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Search Results: 1 - 10 of 32547 matches for " Peter Kraft "
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Families of Group Actions, Generic Isotriviality, and Linearization
Hanspeter Kraft,Peter Russell
Mathematics , 2012,
Abstract: We prove a "Generic Equivalence Theorem which says that two affine morphisms $p: S \to Y$ and $q: T \to Y$ of varieties with isomorphic (closed) fibers become isomorphic under a dominant etale base change $\phi: U \to Y$. A special case is the following result. Call a morphism $\phi: X \to Y$ a "fibration with fiber $F$" if $\phi$ is flat and all fibers are (reduced and) isomorphic to $F$. Then an affine fibration with fiber $F$ admits an etale dominant morphism $\mu: U \to Y$ such that the pull-back is a trivial fiber bundle: $U\times_Y X \simeq U\times F$. As an application we give short proofs of the following two (known) results: (a) Every affine $\A^1$-fibration over a normal variety is locally trivial in the Zariski-topology; (b) Every affine $\A^2$-fibration over a smooth curve is locally trivial in the Zariski-topology. We also study families of reductive group actions on $\A^2$ parametrized by curves and show that every faithful action of a non-finite reductive group on $\AA^3$ is linearizable, i.e. $G$-isomorphic to a representation of $G$.
Research Conducted Using Data Obtained through Online Communities: Ethical Implications of Methodological Limitations
A. Cecile J. W. Janssens ,Peter Kraft
PLOS Medicine , 2012, DOI: 10.1371/journal.pmed.1001328
Abstract:
catena-Poly[[tetra-μ-benzoato-κ8O:O′-dicopper(II)]-μ-[N-(pyridin-4-yl)nicotinamide]-κ2N:N′-[dibenzoato-κ2O-copper(II)]-μ-[N-(pyridin-4-yl)nicotinamide]-κ2N:N′]
Peter E. Kraft,Robert L. LaDuca
Acta Crystallographica Section E , 2012, DOI: 10.1107/s1600536812030437
Abstract: In the polymeric title compound, [Cu3(C7H5O2)6(C11H9N3O)2]n, square-planar-coordinated CuII ions on crystallographic inversion centres are bound by two monodentate benzoate anions. The resulting [Cu(benzoate)]2 fragments are joined to centrosymmetic [Cu2(benzoate)4] paddlewheel clusters [Cu...Cu = 2.6331 (5) ] by means of bridging N-(pyridin-4-yl)nicotinamide (4-pna) ligands [dihedral angle between the aromatic rings = 39.18 (12)°], thereby forming [Cu3(benzoate)6(4-pna)2]n coordination-polymer chains that are arranged parallel to the [30-1] crystal direction. These polymeric chains are anchored into supramolecular layers by N—H...O hydrogen bonding between neighboring 4-pna ligands. These layers aggregate by crystal packing forces to afford the crystal structure of the title compound.
Absence of Evidence for MHC–Dependent Mate Selection within HapMap Populations
Adnan Derti,Can Cenik,Peter Kraft,Frederick P. Roth
PLOS Genetics , 2010, DOI: 10.1371/journal.pgen.1000925
Abstract: The major histocompatibility complex (MHC) of immunity genes has been reported to influence mate choice in vertebrates, and a recent study presented genetic evidence for this effect in humans. Specifically, greater dissimilarity at the MHC locus was reported for European-American mates (parents in HapMap Phase 2 trios) than for non-mates. Here we show that the results depend on a few extreme data points, are not robust to conservative changes in the analysis procedure, and cannot be reproduced in an equivalent but independent set of European-American mates. Although some evidence suggests an avoidance of extreme MHC similarity between mates, rather than a preference for dissimilarity, limited sample sizes preclude a rigorous investigation. In summary, fine-scale molecular-genetic data do not conclusively support the hypothesis that mate selection in humans is influenced by the MHC locus.
COU254, a specific 3-carboxamide-coumarin inhibitor of coagulation factor XII, does not protect mice from acute ischemic stroke
Peter Kraft, Tobias Schwarz, Lionel Pochet, Guido Stoll, Christoph Kleinschnitz
Experimental & Translational Stroke Medicine , 2010, DOI: 10.1186/2040-7378-2-5
Abstract: C57Bl/6 mice were treated with COU254 (40 mg/kg i.p.) or vehicle and subjected to 60 min transient middle cerebral artery occlusion (tMCAO) using the intraluminal filament method. After 24 h infarct volumes were determined from 2,3,5-Triphenyltetrazoliumchloride(TTC)-stained brain sections and functional scores were assessed. Hematoxylin and eosin (H&E) staining was used to estimate the extent of neuronal cell damage. Thrombus formation within the infarcted brain areas was analyzed by immunoblot.Infarct volumes and functional outcomes on day 1 after tMCAO did not significantly differ between COU254 pre-treated mice or untreated controls (p > 0.05). Histology revealed extensive ischemic neuronal damage regularly including the cortex and the basal ganglia in both groups. COU254 treatment did not prevent intracerebral fibrin(ogen) formation.COU254 at the given concentration of 40 mg/kg failed to demonstrate efficacy in acute ischemic stroke in this preliminary study. Further preclinical evaluation of 3-carboxamide-coumarins is needed before the antithrombotic potential of this novel class of FXII inhibitors can be finally judged.Thromboembolic occlusion of intracerebral vessels is responsible for the majority of ischemic strokes [1]. Studies on the early use of anticoagulant drugs (e.g. heparin) in cerebral ischemia failed to demonstrate overall benefit in that reduced lesion progression was counterbalanced by an increase in hemorrhages [2]. In addition, long-term anticoagulation for secondary prevention of cardioembolic stroke, mainly accomplished by warfarin prescription, is inevitably associated with increased bleeding-related morbidity and mortality [3]. Hence, identification of novel targets for more effective and safer anticoagulation in patients with imminent stroke is badly needed.In the classical "waterfall model" of blood coagulation the formation of a fibrin thrombus can be initiated by two distinct pathways, the extrinsic and the intrinsic pathway [4]. Both
Replication in Genome-Wide Association Studies
Peter Kraft,Eleftheria Zeggini,John P. A. Ioannidis
Statistics , 2010, DOI: 10.1214/09-STS290
Abstract: Replication helps ensure that a genotype-phenotype association observed in a genome-wide association (GWA) study represents a credible association and is not a chance finding or an artifact due to uncontrolled biases. We discuss prerequisites for exact replication, issues of heterogeneity, advantages and disadvantages of different methods of data synthesis across multiple studies, frequentist vs. Bayesian inferences for replication, and challenges that arise from multi-team collaborations. While consistent replication can greatly improve the credibility of a genotype-phenotype association, it may not eliminate spurious associations due to biases shared by many studies. Conversely, lack of replication in well-powered follow-up studies usually invalidates the initially proposed association, although occasionally it may point to differences in linkage disequilibrium or effect modifiers across studies.
Von Willebrand Factor Regulation in Patients with Acute and Chronic Cerebrovascular Disease: A Pilot, Case–Control Study
Peter Kraft, Christiane Drechsler, Ignaz Gunreben, Bernhard Nieswandt, Guido Stoll, Peter Ulrich Heuschmann, Christoph Kleinschnitz
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0099851
Abstract: Background and Purpose In animal models, von Willebrand factor (VWF) is involved in thrombus formation and propagation of ischemic stroke. However, the pathophysiological relevance of this molecule in humans, and its potential use as a biomarker for the risk and severity of ischemic stroke remains unclear. This study had two aims: to identify predictors of altered VWF levels and to examine whether VWF levels differ between acute cerebrovascular events and chronic cerebrovascular disease (CCD). Methods A case–control study was undertaken between 2010 and 2013 at our University clinic. In total, 116 patients with acute ischemic stroke (AIS) or transitory ischemic attack (TIA), 117 patients with CCD, and 104 healthy volunteers (HV) were included. Blood was taken at days 0, 1, and 3 in patients with AIS or TIA, and once in CCD patients and HV. VWF serum levels were measured and correlated with demographic and clinical parameters by multivariate linear regression and ANOVA. Results Patients with CCD (158±46%) had significantly higher VWF levels than HV (113±36%, P<0.001), but lower levels than AIS/TIA patients (200±95%, P<0.001). Age, sex, and stroke severity influenced VWF levels (P<0.05). Conclusions VWF levels differed across disease subtypes and patient characteristics. Our study confirms increased VWF levels as a risk factor for cerebrovascular disease and, moreover, suggests that it may represent a potential biomarker for stroke severity, warranting further investigation.
Middle Ordovician graptolite fauna from Praha - erveny vrch (Prague Basin, Czech Republic)
Kraft P,Kraft J
Bulletin of Geosciences , 2003, DOI: 10.3140/bull.geosci.2003.02.129
Abstract: Graptolites collected from a section of the árka Formation at Praha - erveny vrch indicate the uppermost Arenigian (lower part of the Corymbograptus retroflexus Biozone). The pendent Didymograptus cf. spinulosus indicating the Llanvirnian age is recorded from this locality. It is evident that the graptolite faunas span the Arenigian/Llanvirnian boundary interval. Thirteen species of graptolites including seven graptoloid species were found. The succession of graptolite assemblages is compared with the measured section at Rokycany - Drahou used here as a standard for this interval. The data set from Praha - erveny vrch indicates overthrusting within this section of the árka Formation.
The Mitochondrial A10398G Polymorphism, Interaction with Alcohol Consumption, and Breast Cancer Risk
Annamaria Pezzotti, Peter Kraft, Susan E. Hankinson, David J. Hunter, Julie Buring, David G. Cox
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0005356
Abstract: Polymorphisms in the mitochondrial genome are hypothesized to be associated with risk of various diseases, including cancer. However, there has been conflicting evidence for associations between a common polymorphism in the mitochondrial genome (A10398G, G10398A in some prior reports) and breast cancer risk. Reactive oxygen species, a by-product of mitochondrial energy production, can lead to oxidative stress and DNA damage in both the mitochondria and their cells. Alcohol consumption, which may also lead to oxidative stress, is associated with breast cancer risk. Therefore, we hypothesized that polymorphisms in the mitochondrial genome interact with alcohol consumption to alter breast cancer risk. We genotyped the A10398G polymorphism in a case-control study nested within the Nurses' Health Study (NHS, 1,561 cases, 2,209 controls). We observed an interaction between alcohol consumption (yes/no) and A10398G on breast cancer risk (p-int = 0.03). The risk associated with alcohol consumption was limited to carriers of the 10398G allele (Odds Ratio 1.52, 95% Confidence Interval 1.10–2.08 comparing drinkers to non-drinkers). However, we were unable to replicate these findings in the Women's Health Study (WHS, 678 cases, 669 controls), although the power to detect this interaction in the WHS was low (power = 0.57). Further examination of this interaction, such as sufficiently powered epidemiological studies of cancer risk or associations with biomarkers of oxidative stress, may provide further evidence for GxE interactions between the A10398G mitochondrial polymorphism and alcohol consumption on breast cancer risk.
Thrombin-Activatable Fibrinolysis Inhibitor (TAFI) Deficient Mice Are Susceptible to Intracerebral Thrombosis and Ischemic Stroke
Peter Kraft,Tobias Schwarz,Joost C. M. Meijers,Guido Stoll,Christoph Kleinschnitz
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0011658
Abstract: Thrombus formation is a key step in the pathophysiology of acute ischemic stroke and results from the activation of the coagulation cascade. Thrombin plays a central role in this coagulation system and contributes to thrombus stability via activation of thrombin-activatable fibrinolysis inhibitor (TAFIa). TAFIa counteracts endogenous fibrinolysis at different stages and elevated TAFI levels are a risk factor for thrombotic events including ischemic stroke. Although substantial in vitro data on the influence of TAFI on the coagulation-fibrinolysis-system exist, investigations on the consequences of TAFI inhibition in animal models of cerebral ischemia are still lacking. In the present study we analyzed stroke development and post stroke functional outcome in TAFI-/- mice.
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