8,609 research outputs found

    Theory of Linear Spin Wave Emission from a Bloch Domain Wall

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    We report an analytical theory of linear emission of exchange spin waves from a Bloch domain wall, excited by a uniform microwave magnetic field. The problem is reduced to a one-dimensional Schr\"odinger-like equation with a P\"oschl-Teller potential and a driving term of the same profile. The emission of plane spin waves is observed at excitation frequencies above a threshold value, as a result of a linear process. The height-to-width aspect ratio of the P\"oschl-Teller profile for a domain wall is found to correspond to a local maximum of the emission efficiency. Furthermore, for a tailored P\"oschl-Teller potential with a variable aspect ratio, particular values of the latter can lead to enhanced or even completely suppressed emission.Comment: added ancillary file

    The small FNR regulon of Neisseria gonorrhoeae: comparison with the larger Escherichia coli FNR regulon and interaction with the NarQ-NarP regulon

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    BACKGROUND: Neisseria gonorrhoeae can survive during oxygen starvation by reducing nitrite to nitrous oxide catalysed by the nitrite and nitric oxide reductases, AniA and NorB. The oxygen-sensing transcription factor, FNR, is essential for transcription activation at the aniA promoter, and full activation also requires the two-component regulatory system, NarQ-NarP, and the presence of nitrite. The only other gene known to be activated by the gonococcal FNR is ccp encoding a cytochrome c peroxidase, and no FNR-repressed genes have been reported in the gonococcus. In contrast, FNR acts as both an activator and repressor involved in the control of more than 100 operons in E. coli regulating major changes in the adaptation from aerobic to anaerobic conditions. In this study we have performed a microarray-led investigation of the FNR-mediated responses in N. gonorrhoeae to determine the physiological similarities and differences in the role of FNR in cellular regulation in this species. RESULTS: Microarray experiments show that N. gonorrhoeae FNR controls a much smaller regulon than its E. coli counterpart; it activates transcription of aniA and thirteen other genes, and represses transcription of six genes that include dnrN and norB. Having previously shown that a single amino acid substitution is sufficient to enable the gonococcal FNR to complement an E. coli fnr mutation, we investigated whether the gonococcal NarQ-NarP can substitute for E. coli NarX-NarL or NarQ-NarP. A plasmid expressing gonococcal narQ-narP was unable to complement E. coli narQP or narXL mutants, and was insensitive to nitrate or nitrite. Mutations that progressively changed the periplasmic nitrate sensing region, the P box, of E. coli NarQ to the sequence of the corresponding region of gonococcal NarQ resulted in loss of transcription activation in response to the availability of either nitrate or nitrite. However, the previously reported ligand-insensitive ability of gonococcal NarQ, the "locked on" phenotype, to activate either E. coli NarL or NarP was confirmed. CONCLUSION: Despite the sequence similarities between transcription activators of E. coli and N. gonorrhoeae, these results emphasise the fundamental differences in transcription regulation between these two types of pathogenic bacteria

    Primitive Words, Free Factors and Measure Preservation

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    Let F_k be the free group on k generators. A word w \in F_k is called primitive if it belongs to some basis of F_k. We investigate two criteria for primitivity, and consider more generally, subgroups of F_k which are free factors. The first criterion is graph-theoretic and uses Stallings core graphs: given subgroups of finite rank H \le J \le F_k we present a simple procedure to determine whether H is a free factor of J. This yields, in particular, a procedure to determine whether a given element in F_k is primitive. Again let w \in F_k and consider the word map w:G x G x ... x G \to G (from the direct product of k copies of G to G), where G is an arbitrary finite group. We call w measure preserving if given uniform measure on G x G x ... x G, w induces uniform measure on G (for every finite G). This is the second criterion we investigate: it is not hard to see that primitivity implies measure preservation and it was conjectured that the two properties are equivalent. Our combinatorial approach to primitivity allows us to make progress on this problem and in particular prove the conjecture for k=2. It was asked whether the primitive elements of F_k form a closed set in the profinite topology of free groups. Our results provide a positive answer for F_2.Comment: This is a unified version of two manuscripts: "On Primitive words I: A New Algorithm", and "On Primitive Words II: Measure Preservation". 42 pages, 14 figures. Some parts of the paper reorganized towards publication in the Israel J. of Mat

    From paradox to pattern shift: Conceptualising liminal hotspots and their affective dynamics

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    This article introduces the concept of liminal hotspots as a specifically psychosocial and sociopsychological type of wicked problem, best addressed in a process-theoretical framework. A liminal hotspot is defined as an occasion characterised by the experience of being trapped in the interstitial dimension between different forms-of-process. The paper has two main aims. First, to articulate a nexus of concepts associated with liminal hotspots that together provide general analytic purchase on a wide range of problems concerning “troubled” becoming. Second, to provide concrete illustrations through examples drawn from the health domain. In the conclusion, we briefly indicate the sense in which liminal hotspots are part of broader and deeper historical processes associated with changing modes for the management and navigation of liminality

    Mind the gap? The persistence of pathological discourses in urban regeneration policy

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    Urban regeneration policy has historically framed policy problems using a discourse that pathologises areas and spatial communities. Since 2001 in England, and 2002 in Scotland a structural change in policy has occurred where citywide partnerships are now meant overcome structural spatial inequalities, countering pathological explanations. This paper uses historical and discourse analysis to evaluate one of the major community regeneration strategies developed by the Scottish Executive in 2002: Better Communities in Scotland: Closing the Gap. It seeks to ask whether structural change in policy was paralleled by discursive change; what discursive path dependence is evidenced? The text is placed in the historic context of UK urban renewal policies dating back to the launch of the Urban Programme in 1968 and particularly the policy discourse created by the influential Conservative government policy of 1988 New Life for Urban Scotland and the wider discourses of poverty and neighbourhood renewal policy created by Labour governments since 1997. The close textual analysis of the text shows that Better Communities in Scotland continues to pathologise spatial communities. Although this suggests a degree of historical path dependency, the historic breadth of the analysis also problematises simple historical determinism

    Atrial cardiopathy and cognitive impairment

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    Cognitive impairment involves complex interactions between multiple pathways and mechanisms, one of which being cardiac disorders. Atrial cardiopathy (AC) is a structural and functional disorder of the left atrium that may be a substrate for other cardiac disorders such as atrial fibrillation (AF) and heart failure (HF). The association between AF and HF and cognitive decline is clear; however, the relationship between AC and cognition requires further investigation. Studies have shown that several markers of AC, such as increased brain natriuretic peptide and left atrial enlargement, are associated with an increased risk for cognitive impairment. The pathophysiology of cognitive decline in patients with AC is not yet well understood. Advancing our understanding of the relationship between AC and cognition may point to important treatable targets and inform future therapeutic advancements. This review presents our current understanding of the diagnosis of AC, as well as clinical characteristics and potential pathways involved in the association between AC and cognitive impairment
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