Design and development of a deployable self-inflating adaptive membrane

Space structures nowadays are often designed to serve just one objective during their mission life, examples include truss structures that are used as support structures, solar sails for propulsion or antennas for communication. Each and every single one of these structures is optimized to serve just their distinct purpose and are more or less useless for the rest of the mission and therefore dead weight. By developing a smart structure that can change its shape and therefore adapt to different mission requirements in a single structure, the flexibility of the spacecraft can be increased by greatly decreasing the mass of the entire system. This paper will introduce such an adaptive structure called the Self-inflating Adaptive Membrane (SAM) concept which is being developed at the Advanced Space Concepts Laboratory of the University of Strathclyde. An idea presented in this paper is to adapt these basic changeable elements from nature’s heliotropism. Heliotropism describes a movement of a plant towards the sun during a day; the movement is initiated by turgor pressure change between adjacent cells. The shape change of the global structure can be significant by adding up these local changes induced by local elements, for example the cell’s length. To imitate the turgor pressure change between the motor cells in plants to space structures, piezoelectric micro pumps are added between two neighboring cells. A passive inflation technique is used for deploying the membrane at its destination in space. The trapped air in the spheres will inflate the spheres when subjected to vacuum, therefore no pump or secondary active deployment methods are needed. The paper will present the idea behind the adaption of nature’s heliotropism principle to space structures. The feasibility of the residual air inflation method is verified by LS-DYNA simulations and prototype bench tests under vacuum conditions. Additionally, manufacturing techniques and folding patterns are presented to optimize the actual bench test structure and to minimize the required storage volume. It is shown that through a bio-inspired concept, a high ratio of adaptability of the membrane can be obtained. The paper concludes with the design of a technology demonstrator for a sounding rocket experiment to be launched in March 2013 from the Swedish launch side Esrange

Electrochemical Studies on the Leaching of Reduced Ore

Confidentia

Electrochemical Monitoring of Aerators

Confidentia

Metabolism of Synthetic Steroids by the Human Placenta

© 2006 Elsevier Ltd. All rights reserved.Pregnant women with asthma are frequently exposed to synthetic glucocorticoids and glucocorticoids are known to reduce fetal growth. The fetus is normally protected from the harmful effects of maternally derived glucocorticoids by the placental enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2). Whether 11beta-HSD2 inactivates the synthetic glucocorticoids used for asthma treatment during pregnancy (budesonide, beclomethasone dipropionate and fluticasone propionate) remains unknown. To investigate the relationship between steroid use during pregnancy and fetal growth and development, pregnant women with (n=119) and without asthma (n=84) were followed throughout pregnancy. Data on asthma medication use, neonatal size at birth, placental weight and cord blood cortisol and estriol were collected. Placental tissue samples were collected from non-asthmatic women (n=8) for metabolism studies. Placental 11beta-HSD2 activity was determined using beclomethasone dipropionate, budesonide, fluticasone propionate, prednisolone, dexamethasone and betamethasone as steroid substrates. Steroids and their oxidised metabolites were examined using thin layer chromatography and densitometry. Placental 11beta-HSD2 metabolised beclomethasone, prednisolone, dexamethasone and betamethasone, but not budesonide or fluticasone. No association between the use of inhaled steroids for asthma treatment during pregnancy and alterations in neonatal size, placental weight, gestational age at delivery, or umbilical vein estriol concentrations was demonstrated compared to non-asthmatic women. In conclusion, the use of inhaled steroids for asthma treatment does not affect fetal growth, despite differences in placental metabolism by 11beta-HSD2.Murphy VE, Fittock RJ, Zarzycki PK, Delahunty MM, Smith R, Clifton VL.http://www.ncbi.nlm.nih.gov/pubmed/1654919

Metabolism of synthetic steroids by the human placenta

Pregnant women with asthma are frequently exposed to synthetic glucocorticoids and glucocorticoids are known to reduce fetal growth. The fetus is normally protected from the harmful effects of maternally derived glucocorticoids by the placental enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2). Whether 11β-HSD2 inactivates the synthetic glucocorticoids used for asthma treatment during pregnancy (budesonide, beclomethasone dipropionate and fluticasone propionate) remains unknown. To investigate the relationship between steroid use during pregnancy and fetal growth and development, pregnant women with (n = 119) and without asthma (n = 84) were followed throughout pregnancy. Data on asthma medication use, neonatal size at birth, placental weight and cord blood cortisol and estriol were collected. Placental tissue samples were collected from non-asthmatic women (n = 8) for metabolism studies. Placental 11β-HSD2 activity was determined using beclomethasone dipropionate, budesonide, fluticasone propionate, prednisolone, dexamethasone and betamethasone as steroid substrates. Steroids and their oxidised metabolites were examined using thin layer chromatography and densitometry. Placental 11β-HSD2 metabolised beclomethasone, prednisolone, dexamethasone and betamethasone, but not budesonide or fluticasone. No association between the use of inhaled steroids for asthma treatment during pregnancy and alterations in neonatal size, placental weight, gestational age at delivery, or umbilical vein estriol concentrations was demonstrated compared to non-asthmatic women. In conclusion, the use of inhaled steroids for asthma treatment does not affect fetal growth, despite differences in placental metabolism by 11β-HSD2