28 research outputs found

    UK microgeneration. Part I: policy and behavioural aspects

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    A critical review of the literature relating to government policy and behavioural aspects relevant to the uptake and application of microgeneration in the UK is presented. Given the current policy context aspiring to zero-carbon new homes by 2016 and a variety of minimum standards and financial policy instruments supporting microgeneration in existing dwellings, it appears that this class of technologies could make a significant contribution to UK energy supply and low-carbon buildings in the future. Indeed, achievement of a reduction in greenhouse gas emissions by 80% (the UK government's 2050 target) for the residential sector may entail substantial deployment of microgeneration. Realisation of the large potential market for microgeneration relies on a variety of interrelated factors such as microeconomics, behavioural aspects, the structure of supporting policy instruments and well-informed technology development. This paper explores these issues in terms of current and proposed policy instruments in the UK. Behavioural aspects associated with both initial uptake of the technology and after purchase are also considered

    Involvement of endothelium-dependent vasodilator mechanisms in direct STS responses.

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    <p>Mechanisms of vascular responses to STS in mesenteric (A&amp;C) and uterine (B&amp;D) arteries from the pregnant rat (GD 10.9±0.2). Vasodilator responses to STS in the absence (closed circles) or presence of inhibitors of nitric oxide synthase (NOS) (<i>N</i>-nitro-L-arginine methyl ester hydrochloride, L-NAME, 100 μmol/l, open squares), cyclooxygenase (meclofenamate, 1 μmol/l, open circles) or a combination of apamin (100 nmol/l) and TRAM-34 (10 μmol/l) which block SK<sub>Ca</sub> and IK<sub>Ca</sub> channels respectively (open triangles) in A: mesenteric arteries and B: uterine arteries. Sensitivity (negative log of the effective concentration producing 50% of the maximal response) of vascular responses to STS in C: mesenteric arteries or D: uterine arteries. Data analysed by one-way ANOVA with a Bonferroni post-test; ††: p&lt;0.01 vs. control vessel. Mesenteric: control n = 8; L-NAME n = 6; Apa, TRAM n = 7; Meclo n = 4. Uterine: control n = 10; L-NAME n = 6; Apa, TRAM n = 7; Meclo n = 5.</p

    Effect of STS treatment on umbilical artery blood flow velocity in mice.

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    <p>Echocardiographic parameters of umbilical blood flow from control (white bars) and eNOS<sup>-/-</sup> (black bars) late pregnant (GD 18) mice, untreated (open bars) or treated (hatched bars) with STS from GD 12 to 18. STS was given in drinking water at a concentration of approx. 27 mg/kg/day. A: end diastolic velocity (EDV), B: peak systolic velocity (PSV) and C: calculated resistance index (RI). Data analysed by two-way ANOVA with a Bonferroni post-test; **: p&lt;0.01, ***: p&lt;0.001, group genotype effect. Control untreated n = 4; control treated n = 8; eNOS<sup>-/-</sup> untreated n = 6; eNOS<sup>-/-</sup> treated n = 8.</p

    Effect of STS treatment on vasodilator responses in mouse arteries.

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    <p>A: Vascular responses of mouse uterine arteries to MCh from control (circles) and eNOS<sup>-/-</sup> (squares) late pregnant (GD 18) mice, untreated (closed symbols) or treated (open symbols) with STS from GD 12 to 18. STS was given in drinking water at a dose of approx. 27 mg/kg/day. Summary data of B: maximal responses and C: sensitivity (negative log of the effective concentration producing 50% of the maximal response) to MCh. Data analysed by two-way ANOVA with a Bonferroni post-test; **: p&lt;0.01 group treatment effect, ****: p&lt;0.0001 group genotype effect, ††: p&lt;0.01 vs. eNOS<sup>-/-</sup> untreated, †††: p&lt;0.001 vs. control untreated. Control untreated n = 5; control treated n = 5; eNOS<sup>-/-</sup> untreated n = 6; eNOS<sup>-/-</sup> treated n = 4.</p

    Endothelium-independent responses to STS.

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    <p>Vascular responses to STS in A: mesenteric arteries and B: uterine arteries from the pregnant rat (GD 10.9±0.2) with intact endothelium (closed circles) or following endothelial removal using a knotted human hair (open circles). Mesenteric intact n = 6; mesenteric denuded n = 5; uterine intact n = 4; uterine denuded n = 5.</p

    Effect of STS treatment on pregnancy outcomes in mice.

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    <p>Pregnancy outcomes in control (white bars) and eNOS<sup>-/-</sup> (black bars) late pregnant (GD 18) mice, untreated (open bars) or treated (hatched bars) with STS from GD 12 to 18. STS was given in drinking water at a concentration of approx. 27 mg/kg/day. A: pup weight, B: pup crown to rump length, C: maternal systolic blood pressure and D: placental weight. Data analysed by two-way ANOVA with a Bonferroni post-test; **: p&lt;0.01, ***: p&lt;0.001, group genotype or treatment effects; ††: p&lt;0.01 vs. control untreated. Control untreated n = 5(33); control treated n = 8(60); eNOS<sup>-/-</sup> untreated n = 6(30); eNOS<sup>-/-</sup> treated n = 7(43); where n = dams(pups).</p

    Direct vasodilator effects of STS in rat arteries.

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    <p>Vascular responses to STS in the carotid (open squares, n = 8), uterine (open circles, n = 10), and mesenteric arteries (closed circles, n = 8) from the pregnant rat (GD 10.9±0.2).</p
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