The Influence of Epistemology on the Design of Artificial Agents

Lee, M. H., Lacey, N. J. (2003). The Influence of Epistemology on the Design of Artificial Agents. Minds and Machines, 13 (3), 367-395

Studies of the solar mean magnetic field with the Birmingham Solar-Oscillations Network (BiSON)

Chaplin, W. J.; Dumbill, A. M.; Elsworth, Y.; Isaak, G. R.; McLeod, C. P.; Miller, B. A.; New, R.; Pint?r, B., Studies of the solar mean magnetic field with the Birmingham Solar-Oscillations Network (BiSON), Monthly Notice of the Royal Astronomical Society, Volume 343, Issue 3, pp. 813-818. RAE2008

Rhywfaint o Anfarwoldeb: Bywgraffiad Islwyn Ffowc Elis

Chapman, T. (2003). Rhywfaint o Anfarwoldeb: Bywgraffiad Islwyn Ffowc Elis. Llandysul: Gwasg Gomer.

The rheology of collapsing zeolites amorphized by temperature and pressure

Greaves, G.; Meneau, F.; ap Gwynn, I.A.; Wade, S., (2003). The rheology of collapsing zeolites amorphized by temperature and pressure. Nature Materials 2, 622-629. RAE2008

An experimental study of the peeling of dough from solid surfaces

Binding, David; Couch, M.A., (2003) 'An experimental study of the peeling of dough from solid surfaces', Journal of Food Engineering 58(2) pp.299-309 RAE2008

Analysis of Sequence Periodicity in E. coli Proteins: Empirical Investigation of the ?Duplication and Divergence? Theory of Protein Evolution

Gatherer, D., and McEwan, N.R. (2003). Analysis of sequence periodicity in E. coli proteins: empirical investigation of the 'duplication and divergence' theory of protein evolution. Journal of Molecular Evolution 57, 149-158. RAE2008

Proteomic analysis of the larval stage of the parasite Echinococcus granulosus: causative agent of cystic hydatid disease

Gustavo Chemale, Arjan J. van Rossum, James R. Jefferies, John Barrett, Peter M. Brophy, Henrique B. Ferreira, Arnaldo Zaha (2003). Proteomic analysis of the larval stage of the parasite Echinococcus granulosus: causative agent of cystic hydatid disease. Proteomics, 3(8), 1633-1636. Sponsorship: CNPq / PADCT/CNPq / FAPERGS (Brazil)/ BBSRC (UK) RAE2008

Asesoría en diseño de joyería en plata en Santafé de Antioquia, Antioquia, Regional Occidente y en diseño de artesanía en cobre en Bogotá.

60 hojas: ilustraciones.

Dynamic Window-Constrained Scheduling for Real-Time Media Streaming

This paper describes an algorithm for scheduling packets in real-time multimedia data streams. Common to these classes of data streams are service constraints in terms of bandwidth and delay. However, it is typical for real-time multimedia streams to tolerate bounded delay variations and, in some cases, finite losses of packets. We have therefore developed a scheduling algorithm that assumes streams have window-constraints on groups of consecutive packet deadlines. A window-constraint defines the number of packet deadlines that can be missed in a window of deadlines for consecutive packets in a stream. Our algorithm, called Dynamic Window-Constrained Scheduling (DWCS), attempts to guarantee no more than x out of a window of y deadlines are missed for consecutive packets in real-time and multimedia streams. Using DWCS, the delay of service to real-time streams is bounded even when the scheduler is overloaded. Moreover, DWCS is capable of ensuring independent delay bounds on streams, while at the same time guaranteeing minimum bandwidth utilizations over tunable and finite windows of time. We show the conditions under which the total demand for link bandwidth by a set of real-time (i.e., window-constrained) streams can exceed 100% and still ensure all window-constraints are met. In fact, we show how it is possible to guarantee worst-case per-stream bandwidth and delay constraints while utilizing all available link capacity. Finally, we show how best-effort packets can be serviced with fast response time, in the presence of window-constrained traffic.

A Neural Model of Surface Perception: Lightness, Anchoring, and Filling-in

This article develops a neural model of how the visual system processes natural images under variable illumination conditions to generate surface lightness percepts. Previous models have clarified how the brain can compute the relative contrast of images from variably illuminate scenes. How the brain determines an absolute lightness scale that "anchors" percepts of surface lightness to us the full dynamic range of neurons remains an unsolved problem. Lightness anchoring properties include articulation, insulation, configuration, and are effects. The model quantatively simulates these and other lightness data such as discounting the illuminant, the double brilliant illusion, lightness constancy and contrast, Mondrian contrast constancy, and the Craik-O'Brien-Cornsweet illusion. The model also clarifies the functional significance for lightness perception of anatomical and neurophysiological data, including gain control at retinal photoreceptors, and spatioal contrast adaptation at the negative feedback circuit between the inner segment of photoreceptors and interacting horizontal cells. The model retina can hereby adjust its sensitivity to input intensities ranging from dim moonlight to dazzling sunlight. A later model cortical processing stages, boundary representations gate the filling-in of surface lightness via long-range horizontal connections. Variants of this filling-in mechanism run 100-1000 times faster than diffusion mechanisms of previous biological filling-in models, and shows how filling-in can occur at realistic speeds. A new anchoring mechanism called the Blurred-Highest-Luminance-As-White (BHLAW) rule helps simulate how surface lightness becomes sensitive to the spatial scale of objects in a scene. The model is also able to process natural images under variable lighting conditions.

Beta-arrestin-2 regulates the development of allergic asthma.

Asthma is a chronic inflammatory disorder of the airways that is coordinated by Th2 cells in both human asthmatics and animal models of allergic asthma. Migration of Th2 cells to the lung is key to their inflammatory function and is regulated in large part by chemokine receptors, members of the seven-membrane-spanning receptor family. It has been reported recently that T cells lacking beta-arrestin-2, a G protein-coupled receptor regulatory protein, demonstrate impaired migration in vitro. Here we show that allergen-sensitized mice having a targeted deletion of the beta-arrestin-2 gene do not accumulate T lymphocytes in their airways, nor do they demonstrate other physiological and inflammatory features characteristic of asthma. In contrast, the airway inflammatory response to LPS, an event not coordinated by Th2 cells, is fully functional in mice lacking beta-arrestin-2. beta-arrestin-2-deficient mice demonstrate OVA-specific IgE responses, but have defective macrophage-derived chemokine-mediated CD4+ T cell migration to the lung. This report provides the first evidence that beta-arrestin-2 is required for the manifestation of allergic asthma. Because beta-arrestin-2 regulates the development of allergic inflammation at a proximal step in the inflammatory cascade, novel therapies focused on this protein may prove useful in the treatment of asthma.

β-Arrestin-2 regulates the development of allergic asthma

Asthma is a chronic inflammatory disorder of the airways that is coordinated by Th2 cells in both human asthmatics and animal models of allergic asthma. Migration of Th2 cells to the lung is key to their inflammatory function and is regulated in large part by chemokine receptors, members of the seven-membrane-spanning receptor family. It has been reported recently that T cells lacking β-arrestin-2, a G protein-coupled receptor regulatory protein, demonstrate impaired migration in vitro. Here we show that allergen-sensitized mice having a targeted deletion of the β-arrestin-2 gene do not accumulate T lymphocytes in their airways, nor do they demonstrate other physiological and inflammatory features characteristic of asthma. In contrast, the airway inflammatory response to LPS, an event not coordinated by Th2 cells, is fully functional in mice lacking β-arrestin-2. β-arrestin-2-deficient mice demonstrate OVA-specific IgE responses, but have defective macrophage-derived chemokine-mediated CD4+ T cell migration to the lung. This report provides the first evidence that β-arrestin-2 is required for the manifestation of allergic asthma. Because β-arrestin-2 regulates the development of allergic inflammation at a proximal step in the inflammatory cascade, novel therapies focused on this protein may prove useful in the treatment of asthma.