Ordnungstheorie – Ordnungspolitik: Was ist Neoliberalismus?

Der Begriff Neoliberalismus ist angesichts der Finanzkrise in Misskredit geraten. Aber was bedeutet eigentlich Neoliberalismus? Viktor J. Vanberg, Walter Eucken Institut, Freiburg, definiert Ordnungstheorie als das wirtschafts- und rechtswissenschaftliche Forschungsprogramm der Freiburger Schule und ihr verwandter Denkansätze, das das Augenmerk auf die Steuerungswirkungen richtet, die die rechtlich-institutionellen Rah-menbedingungen auf die in ihnen stattfindenden wirtschaftlichen Prozessabläufe aus-üben. Ordnungspolitik ist der angewandte Zweig dieses Forschungsprogramms. Die ordoliberale Ordnungsökonomik richte ihr Forschungsinteresse auf die Frage, wie die institutionellen Rahmenbedingungen, unter denen Individuen agieren und kooperieren, in einer Weise gestaltet werden können, die ihnen bestmögliche Aussichten biete, in wechselseitig kompatibler Freiheit ihre eigenen Zwecke zu verfolgen. Für Wernhard Möschel, Universität Tübingen, ist eine marktwirtschaftliche Ordnung nicht denkbar ohne inhaltliche Normierungen. Auch bei einem neoliberalen Ansatz bleibe Raum für ergänzende und für korrigierende Politiken. Heiner Flassbeck, UNCTAD, und Friederi-ke Spiecker sehen dagegen den Neoliberalismus »mit seiner undifferenzierten Vorstel-lung, den Staat auf ein ordnungspolitisches Minimum zur Organisation des freien Wett-bewerbs auf freien Märkten zu reduzieren«, als gescheitert an. Der Wirtschaftspolitik sollte ein klares Primat gegenüber spekulationsanfälligen Märkten eingeräumt werden. Peter Hampe, Technische Universität Dresden und Münchner Hochschule für Politik, betrachtet die Entstehungsgeschichte des Neoliberalismus und erläutert die Differenz zwischen Neo- und Paleoliberalismus. Hans-Werner Sinn erklärt die Position des Neo-liberalismus anhand eines Fußballspiels.Wirtschaftsliberalismus, Ordnungstheorie, Ordnungspolitik

Efficacy assessment of SNP sets for genome-wide disease association studies

The power of a genome-wide disease association study depends critically upon the properties of the marker set used, particularly the number and physical spacing of markers, and the level of inter-marker association due to linkage disequilibrium. Extending our previously devised theoretical framework for the entropy-based selection of genetic markers, we have developed a local measure of the efficacy of a marker set, relative to including a maximally polymorphic single nucleotide polymorphism (SNP) at the map position of interest. Using this quantitative criterion, we evaluated five currently available SNP sets, namely Affymetrix 100K and 500K, and Illumina 100K, 300K and 550K in the CEU, YRI and JPT + CHB HapMap populations. At 50% relative efficacy, the commercial marker sets cover between 19 and 68% of the human genome, depending upon the population under study. An optimal technology-independent 500K marker set constructed from HapMap for Caucasians, in contrast, would achieve 73% coverage at the same relative efficacy

Arbeitslosigkeit ohne Ende? Die Arbeitsmarkt- und Beschäftigungspolitik der neuen Bundesregierung in der Kontroverse

Am 24. und 25. März 2006 fand an der Akademie für Politische Bildung Tutzing unter der Leitung von Dr. Wolfgang Quaisser und Karl-Heinz Willenborg die Tagung "Arbeitslosigkeit ohne Ende? Die Arbeitsmarkt- und Beschäftigungspolitik der neuen Bundesregierung in der Kontroverse" statt. Im Zentrum der Tagung standen die im Koalitionsvertrag vorgeschlagenen arbeitsmarktpolitischen Maßnahmen. Als Mitglied der Bundesregierung erläutert Franz Müntefering, Bundesminister für Arbeit und Soziales, die Arbeitsmarkt- und Beschäftigungspolitik der Bundesregierung. Hermann Otto Solms, FDP-Bundestagsfraktion, Heike Maria Kunstmann, Gesamtmetall, und Wilhelm Adamy, DGB, nehmen als Vertreter der Opposition, der Arbeitgeber und der Arbeitnehmer Stellung dazu. Joachim Möller, Universität Regensburg, legt seine Bewertung aus wissenschaftlicher Sicht dar. Im Anschluss daran prüfen Peter Hampe, TU Dresden, und Ulrich Walwei, Michael Feil und Lisa Tillmann, IAB, Nürnberg, ob aus der deutschen Wirtschafts- und Arbeitsmarktpolitik seit der Wiedervereinigung Lehren für Deutschland im Kampf gegen die Arbeitslosigkeit gezogen werden können. Zum Abschluss berichten Michael Knogler, Osteuropa-Institut München, und Wolfgang Quaisser, Politische Akademie Tutzing, Wolfgang Ochel, ifo Institut, und Henry Werner, dänische Botschaft, Berlin, über die Arbeitsmarktpolitik der neuen EU-Mitgliedstaaten, der USA sowie Dänemarks.Arbeitslosigkeit, Arbeitsmarktpolitik, Beschäftigungspolitik, Regierung, Deutschland

Long-Lived Plasma Cells and Memory B Cells Produce Pathogenic Anti-GAD65 Autoantibodies in Stiff Person Syndrome

Stiff person syndrome (SPS) is a rare, neurological disorder characterized by sudden cramps and spasms. High titers of enzyme-inhibiting IgG autoantibodies against the 65 kD isoform of glutamic acid decarboxylase (GAD65) are a hallmark of SPS, implicating an autoimmune component in the pathology of the syndrome. Studying the B cell compartment and the anti-GAD65 B cell response in two monozygotic twins suffering from SPS, who were treated with the B cell-depleting monoclonal anti-CD20 antibody rituximab, we found that the humoral autoimmune response in SPS is composed of a rituximab-sensitive part that is rapidly cleared after treatment, and a rituximab-resistant component, which persists and acts as a reservoir for autoantibodies inhibiting GAD65 enzyme activity. Our data show that these potentially pathogenic anti-GAD65 autoantibodies are secreted by long-lived plasma cells, which may either be persistent or develop from rituximab-resistant memory B lymphocytes. Both subsets represent only a fraction of anti-GAD65 autoantibody secreting cells. Therefore, the identification and targeting of this compartment is a key factor for successful treatment planning of SPS and of similar autoimmune diseases

Systematic Association Mapping Identifies NELL1 as a Novel IBD Disease Gene

Crohn disease (CD), a sub-entity of inflammatory bowel disease (IBD), is a complex polygenic disorder. Although recent studies have successfully identified CD-associated genetic variants, these susceptibility loci explain only a fraction of the heritability of the disease. Here, we report on a multi-stage genome-wide scan of 393 German CD cases and 399 controls. Among the 116,161 single-nucleotide polymorphisms tested, an association with the known CD susceptibility gene NOD2, the 5q31 haplotype, and the recently reported CD locus at 5p13.1 was confirmed. In addition, SNP rs1793004 in the gene encoding nel-like 1 precursor (NELL1, chromosome 11p15.1) showed a consistent disease-association in independent German population- and family-based samples (942 cases, 1082 controls, 375 trios). Subsequent fine mapping and replication in an independent sample of 454 French/Canadian CD trios supported the authenticity of the NELL1 association. Further confirmation in a large German ulcerative colitis (UC) sample indicated that NELL1 is a ubiquitous IBD susceptibility locus (combined p<10−6; OR = 1.66, 95% CI: 1.30–2.11). The novel 5p13.1 locus was also replicated in the French/Canadian sample and in an independent UK CD patient panel (453 cases, 521 controls, combined p<10−6 for SNP rs1992660). Several associations were replicated in at least one independent sample, point to an involvement of ITGB6 (upstream), GRM8 (downstream), OR5V1 (downstream), PPP3R2 (downstream), NM_152575 (upstream) and HNF4G (intron)

Open Surgical versus Minimal Invasive Necrosectomy of the Pancreas-A Retrospective Multicenter Analysis of the German Pancreatitis Study Group

Background Necrotising pancreatitis, and particularly infected necrosis, are still associated with high morbidity and mortality. Since 2011, a step-up approach with lower morbidity rates compared to initial open necrosectomy has been established. However, mortality and complication rates of this complex treatment are hardly studied thereafter. Methods The German Pancreatitis Study Group performed a multicenter, retrospective study including 220 patients with necrotising pancreatitis requiring intervention, treated at 10 hospitals in Germany between January 2008 and June 2014. Data were analysed for the primary endpoints "severe complications" and "mortality" as well as secondary endpoints including "length of hospital stay", "follow up", and predisposing or prognostic factors. Results Of all patients 13.6% were treated primarily with surgery and 86.4% underwent a step-up approach. More men (71.8%) required intervention for necrotising pancreatitis. The most frequent etiology was biliary (41.4%) followed by alcohol (29.1%). Compared to open necrosectomy, the step-up approach was associated with a lower number of severe complications (primary composite endpoint including sepsis, persistent multiorgan dysfunction syndrome (MODS) and erosion bleeding: 44.7% vs. 73.3%), lower mortality (10.5% vs. 33.3%) and lower rates of diabetes mellitus type 3c (4.7% vs. 33.3%). Low hematocrit and low blood urea nitrogen at admission as well as a history of acute pancreatitis were prognostic for less complications in necrotising pancreatitis. A combination of drainage with endoscopic necrosectomy resulted in the lowest rate of severe complications. Conclusion A step-up approach starting with minimal invasive drainage techniques and endoscopic necrosectomy results in a significant reduction of morbidity and mortality in necrotising pancreatitis compared to a primarily surgical intervention

Autoimmunity plays a role in the onset of diabetes after 40 years of age

Funder: Umea UniversityAbstract: Aims/hypothesis: Type 1 and type 2 diabetes differ with respect to pathophysiological factors such as beta cell function, insulin resistance and phenotypic appearance, but there may be overlap between the two forms of diabetes. However, there are relatively few prospective studies that have characterised the relationship between autoimmunity and incident diabetes. We investigated associations of antibodies against the 65 kDa isoform of GAD (GAD65) with type 1 diabetes and type 2 diabetes genetic risk scores and incident diabetes in adults in European Prospective Investigation into Cancer and Nutrition (EPIC)-InterAct, a case-cohort study nested in the EPIC cohort. Methods: GAD65 antibodies were analysed in EPIC participants (over 40 years of age and free of known diabetes at baseline) by radioligand binding assay in a random subcohort (n = 15,802) and in incident diabetes cases (n = 11,981). Type 1 diabetes and type 2 diabetes genetic risk scores were calculated. Associations between GAD65 antibodies and incident diabetes were estimated using Prentice-weighted Cox regression. Results: GAD65 antibody positivity at baseline was associated with development of diabetes during a median follow-up time of 10.9 years (HR for GAD65 antibody positive vs negative 1.78; 95% CI 1.43, 2.20) after adjustment for sex, centre, physical activity, smoking status and education. The genetic risk score for type 1 diabetes but not type 2 diabetes was associated with GAD65 antibody positivity in both the subcohort (OR per SD genetic risk 1.24; 95% CI 1.03, 1.50) and incident cases (OR 1.97; 95% CI 1.72, 2.26) after adjusting for age and sex. The risk of incident diabetes in those in the top tertile of the type 1 diabetes genetic risk score who were also GAD65 antibody positive was 3.23 (95% CI 2.10, 4.97) compared with all other individuals, suggesting that 1.8% of incident diabetes in adults was attributable to this combination of risk factors. Conclusions/interpretation: Our study indicates that incident diabetes in adults has an element of autoimmune aetiology. Thus, there might be a reason to re-evaluate the present subclassification of diabetes in adulthood

Genetic Evidence Supporting the Association of Protease and Protease Inhibitor Genes with Inflammatory Bowel Disease: A Systematic Review

As part of the European research consortium IBDase, we addressed the role of proteases and protease inhibitors (P/PIs) in inflammatory bowel disease (IBD), characterized by chronic mucosal inflammation of the gastrointestinal tract, which affects 2.2 million people in Europe and 1.4 million people in North America. We systematically reviewed all published genetic studies on populations of European ancestry (67 studies on Crohn's disease [CD] and 37 studies on ulcerative colitis [UC]) to identify critical genomic regions associated with IBD. We developed a computer algorithm to map the 807 P/PI genes with exact genomic locations listed in the MEROPS database of peptidases onto these critical regions and to rank P/PI genes according to the accumulated evidence for their association with CD and UC. 82 P/PI genes (75 coding for proteases and 7 coding for protease inhibitors) were retained for CD based on the accumulated evidence. The cylindromatosis/turban tumor syndrome gene (CYLD) on chromosome 16 ranked highest, followed by acylaminoacyl-peptidase (APEH), dystroglycan (DAG1), macrophage-stimulating protein (MST1) and ubiquitin-specific peptidase 4 (USP4), all located on chromosome 3. For UC, 18 P/PI genes were retained (14 proteases and 4protease inhibitors), with a considerably lower amount of accumulated evidence. The ranking of P/PI genes as established in this systematic review is currently used to guide validation studies of candidate P/PI genes, and their functional characterization in interdisciplinary mechanistic studies in vitro and in vivo as part of IBDase. The approach used here overcomes some of the problems encountered when subjectively selecting genes for further evaluation and could be applied to any complex disease and gene family