Bijectivity of the canonical map for the noncommutative instanton bundle

It is shown that the quantum instanton bundle introduced in Commun. Math. Phys. 226, 419-432 (2002) has a bijective canonical map and is, therefore, a coalgebra Galois extension.Comment: Latex, 12 pages. Published versio

Quantum planes and quantum cylinders from Poisson homogeneous spaces

Quantum planes and a new quantum cylinder are obtained as quantization of Poisson homogeneous spaces of two different Poisson structures on classical Euclidean group E(2).Comment: 13 pages, plain Tex, no figure

Protection against oxidative damage of erythrocyte membrane by the flavonoid quercetin and its relation to iron chelating activity

AbstractIncubation of glutathione (GSH) depleted mouse erythrocytes with the oxidants phenylhydrazine, acrolein, divicine and isouramil resulted in the release of free iron and in lipid peroxidation and hemolysis. The addition of the flavonoid quercetin, which chelates iron and penetrates erythrocytes, resulted in remarkable protection against lipid peroxidation and hemolysis. The protection seems to be due to intracellular chelation of iron, since a semi-stoichiometric ratio between released iron and the amount of quercetin necessary to prevent lipid peroxidation and hemolysis was found. Incubation of GSH depleted human erythrocytes with divicine and isouramil did not induce lipid peroxidation and hemolysis in spite of a substantial release of iron. However, divicine and isouramil produced alterations of membrane proteins, such as spectrin and band 3, as well as formation of senescent cell antigen. The addition of quercetin prevented these alterations

Persistent Unresolved Inflammation in the Mecp2-308 Female Mutated Mouse Model of Rett Syndrome

Rett syndrome (RTT) is a rare neurodevelopmental disorder usually caused by mutations in the X-linked gene methyl-CpG-binding protein 2 (MECP2). Several Mecp2 mutant mouse lines have been developed recapitulating part of the clinical features. In particular, Mecp2-308 female heterozygous mice, bearing a truncating mutation, are a validated model of the disease. While recent data suggest a role for inflammation in RTT, little information on the inflammatory status in murine models of the disease is available. Here, we investigated the inflammatory status by proteomic 2-DE/MALDI-ToF/ToF analyses in symptomatic Mecp2-308 female mice. Ten differentially expressed proteins were evidenced in the Mecp2-308 mutated plasma proteome. In particular, 5 positive acute-phase response (APR) proteins increased (i.e., kininogen-1, alpha-fetoprotein, mannose-binding protein C, alpha-1-antitrypsin, and alpha-2-macroglobulin), and 3 negative APR reactants were decreased (i.e., serotransferrin, albumin, and apolipoprotein A1). CD5 antigen-like and vitamin D-binding protein, two proteins strictly related to inflammation, were also changed. These results indicate for the first time a persistent unresolved inflammation of unknown origin in the Mecp2-308 mouse model

statistics biomedicine and scientific fraud

A consistent fraction of published data on scientific journals is not reproducible mainly due to insufficient knowledge of statistical methods. Here, we discuss on the use of proper statistical tools in biomedical research and statistical pitfalls potentially undermining the scientific validity of published data. Apart from unaware errors, a growing concern exists regarding data fabrication and scientific misconduct. Indeed, the social impact of false scientific data can be largely unpredictable and devastating, as shown by the worldwide dramatic effects on vaccinations coverage following a retracted paper published on a highly authoritative medical journal. Unfortunately, statistics shows a quite limited power in detecting false science, although a few statistical tools, such as the Benford's law, are known. Taken together, statistics in biomedical sciences i) is a powerful tool to interpret experimental data; ii) has limited power in detecting false science; and iii) first and foremost, is not the result of a simple "click of a mouse", but should be the result of accurate research planning by experienced and knowledgeable users

Free q-Schrodinger Equation from Homogeneous Spaces of the 2-dim Euclidean Quantum Group

After a preliminary review of the definition and the general properties of the homogeneous spaces of quantum groups, the quantum hyperboloid qH and the quantum plane qP are determined as homogeneous spaces of Fq(E(2)). The canonical action of Eq(2) is used to define a natural q-analog of the free Schro"dinger equation, that is studied in the momentum and angular momentum bases. In the first case the eigenfunctions are factorized in terms of products of two q-exponentials. In the second case we determine the eigenstates of the unitary representation, which, in the qP case, are given in terms of Hahn-Exton functions. Introducing the universal T-matrix for Eq(2) we prove that the Hahn-Exton as well as Jackson q-Bessel functions are also obtained as matrix elements of T, thus giving the correct extension to quantum groups of well known methods in harmonic analysis.Comment: 19 pages, plain tex, revised version with added materia

MtDNA mutagenesis impairs elimination of mitochondria during erythroid maturation leading to enhanced erythrocyte destruction

Haematopoietic progenitor cells show special sensitivity to mitochondrial DNA (mtDNA) mutagenesis, which suggests that increased mtDNA mutagenesis could underlie anemias. Here we show that elevated mtDNA mutagenesis in mice with a proof-reading deficient mtDNA polymerase (PolG) leads to incomplete mitochondrial clearance, with asynchronized iron loading in erythroid precursors, and increased total and free cellular iron content. The resulting Fenton chemistry leads to oxidative damage and premature destruction of erythrocytes by splenic macrophages. Our data indicate that mitochondria actively contribute to their own elimination in reticulocytes and modulate iron loading. Asynchrony of this sequence of events causes severe mitochondrial anaemia by depleting the organism of red blood cells and the bone marrow of iron. Our findings account for the anaemia development in a progeroid mouse model and may have direct relevance to the anemias associated with human mitochondrial disease and ageing.Peer reviewe