808 resultados para Engineering and Physical Sciences Research Council (EPSRC)
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When individual quantum spins are placed in close proximity to conducting substrates, the localized spin is coupled to the nearby itinerant conduction electrons via Kondo exchange. In the strong coupling limit this can result in the Kondo effect — the formation of a correlated, many body singlet state — and a resulting renormalization of the density of states near the Fermi energy. However, even when Kondo screening does not occur, Kondo exchange can give rise to a wide variety of other phenomena. In addition to the well known renormalization of the g factor and the finite spin decoherence and relaxation times, Kondo exchange has recently been found to give rise to a newly discovered effect: the renormalization of the single ion magnetic anisotropy. Here we put these apparently different phenomena on equal footing by treating the effect of Kondo exchange perturbatively. In this formalism, the central quantity is ρJ, the product of the density of states at the Fermi energy ρ and the Kondo exchange constant J. We show that perturbation theory correctly describes the experimentally observed exchange induced shifts of the single spin excitation energies, demonstrating that Kondo exchange can be used to tune the effective magnetic anisotropy of a single spin.
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Edge detection is crucial in visual processing. Previous computational and psychophysical models have often used peaks in the gradient or zero-crossings in the 2nd derivative to signal edges. We tested these approaches using a stimulus that has no such features. Its luminance profile was a triangle wave, blurred by a rectangular function. Subjects marked the position and polarity of perceived edges. For all blur widths tested, observers marked edges at or near 3rd derivative maxima, even though these were not 1st derivative maxima or 2nd derivative zero-crossings, at any scale. These results are predicted by a new nonlinear model based on 3rd derivative filtering. As a critical test, we added a ramp of variable slope to the blurred triangle-wave luminance profile. The ramp has no effect on the (linear) 2nd or higher derivatives, but the nonlinear model predicts a shift from seeing two edges to seeing one edge as the ramp gradient increases. Results of two experiments confirmed such a shift, thus supporting the new model. [Supported by the Engineering and Physical Sciences Research Council].
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Funded by •Parkinson's UK •Scottish Chief Scientist Office •BMA Doris Hillier Award •RS Macdonald Trust •BUPA Foundation •NHS Grampian Endowments •SPRING •National Institute of Health Research, and Engineering and Physical Sciences Research Council
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Funded by •Parkinson's UK •Scottish Chief Scientist Office •BMA Doris Hillier Award •RS Macdonald Trust •BUPA Foundation •NHS Grampian Endowments •SPRING •National Institute of Health Research, and Engineering and Physical Sciences Research Council
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This work was supported by the Engineering and Physical Sciences Research Council [grant number EP/K006428/1]; and the European Regional Development Fund [grant number LUPS/ERDF/2010/4/1/0164].
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Cities may be responsible for up to 70% of global carbon emissions and 75% of global energy consumption and by 2050 it is estimated that 70% of the world's population could live in cities. The critical challenge for contemporary urbanism, therefore, is to understand how to develop the knowledge, capacity and capability for public agencies, the private sector and multiple users in city regions systemically to re-engineer their built environment and urban infrastructure in response to climate change and resource constraints. Re-Engineering the City 2020–2050: Urban Foresight and Transition Management (Retrofit 2050) is a major new interdisciplinary project funded under the Engineering and Physical Science Research Council's (EPSRC) Sustainable Urban Environments Programme which seeks to address this challenge. This briefing describes the background and conceptual framing of Retrofit 2050 project, its aims and objectives and research approach.
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Mode of access: Internet.
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Cover title: Model learning objectives: Biological & physical sciences.
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The authors would like to thank the participants of the Aberdeen 1936 Birth Cohort (ABC36). Image acquisition and image analysis for ABC36 were funded by the Alzheimer’s Research Trust (now Alzheimer’s Research UK). A.D.M., C.J.M., S.S., L.J.W., and R.T.S. have received grants from: Chief Scientist Office, Department of Health, Scottish Government; Biotechnology and Biological Sciences Research Council
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The authors would like to thank the participants of the Aberdeen 1936 Birth Cohort (ABC36). Image acquisition and image analysis for ABC36 were funded by the Alzheimer’s Research Trust (now Alzheimer’s Research UK). A.D.M., C.J.M., S.S., L.J.W., and R.T.S. have received grants from: Chief Scientist Office, Department of Health, Scottish Government; Biotechnology and Biological Sciences Research Council
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RpfG is a paradigm for a class of widespread bacterial two-component regulators with a CheY-like receiver domain attached to a histidine-aspartic acid-glycine-tyrosine-proline (HD-GYP) cyclic di-GMP phosphodiesterase domain. In the plant pathogen Xanthomonas campestris pv. campestris (Xcc), a two-component system comprising RpfG and the complex sensor kinase RpfC is implicated in sensing and responding to the diffusible signaling factor (DSF), which is essential for cell-cell signaling. RpfF is involved in synthesizing DSF, and mutations of rpfF, rpfG, or rpfC lead to a coordinate reduction in the synthesis of virulence factors such as extracellular enzymes, biofilm structure, and motility. Using yeast two-hybrid analysis and fluorescence resonance energy transfer experiments in Xcc, we show that the physical interaction of RpfG with two proteins with diguanylate cyclase (GGDEF) domains controls a subset of RpfG-regulated virulence functions. RpfG interactions were abolished by alanine substitutions of the three residues of the conserved GYP motif in the HD-GYP domain. Changing the GYP motif or deletion of the two GGDEF-domain proteins reduced Xcc motility but not the synthesis of extracellular enzymes or biofilm formation. RpfG-GGDEF interactions are dynamic and depend on DSF signaling, being reduced in the rpfF mutant but restored by DSF addition. The results are consistent with a model in which DSF signal transduction controlling motility depends on a highly regulated, dynamic interaction of proteins that influence the localized expression of cyclic di-GMP.
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RpfG is a member of a class of wide spread bacterial two-component regulators with an HD-GYP cyclic di-GMP phosphodiesterase domain. In the plant pathogen Xanthomonas campestris, RpfG together with the sensor kinase RpfC regulates multiple factors as a response to the cell-to-cell Diffusible Signalling Factor (DSF). A dynamic physical interaction of RpfG with two diguanylate cyclase (GGDEF) domain proteins controls motility. Here we show that, contrary to expectation, regulation of motility by the GGDEF domain proteins does not depend upon their cyclic di-GMP synthetic activity. Furthermore we show that the complex of RpfG and GGDEF domain proteins recruits a specific PilZ domain adaptor protein, and this complex then interacts with the pilus motor proteins PilU and PiIT. The results support a model in which DSF signalling influences motility through the highly regulated dynamic interaction of proteins that affect pilus action. A specific motif that we identify to be required for HD-GYP domain interaction is conserved in a number of GGDEF domain proteins, suggesting that regulation via interdomain interactions is of broad relevance.
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The authors thank M. C. Romano, I. Stansfield, L. Ciandrini, A. Kort, and M. Rehberg for helpful discussions. This work was funded by BBSRC grants BB/F00513/X1 and BB/G010722, and the Scottish Universities Life Science Alliance (SULSA).
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The authors thank M. C. Romano, I. Stansfield, L. Ciandrini, A. Kort, and M. Rehberg for helpful discussions. This work was funded by BBSRC grants BB/F00513/X1 and BB/G010722, and the Scottish Universities Life Science Alliance (SULSA).
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The cytokine hormone leptin is a key signalling molecule in many pathways that control physiological functions. Although leptin demonstrates structural conservation in mammals, there is evidence of positive selection in primates, lagomorphs and chiropterans. We previously reported that the leptin genes of the grey and harbour seals (phocids) have significantly diverged from other mammals. Therefore we further investigated the diversification of leptin in phocids, other marine mammals and terrestrial taxa by sequencing the leptin genes of representative species. Phylogenetic reconstruction revealed that leptin diversification was pronounced within the phocid seals with a high dN/dS ratio of 2.8, indicating positive selection. We found significant evidence of positive selection along the branch leading to the phocids, within the phocid clade, but not over the dataset as a whole. Structural predictions indicate that the individual residues under selection are away from the leptin receptor (LEPR) binding site. Predictions of the surface electrostatic potential indicate that phocid seal leptin is notably different to other mammalian leptins, including the otariids. Cloning the grey seal leptin binding domain of LEPR confirmed that this was structurally conserved. These data, viewed in toto, support a hypothesis that phocid leptin divergence is unlikely to have arisen by random mutation. Based upon these phylogenetic and structural assessments, and considering the comparative physiology and varying life histories among species, we postulate that the unique phocid diving behaviour has produced this selection pressure. The Phocidae includes some of the deepest diving species, yet have the least modified lung structure to cope with pressure and volume changes experienced at depth. Therefore, greater surfactant production is required to facilitate rapid lung re-inflation upon surfacing, while maintaining patent airways. We suggest that this additional surfactant requirement is met by the leptin pulmonary surfactant production pathway which normally appears only to function in the mammalian foetus.