Modelling the reorientation of sea-ice faults as the wind changes direction

A discrete-element model of sea ice is used to study how a 90° change in wind direction alters the pattern of faults generated through mechanical failure of the ice. The sea-ice domain is 400km in size and consists of polygonal floes obtained through a Voronoi tessellation. Initially the floes are frozen together through viscous–elastic joints that can break under sufficient compressive, tensile and shear deformation. A constant wind-stress gradient is applied until the initially frozen ice pack is broken into roughly diamond-shaped aggregates, with crack angles determined by wing-crack formation. Then partial refreezing of the cracks delineating the aggregates is modelled through reduction of their length by a particular fraction, the ice pack deformation is neglected and the wind stress is rotated by 90°. New cracks form, delineating aggregates with a different orientation. Our results show the new crack orientation depends on the refrozen fraction of the initial faults: as this fraction increases, the new cracks gradually rotate to the new wind direction, reaching 90° for fully refrozen faults. Such reorientation is determined by a competition between new cracks forming at a preferential angle determined by the wing-crack theory and at old cracks oriented at a less favourable angle but having higher stresses due to shorter contacts across the joints

Failure of a control strategy for a hybrid air-conditioning and wind catchers/towers system at Bluewater shopping malls in Kent

Purpose – To evaluate the control strategy for a hybrid natural ventilation wind catchers and air-conditioning system and to assess the contribution of wind catchers to indoor air environments and energy savings if any. Design/methodology/approach – Most of the modeling techniques for assessing wind catchers performance are theoretical. Post-occupancy evaluation studies of buildings will provide an insight into the operation of these building components and help to inform facilities managers. A case study for POE was presented in this paper. Findings – The monitoring of the summer and winter month operations showed that the indoor air quality parameters were kept within the design target range. The design control strategy failed to record data regarding the operation, opening time and position of wind catchers system. Though the implemented control strategy was working effectively in monitoring the operation of mechanical ventilation systems, i.e. AHU, did not integrate the wind catchers with the mechanical ventilation system. Research limitations/implications – Owing to short-falls in the control strategy implemented in this project, it was found difficult to quantify and verify the contribution of the wind catchers to the internal conditions and, hence, energy savings. Practical implications – Controlling the operation of the wind catchers via the AHU will lead to isolation of the wind catchers in the event of malfunctioning of the AHU. Wind catchers will contribute to the ventilation of space, particularly in the summer months. Originality/value – This paper demonstrates the value of POE as indispensable tool for FM professionals. It further provides insight into the application of natural ventilation systems in building for healthier indoor environments at lower energy cost. The design of the control strategy for natural ventilation and air-conditioning should be considered at the design stage involving the FM personnel.

Nuclear accumulation of myocyte muscle LIM protein is regulated by heme oxygenase 1 and correlates with cardiac function in the transition to failure

Impaired mechanosensing leads to heart failure and we have previously shown that a decreased ratio of cytoplasmic to nuclear CSRP3/Muscle LIM protein (MLP ratio) is associated with a loss of mechanosensitivity. Here we tested whether passive or active stress/strain was important in modulating the MLP ratio and determined whether this correlated with heart function during the transition to failure. We exposed cultured neonatal rat myocytes to 10% cyclic mechanical stretch at 1 Hz, or electrically paced myocytes at 6.8 V (1 Hz) for 48 h. The MLP ratio decreased 50% (P < 0.05, n = 4) only in response to electrical pacing, suggesting impaired mechanosensitivity. Inhibition of contractility with 10 μM blebbistatin resulted in a ∼3 fold increase in the MLP ratio (n = 8, P < 0.05), indicating that myocyte contractility regulates nuclear MLP. Inhibition of histone deacetylase (HDAC) signaling with trichostatin A increased nuclear MLP following passive stretch, suggesting that HDACs block MLP nuclear accumulation. Inhibition of heme-oxygenase1 (HO-1) activity with PPZII blocked MLP nuclear accumulation. To examine how mechanosensitivity changes during the transition to heart failure, we studied a guinea pig model of angiotensin II infusion (400 ng/kg/min) over 12 weeks. Using subcellular fractionation we showed that the MLP ratio increased 88% (n = 4, P < 0.01) during compensated hypertrophy, but decreased significantly during heart failure (P < 0.001, n = 4). The MLP ratio correlated significantly with the E/A ratio (r = 0.71, P < 0.01 n = 12), a clinical measure of diastolic function. These data indicate for the first time that myocyte mechanosensitivity as indicated by the MLP ratio is regulated primarily by myocyte contractility via HO-1 and HDAC signaling.