenschaften und Künste, die Akademie der Volksrepublik Rumänien, die Ungarische Akademie der Wissenschaften, die Polnische Akademie der Wissenschaften, die Tschechoslowakische Akademie der Wissenschaften und die Slowakische Akademie der Wissenschaften), Akademien der Wissenschaften im geteilten Deutschland (die Deutsche Akademie der Wissenschaften zu Berlin [Akademie der Wissenschaften der DDR], die Sächsische Akademie der Wissenschaften, die Akademie der Landwirtschaftswissenschaften der DDR, die Bayerische Akademie der Wissenschaften, die Heidelberger Akademie der Wissenschaften und schließlich die Leopoldina in Halle/Saale als gesamtdeutsche Akademie der Naturforscher) sowie die Österreichische Akademie der Wissenschaften

A Flexible Patch-Based Lattice Boltzmann Parallelization Approach for Heterogeneous GPU-CPU Clusters

Sustaining a large fraction of single GPU performance in parallel computations is considered to be the major problem of GPU-based clusters. In this article, this topic is addressed in the context of a lattice Boltzmann flow solver that is integrated in the WaLBerla software framework. We propose a multi-GPU implementation using a block-structured MPI parallelization, suitable for load balancing and heterogeneous computations on CPUs and GPUs. The overhead required for multi-GPU simulations is discussed in detail and it is demonstrated that the kernel performance can be sustained to a large extent. With our GPU implementation, we achieve nearly perfect weak scalability on InfiniBand clusters. However, in strong scaling scenarios multi-GPUs make less efficient use of the hardware than IBM BG/P and x86 clusters. Hence, a cost analysis must determine the best course of action for a particular simulation task. Additionally, weak scaling results of heterogeneous simulations conducted on CPUs and GPUs simultaneously are presented using clusters equipped with varying node configurations.Comment: 20 pages, 12 figure

Die Akademien der Wissenschaften in Zentraleuropa im Kalten Krieg

During the Cold War, the systemic rivalry between East and West was also carried out in the field of scholarship. This volume examines the Academies of Sciences in Central Europe on either side of the Iron Curtain in the early stages of the Cold War (and in some cases beyond). These include academies in the Socialist states (the Slovenian Academy of Sciences and Arts, the Romanian People’s Republic Academy, the Hungarian Academy of Sciences, the Polish Academy of Sciences, the Czechoslovakian Academy of Sciences, and the Slovakian Academy of Sciences), academies in divided Germany (the German Academy of Sciences at Berlin [Academy of Sciences of the GDR], the Saxon Academy of Sciences, the Academy of Agricultural Sciences of the GDR, the Bavarian Academy of Sciences and Humanities, the Heidelberg Academy of Sciences and Humanities, and finally the Leopoldina in Halle/Saale as the all-German Academy of Sciences), and the Austrian Academy of Sciences.Der vorliegende Band ermöglicht erstmals einen vergleichenden Blick auf Akademien der Wissenschaften in Zentraleuropa im Kalten Krieg

The first knock-in rat model for glutaric aciduria type I allows further insights into pathophysiology in brain and periphery.

Glutaric aciduria type I (GA-I, OMIM # 231670) is an inborn error of metabolism caused by a deficiency of glutaryl-CoA dehydrogenase (GCDH). Patients develop acute encephalopathic crises (AEC) with striatal injury most often triggered by catabolic stress. The pathophysiology of GA-I, particularly in brain, is still not fully understood. We generated the first knock-in rat model for GA-I by introduction of the mutation p.R411W, the rat sequence homologue of the most common Caucasian mutation p.R402W, into the Gcdh gene of Sprague Dawley rats by CRISPR/CAS9 technology. Homozygous Gcdhki/ki rats revealed a high excretor phenotype, but did not present any signs of AEC under normal diet (ND). Exposure to a high lysine diet (HLD, 4.7%) after weaning resulted in clinical and biochemical signs of AEC. A significant increase of plasmatic ammonium concentrations was found in Gcdhki/ki rats under HLD, accompanied by a decrease of urea concentrations and a concomitant increase of arginine excretion. This might indicate an inhibition of the urea cycle. Gcdhki/ki rats exposed to HLD showed highly diminished food intake resulting in severely decreased weight gain and moderate reduction of body mass index (BMI). This constellation suggests a loss of appetite. Under HLD, pipecolic acid increased significantly in cerebral and extra-cerebral liquids and tissues of Gcdhki/ki rats, but not in WT rats. It seems that Gcdhki/ki rats under HLD activate the pipecolate pathway for lysine degradation. Gcdhki/ki rat brains revealed depletion of free carnitine, microglial activation, astroglyosis, astrocytic death by apoptosis, increased vacuole numbers, impaired OXPHOS activities and neuronal damage. Under HLD, Gcdhki/ki rats showed imbalance of intra-and extracellular creatine concentrations and indirect signs of an intracerebral ammonium accumulation. We successfully created the first rat model for GA-I. Characterization of this Gcdhki/ki strain confirmed that it is a suitable model not only for the study of pathophysiological processes, but also for the development of new ther-apeutic interventions. We further brought up interesting new insights into the pathophysiology of GA-I in brain and periphery

PPA1 Deficiency Causes a Deranged Galactose Metabolism Recognizable in Neonatal Screening

Two siblings showed increased galactose and galactose-related metabolites in neonatal screening. Diagnostic workup did not reveal abnormalities in any of the known disease-causing enzymes involved in galactose metabolism. Using whole-exome sequencing, we identified a homozygous missense variant in PPA1 encoding the cytosolic pyrophosphatase 1 (PPA1), c.557C>T (p.Thr186Ile). The enzyme activity of PPA1 was determined using a colorimetric assay, and the protein content was visualized via western blotting in skin fibroblasts from one of the affected individuals. The galactolytic activity of the affected fibroblasts was determined by measuring extracellular acidification with a Seahorse XFe96 analyzer. PPA1 activity decreased to 22% of that of controls in the cytosolic fraction of homogenates from patient fibroblasts. PPA1 protein content decreased by 50% according to western blot analysis, indicating a reduced stability of the variant protein. The extracellular acidification rate was reduced in patient fibroblasts when galactose was used as a substrate. Untargeted metabolomics of blood samples revealed an elevation of other metabolites related to pyrophosphate metabolism. Besides hyperbilirubinemia in the neonatal period in one child, both children were clinically unremarkable at the ages of 3 and 14 years, respectively. We hypothesize that the observed metabolic derangement is a possible mild manifestation of PPA1 deficiency. Unresolved abnormalities in galactosemia screening might result in the identification of more individuals with PPA1 deficiency, a newly discovered inborn metabolic disorder (IMD)