192 research outputs found
Has Health Capital Formation Cured 'Baumol’s Disease'? – Panel Granger Causality Evidence for OECD Countries: Panel Granger Causality Evidence for OECD Countries
A large body of both theoretical and empirical literature has affirmed a positive impact of human capital accumulation in the form of health on economic growth. Yet Baumol (1967) has presented a model in which imbalances in productivity growth between a ‘progressive’ (manufacturing) sector and a ‘nonprogressive’ sector of the economy (of which health care forms an integral part) lead to perpetual expenditure shifts into the latter and, as a consequence, to a decline in overall GDP growth. Which of the two views has an empirical grounding is here tested by means of Granger causality analysis of a panel of 21 OECD countries. The results do not lend support to the hypothesis that health capital formation fosters economic growth in rich countries. They are more in line with the predictions of Baumol’s model of unbalanced growth
Marx's reproduction schemes and the Keynesian multiplier: a reply to Sardoni
In a recent contribution to this journal, C. Sardoni takes issue with the identification by Trigg, in a 2006 publication, of a role for the Keynesian investment multiplier in Marx's schemes of reproduction. Indirectly, Sardoni also expresses his disagreement with Hartwig (by attributing one of his statements to Trigg). We appreciate the opportunity to defend our view against Sardoni's critique. This reply shows that a bridging point between Marx and Keynes can be established without recourse to microfoundations. As suggested by both Trigg, in 2006, and Hartwig, in 2004, the well known Harrod-Domar model of economic growth provides an interpretation of Marx's reproduction schemes that has the Keynesian multiplier as a constituent element. This note will further explore the assumptions underlying the interface between Marx and Keynes, in response to the challenging questions raised in Sardoni's contributio
Petty - oder: die Geburt der Arbeitswertlehre aus ökonomischen Problemen des frühen Kapitalismus
Der Autor rekonstruiert die ökonomische Theorie des englischen Universalgelehrten Sir William Petty (1623-1687), der von Marx als Begründer der klassischen politischen Ökonomie benannt wurde. Vor allem die Begründung der Arbeitswertlehre, die das Hauptparadigma der klassischen Wirtschaftstheorie bildete, sicherte Petty einen Platz unter den politischen Ökonomen jener Zeit. Petty stellte sich als Wirtschaftstheoretiker die Aufgabe, die Erscheinungen über ein begründetes Aussagensystem auf ihr Wesen zurückzuführen. Der Autor skizziert zunächst die für die Theorieentwicklung Pettys wesentlichen Ereignisse, Prozesse und Strukturen im England des 17. Jahrhunderts. Am Beispiel von zwei Problemkreisen - der Besteuerung und des Bodenwerts - wird anschließend die Bedeutung Pettys als praxisbezogener Theoretiker dargestellt. Eine Verknüpfung der beiden Problemkreise führt ferner zum Problem der Inflation, das ebenso diskutiert wird wie das Konzept der 'Sozialen Arbeitsteilung' von Tony Aspromourgos. Der Autor macht in diesem Zusammenhang auch auf eine problematische Petty-Rekonstruktion bei Marx aufmerksam. (ICI)'This paper aims at reconstructing the economic theory of Sir William Petty (1623-1687), whom Marx has designated as founder of political economy. Two features distinguish the present paper from the bulk of the literature on Petty. Firstly, Petty's theory is interpreted as a set of specific answers to economic problems of his time. To this end the socio-economic development of England and Ireland between the 15th and 17th century is briefly spelled out. Petty's theoretical innovations, especially his new labour theory of value, are then interpreted as a foundation for public policy recommendations aiming at the solution of the most urgent economic problems of his time, such as inflation, just taxation, and finding criteria for an adequate distribution of the Irish soil to those who financed the suppression of the Irish upheaval of 1649-1652. The second distinctive feature of this paper is its focus on Marx's reinterpretation of Petty's theory. It is argued that, in an attempt to present Petty as a thorough predecessor of himself, Marx strains the similarities too much while understating important differences.' (author's abstract
In-line Raman spectroscopy and advanced process control for the extraction of anethole and fenchone from fennel (<i>Foeniculum vulgare</i> L. MILL.)
Simvastatin Reduces Endotoxin-Induced Acute Lung Injury by Decreasing Neutrophil Recruitment and Radical Formation
Treatment of acute lung injury (ALI) remains an unsolved problem in intensive care medicine. As simvastatin exerts protective effects in inflammatory diseases we explored its effects on development of ALI and due to the importance of neutrophils in ALI also on neutrophil effector functions.
C57Bl/6 mice were exposed to aerosolized LPS (500 µg/ml) for 30 min. The count of alveolar, interstitial, and intravasal neutrophils were assessed 4 h later by flow cytometry. Lung permeability changes were assessed by FITC-dextran clearance and albumin content in the BAL fluid. In vitro, we analyzed the effect of simvastatin on neutrophil adhesion, degranulation, apoptosis, and formation of reactive oxygen species. To monitor effects of simvastatin on bacterial clearance we performed phagocytosis and bacterial killing studies in vitro as well as sepsis experiments in mice.
Simvastatin treatment before and after onset of ALI reduces neutrophil influx into the lung as well as lung permeability indicating the protective role of simvastatin in ALI. Moreover, simvastatin reduces the formation of ROS species and adhesion of neutrophils without affecting apoptosis, bacterial phagocytosis and bacterial clearance.
Simvastatin reduces recruitment and activation of neutrophils hereby protecting from LPS-induced ALI. Our results imply a potential role for statins in the management of ALI
Seminal plasma as a source of prostate cancer peptide biomarker candidates for detection of indolent and advanced disease
Background:Extensive prostate specific antigen screening for prostate cancer generates a high number of unnecessary biopsies and over-treatment due to insufficient differentiation between indolent and aggressive tumours. We hypothesized that seminal plasma is a robust source of novel prostate cancer (PCa) biomarkers with the potential to improve primary diagnosis of and to distinguish advanced from indolent disease.
<br>Methodology/Principal Findings: In an open-label case/control study 125 patients (70 PCa, 21 benign prostate hyperplasia, 25 chronic prostatitis, 9 healthy controls) were enrolled in 3 centres. Biomarker panels a) for PCa diagnosis (comparison of PCa patients versus benign controls) and b) for advanced disease (comparison of patients with post surgery Gleason score <7 versus Gleason score >>7) were sought. Independent cohorts were used for proteomic biomarker discovery and testing the performance of the identified biomarker profiles. Seminal plasma was profiled using capillary electrophoresis mass spectrometry. Pre-analytical stability and analytical precision of the proteome analysis were determined. Support vector machine learning was used for classification. Stepwise application of two biomarker signatures with 21 and 5 biomarkers provided 83% sensitivity and 67% specificity for PCa detection in a test set of samples. A panel of 11 biomarkers for advanced disease discriminated between patients with Gleason score 7 and organ-confined (<pT3a) or advanced (≥pT3a) disease with 80% sensitivity and 82% specificity in a preliminary validation setting. Seminal profiles showed excellent pre-analytical stability. Eight biomarkers were identified as fragments of N-acetyllactosaminide beta-1,3-N-acetylglucosaminyltransferase​,prostatic acid phosphatase, stabilin-2, GTPase IMAP family member 6, semenogelin-1 and -2. Restricted sample size was the major limitation of the study.</br>
<br>Conclusions/Significance: Seminal plasma represents a robust source of potential peptide makers for primary PCa diagnosis. Our findings warrant further prospective validation to confirm the diagnostic potential of identified seminal biomarker candidates.</br>
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