3,803 research outputs found

    Differentiating the effects of negative state on optimism and the implicit perception of everyday injury risk

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    To date no research has examined the effects of negative state on the perception of everyday injury risk. Instead, studies have focussed more broadly on the relationship between mood and self- reported optimism. The present study had two aims. Firstly, to assess the effect of incidental anxiety on implicit injury risk perception using a modified Implicit Association Test (IAT). Secondly, it sought to compare any effect with that on a conventional measure of risk perception (optimism). In line with previous research, anxious participants perceived more risk (were less optimistic). In contrast, there was no significant correlation between anxiety and the implicit perception of everyday injury risk. Theoretical and practical implications are discussed

    The Collaboration of a Principal and a Mathematics Specialist

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    This article describes the importance of the collaboration between the principal, Patty Granada, and the Mathematics Specialist, Susan Garthwaite, in fostering a highly functioning mathematics program. While many aspects of the collaboration as facilitators for a mathematics program are logical, the messy aspects provide greater challenges. Through continued collaboration, they have come to embrace the messiness which has contributed to an awareness of similar belief systems in their roles. These beliefs include openness to learning and a sincere commitment to bringing out the best in students and teachers. The principal and the Mathematics Specialist share their continued journey in this collaborative relationship that is essential to the success of the mathematics program

    Tonic and phasic nitric oxide signals in hippocampal long-term potentiation

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    Nitric oxide ( NO) participates in long-term potentiation (LTP) and other forms of synaptic plasticity in many different brain areas but where it comes from and how it acts remain controversial. Using rat and mouse hippocampal slices, we tested the hypothesis that tonic and phasic NO signals are needed and that they derive from different NO synthase isoforms. NMDA increased NO production in a manner that was potently inhibited by three different neuronal NO synthase ( nNOS) inhibitors. Tonic NO could be monitored after sensitizing guanylyl cyclase-coupled NO receptors, allowing the very low ambient NO concentrations to be detected by cGMP measurement. The levels were unaffected by inhibition of NMDA receptors, nNOS, or the inducible NO synthase ( iNOS). iNOS was also undetectable in protein or activity assays. Tonic NO was susceptible to agents inhibiting endothelial NO synthase ( eNOS) and was missing in eNOS knock-out mice. The eNOS knock-out sexhibited a deficiency in LTP resembling that seen in wild-types treated with a NO synthase inhibitor. LTP in the knock-outs could be fully restored by supplying a low level of NO exogenously. Inhibition of nNOS also caused a major loss of LTP, particularly of late-LTP. Again, exogenous NO could compensate, but higher concentrations were needed compared with those restoring LTP in the eNOS knock-outs. It is concluded that tonic and phasic NO signals are both required for hippocampal LTP and the two are generated, respectively, by eNOS and nNOS, the former in blood vessels and the latter in neurons

    Zeros of weakly holomorphic modular forms of levels 2 and 3

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    Let Mk(N)M_k^\sharp(N) be the space of weakly holomorphic modular forms for Γ0(N)\Gamma_0(N) that are holomorphic at all cusps except possibly at \infty. We study a canonical basis for Mk(2)M_k^\sharp(2) and Mk(3)M_k^\sharp(3) and prove that almost all modular forms in this basis have the property that the majority of their zeros in a fundamental domain lie on a lower boundary arc of the fundamental domain.Comment: Added a reference, corrected typo

    Signaling from blood vessels to CNS axons through nitric oxide

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    Brain function is usually perceived as being performed by neurons with the support of glial cells, the network of blood vessels situated nearby serving simply to provide nutrient and to dispose of metabolic waste. Revising this view, we find from experiments on a rodent central white matter tract (the optic nerve) in vitro that microvascular endothelial cells signal persistently to axons using nitric oxide (NO) derived from the endothelial NO synthase (eNOS). The endogenous NO acts to stimulate guanylyl cyclase-coupled NO receptors in the axons, leading to a raised cGMP level which then causes membrane depolarization, apparently by directly engaging hyperpolarization-activated cyclic nucleotide-gated ion channels. The tonic depolarization and associated endogenous NO-dependent cGMP generation was absent in optic nerves from mice lacking eNOS, although such nerves responded to exogenous NO, with raised cGMP generation in the axons and associated depolarization. In addition to the tonic activity, exposure of optic nerves to bradykinin, a classical stimulator of eNOS in endothelial cells, elicited reversible NO- and cGMP-dependent depolarization through activation of bradykinin B-2 receptors, to which eNOS is physically complexed. No contribution of other NO synthase isoforms to either the action of bradykinin or the continuous ambient NO level could be detected. The results suggest that microvascular endothelial cells participate in signal processing in the brain and can do so by generating both tonic and phasic NO signals

    Cytochrome P450 oxidoreductase participates in nitric oxide consumption by rat brain

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    In low nanomolar concentrations, NO (nitric oxide) functions as a transmitter in brain and other tissues, whereas near-micromolar NO concentrations are associated with toxicity and cell death. Control of the NO concentration, therefore, is critical for proper brain function, but, although its synthesis pathway is well-characterized, the major route of breakdown of NO in brain is unclear. Previous observations indicate that brain cells actively consume NO at a high rate. The mechanism of this consumption was pursued in the present study. NO consumption by a preparation of central glial cells was abolished by cell lysis and recovered by addition of NADPH. NADPH-dependent consumption of NO localized to cell membranes and was inhibited by proteinase K, indicating the involvement of a membrane-bound protein. Purification of this activity yielded CYPOR (cytochrome P450 oxidoreductase). Antibodies against CYPOR inhibited NO consumption by brain membranes and the amount of CYPOR in several cell types correlated with their rate of NO consumption. NO was also consumed by purified CYPOR but this activity was found to depend on the presence of the vitamin E analogue Trolox (6-hydroxy-2,5,7,8-tetramethylchromane-2-carboxylic acid), included in the buffer as a precaution against inadvertent NO consumption by lipid peroxidation. In contrast, NO consumption by brain membranes was independent of Trolox. Hence, it appears that, during the purification process, CYPOR becomes separated from a partner needed for NO consumption. Cytochrome P450 inhibitors inhibited NO consumption by brain membranes, making these proteins likely candidates

    Using discovered, polyphonic patterns to filter computer-generated music

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    A metric for evaluating the creativity of a music-generating system is presented, the objective being to generate mazurka-style music that inherits salient patterns from an original excerpt by Frédéric Chopin. The metric acts as a filter within our overall system, causing rejection of generated passages that do not inherit salient patterns, until a generated passage survives. Over fifty iterations, the mean number of generations required until survival was 12.7, with standard deviation 13.2. In the interests of clarity and replicability, the system is described with reference to specific excerpts of music. Four concepts–Markov modelling for generation, pattern discovery, pattern quantification, and statistical testing–are presented quite distinctly, so that the reader might adopt (or ignore) each concept as they wish
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