16 research outputs found

    On the origin of A-tents (pop-ups), sheet structures, and associated forms

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    Copyright © 2009 by SAGE PublicationsA-tents are also known as pop-ups and by several other local names. They consist of raised slabs or plates of various thicknesses and origins. Laminae are caused by weathering, and spall plates or slabs may be caused in part by freeze-thaw acting on water held in pre-existing partings which are, however, like the sheet fractures that define the thicker sheet structures, probably of tectonic origin. A-tents are the result of the buckling of such laminae, plates and slabs. Again, tectonism in the form of compressive horizontal stress, appears the most likely and common causation, though decreases in lithostatic pressure consequent on unloading and, in particular cases, surficial expansion of plates caused by the intense heat of fires, may also contribute to rock failure and rupture. All A-tents are of Holocene age and are, therefore, neotectonic forms. Some have developed in living memory, and some are known to be developing from blisters. There is some evidence of continued dislocation along sheet fractures and of the transformation of blisters or arches into A-tents under the influence of continued lateral compression. This review demonstrates, therefore, that A-tents, sheet structures, and associated forms share a common heritage

    The Na+-K+-2Cl- cotransporter and the osmotic stress response in a model salt transport epithelium.

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    Epithelia are physiologically exposed to osmotic stress resulting in alteration of cell volume in several aspects of their functioning; therefore, the activation of ‘emergency’ systems of rapid cell volume regulation is fundamental in their physiology. In this review, the physiological response to osmotic stress, particularly hypertonic stress, was described in a salt-transporting epithelium, the intestine of the euryhaline teleost European eel. This epithelium is physiologically exposed to changes in extracellular osmolarity and represents a good physiological model for functional studies on cellular volume regulation, permitting the study of volume regulated ion transport mechanisms in a native tissue. An absorptive form of the cotransporter, homologue of the renal NKCC2, localized on the apical membrane, was found in the intestine of the euryhaline teleost European eel. This cotransporter accounts for the luminal uptake of Cl); it operates in series with a basolateral Cl) conductance and presumably a basolateral electroneutral KCl cotransport and in parallel with a luminal K+ conductance. The ion transport model described for eel intestine, based on the operation of an absorptive luminal Na+–K+– 2Cl), is basically the same as the model that has been proposed for the thick ascending limb (cTAL) of the mammalian renal cortex. This paper focuses on the role of Na+–K+–2Cl) cotransport in the responses to hypertonic stress in the eel intestine and the role of cytoskeleton (either actin-based or tubulin based) is discussed
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