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The Global ETD Search service is a free service for researchers
to find electronic theses and dissertations. This service is
provided by the
Networked Digital Library of Theses and Dissertations.
Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
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Showing 31 to 40 of 151 (0.008 seconds)| 31 |
The role of serum- and glucocorticoid kinase in the hormonal control of sodium transport in pulmonary epitheliaWatt, Gordon B. January 2011 (has links)
In the hormonal control of sodium transport in the lung via glucocorticoids there is substantial evidence that supports a central role for serum- and glucocorticoid-kinase(SGK1). The activity of this kinase is dependent upon phosphorylation of two distinct residues by the target of rapamycin complex 2 (TORC2) and phosphoinositidedependent Kinase 1 (PDK1), both of which are dependent upon Phosphoinositide-3-Kinase (PI3K). However, SGK1 knockout mice do not display any pulmonary abnormalities. Thus the role that SGK1 plays is not fully understood. In this thesis I have explored the role of this kinase in dexamethasone-induced ENaC activity in the H441 human bronchiolar cell model. Dexamethasone-deprived cells do not display ENaC activity as there is no amiloride sensitive current in these cells. Groups of dexamethasone-treated H441 cells do display ENaC activity; however single cells do not display ENaC activity despite displaying an increase in current. Thus cell-cell contact is vital to the development of amiloride sensitivity. SGK1 activity does not mimic the electrophysiological effects of dexamethasone-stimulation as there is no amiloride sensitivity seen after ~3 hours despite a clear increase in SGK1 activity. Furthermore after ~24 hours stimulation, there is a clear amiloride sensitive current although SGK1 activity is comparable to that of dexamethasone-deprived cells. These findings further question whether SGK1 is required for dexamethasone-evoked ENaC activity. Inhibition of PI3K, TORC2 and SGK1 abolished ENaC activity. However inhibition of TORC1 had no effect upon dexamethasone induced ENaC activity. Thus demonstrates that the maintenance of glucocorticoid induced ENaC activity, in pulmonary epithelium, is dependent upon the PI3K-TORC2-SGK1 signalling pathway. Furthermore PI3K plays a permissive, but critical role as its activity is required for SGK1 activity. However without SGK1 activity dexamethasone induced ENaC activity cannot be maintained.
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The study of respiratory and cardiovascular reflex mechanisms involving the lungsPaintal, A. S. January 1952 (has links)
No description available.
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Modelling the ventilation of human maxillary sinusesHood, Christina Mary January 2010 (has links)
No description available.
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Regulation of oxidant and antioxidant enzyme expression by TGF-[beta] in airway smooth muscle cellsMichaeloudes, Charalambos January 2009 (has links)
No description available.
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CO2 retention in respiratory disease : Investigations into potential pre-existing mechanisms in healthy yang subjects using added external dead-spaceDunroy, Helen Mary Agnes January 2007 (has links)
No description available.
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Novel methods to evaluate the impact of cigarette smoking and COPD on lung physiologyRuparelia, Prina January 2009 (has links)
No description available.
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The functional assessment of pulmonary circulation in manBush, A. January 1987 (has links)
No description available.
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The role of serine esterase in extracellular surfactant metabolismClark, H. W. January 2000 (has links)
No description available.
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The assessment of pulmonary functionBates, D. V. January 1954 (has links)
No description available.
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Respiratory tract fluidBlanshard, G. P. January 1955 (has links)
No description available.
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