10 research outputs found

    Slatted-blade Savonius wind-rotors

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    The Savonius rotor can develop a relatively high torque at low rotational speeds and is cheap to build, but it harnesses only a small fraction of the wind energy incident upon it. One initially attractive proposal for augmenting its harnessing effectiveness, was to fit an array of hinged flaps in place of the curved parts of the turbine's blades. The flaps open automatically as a result of wind pressure when they advance into the wind (and hence experience less flow-resistance), but close (again automatically) when retreating from the wind, i.e. during the power-harnessing part of the cycle. It had been found previously that this arrangement, as required, significantly enhances the static torque imposed by the wind on the rotor. So, in this study, dynamic-torque and power-harnessing tests were carried out for a Savonius rotor as well as for rotors modified with 8 or subsequently 16 hinged flaps. The modified rotors displayed slightly increased torques at low rotational speeds, but the traditional Savonius rotor developed a peak power-coefficient of 18% compared with only 5% for the slatted turbines.

    Biomass-fuelled indirect air heater for agro-processing industries Design approach

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    SIGLEAvailable from British Library Document Supply Centre- DSC:GPC/05290 / BLDSC - British Library Document Supply CentreGBUnited Kingdo

    Biomass combustion systems A guide for monitoring and efficient operation

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    SIGLEAvailable from British Library Document Supply Centre- DSC:GPC/05800 / BLDSC - British Library Document Supply CentreGBUnited Kingdo

    Review of the activated carbon industry and scope for oil palm kernel shell as a raw material

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    SIGLEAvailable from British Library Document Supply Centre- DSC:GPC/06749 / BLDSC - British Library Document Supply CentreGBUnited Kingdo

    Positive end-expiratory pressure and mechanical power

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    Editor's Perspective What We Already Know about This Topic Positive end-expiratory pressure protects against ventilation-induced lung injury by improving homogeneity of ventilation, but positive end-expiratory pressure contributes to the mechanical power required to ventilate the lung What This Article Tells Us That Is New This in vivo study (36 pigs mechanically ventilated in the prone position) suggests that low levels of positive end-expiratory pressure reduce injury associated with atelectasis, and above a threshold level of power, positive end-expiratory pressure causes lung injury and adverse hemodynamics Background: Positive end-expiratory pressure is usually considered protective against ventilation-induced lung injury by reducing atelectrauma and improving lung homogeneity. However, positive end-expiratory pressure, together with tidal volume, gas flow, and respiratory rate, contributes to the mechanical power required to ventilate the lung. This study aimed at investigating the effects of increasing mechanical power by selectively modifying its positive end-expiratory pressure component. Methods: Thirty-six healthy piglets (23.3 \ub1 2.3 kg) were ventilated prone for 50 h at 30 breaths/min and with a tidal volume equal to functional residual capacity. Positive end-expiratory pressure levels (0, 4, 7, 11, 14, and 18 cm H2O) were applied to six groups of six animals. Respiratory, gas exchange, and hemodynamic variables were recorded every 6 h. Lung weight and wet-to-dry ratio were measured, and histologic samples were collected. Results: Lung mechanical power was similar at 0 (8.8 \ub1 3.8 J/min), 4 (8.9 \ub1 4.4 J/min), and 7 (9.6 \ub1 4.3 J/min) cm H2O positive end-expiratory pressure, and it linearly increased thereafter from 15.5 \ub1 3.6 J/min (positive end-expiratory pressure, 11 cm H2O) to 18.7 \ub1 6 J/min (positive end-expiratory pressure, 14 cm H2O) and 22 \ub1 6.1 J/min (positive end-expiratory pressure, 18 cm H2O). Lung elastances, vascular congestion, atelectasis, inflammation, and septal rupture decreased from zero end-expiratory pressure to 4 to 7 cm H2O (P < 0.0001) and increased progressively at higher positive end-expiratory pressure. At these higher positive end-expiratory pressure levels, striking hemodynamic impairment and death manifested (mortality 0% at positive end-expiratory pressure 0 to 11 cm H2O, 33% at 14 cm H2O, and 50% at 18 cm H2O positive end-expiratory pressure). From zero end-expiratory pressure to 18 cm H2O, mean pulmonary arterial pressure (from 19.7 \ub1 5.3 to 32.2 \ub1 9.2 mmHg), fluid administration (from 537 \ub1 403 to 2043 \ub1 930 ml), and noradrenaline infusion (0.04 \ub1 0.09 to 0.34 \ub1 0.31 \u3bcg \ub7 kg-1 \ub7 min-1) progressively increased (P < 0.0001). Lung weight and lung wet-to-dry ratios were not significantly different across the groups. The lung mechanical power level that best discriminated between more versus less severe damage was 13 \ub1 1 J/min. Conclusions: Less than 7 cm H2O positive end-expiratory pressure reduced atelectrauma encountered at zero end-expiratory pressure. Above a defined power threshold, sustained positive end-expiratory pressure contributed to potentially lethal lung damage and hemodynamic impairment
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