943 research outputs found

    The molecular epidemiology of human immunodeficiency virus type 1 in six cities in Britain and Ireland

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    The authors sequenced the p17 coding regions of the gag gene from 211 patients infected either through injecting drug use (IDU) or by sexual intercourse between men from six cities in Scotland, N. England, N. Ireland, and the Republic of Ireland. All sequences were of subtype 5. Phylogenetic analysis revealed substantial heterogeneity in the sequences from homosexual men. In contrast, sequence from over 80% of IDUs formed a relatively tight cluster, distinct both from those of published isolates and of the gay men. There was no large-scale clustering of sequences by city in either risk group, although a number of close associations between pairs of individuals were observed. From the known date of the HIV-1 epidemic among IDUs in Edinburgh, the rate of sequence divergence at synonymous sites is estimated to be about 0.8%. On this basis it has been estimated that the date of divergence of the sequences among homosexual men to be about 1975, which may correspond to the origin of the B subtype epidemic

    Hard measures for soft stuff: citizenship indicators and educational policy under the Lisbon Strategy

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    How far is the European Union a vehicle for inclusion and empowerment of a new range of policy actors in education? This article explores the role of actors in policy formation through a case study. It examines European Union attempts since 2000 to develop indicators of ‘active citizenship’ and ‘education and training for active citizenship’. It is based on two main sources: policy documents on the development of indicators and benchmarks; and a case study of an exercise (2005-07) to develop such indicators, initiated by the European Commission’s Directorate General for Education and Culture. It shows that policy actors have attempted to take advantage of the Open Method of Coordination, often seen as a neo-liberal control mechanism, to ensure that citizenship remains on the policy agenda

    Gravitation and inertia; a rearrangement of vacuum in gravity

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    We address the gravitation and inertia in the framework of 'general gauge principle', which accounts for 'gravitation gauge group' generated by hidden local internal symmetry implemented on the flat space. We connect this group to nonlinear realization of the Lie group of 'distortion' of local internal properties of six-dimensional flat space, which is assumed as a toy model underlying four-dimensional Minkowski space. The agreement between proposed gravitational theory and available observational verifications is satisfactory. We construct relativistic field theory of inertia and derive the relativistic law of inertia. This theory furnishes justification for introduction of the Principle of Equivalence. We address the rearrangement of vacuum state in gravity resulting from these ideas.Comment: 17 pages, no figures, revtex4, Accepted for publication in Astrophys. Space Sc

    WMAP constraints on scalar-tensor cosmology and the variation of the gravitational constant

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    We present observational constraints on a scalar-tensor gravity theory by χ2\chi^2 test for CMB anisotropy spectrum. We compare the WMAP temperature power spectrum with the harmonic attractor model, in which the scalar field has its harmonic effective potential with curvature β\beta in the Einstein conformal frame and the theory relaxes toward Einstein gravity with time. We found that the present value of the scalar coupling, i.e. the present level of deviation from Einstein gravity (α02)(\alpha_0^2), is bounded to be smaller than 5×10−4−7β5\times 10^{-4-7\beta} (2σ2\sigma), and 10−2−7β10^{-2-7\beta} (4σ4\sigma) for 0<β<0.450< \beta<0.45. This constraint is much stronger than the bound from the solar system experiments for large β\beta models, i.e., β>0.2\beta> 0.2 and 0.3 in 2σ2\sigma and 4σ4\sigma limits, respectively. Furthermore, within the framework of this model, the variation of the gravitational constant at the recombination epoch is constrained as ∣G(z=zrec)−G0∣/G0<0.05(2σ)|G(z=z_{rec})-G_0|/G_0 < 0.05(2\sigma), and 0.23(4σ)0.23(4\sigma).Comment: 7 page

    Child caries management: A randomized controlled trial in dental practice

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    This multicenter 3-arm, parallel-group, patient-randomized controlled trial compared clinical effectiveness of 3 treatment strategies over 3 y for managing dental caries in primary teeth in UK primary dental care. Participants aged 3 to 7 y with at least 1 primary molar with dentinal carious lesion were randomized across 3 arms (1:1:1 via centrally administered system with variable-length random permuted blocks): C+P, conventional carious lesion management (complete carious tooth tissue removal and restoration placement) with prevention; B+P, biological management (sealing in carious tooth tissue restoratively) with prevention; and PA, prevention alone (diet, plaque removal, fluorides, and fissure sealants). Parents, children, and dentists were not blind to allocated arm. Co–primary outcomes were 1) the proportion of participants with at least 1 episode of dental pain and/or infection and 2) the number of episodes of dental pain and/or infection during follow-up (minimum, 23 mo). In sum, 1,144 participants were randomized (C+P, n = 386; B+P, n = 381; PA, n = 377) by 72 general dental practitioners, of whom 1,058 (C+P, n = 352; B+P, n = 352; PA, n = 354) attended at least 1 study visit and were included in the primary analysis. The median follow-up was 33.8 mo (interquartile range, 23.8 to 36.7). Proportions of participants with at least 1 episode of dental pain and/or infection were as follows: C+P, 42%; B+P, 40%; PA, 45%. There was no evidence of a difference in incidence of dental pain and/or infection when B+P (adjusted risk difference [97.5% CI]: −2% [−10% to 6%]) or PA (4% [−4% to 12%]) was compared with C+P. The mean (SD) number of episodes of dental pain and/or infection were as follows: C+P, 0.62 (0.95); B+P, 0.58 (0.87); and PA, 0.72 (0.98). Superiority could not be concluded for number of episodes between B+P (adjusted incident rate ratio (97.5% CI): 0.95 [0.75 to 1.21]) or PA (1.18 [0.94 to 1.48]) and C+P. In conclusion, there was no evidence of a difference among the 3 treatment approaches for incidence or number of episodes of dental pain and/or infection experienced by these participants with high caries risk and established disease (trial registration: ISRCTN77044005)

    Questioning Glutamate Excitotoxicity in Acute Brain Damage: The Importance of Spreading Depolarization

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    Background: Within 2 min of severe ischemia, spreading depolarization (SD) propagates like a wave through compromised gray matter of the higher brain. More SDs arise over hours in adjacent tissue, expanding the neuronal damage. This period represents a therapeutic window to inhibit SD and so reduce impending tissue injury. Yet most neuroscientists assume that the course of early brain injury can be explained by glutamate excitotoxicity, the concept that immediate glutamate release promotes early and downstream brain injury. There are many problems with glutamate release being the unseen culprit, the most practical being that the concept has yielded zero therapeutics over the past 30 years. But the basic science is also flawed, arising from dubious foundational observations beginning in the 1950s Methods: Literature pertaining to excitotoxicity and to SD over the past 60 years is critiqued. Results: Excitotoxicity theory centers on the immediate and excessive release of glutamate with resulting neuronal hyperexcitation. This instigates poststroke cascades with subsequent secondary neuronal injury. By contrast, SD theory argues that although SD evokes some brief glutamate release, acute neuronal damage and the subsequent cascade of injury to neurons are elicited by the metabolic stress of SD, not by excessive glutamate release. The challenge we present here is to find new clinical targets based on more informed basic science. This is motivated by the continuing failure by neuroscientists and by industry to develop drugs that can reduce brain injury following ischemic stroke, traumatic brain injury, or sudden cardiac arrest. One important step is to recognize that SD plays a central role in promoting early neuronal damage. We argue that uncovering the molecular biology of SD initiation and propagation is essential because ischemic neurons are usually not acutely injured unless SD propagates through them. The role of glutamate excitotoxicity theory and how it has shaped SD research is then addressed, followed by a critique of its fading relevance to the study of brain injury. Conclusions: Spreading depolarizations better account for the acute neuronal injury arising from brain ischemia than does the early and excessive release of glutamate.Grants to RDA from the Canadian Heart & Stroke Foundation, National Science Engineering and Research Council and the New Frontiers in Research Fund, to E.F from the National Research, Development and Innovation Office of Hungary, grant no. K134377; and the EU’s Horizon 2020 research and innovation program under grant agreement No. 739593, and to JPD from the DFG (German research Council) (DFG DR323/5-1,DFG DR 323/10-1) BMBF Bundesministerium fuer Bildung und Forschung (Era-Net Neuron EBio2, with funds from BMBF 01EW2004)

    Determination of Omega_b From Big Bang Nucleosynthesis in the Presence of Regions of Antimatter

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    Production of regions of antimatter in the early universe is predicted in many baryogenesis models. Small scale antimatter regions would annihilate during or soon after nucleosynthesis, affecting the abundances of the light elements. In this paper we study how the acceptable range in Omega_b changes in the presence of antimatter regions, as compared to the standard big bang nucleosynthesis. It turns out that it is possible to produce at the same time both a low 4He value (Y_p < 0.240) and a low D/H value (D/H < 4e-5), but overproduction of 7Li is unavoidable at large Omega_b.Comment: 9 pages, PRD version, ref. 6 correcte
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