Visual surveillance for moving vehicles

An overview is given of a vision system for locating, recognising and tracking multiple vehicles, using an image sequence taken by a single camera mounted on a moving vehicle. The camera motion is estimated by matching features on the ground plane from one image to the next. Vehicle detection and hypothesis generation are performed using template correlation and a 3D wire frame model of the vehicle is fitted to the image. Once detected and identified, vehicles are tracked using dynamic filtering. A separate batch mode filter obtains the 3D trajectories of nearby vehicles over an extended time. Results are shown for a motorway image sequence.

Bottom-up, not top-down, modulation of imitation by human and robotic models

Visual observation of human actions provokes more motor activation than observation of robotic actions. We investigated the extent to which this visuomotor priming effect is mediated by bottom-up or top-down processing. The bottom-up hypothesis suggests that robotic movements are less effective in activating the ‘mirror system’ via pathways from visual areas via the superior temporal sulcus to parietal and premotor cortices. The top-down hypothesis postulates that beliefs about the animacy of a movement stimulus modulate mirror system activity via descending pathways from areas such as the temporal pole and prefrontal cortex. In an automatic imitation task, subjects performed a prespecified movement (e.g. hand opening) on presentation of a human or robotic hand making a compatible (opening) or incompatible (closing) movement. The speed of responding on compatible trials, compared with incompatible trials, indexed visuomotor priming. In the first experiment, robotic stimuli were constructed by adding a metal and wire ‘wrist’ to a human hand. Questionnaire data indicated that subjects believed these movements to be less animate than those of the human stimuli but the visuomotor priming effects of the human and robotic stimuli did not differ. In the second experiment, when the robotic stimuli were more angular and symmetrical than the human stimuli, human movements elicited more visuomotor priming than the robotic movements. However, the subjects’ beliefs about the animacy of the stimuli did not affect their performance. These results suggest that bottom-up processing is primarily responsible for the visuomotor priming advantage of human stimuli.

Thromboxane A2 inhibition of SKCa after NO synthase block in rat middle cerebral artery

NO/prostanoid independent, EDHF-mediated hyperpolarization and dilation in rat middle cerebral arteries is mediated solely by endothelial cell IK(Ca). However, when the NO-pathway is also active, both SK(Ca) and IK(Ca) contribute to EDHF responses. As the SK(Ca) component can be inhibited by stimulation of thromboxane A(2) (TxA(2)) TP receptors and NO has the potential ability to inhibit thromboxane synthesis, we investigated whether TxA(2) might explain loss of functional input from SK(Ca) during NOS inhibition in cerebral arteries. EXPERIMENTAL APPROACH: Rat middle cerebral arteries were mounted in a wire myograph. Endothelium-dependent responses to the PAR2 agonist, SLIGRL were assessed as simultaneous changes in smooth muscle membrane potential and tension. KEY RESULTS: Responses were obtained in the presence of L-NAME as appropriate. Inhibition of TP receptors with either ICI 192,605 or SQ 29,548, did not affect EDHF mediated hyperpolarization and relaxation, but in their presence neither TRAM-34 nor apamin (to block IK(Ca) and SK(Ca) respectively) individually affected the EDHF response. However, in combination they virtually abolished it. Similar effects were obtained in the presence of the thromboxane synthase inhibitor, furegrelate, which additionally revealed an iberiotoxin-sensitive residual EDHF hyperpolarization and relaxation in the combined presence of TRAM-34 and apamin. CONCLUSIONS AND IMPLICATIONS: In the rat middle cerebral artery, inhibition of NOS leads to a loss of the SK(Ca) component of EDHF responses. Either antagonism of TP receptors or block of thromboxane synthase restores an input through SK(Ca). These data indicate that NO normally enables SK(Ca) activity in rat middle cerebral arteries.

Evidence for involvement of both IKCa and SKCa channels in hyperpolarizing responses of the rat middle cerebral artery

Endothelium-derived hyperpolarizing factor responses in the rat middle cerebral artery are blocked by inhibiting IKCa channels alone, contrasting with peripheral vessels where block of both IKCa and SKCa is required. As the contribution of IKCa and SKCa to endothelium-dependent hyperpolarization differs in peripheral arteries, depending on the level of arterial constriction, we investigated the possibility that SKCa might contribute to equivalent hyperpolarization in cerebral arteries under certain conditions. METHODS: Rat middle cerebral arteries (approximately 175 microm) were mounted in a wire myograph. The effect of KCa channel blockers on endothelium-dependent responses to the protease-activated receptor 2 agonist, SLIGRL (20 micromol/L), were then assessed as simultaneous changes in tension and membrane potential. These data were correlated with the distribution of arterial KCa channels revealed with immunohistochemistry. RESULTS: SLIGRL hyperpolarized and relaxed cerebral arteries undergoing variable levels of stretch-induced tone. The relaxation was unaffected by specific inhibitors of IKCa (TRAM-34, 1 micromol/L) or SKCa (apamin, 50 nmol/L) alone or in combination. In contrast, the associated smooth-muscle hyperpolarization was inhibited, but only with these blockers in combination. Blocking nitric oxide synthase (NOS) or guanylyl cyclase evoked smooth-muscle depolarization and constriction, with both hyperpolarization and relaxation to SLIGRL being abolished by TRAM-34 alone, whereas apamin had no effect. Immunolabeling showed SKCa and IKCa within the endothelium. CONCLUSIONS: In the absence of NO, IKCa underpins endothelium-dependent hyperpolarization and relaxation in cerebral arteries. However, when NOS is active SKCa contributes to hyperpolarization, whatever the extent of background contraction. These changes may have relevance in vascular disease states where NO release is compromised and when the levels of SKCa expression may be altered.

Endosomal proteolysis regulates calcitonin gene-related peptide responses in mesenteric arteries

Background and Purpose: Calcitonin gene‐related peptide (CGRP) is a potent vasodilator, implicated in the pathogenesis of migraine. CGRP activates a receptor complex comprising, calcitonin receptor‐like receptor (CLR) and receptor activity‐modifying protein 1 (RAMP1). In vitro studies indicate recycling of CLR•RAMP1 is regulated by degradation of CGRP in early endosomes by endothelin‐converting enzyme‐1 (ECE‐1). However, it is not known if ECE‐1 regulates the resensitization of CGRP‐induced responses in functional arterial tissue. Experimental Approach: CLR, ECE‐1a‐d and RAMP1 expression in rat mesenteric artery smooth muscle cells (RMA‐SMCs) and mesenteric arteries was analyzed by RT‐PCR and by immunofluorescence and confocal microscopy. CGRP‐induced signaling in cells was examined by measuring cAMP production and ERK activation. CGRP‐induced relaxation of arteries was measured by isometric wire myography. ECE‐1 was inhibited using the specific inhibitor, SM‐19712. Key Results: RMA‐SMCs and arteries contained mRNA for CLR, ECE‐1a‐d and RAMP1. ECE‐1 was present in early endosomes of RMA‐SMCs and in the smooth muscle layer of arteries. CGRP induced endothelium‐independent relaxation of arteries. ECE‐1 inhibition had no effect on initial CGRP‐induced responses but reduced cAMP generation in RMA‐SMCs and vasodilation in mesenteric arteries responses to subsequent CGRP challenges. Conclusions and Implications: ECE‐1 regulates the resensitization of responses to CGRP in RMA‐SMCs and mesenteric arteries. CGRP‐induced relaxation does not involve endothelium‐derived pathways. This is the first report of ECE‐1 regulating CGRP responses in SMCs and arteries. ECE‐1 inhibitors may attenuate an important vasodilatory pathway, implicated in primary headaches and may represent a new therapeutic approach for the treatment of migraine.

Possible role for K+ in endothelium-derived hyperpolarizing factor–linked dilatation in rat middle cerebral artery

Background and Purpose— Endothelium-derived hyperpolarizing factor (EDHF) and K+ are vasodilators in the cerebral circulation. Recently, K+ has been suggested to contribute to EDHF-mediated responses in peripheral vessels. The EDHF response to the protease-activated receptor 2 ligand SLIGRL was characterized in cerebral arteries and used to assess whether K+ contributes as an EDHF. Methods— Rat middle cerebral arteries were mounted in either a wire or pressure myograph. Concentration-response curves to SLIGRL and K+ were constructed in the presence and absence of a variety of blocking agents. In some experiments, changes in tension and smooth muscle cell membrane potential were recorded simultaneously. Results— SLIGRL (0.02 to 20 μmol/L) stimulated concentration and endothelium-dependent relaxation. In the presence of NG-nitro-L-arginine methyl ester, relaxation to SLIGRL was associated with hyperpolarization and sensitivity to a specific inhibitor of IKCa, 1-[(2-chlorophenyl)diphenylmethyl]-1H-pyrazole (1μmol/L), reflecting activation of EDHF. Combined inhibition of KIR with Ba2+ (30μmol/L) and Na+/K+-ATPase with ouabain (1 μmol/L) markedly attenuated the relaxation to EDHF. Raising extracellular [K+] to 15 mmol/L also stimulated smooth muscle relaxation and hyperpolarization, which was also attenuated by combined application of Ba2+ and ouabain. Conclusions— SLIGRL evokes EDHF-mediated relaxation in the rat middle cerebral artery, underpinned by hyperpolarization of the smooth muscle. The profile of blockade of EDHF-mediated hyperpolarization and relaxation supports a pivotal role for IKCa channels. Furthermore, similar inhibition of responses to EDHF and exogenous K+ with Ba2+ and ouabain suggests that K+ may contribute as an EDHF in the middle cerebral artery.

Statins and selective inhibition of Rho kinase protect small conductance calcium-activated potassium channel function (KCa2.3) in cerebral arteries

Background: In rat middle cerebral and mesenteric arteries the KCa2.3 component of endothelium-dependent hyperpolarization (EDH) is lost following stimulation of thromboxane (TP) receptors, an effect that may contribute to the endothelial dysfunction associated with cardiovascular disease. In cerebral arteries, KCa2.3 loss is associated with NO synthase inhibition, but is restored if TP receptors are blocked. The Rho/Rho kinase pathway is central for TP signalling and statins indirectly inhibit this pathway. The possibility that Rho kinase inhibition and statins sustain KCa2.3 hyperpolarization was investigated in rat middle cerebral arteries (MCA). Methods: MCAs were mounted in a wire myograph. The PAR2 agonist, SLIGRL was used to stimulate EDH responses, assessed by simultaneous measurement of smooth muscle membrane potential and tension. TP expression was assessed with rt-PCR and immunofluorescence. Results: Immunofluorescence detected TP in the endothelial cell layer of MCA. Vasoconstriction to the TP agonist, U46619 was reduced by Rho kinase inhibition. TP receptor stimulation lead to loss of KCa2.3 mediated hyperpolarization, an effect that was reversed by Rho kinase inhibitors or simvastatin. KCa2.3 activity was lost in L-NAME-treated arteries, but was restored by Rho kinase inhibition or statin treatment. The restorative effect of simvastatin was blocked after incubation with geranylgeranyl-pyrophosphate to circumvent loss of isoprenylation. Conclusions: Rho/Rho kinase signalling following TP stimulation and L-NAME regulates endothelial cell KCa2.3 function. The ability of statins to prevent isoprenylation and perhaps inhibit of Rho restores/protects the input of KCa2.3 to EDH in the MCA, and represents a beneficial pleiotropic effect of statin treatment.

‘The Making of the Book’: Roy Fisher, the Circle Press and the poetics of book art

Between 1972 and 2001, the English late-modernist poet Roy Fisher provided the text for nine separate artist's books produced by Ron King at the Circle Press. Taken together, as Andrew Lambirth has written, the Fisher-King collaborations represent a sustained investigation of the various ways in which text and image can be integrated, breaking the mould of the codex or folio edition, and turning the book into a sculptural object. From the three-dimensional pop-up designs of Bluebeard's Castle (1973), each representing a part of the edifice (the portcullis, the armoury and so on), to ‘alphabet books’ such as The Half-Year Letters (1983), held in an ingenious french-folded concertina which can be stretched to over a metre long or compacted to a pocketbook, the project of these art books is to complicate their own bibliographic codes, and rethink what a book can be. Their folds and reduplications give a material form to the processes by which meanings are produced: from the discovery, in Top Down, Bottom Up (1990), of how to draw on both sides of the page at the same time, to the developments of The Left-Handed Punch (1987) and Anansi Company (1992), where the book becomes first a four-dimensional theatre space, in which a new version of Punch and Judy is played out by twelve articulated puppets, and then a location for characters that are self-contained and removable, in the form of thirteen hand-made wire and card rod-puppets. Finally, in Tabernacle (2001), a seven-drawer black wooden cabinet that stands foursquare like a sculpture (and sells to galleries and collectors for over three thousand pounds), the conception of the book and the material history of print are fully undone and reconstituted. This paper analyses how the King-Fisher art books work out their radically material poetics of the book; how their emphasis on collaboration, between artist and poet, image and text, and also book and reader – the construction of meaning becoming a co-implicated process – continuously challenges hierarchies and fixities in our conception of authorship; and how they re-think the status of poetic text and the construction of the book as material object.

Regulation of KCa2.3 andendothelium-dependent hyperpolarization (EDH) in the rat middle cerebral artery: the role of lipoxygenase metabolites and isoprostanes

Background and Purpose. In rat middle cerebral arteries, endothelium-dependent hyperpolarization (EDH) is mediated by activation of calcium-activated potassium(KCa) channels specifically KCa2.3 and KCa3.1. Lipoxygenase (LOX) products function as endothelium-derived hyperpolarizing factors (EDHFs) in rabbit arteries by stimulating KCa2.3. We investigated if LOX products contribute to EDH in rat cerebral arteries. Methods. Arachidonic acid (AA) metabolites produced in middle cerebral arteries were measured using HPLC and LC/MS. Vascular tension and membrane potential responses to SLIGRL were simultaneously recorded using wire myography and intracellular microelectrodes. Results. SLIGRL, an agonist at PAR2 receptors, caused EDH that was inhibited by a combination of KCa2.3 and KCa3.1 blockade. Non-selective LOX-inhibition reduced EDH, whereas inhibition of 12-LOX had no effect. Soluble epoxide hydrolase (sEH) inhibition enhanced the KCa2.3 component of EDH. Following NO synthase (NOS) inhibition, the KCa2.3 component of EDH was absent. Using HPLC, middle cerebral arteries metabolized 14C-AA to 15- and 12-LOX products under control conditions. With NOS inhibition, there was little change in LOX metabolites, but increased F-type isoprostanes. 8-iso-PGF2α inhibited the KCa2.3 component of EDH. Conclusions. LOX metabolites mediate EDH in rat middle cerebral arteries. Inhibition of sEH increases the KCa2.3 component of EDH. Following NOS inhibition,loss of KCa2.3 function is independent of changes in LOX production or sEH inhibition but due to increased isoprostane production and subsequent stimulation of TP receptors. These findings have important implications in diseases associated with loss of NO signaling such as stroke; where inhibition of sEH and/or isoprostane formation may of benefit.

Do turning biases by the 7-spot ladybird, Coccinella septempunctata, increase their foraging efficiency?

The hypothesis that foraging male and female Coccinella septempunctata L. would exhibit a turning bias when walking along a branched linear wire in a Y-maze was tested. Individuals were placed repeatedly in the maze. Approximately 45% of all individuals tested displayed significant turning biases, with a similar number of individuals biased to the left and right. In the maze right-handed individuals turned right at 84.4% of turns and the left-handed individuals turned left at 80.2% of turns. A model of the searching efficiency of C. septempunctata in dichotomous branched environments showed that model coccinellids with greater turning biases discovered a higher proportion of the plant for a given number of searches than those with no bias. A modification of the model to investigate foraging efficiency, by calculating the mean time taken by individuals to find randomly distributed aphid patches, suggested that on four different sizes of plants, with a variety of aphid patch densities, implementing a turning bias was a significantly more efficient foraging strategy than no bias. In general the benefits to foraging of implementing a turning bias increased with the degree of the bias. It may be beneficial for individuals in highly complex branched environments to have a turning bias slightly lower than 100% in order to benefit from increased foraging efficiency without walking in circles. Foraging bias benefits increased with increasing plant size and decreasing aphid density. In comparisons of two different plant morphologies, one with a straight stem and side branches and one with a symmetrically branched morphology, there were few significant differences in the effects of turning biases on foraging efficiency between morphologies

Foraging strategies of natural enemies of the peach-potato aphid Myzus persicae

The foraging strategies of two natural enemies of the peach-potato aphid Myzus persicae: the seven-spot ladybird Coccinella septempunctata and the parasitoid wasp Diaeretiella rapae, were investigated. Specifically the roles of plant semiochemicals in the location of plants infested with M. persicae by these natural enemies were examined. I investigated the olfactory responses of female C. septempunctata to volatiles collected from M. persicae and four Brassica cultivars; Brassica rapa, B. juncea, B. napus cultivar ‘Apex’ and B. napus cultivar ‘Courage’ and wild-type Arabidopsis thaliana that were: undamaged, previously infested by M. persicae and infested with M. persicae. C. septempunctata showed no attraction to volatiles from M. persicae alone. C. septempunctata significantly changed its searching behaviour in response to plant volatiles from B. rapa, B. napus cv. ‘Apex’ and Arabidopsis infested with M. persicae. C. septempunctata was also found to display a significant turning bias when foraging on a branching horizontal wire stem. A model was developed to investigate how turning biases affect the foraging efficiency of C. septempunctata in dichotomous branched environments. Simulations using this model indicated that turning biases could potentially increase searching efficiency. D. rapae showed a significant preference for volatiles from M. persicae infested wild-type Arabidopsis but no preference to volatiles from M. persicae alone or M. persicae honeydew. Volatile emissions by Arabidopsis were shown to be localised to the area of aphid-infestation rather than systemic. Using gas chromatography plants infested with M. persicae were shown to emit a quantitatively different volatile blend than undamaged plants. In experiments with jasmonate mutants of Arabidopsis the jasmonate (octadecanoid) wound response pathway was implicated as being important for the production of M. persicae induced volatiles, attractive to D. rapae. Other wound response pathways were also found to be involved in the production of the full blend of M. persicae induced volatiles.

Playing Kant at the Court of King Arthur

This article contrasts the sense in which those whom Bernard Williams called ‘political realists’ and John Rawls are committed to the idea that political philosophy has to be distinctively political. Distinguishing the realist critique of political moralism from debates over ideal and non-ideal theory, it is argued that Rawls is more realist than many realists realise, and that realists can learn more about how to make a distinctively political vision of how our life together should be organised from his theorising, although it also points to a worrying tendency among Rawlsians to reach for inappropriately moralised arguments. G. A. Cohen’s advocacy of socialism and the second season of HBO’s The Wire are used as examples to illustrate these points.

Long-Term Ouabain Treatment Impairs Vascular Function in Resistance Arteries

Background/Aims: The purpose of this study was to examine the cardiovascular effects of long-term ouabain treatment at different time points. Methods: Systolic blood pressure (SBP) was measured by tail-cuff method in male Wistar rats treated with ouabain (approx. 8.0 mu g.day(-1)) or vehicle for 5, 10 and 20 weeks. Afterwards, vascular function was assessed in mesenteric resistance arteries (MRA) using a wire myograph. ROS production and COX-1 and COX-2, TNF-alpha, and IL-6 protein expression were investigated. Results: SBP was increased by ouabain treatment up to the 6th week and remained stable until the 20th week. However, noradrenaline-induced contraction increased only in MRA in rats treated with ouabain for 20 weeks. NOS inhibition and endothelium removal increased the noradrenaline response, but to a smaller magnitude in MRA in the ouabain group. Moreover, inhibition of COX-2 or incubation with superoxide dismutase restores noradrenaline-induced contraction in the 20-week ouabain group to control levels. ROS production as well as COX-2, IL-6 and TNF-alpha protein expression increased in MRA in this group. Conclusion: Although ouabain treatment induced hypertension in all groups, a larger noradrenaline induced contraction was observed over 20 weeks of treatment. This vascular dysfunction was related to COX-2-derived prostanoids and oxidative stress, increased pro-inflammatory cytokines and reduced NO bioavailability. Copyright (C) 2011 S. Karger AG, Basel

Integrable maps with non-trivial topology: application to divertor configurations

We explore a method for constructing two-dimensional area-preserving, integrable maps associated with Hamiltonian systems, with a given set of fixed points and given invariant curves. The method is used to find an integrable Poincare map for the field lines in a large aspect ratio tokamak with a poloidal single-null divertor. The divertor field is a superposition of a magnetohydrodynamic equilibrium with an arbitrarily chosen safety factor profile, with a wire carrying an electric current to create an X-point. This integrable map is perturbed by an impulsive perturbation that describes non-axisymmetric magnetic resonances at the plasma edge. The non-integrable perturbed map is applied to study the structure of the open field lines in the scrape-off layer, reproducing the main transport features obtained by integrating numerically the magnetic field line equations, such as the connection lengths and magnetic footprints on the divertor plate.

Magnetic Susceptibility Measurements at Ultra-low Temperatures

We report the design and operation of a device for ac magnetic susceptibility measurements that can operate down to 1 mK. The device, a modification of the standard mutual inductance bridge, is designed with detailed consideration of the thermalization and optimization of each element. First, in order to reduce local heating, the primary coil is made with superconducting wire. Second, a low-temperature transformer which is thermally anchored to the mixing chamber of a dilution refrigerator, is used to match the output of the secondary coil to a high-sensitivity bridge detector. The careful thermal anchoring of the secondary coil and the matching transformer is required to reduce the overall noise temperature and maximize sensitivity. The sample is immersed in liquid (3)He to minimize the Kapitza thermal resistance. The magnetic susceptibility of several magnetic compounds, such as the well-known spin gap compound NiCl(2)-4SC(NH(2))(2) and other powdered samples, have been successfully measured to temperatures well below 10 mK.