Sara Borazjani, Abolfazl Hashemi, Cuong Nguyen
et al.
Abstract The paper presents a strength-failure mechanism for colloidal detachment by breakage and permeability decline in reservoir rocks. The current theory for permeability decline due to colloidal detachment, including microscale mobilisation mechanisms, mathematical and laboratory modelling, and upscaling to natural reservoirs, is developed only for detrital particles with detachment that occurs against electrostatic attraction. We establish a theory for detachment of widely spread authigenic particles due to breakage of the particle-rock bonds, by integrating beam theory of particle deformation, failure criteria, and creeping flow. Explicit expressions for stress maxima in the beam yield a graphical technique to determine the failure regime. The core-scale model for fines detachment by breakage has a form of maximum retention concentration of the fines, expressing rock capacity to produce breakable fines. This closes the governing system for authigenic fines transport in rocks. Matching of the lab coreflood data by the analytical model for 1D flow exhibits two-population particle behaviour, attributed to simultaneous detachment and migration of authigenic and detrital fines. High agreement between the laboratory and modelling data for 16 corefloods validates the theory. The work is concluded by geo-energy applications to (i) clay breakage in geological faults, (ii) typical reservoir conditions for kaolinite breakage, (iii) well productivity damage due to authigenic fines migration, and (iv) feasibility of fines breakage in various geo-energy extraction technologies.
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The mechanisms underlying cytoplasmic pH (pHi) regulation in rat thymic lymphocytes were studied using trapped fluorescein derivatives as pHi indicators. Cells that were acid-loaded with nigericin in choline+ media recovered normal pHi upon addition of extracellular Na+ (Nao+). The cytoplasmic alkalinization was accompanied by medium acidification and an increase in cellular Na+ content and was probably mediated by a Nao+/Hi+ antiport. At normal [Na+]i, Nao+/Hi+ exchange was undetectable at pHi greater than or equal to 6.9 but was markedly stimulated by internal acidification. Absolute rates of H+ efflux could be calculated from the Nao+-induced delta pHi using a buffering capacity of 25 mmol X liter-1 X pH-1, measured by titration of intact cells with NH4+. At pHi = 6.3, pHo = 7.2, and [Na+]o = 140 mM, H+ extrusion reached 10 mmol X liter-1 X min-1. Nao+/Hi+ exchange was stimulated by internal Na+ depletion and inhibited by lowering pHo and by addition of amiloride (apparent Ki = 2.5 microM). Inhibition by amiloride was competitive with respect to Nao+. Hi+ could also exchange for Lio+, but not for K+, Rb+, Cs+, or choline+. Nao+/Hi+ countertransport has an apparent 1:1 stoichiometry and is electrically silent. However, a small secondary hyperpolarization follows recovery from acid-loading in Na+ media. This hyperpolarization is amiloride- and ouabain-sensitive and probably reflects activation of the electrogenic Na+-K+ pump. At normal Nai+ values, the Nao+/Hi+ antiport of thymocytes is ideally suited for the regulation of pHi. The system can also restore [Na+]i in Na+-depleted cells. In this instance the exchanger, in combination with the considerable cytoplasmic buffering power, will operate as a [Na+]i- regulatory mechanism.
Human skin has an acid mantle of pH 4-6, contrasting with the almost neutral pH of the interior body and implying the existence of a pH gradient over the horny layer that might influence a variety of epidermal processes. In an attempt to characterize the pH gradient, we applied a glass electrode to the volar surface of the forearm before and after consecutive strippings with sello-tape. Before stripping, the surface pH (mean +/- SD) was 4.5 +/- 0.2 in men (n = 7) and 5.3 +/- 0.5 in women (n = 7), the values gradually increasing to pH 6.9 +/- 0.4 in men and 6.8 +/- 0.5 in women after about 100-120 tape strippings, which completely removed the stratum corneum. When plotted against the number of strippings, the pH values usually conformed to a sigmoid curve with inflection (50% change) after about 60 strippings, at a level corresponding histologically to the lower third of stratum corneum. Similar gradients were found also in skin of the abdomen and calf. Stripping with cyanoacrylate resin produced a similar gradient, even though this form of stripping was 10 times more effective. The healing process after tape stripping was studied by determining pH and transepidermal water loss in 5 persons over a period of 14 days. The importance of the re-established pH gradient is discussed in relation to the many pH-dependent enzymes operating in stratum corneum.
We have previously proposed that acidification-induced regulation of the cardiac gap junction protein connexin43 (Cx43) may be modeled as a particle-receptor interaction between two separate domains of Cx43: the carboxyl terminal (acting as a particle), and a region including histidine 95 (acting as a receptor). Accordingly, intracellular acidification would lead to particle-receptor binding, thus closing the channel. A premise of the model is that the particle can bind its receptor, even if the particle is not covalently bound to the rest of the protein. The latter hypothesis was tested in antisense-injected Xenopus oocyte pairs coexpressing mRNA for a pH-insensitive Cx43 mutant truncated at amino acid 257 (i.e., M257) and mRNA coding for the carboxyl terminal region (residues 259-382). Intracellular pH (pHo) was recorded using the dextran form of the proton-sensitive dye seminaphthorhodafluor (SNARF). Junctional conductance (Gj) was measured with the dual voltage clamp technique. Wild-type Cx43 channels showed their characteristic pH sensitivity. M257 channels were not pH sensitive (pHo tested: 7.2 to 6.4). However, pH sensitivity was restored when the pH-insensitive channel (M257) was coexpressed with mRNA coding for the carboxyl terminal. Furthermore, coexpression of the carboxyl terminal of Cx43 enhanced the pH sensitivity of an otherwise less pH-sensitive connexin (Cx32). These data are consistent with a model of intramolecular interactions in which the carboxyl terminal acts as an independent domain that, under the appropriate conditions, binds to a separate region of the protein and closes the channel. These interactions may be direct (as in the ball-and-chain mechanism of voltage-dependent gating of potassium channels) or mediated through an intermediary molecule. The data further suggest that the region of Cx43 that acts as a receptor for the particle is conserved among connexins. A similar molecular mechanism may mediate chemical regulation of other channel proteins.