551 research outputs found

    Equivalence of block sequences in Schreier spaces and their duals

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    We prove that any normalized block sequence in a Schreier space XξX_\xi, of arbitrary order ξ<ω1\xi<\omega_1, admits a subsequence equivalent to a subsequence of the canonical basis of some Schreier space. The analogous result is proved for dual spaces to Schreier spaces. Basing on these results, we examine the structure of strictly singular operators on Schreier spaces and show that there are 2c2^\mathfrak{c} many closed operator ideals on a Schreier space of any order, its dual and bidual space.Comment: Corrected citatio

    Forms and objects of thought

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    Abstract It is generally assumed that if it is possible to believe that p without believing that q, then there is some difference between the object of the thought that p and the object of the thought that q. This assumption is challenged in the present paper, opening the way to an account of epistemic opacity that improves on existing accounts, not least because it casts doubt on various arguments that attempt to derive startling ontological conclusions from seemingly innocent epistemic premises. Keyword Propositional attitudes Propositional attitudes and the language we use to ascribe them are a perennial source of interest to both linguists and philosophers. Linguistically, the practice of ascribing propositional attitudes defies regimentation of the kind to which it seems possible to subject much of the remainder of human discourse. In particular, our use of such indispensable verbs as &apos;&apos;believes&apos;&apos; and &apos;&apos;wants&apos;&apos; appears to violate the otherwise fruitful and well-confirmed principle that the semantic value of a sentence is a function of the semantic values of its component expressions together with their mode of composition. Philosophically, propositional attitudes are of interest as the prime candidates for underived intentionality. Here we find the roots of the compositionality problem in the apparent possibility for a thinker to have one belief to the effect that the world is a certain way without having all the beliefs he could have to the effect that it is that way. In this paper I survey existing attempts to solve these problems, and propose an alternative solution. What makes this solution an alternative is not that it comports with the available linguistic or psychological data better than existing theories; indeed, the theory I favor-I call it the multiple relation theory-seems to b

    Mitigation of 42^{42}Ar/42^{42}K background for the GERDA Phase II experiment

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    Background coming from the 42^{42}Ar decay chain is considered to be one of the most relevant for the GERDA experiment, which aims to search of the neutrinoless double beta decay of 76^{76}Ge. The sensitivity strongly relies on the absence of background around the Q-value of the decay. Background coming from 42^{42}K, a progeny of 42^{42}Ar, can contribute to that background via electrons from the continuous spectrum with an endpoint of 3.5 MeV. Research and development on the suppression methods targeting this source of background were performed at the low-background test facility LArGe. It was demonstrated that by reducing 42^{42}K ion collection on the surfaces of the broad energy germanium detectors in combination with pulse shape discrimination techniques and an argon scintillation veto, it is possible to suppress the 42^{42}K background by three orders of magnitude. This is sufficient for Phase II of the GERDA experiment

    Andrzej Pelczar

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    KATANA - a charge-sensitive triggering system for the Sπ\piRIT experiment

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    KATANA - the Krakow Array for Triggering with Amplitude discrimiNAtion - has been built and used as a trigger and veto detector for the Sπ\piRIT TPC at RIKEN. Its construction allows operating in magnetic field and providing fast response for ionizing particles, giving the approximate forward multiplicity and charge information. Depending on this information, trigger and veto signals are generated. The article presents performance of the detector and details of its construction. A simple phenomenological parametrization of the number of emitted scintillation photons in plastic scintillator is proposed. The effect of the light output deterioration in the plastic scintillator due to the in-beam irradiation is discussed.Comment: 14 pages, 11 figure

    Quantitative reduction of RyR1 protein caused by a single-allele frameshift mutation in RYR1 ex36 impairs the strength of adult skeletal muscle fibres

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    Here we characterized a mouse model knocked-in for a frameshift mutation in RYR1 exon 36 (p.Gln1970fsX16) that is isogenic to that identified in one parent of a severely affected patient with recessively inherited multiminicore disease. This individual carrying the RYR1 frameshifting mutation complained of mild muscle weakness and fatigability. Analysis of the RyR1 protein content in a muscle biopsy from this individual showed a content of only 20% of that present in a control individual. The biochemical and physiological characteristics of skeletal muscles from RyR1Q1970fsX16 heterozygous mice recapitulates that of the heterozygous parent. RyR1 protein content in the muscles of mutant mice reached 38% and 58% of that present in total muscle homogenates of fast and slow muscles from wild-type (WT) littermates. The decrease of RyR1 protein content in total homogenates is not accompanied by a decrease of Cav1.1 content, whereby the Cav1.1/RyR1 stoichiometry ratio in skeletal muscles from RyR1Q1970fsX16 heterozygous mice is lower compared to that from WT mice. Electron microscopy (EM) revealed a 36% reduction in the number/area of calcium release units accompanied by a 2.5-fold increase of dyads (triads that have lost one junctional sarcoplasmic reticulum element); both results suggest a reduction of the RyR1 arrays. Compared to WT, muscle strength and depolarization-induced calcium transients in RyR1Q1970fsX16 heterozygous mice muscles were decreased by 20% and 15%, respectively. The RyR1Q1970fsX16 mouse model provides mechanistic insight concerning the phenotype of the parent carrying the RYR1 ex36 mutation and suggests that in skeletal muscle fibres there is a functional reserve of RyR1

    TNF-α protects from exacerbated myocarditis and cardiac death by suppressing expansion of activated heart-reactive CD4+ T cells

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    BACKGROUND AND AIMS Tumour necrosis factor α (TNF-α) represents a classical proinflammatory cytokine and its increased levels positively correlate with the severity of many cardiovascular diseases. Surprisingly, some heart failure patients receiving high doses of anti- TNF-α antibodies showed serious health worsening. This work aimed to examine the role of TNF-α signalling on the development and progression of myocarditis and heart-specific autoimmunity. METHODS AND RESULTS Mice with genetic deletion of TNF-α (Tnf+/- and Tnf-/-) and littermate controls (Tnf+/+) were used to study myocarditis in the inducible and the transgenic T cell receptor (TCR-M) models. Tnf+/- and Tnf-/- mice immunized with α-myosin heavy chain peptide (αMyHC) showed reduced myocarditis incidence but the susceptible animals developed extensive inflammation in the heart. In the TCR-M model, defective TNF-α production was associated with increased mortality at a young age due to cardiomyopathy and cardiac fibrosis. We could confirm that TNF-α as well as the secretome of antigen-activated heart-reactive effector CD4+ T (Teff) cells effectively activated the adhesive properties of cardiac microvascular endothelial cells (cMVECs). Our data suggested that TNF-α produced by endothelial in addition to Teff cells promoted leucocyte adhesion to activated cMVECs. Analysis of CD4+ T lymphocytes from both models of myocarditis showed a strongly increased fraction of Teff cells in hearts, spleens, and in the blood of Tnf+/- and Tnf-/- mice. Indeed, antigen-activated Tnf-/- Teff cells showed prolonged long-term survival and TNF-α cytokine-induced cell death of heart-reactive Teff. CONCLUSIONS TNF-α signalling promotes myocarditis development by activating cardiac endothelial cells. However, in the case of established disease, TNF-α protects from exacerbating cardiac inflammation by inducing activation-induced cell death of heart-reactive Teff. These data might explain the lack of success of standard anti-TNF-α therapy in heart failure patients and open perspectives for T cell-targeted approaches
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