Academic literature on the topic 'Cell membranes. Biological transport. Chlorides'

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Journal articles on the topic "Cell membranes. Biological transport. Chlorides"

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Naftalin, R. J. "Chloride transport coupling in biological membranes and epithelia." FEBS Letters 196, no. 1 (February 3, 1986): 182–83. http://dx.doi.org/10.1016/0014-5793(86)80240-x.

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Cabantchik, Z. I., and R. Greger. "Chemical probes for anion transporters of mammalian cell membranes." American Journal of Physiology-Cell Physiology 262, no. 4 (April 1, 1992): C803—C827. http://dx.doi.org/10.1152/ajpcell.1992.262.4.c803.

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Mammalian cell membranes harbor several types of chloride channels, chloride-cation symporters/cotransporters, and several classes of anion exchangers/antiporters. These transport systems subserve different cellular or organismic functions, depending on the nature of the cell, the spatial organization of transporters, and their functional interplay. Chemical probing has played a central role in the structural and functional delineation of the various anion transport systems. The design of specific probes or their selection from existing sources coupled with their judicious application to the most appropriate biological system had led to the identification of specific anion transporters and to the elucidation of the underlying molecular transport mechanism. In many instances, chemical probing has remained the major or exclusive analytical tool for the functional definition or identification of a given transport system, particularly for discerning among the various anion transporters which operate in highly heterogeneous cell membrane systems. This work critically reviews the present state of the chemical armamentarium available for the most common anion transporters found in mammalian cell membranes. It encompasses the description of the most useful or commonly used probes in terms of their chemical, biochemical, physiological, and pharmacological properties. The review deals primarily with what chemical probes tell about anion transporters and, most importantly, with the limitations inherent in the use of probes in transport studies.
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Gałczyńska, Katarzyna, Jarosław Rachuna, Karol Ciepluch, Magdalena Kowalska, Sławomir Wąsik, Tadeusz Kosztołowicz, Katarzyna D. Lewandowska, Jacek Semaniak, Krystyna Kurdziel, and Michał Arabski. "Experimental and Theoretical Analysis of Metal Complex Diffusion through Cell Monolayer." Entropy 23, no. 3 (March 17, 2021): 360. http://dx.doi.org/10.3390/e23030360.

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The study of drugs diffusion through different biological membranes constitutes an essential step in the development of new pharmaceuticals. In this study, the method based on the monolayer cell culture of CHO-K1 cells has been developed in order to emulate the epithelial cells barrier in permeability studies by laser interferometry. Laser interferometry was employed for the experimental analysis of nickel(II) and cobalt(II) complexes with 1-allylimidazole or their chlorides’ diffusion through eukaryotic cell monolayers. The amount (mol) of nickel(II) and cobalt(II) chlorides transported through the monolayer was greater than that of metals complexed with 1-allylimidazole by 4.34-fold and 1.45-fold, respectively, after 60 min. Thus, laser interferometry can be used for the quantitative analysis of the transport of compounds through eukaryotic cell monolayers, and the resulting parameters can be used to formulate a mathematical description of this process.
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Verkman, A. S. "Development and biological applications of chloride-sensitive fluorescent indicators." American Journal of Physiology-Cell Physiology 259, no. 3 (September 1, 1990): C375—C388. http://dx.doi.org/10.1152/ajpcell.1990.259.3.c375.

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Chloride movement across cell plasma and internal membranes, is of central importance for regulation of cell volume and pH, vectorial salt movement in epithelia, and, probably, intracellular traffic. Quinolinium-based chloride-sensitive fluorescent indicators provide a new approach to study chloride transport mechanisms and regulation that is complementary to 36Cl tracer methods, intracellular microelectrodes, and patch clamp. Indicator fluorescence is quenched by chloride by a collisional mechanism with Stern-Volmer constants of up to 220 M-1. Fluorescence is quenched selectively by chloride in physiological systems and responds to changes in chloride concentration in under 1 ms. The indicators are nontoxic and can be loaded into living cells for continuous measurement of intracellular chloride concentration by single-cell fluorescence microscopy. In this review, the structure-activity relationships for chloride-sensitive fluorescent indicators are described. Methodology for measurement of chloride transport in isolated vesicle and liposome systems and in intact cells is evaluated critically by use of examples from epithelial cell physiology. Future directions for synthesis of tailored chloride-sensitive indicators and new applications of indicators for studies of transport regulation and intracellular ion gradients are proposed.
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Fahlke, Christoph. "Ion permeation and selectivity in ClC-type chloride channels." American Journal of Physiology-Renal Physiology 280, no. 5 (May 1, 2001): F748—F757. http://dx.doi.org/10.1152/ajprenal.2001.280.5.f748.

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Voltage-gated anion channels are present in almost every living cell and have many physiological functions. Recently, a novel gene family encoding voltage-gated chloride channels, the ClC family, was identified. The knowledge of primary amino acid sequences has allowed for the study of these anion channels in heterologous expression systems and made possible the combination of site-directed mutagenesis and high-resolution electrophysiological measurements as a means of gaining insights into the molecular basis of channel function. This review focuses on one particular aspect of chloride channel function, the selective transport of anions through biological membranes. I will describe recent experiments using a combination of cellular electrophysiology, molecular genetics, and recombinant DNA technology to study the molecular basis of ion permeation and selection in ClC-type chloride channels. These novel tools have provided new insights into basic mechanisms underlying the function of these biologically important channels.
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El-Etri, M., and J. Cuppoletti. "Metalloporphyrin chloride ionophores: induction of increased anion permeability in lung epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 3 (March 1, 1996): L386—L392. http://dx.doi.org/10.1152/ajplung.1996.270.3.l386.

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5,10,15,20-Tetraphenyl-21H,23H-porphine manganese (III) chloride [TPPMn(III)] is a positively charged lipophilic anion carrier that is widely used as a Cl- sensor. TPPMn(III) increased anion permeability of cultured mouse lung epithelial (MLE) cells as measured by short-circuit current (ISC) to a level similar to that induced by forskolin analogues. Anion permeability was also studied in cultured human lung epithelial (A549) cells by measurement of the rates of change of fluorescence of the anion sensitive fluorescent dye, 6-methoxy-N-(3-sulfopropyl)quinolinium (SPQ). In these studies, cells were incubated with SPQ in SO2-4- medium, washed free of extracellular SPQ, and then perfused with medium containing anions that are known to quench SPQ fluorescence. The effect of TPPMn(III) on anion transport was then determined either microscopically in single cell studies or using cell monolayers mounted in a front face fluorimeter. TPPMn(III) in the range from 1 to 100 micrograms/ml induced a dose-dependent increase in Br- transport. The half-maximal quenching effect was estimated to be approximate 5 micrograms/ml. TPPMn(III) increased the rates of fluorescence quench of anions by up to fourfold. TPPMn(III) was without effect on -Ca2+-i level in A549 cells as measured with fura 2-AM. This indicates that TPPMn(III) effects were not mediated through effects on Ca+2 -activated Cl- channels, or by compromise of energy metabolism or membrane integrity of the cells. This study suggests that TPPMn(III) and, by extension, other lipophilic Mn(III) or Co(III) derivatives wherein the selectivity of lipophilicity is altered, could increase the anion permeability of biological membranes, and suggests a new approach for treatment of diseases such as cystic fibrosis, where transport of Cl- is defective.
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Jentsch, Thomas J., and Michael Pusch. "CLC Chloride Channels and Transporters: Structure, Function, Physiology, and Disease." Physiological Reviews 98, no. 3 (July 1, 2018): 1493–590. http://dx.doi.org/10.1152/physrev.00047.2017.

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CLC anion transporters are found in all phyla and form a gene family of eight members in mammals. Two CLC proteins, each of which completely contains an ion translocation parthway, assemble to homo- or heteromeric dimers that sometimes require accessory β-subunits for function. CLC proteins come in two flavors: anion channels and anion/proton exchangers. Structures of these two CLC protein classes are surprisingly similar. Extensive structure-function analysis identified residues involved in ion permeation, anion-proton coupling and gating and led to attractive biophysical models. In mammals, ClC-1, -2, -Ka/-Kb are plasma membrane Cl−channels, whereas ClC-3 through ClC-7 are 2Cl−/H+-exchangers in endolysosomal membranes. Biological roles of CLCs were mostly studied in mammals, but also in plants and model organisms like yeast and Caenorhabditis elegans. CLC Cl−channels have roles in the control of electrical excitability, extra- and intracellular ion homeostasis, and transepithelial transport, whereas anion/proton exchangers influence vesicular ion composition and impinge on endocytosis and lysosomal function. The surprisingly diverse roles of CLCs are highlighted by human and mouse disorders elicited by mutations in their genes. These pathologies include neurodegeneration, leukodystrophy, mental retardation, deafness, blindness, myotonia, hyperaldosteronism, renal salt loss, proteinuria, kidney stones, male infertility, and osteopetrosis. In this review, emphasis is laid on biophysical structure-function analysis and on the cell biological and organismal roles of mammalian CLCs and their role in disease.
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Su, Xianbin, Ruihong Li, Ka-Fai Kong, and Jimmy S. H. Tsang. "Transport of haloacids across biological membranes." Biochimica et Biophysica Acta (BBA) - Biomembranes 1858, no. 12 (December 2016): 3061–70. http://dx.doi.org/10.1016/j.bbamem.2016.09.017.

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Fuliński, A. "Noise-stimulated active transport in biological cell membranes." Physics Letters A 193, no. 3 (October 1994): 267–73. http://dx.doi.org/10.1016/0375-9601(94)90595-9.

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McPherson, M. A., D. K. Shori, and R. L. Dormer. "Defective regulation of apical membrane chloride transport and exocytosis in cystic fibrosis." Bioscience Reports 8, no. 1 (February 1, 1988): 27–33. http://dx.doi.org/10.1007/bf01128969.

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A biochemical link is proposed between recent observations on defective regulation of Cl− transport in CF respiratory epithelial cells and studies showing altered biological activity of calmodulin in exocrine glands from CF patients. A consensus is emerging that defective β-adrenergic secretory responsiveness in CF cells is caused by a defect in a regulator protein at a site distal to cyclic AMP formation. Our results indicate that this protein might be a specific calmodulin acceptor protein which modifies the activity of calmodulin in epithelial cells. Alteration in Ca2+/calmodulin dependent regulation of Cl− transport and protein secretion could explain (i) alterations in Ca2+ homeostasis seen in CF, (ii) defective β-adrenergic responses of CF cells, and (iii) the observed inability of cyclic AMP (acting via its specific protein kinase, A-kinase) to open apical membrane Cl− channels in CF epithelial cells. Most of the physiological abnormalities of CF including elevated sweat electrolytes and hyperviscous mucus can be explained on this basis.
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Dissertations / Theses on the topic "Cell membranes. Biological transport. Chlorides"

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Liou, Chen-Chen. "Zinc transport across cell membranes." Thesis, University of Oxford, 1992. http://ora.ox.ac.uk/objects/uuid:176943c5-b0bc-45d7-abe1-3240f6710b54.

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The mechanism of zinc transport has been investigated in red cells from normal humans, lampreys, sheep, sickle cell anaemia patients and in bovine chondrocytes. In all the cell types investigated except for lamprey red cells, zinc transport is mainly via the anion exchanger (band 3), which accounts for over 80% of total measured zinc uptake, when the medium contains no zinc binding ligands. Zinc uptake via the band 3 pathway is stimulated by the presence of bicarbonate (5mM) and inhibited by treatment with DIDS or SITS (10andmu;M). This anion-dependent mechanism represents the major route for zinc transport across the cell membrane in vitro. The presence of the zinc binding ligands albumin and histidine in the media greatly reduced the uptake of zinc via the anion exchanger due to the decrease in free zinc concentration. Histidine, in addition to its chelating effect, shows a specific facilitating effect on zinc uptake in all the cell types. This stimulating effect of histidine was stereospecific (significantly different between L-, and D-histidine) in red cells from normal humans and sickle cell anaemia patients, but not in red cells from lampreys, sheep, and bovine chondrocytes. Evidence from all cell types strongly suggests that the stimulus is due to the cotransport of zinc and histidine via the histidine transport systems, which are system L, and y* in normal human and sickle red cells; a non-stereospecific L-like system in lamprey red cells and bovine chondrocytes; system C or unknown specific histidine transporter in sheep red cells. The amino acid linked zinc uptake may represent a physiologically significant mechanism for zinc transport into cells.
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Hsu, Viktoria R. T. "Ion transport through biological cell membranes : from electro-diffusion to Hodgkin-Huxley via a quasi steady-state approach /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/6755.

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Teh, Ooi-kock. "Characterisation of membrane trafficking mutants in Arabidopsis thaliana." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670105.

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Couch, Richard A. "A new method to study transport across membranes and interfaces using spacially resolved spectroscopy with laser excitation and diode array detection /." The Ohio State University, 1986. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487266011221019.

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Mahey, Rajesh. "Calcium transport and ATP hydrolytic activities in guinea-pig pancreatic acinar plasma membranes." Thesis, University of British Columbia, 1991. http://hdl.handle.net/2429/31044.

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The aim of the present investigation was to determine whether a plasma membrane high affinity Ca²+-ATPase plays an integral role in the maintenance of cytoplasmic free Ca²+ in pancreatic acinar cells. To achieve this, the Ca²+-transport and Ca²+-ATPase activities were characterized and their properties compared. Plasma membranes from guinea-pig pancreatic acini were shown to contain an ATP-dependent high affinity Ca²+-pump and a high affinity Ca²+-dependent ATPase activity. In addition, a low affinity ATPase activity was also observed. The high affinity Ca²+-ATPase activity as well as the Ca²+-transport were found to be dependent on Mg²+, whereas the low affinity ATPase activity appeared to be inhibited by Mg²+. The high affinity ATPase activity was 7-fold greater in magnitude than the Ca²+-transport. Whereas the Ca²+-transport was very specific for ATP as a substrate, the high affinity Ca²+-ATPase showed little specificity for various nucleotide triphosphates. These data would suggest that the Ca²+-transport and the high affinity Ca²+-dependent ATPase in guinea-pig pancreatic acinar plasma membranes may be two distinct activities To further investigate whether the two activities were related, we investigated how the Ca²+-transport and Ca²+-ATPase activities were regulated by intracellular mediators. Regulation of the two activities by calmodulin, cyclic AMP-dependent protein kinase, Protein kinase C and inositol phosphates was investigated. Calmodulin failed to stimulate either activity. In addition, calmodulin antagonists, trifluoperazine and compound 48/80 produced a concentration-dependent inhibition of Ca²+-transport. These data suggested the presence of endogenous calmodulin. Both antagonists failed to influence the Ca²+-dependent ATPase activity. Experiments using boiled extracts from guinea-pig pancreatic acinar plasma membranes and erythrocyte plasma membranes Ca²+-ATPase confirmed the presence of endogenous calmodulin. The catalytic subunit of cyclic AMP-dependent protein kinase stimulated Ca²+ transport, suggesting that cyclic AMP may have a role in the regulation of Ca²+-pump-mediated Ca²+ efflux from pancreatic acini. Ca²+-dependent ATPase activity, on the other hand, was not affected by the catalytic subunit. HA 1004, a specific inhibitor of cAMP-dependent protein kinase, failed to inhibit the Ca²+-transport and Ca²+-dependent ATPase activities. Since, this inhibitor was also ineffective at inhibiting the catalytic-subunit-stimulated Ca²+ transport, it may be concluded that HA 1004 is ineffective in blocking the actions of cAMP-dependent protein kinase in pancreatic acinar plasma membranes. In our studies, purified protein kinase C, the phorbol ester TPA and the diacylglycerol derivative, SA-DG, failed to stimulate the Ca²+-uptake activity. However, these agents produced stimulation of the Ca²+-dependent ATPase activity in the presence of phosphatidylserine. CGP 41 251, a potent and selective inhibitor of protein kinase C, did not inhibit the Ca²+-transport or Ca²+-dependent ATPase activities. These observations suggest that protein kinase C may not be involved in the regulation of the plasma membrane Ca²+-pump in guinea-pig pancreatic acinar cells. These results also point to another difference between Ca²+-transport and the Ca²+-ATPase activities in guinea-pig pancreatic acinar plasma membranes. Neither inositol trisphosphate nor inositol tetrakisphosphate produced a statistically significant effect on Ca²+-uptake, suggesting that IP₃- and/or IP₄-mediated Ca²+ releasing pathways may not operate in the isolated guinea-pig pancreatic acinar plasma membrane vesicles. In summary, the results presented here provide evidence to suggest that the high affinity Ca²+-ATPase is not the biochemical expression of plasma membrane Ca²+-transport in panreatic acini. Our results imply a role for calmodulin and cAMP-dependent protein kinase, but not protein kinase C, in the regulation of Ca²+ efflux from pancreatic acinar cells.
Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
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Manrique, Blanco Thibaldo Javier. "The partial purification and characterization of a soluble activator for the sodium adenosinetriphosphatase from rat cerebral cortex and the effect of cholinergic agents." Scholarly Commons, 1986. https://scholarlycommons.pacific.edu/uop_etds/2117.

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Fervenza, Fernando Custodio. "Membrane transport abnormalities in patients with renal failure." Thesis, University of Oxford, 1990. http://ora.ox.ac.uk/objects/uuid:9c345fc7-7e25-4f47-b41d-feddb8bc5cb7.

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The possibility that changes in membrane transport systems may contribute to the pathophysiology of the uraeraic syndrome has not been extensively studied. This thesis presents a study of eight erythrocyte membrane transport systems, namely the Na/K pump, the amino acid systems y+, ASC, gly, L and T, the nucleoside and choline transporters. The results indicate that, compared to normal controls, K+ flux through the Na/K pump was reduced in chronic renal failure patients (CRF), on haemodialysis (HD), and on continuous ambulatory peritoneal dialysis (CAPD), but was normal in functional transplant (FT) patients' erythrocytes. The number of Na/K pumps per erythrocyte was decreased in CRF and CAPD but showed no differences between HD, FT and Normal controls. The mean turnover rate per pump site was reduced in patients on HD, whereas other groups were not significantly different from controls. Cross-incubation experiments suggest that the lowered pump flux seen in the HD group was due to plasma factors since reversibility of the defect was achieved when those cells were incubated in normal plasma. The defect was completely reversed with a successful transplant. Erythrocytes from haemodialysis patients exhibited an increased uptake of L-lysine through the y+ system. The uptake of L-serine was decreased and the affinity of the ASC system for L-serine was increased in these patients compared with controls. The glycine transporter showed a significant increase in affinity for glycine. The flux of L-leucine and L-tryptophan showed no differences from control cells. Erythrocyte membrane transport of uridine was similar in normal control cells and in those obtained from uraemic patients. Choline influx rates were significantly increased and affinity of the transporter for choline reduced in dialysis patients' erythrocytes. Renal transplant and CRF patients showed variable influx rates which gave a significant negative correlation with creatinine clearance. These results show that there are selective abnormalities in some membrane transport system of the erythrocyte in patients with renal failure. The mechanism and possible significance of these changes are discussed.
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Spelbrink, Robert G. "The role of the yeast GRD20 protein in membrane trafficking and actin organization /." free to MU campus, to others for purchase, 2000. http://wwwlib.umi.com/cr/mo/fullcit?p9974686.

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Godenir, Nicole. "Membrane shedding in kidney (MDCK) cells as revealed by covalent markers during quantification of endocytosis and transcytosis." Master's thesis, University of Cape Town, 1991. http://hdl.handle.net/11427/27141.

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Membrane traffic in polarised cells was investigated by growing Madin-Darby canine kidney (MOCK) cells on ·permeable polycarbonate filter supports which allowed access to both sides of the cell monolayer. Membrane glycoconjugates on the apical and basolateral cell surfaces were labelled enzymatically with ³H- and ¹⁴C-galactose, respectively, to provide covalent membrane markers. Experiments were done to quantitate membrane traffic during endocytosis at the respective plasma membrane domains and that due to transcytosis. Internalized label was quantitatively distinguished from label on the respective cell surface by its resistance to removal by glycosidases.
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Eller, Leah Renee Sessler Jonathan L. "Anions in hydrophobic environments liquid-liquid extraction of sulfate and chloride, and membrane transport of chloride /." 2005. http://repositories.lib.utexas.edu/bitstream/handle/2152/1542/ellerl50469.pdf.

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Books on the topic "Cell membranes. Biological transport. Chlorides"

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R, Lieb W., ed. Transport and diffusion across cell membranes. Orlando: Academic Press, 1986.

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J, Garrahan Patricio, ed. The Ca2+ pump of plasma membranes. Boca Raton, Fla: CRC Press, 1986.

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Winkle, Lon J. Van. Biomembrane transport. San Diego, Calif: Academic Press, 1999.

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Winkle, Lon J. Van. Biomembrane transport. San Diego: Academic Press, 1999.

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Biomembrane transport. San Diego, Calif: Academic, 1999.

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Winkle, Lon J. Van. Biomembrane transport. San Diego, Calif: Academic, 1999.

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J, Dainty, ed. Plant membrane transport: The current position. Amsterdam: Elsevier, 1989.

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Keränen, Sirkka, and Jussi Jäntti. Regulatory mechanisms of intracellular membrane transport. Berlan: Springer-Verlag, 2004.

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Society of General Physiologists. (40th 1986 Marine Biological Laboratory). Cell calcium and the control of membrane transport: A symposium held at the Marine Biological Laboratory, Woods Hole, Mass., 3-7 Sept., 1986. New York: Rockefeller University Press, 1987.

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Protein secretion: A critical analysis of the vesicle model. New York: J. Wiley, 1985.

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Book chapters on the topic "Cell membranes. Biological transport. Chlorides"

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Friedman, Morton H. "Models of Transport Across Cell Membranes." In Principles and Models of Biological Transport, 1–34. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-79240-8_7.

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Friedman, Morton H. "Models of Transport Across Cell Membranes." In Principles and Models of Biological Transport, 134–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-662-02467-6_6.

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Sarkadi, B., and G. Gárdos. "Calcium-Induced Potassium Transport in Cell Membranes." In The Enzymes of Biological Membranes, 193–234. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4601-2_5.

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Kulbacka, Julita, Anna Choromańska, Joanna Rossowska, Joanna Weżgowiec, Jolanta Saczko, and Marie-Pierre Rols. "Cell Membrane Transport Mechanisms: Ion Channels and Electrical Properties of Cell Membranes." In Transport Across Natural and Modified Biological Membranes and its Implications in Physiology and Therapy, 39–58. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56895-9_3.

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Tarek, Mounir. "Atomistic Simulations of Electroporation of Model Cell Membranes." In Transport Across Natural and Modified Biological Membranes and its Implications in Physiology and Therapy, 1–15. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56895-9_1.

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Saczko, Jolanta, Olga Michel, Agnieszka Chwiłkowska, Ewa Sawicka, Justyna Mączyńska, and Julita Kulbacka. "Estrogen Receptors in Cell Membranes: Regulation and Signaling." In Transport Across Natural and Modified Biological Membranes and its Implications in Physiology and Therapy, 93–105. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56895-9_6.

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Azan, Antoine, Florian Gailliègue, Lluis M. Mir, and Marie Breton. "Cell Membrane Electropulsation: Chemical Analysis of Cell Membrane Modifications and Associated Transport Mechanisms." In Transport Across Natural and Modified Biological Membranes and its Implications in Physiology and Therapy, 59–71. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56895-9_4.

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Subczynski, Witold Karol, Justyna Widomska, and Laxman Mainali. "Factors Determining the Oxygen Permeability of Biological Membranes: Oxygen Transport Across Eye Lens Fiber-Cell Plasma Membranes." In Advances in Experimental Medicine and Biology, 27–34. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55231-6_5.

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Gibot, Laure, Muriel Golzio, and Marie-Pierre Rols. "How Imaging Membrane and Cell Processes Involved in Electropermeabilization Can Improve Its Development in Cell Biology and in Clinics." In Transport Across Natural and Modified Biological Membranes and its Implications in Physiology and Therapy, 107–18. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56895-9_7.

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Jakutavičiūtė, Milda, Paulius Ruzgys, Mindaugas Tamošiūnas, Martynas Maciulevičius, and Saulius Šatkauskas. "Physical Methods for Drug and Gene Delivery Through the Cell Plasma Membrane." In Transport Across Natural and Modified Biological Membranes and its Implications in Physiology and Therapy, 73–92. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56895-9_5.

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Conference papers on the topic "Cell membranes. Biological transport. Chlorides"

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Grattoni, Alessandro, Xuewu Liu, Zongxing Wang, Jaskaran Gill, Arturas Ziemys, and Mauro Ferrari. "Electrokinetic Transport of Molecules Through Nanochanneled Membranes." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13236.

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Our research group was the first one to microfabricate and demonstrate nano-channels in silicon membranes (1, 2). We employed nano-channeled chips to provide immuno-isolation for cell transplantation towards the treatment of diabetes (3), for biomolecular separation (4), and for the controlled passive and active release of drug molecules from implanted capsules (5). We showed that the constraints placed upon molecular agitation in nano-channels affected their concentration-driven transport kinetics (6, 7). A zero-order passive release of biological molecules was achieved, by the rational tailoring of nano-channels dimensions. This achievement allowed releasing of a constant amount of drugs over a long period of time. However, the development and optimization of many drug therapies require long-term drug delivery with controlled but variable dosage using miniaturized systems (8). Moreover, application such as drug release from implanted devices requires tight operational control, of regulatory agency caliber. We have engaged in the development and characterization of elecroosmotic nano-channels membranes, and present our results in this communication. These include the influence of the drug release rate on nanochannel size, membrane configuration, and applied voltage.
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Rosengarten, Gary. "Can We Learn From Nature to Design Membranes? The Intricate Pore Structure of the Diatom." In ASME 2009 7th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2009. http://dx.doi.org/10.1115/icnmm2009-82148.

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Membranes are ubiquitous functional elements used in separation processes. An ideal membrane will stop certain species penetrating it while having excellent transport properties for others. Membranes are used in synthetic systems such as fuel cells and desalination plants, but are also formed naturally in biological systems. For example all cells use a membrane to contain the cellular contents, while allowing transport of nutrients though the cell wall. I will present our recent work on examining diatoms, which are unicellular algae that grow in water. They have a self assembled silica membrane wall with a regular array of nanopores whose function is very poorly understood. I will outline the unique structure of the pores and our experimental work on understanding their structure to help develop membranes with better performance.
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3

Guan, Yingxue, Aili Zhang, and Lisa X. Xu. "Study of Interaction Energy Between Nanoparticles and Cell Membrane." In 2010 14th International Heat Transfer Conference. ASMEDC, 2010. http://dx.doi.org/10.1115/ihtc14-23187.

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Applications of nanoparticles in the bio-medical field like nano-medicine, molecular imaging probes, fluorescence marker, gene carriers, are developing quickly owing to the unique characteristics of nanoparticles. Among these applications, the interaction of nano-particles with the living cells is of critical importance. The complex chemical properties and biological activities of the particles bring about undesirable cytotoxic potentials and special cell internalization. According to previous studies, the cell uptake kinetics of nanoparticles mainly depend on the concentration difference between extracellular and intracellular nanoparticles, the surface electric charge of the nanoparticle, and the active transport of the cell. For example, Ginzburg’s thermodynamic simulation and Park’s three-dimensional phase-field model quantitatively explain the transitions in membrane morphology after exposure to nanoparticles with different surface charge, respectively. However, recent studies have shown that the gold nanoparticles coated with hydrophilic and hydrophobic functional groups with the same concentration but in different orders, completely exhibit quite different intrusion ability at 4°C when the active transport of the cell is greatly inhibited. The results suggest that the interaction energy of nanoparticles and cell membranes may be another driving force for the nanopartcles’ mass transfer across the cell membrane. Thus, in this paper, the interaction energy of the differently coated nanoparticles (P) with cell membrane (M) in water (W) is studied theoretically and results are used to explain the former experimental findings.
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Banneyake, B. M. R. U., and Debjyoti Banerjee. "Microfluidic Device for Synthesis of Lipid Bi-Layers." In ASME 2008 Fluids Engineering Division Summer Meeting collocated with the Heat Transfer, Energy Sustainability, and 3rd Energy Nanotechnology Conferences. ASMEDC, 2008. http://dx.doi.org/10.1115/fedsm2008-55219.

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Lipid bi-layers are ubiquitous components of biological cells — and are found in variety of cell components ranging from cell membranes to membranes of organelles inside the cells. In biological membranes, lipid bi-layer membranes carry membrane proteins, which serve as single channel nanopores that are used to study transport of proteins and characterize the properties of proteins. However, lipid bi-layers have very short half lives, which are usually less than an hour. The lipid bi-layers are usually obtained by physico-chemical interactions between a lipid containing organic solvent, an aqueous buffer solution and a hydrophobic surface. We have developed a continuous flow through microfluidic device using pressure driven flow (by means of a tandem syringe pump system) for synthesis of lipid bi-layers. The microfluidic device consists of two glass substrates with micro-channels and microchambers microfabricated using photolithography and wet glass etching. The microchannels in each substrate is in the form of “+” shape and form a mirror image of each other. A Teflon sheet (∼200 microns thickness) is sandwiched between the glass substrates with a ∼200 microns diameter hole etched in the center to communicate with the two sets of microchannels. A lipid solution in an organic solvent (Pentane) and KCl buffer solution are alternately flown through the legs of the microchannel. The conductivity of the buffer is monitored using a current amplifier. The formation of the lipid bi-layer is confirmed by monitoring the resistivity and the impedance to high frequency electrical oscillations. The flow rate in the microfluidic device is optimized to obtain the lipid bi-layer.
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