Relevant bibliographies by topics / Osmotic cell swelling

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Osmotic cell swelling'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 February 2022

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Journal articles on the topic "Osmotic cell swelling"

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Lepple-Wienhues, Albrecht, Ildikò Szabò, Tilmann Laun, Nubia Kristen Kaba, Erich Gulbins, and Florian Lang. "The Tyrosine Kinase p56lck Mediates Activation of Swelling-induced Chloride Channels in Lymphocytes." Journal of Cell Biology 141, no. 1 (April 6, 1998): 281–86. http://dx.doi.org/10.1083/jcb.141.1.281.

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Osmotic cell swelling activates Cl− channels to achieve anion efflux. In this study, we find that both the tyrosine kinase inhibitor herbimycin A and genetic knockout of p56lck, a src-like tyrosine kinase, block regulatory volume decrease (RVD) in a human T cell line. Activation of a swelling-activated chloride current (ICl−swell) by osmotic swelling in whole-cell patch-clamp experiments is blocked by herbimycin A and lavendustin. Osmotic activation of ICl−swell is defective in p56lck-deficient cells. Retransfection of p56lck restores osmotic current activation. Furthermore, tyrosine kinase activity is sufficient for activation of ICl−swell. Addition of purified p56lck to excised patches activates an outwardly rectifying chloride channel with 31 pS unitary conductance. Purified p56lck washed into the cytoplasm activates ICl−swell in native and p56lck-deficient cells even when hypotonic intracellular solutions lead to cell shrinkage. When whole-cell currents are activated either by swelling or by p56lck, slow single-channel gating events can be observed revealing a unitary conductance of 25–28 pS. In accordance with our patch-clamp data, osmotic swelling increases activity of immunoprecipitated p56lck. We conclude that osmotic swelling activates ICl−swell in lymphocytes via the tyrosine kinase p56lck.
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Tomassen, Sebastian F. B., Thea van der Wijk, Hugo R. de Jonge, and Ben C. Tilly. "Activation of phospholipase D by osmotic cell swelling." FEBS Letters 566, no. 1-3 (May 4, 2004): 287–90. http://dx.doi.org/10.1016/j.febslet.2004.04.063.

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Häussinger, D., C. Hallbrucker, N. Saha, F. Lang, and W. Gerok. "Cell volume and bile acid excretion." Biochemical Journal 288, no. 2 (December 1, 1992): 681–89. http://dx.doi.org/10.1042/bj2880681.

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The interaction between cell volume and taurocholate excretion into bile was studied in isolated perfused rat liver. Cell swelling due to hypo-osmotic exposure, addition of amino acids or insulin stimulated taurocholate excretion into bile and bile flow, whereas hyperosmotic cell shrinkage inhibited these. These effects were explained by changes in Vmax of taurocholate excretion into bile: Vmax. increased from about 300 to 700 nmol/min per g after cell swelling by 12-15% caused by either hypo-osmotic exposure or addition of amino acids under normo-osmotic conditions. Steady-state taurocholate excretion into bile was not affected when the influent K+ concentration was increased from 6 to 46 mM or decreased to 1 mM with iso-osmoticity being maintained by corresponding changes in the influent Na+ concentration. Replacement of 40 mM-NaCl by 80 mM-sucrose decreased taurocholate excretion into bile by about 70%; subsequent hypo-osmotic exposure by omission of sucrose increased taurocholate excretion to 160%. Only minor, statistically insignificant, effects of aniso-osmotic cell volume changes on the appearance of bolus-injected horseradish peroxidase in bile were observed. Taurocholate (400 microM) exhibited a cholestatic effect during hyperosmotic cell shrinkage, but not during hypo-osmotic cell swelling. Both taurocholate and tauroursodeoxycholate increased liver cell volume. Tauroursodeoxycholate stimulated taurocholate (100 microM) excretion into bile. This stimulatory effect was strongly dependent on the extent of tauroursodeoxycholate-induced cell swelling. During continuous infusion of taurocholate (100 microM) further addition of tauroursodeoxycholate at concentrations of 20, 50 and 100 microM increased cell volume by 10, 8 and 2% respectively, in parallel with a stimulation of taurocholate excretion into bile by 29, 27 and 9% respectively. There was a close relationship between the extent of cell volume changes and taurocholate excretion into bile, regardless of whether cell volume was modified by tauroursodeoxycholate, amino acids or aniso-osmotic exposure. The data suggest that: (i) liver cell volume is one important factor determining bile flow and biliary taurocholate excretion; (ii) swelling-induced stimulation of taurocholate excretion into bile is probably not explained by alterations of the membrane potential; (iii) bile acids modulate liver cell volume; (iv) taurocholate-induced cholestasis may depend on cell volume; (v) stimulation of taurocholate excretion into bile by tauroursodeoxycholate can largely be explained by tauroursodeoxycholate-induced cell swelling.
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Häussinger, D., C. Hallbrucker, S. vom Dahl, F. Lang, and W. Gerok. "Cell swelling inhibits proteolysis in perfused rat liver." Biochemical Journal 272, no. 1 (November 15, 1990): 239–42. http://dx.doi.org/10.1042/bj2720239.

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Exposure of isolated single-pass-perfused rat liver to hypo-osmotic media resulted in liver cell swelling and an inhibition of release of branched-chain amino acids. Similarly, cell swelling inhibited [3H]leucine release from perfused livers from rats in which liver proteins were prelabelled in vivo by intraperitoneal injection of L-[4,5-3H]leucine 16-20 h before the experiment. The effects of cell swelling on [3H]leucine release were fully reversible. [3H]Leucine release was also inhibited when cell swelling was induced by addition of glutamine (0.5-2 mM). There was a close relationship between the inhibition of [3H]leucine release and the degree of liver cell swelling, regardless of whether cell swelling was induced by hypo-osmotic perfusion or addition of glutamine. The data suggest that the known anti-proteolytic effect of glutamine is in large part due to glutamine-induced hepatocyte swelling.
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Ahkong, Q. F., and J. A. Lucy. "Localized osmotic swelling and cell fusion in erythrocytes: possible implications for exocytosis." Journal of Cell Science 91, no. 4 (December 1, 1988): 597–601. http://dx.doi.org/10.1242/jcs.91.4.597.

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Factors that govern the experimentally induced fusion of erythrocytes with one another may generally be relevant to whether or not osmotic forces drive membrane fusion in exocytosis because, under appropriate conditions, osmotic swelling can drive the fusion of erythrocytes. It is now reported that these cells fuse when they are subjected to osmotic swelling caused by exposure to small permeant molecules. The behaviour of erythrocytes in fusion induced by treatment with a concentrated solution of high molecular weight poly(ethylene glycol) (PEG) is also of specific interest in relation to exocytosis because the haemoglobin of erythrocytes that are dehydrated by concentrated solutions of the polymer may be regarded as a model for the tightly packed, dehydrated contents of the granules in secretory cells. We have observed that, under certain conditions of rehydration, the swelling of aqueous microdroplets between the dehydrated haemoglobin and the plasma membrane is closely associated with the fusion of partially rehydrated but still shrunken, PEG-treated erythrocytes. It is therefore apparent that osmotic forces, acting locally at the sites of aqueous microdroplets, can drive the fusion of membranes that encapsulate a dehydrated, concentrated protein, even though gross osmotic swelling at the level of the light microscope is absent. This finding is consistent with the possibility that osmotic swelling may play a role in exocytotic membrane fusion if it is restricted to a small zone immediately under the granule membrane.
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van der Wijk, Thea, Sebastian F. B. Tomassen, Adriaan B. Houtsmuller, Hugo R. de Jonge, and Ben C. Tilly. "Increased Vesicle Recycling in Response to Osmotic Cell Swelling." Journal of Biological Chemistry 278, no. 41 (July 18, 2003): 40020–25. http://dx.doi.org/10.1074/jbc.m307603200.

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Barfod, Elisabeth T., Ann L. Moore, Benjamin G. Van de Graaf, and Steven D. Lidofsky. "Myosin light chain kinase and Src control membrane dynamics in volume recovery from cell swelling." Molecular Biology of the Cell 22, no. 5 (March 2011): 634–50. http://dx.doi.org/10.1091/mbc.e10-06-0514.

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The expansion of the plasma membrane, which occurs during osmotic swelling of epithelia, must be retrieved for volume recovery, but the mechanisms are unknown. Here we have identified myosin light chain kinase (MLCK) as a regulator of membrane internalization in response to osmotic swelling in a model liver cell line. On hypotonic exposure, we found that there was time-dependent phosphorylation of the MLCK substrate myosin II regulatory light chain. At the sides of the cell, MLCK and myosin II localized to swelling-induced membrane blebs with actin just before retraction, and MLCK inhibition led to persistent blebbing and attenuated cell volume recovery. At the base of the cell, MLCK also localized to dynamic actin-coated rings and patches upon swelling, which were associated with uptake of the membrane marker FM4-64X, consistent with sites of membrane internalization. Hypotonic exposure evoked increased biochemical association of the cell volume regulator Src with MLCK and with the endocytosis regulators cortactin and dynamin, which colocalized within these structures. Inhibition of either Src or MLCK led to altered patch and ring lifetimes, consistent with the concept that Src and MLCK form a swelling-induced protein complex that regulates volume recovery through membrane turnover and compensatory endocytosis under osmotic stress.
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Okada, Yasunobu, Akihiro Hazama, Akira Hashimoto, Yoshio Maruyama, and Machiko Kubo. "Exocytosis upon osmotic swelling in human epithelial cells." Biochimica et Biophysica Acta (BBA) - Biomembranes 1107, no. 1 (June 1992): 201–5. http://dx.doi.org/10.1016/0005-2736(92)90348-p.

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Granitzer, Marita, Peter Bakos, Wolfram Nagel, and Jean Crabbé. "Osmotic swelling and membrane conductances in A6 cells." Biochimica et Biophysica Acta (BBA) - Biomembranes 1110, no. 2 (October 1992): 239–42. http://dx.doi.org/10.1016/0005-2736(92)90365-s.

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Maloney, John M., and Krystyn J. Van Vliet. "Chemoenvironmental modulators of fluidity in the suspended biological cell." Soft Matter 10, no. 40 (2014): 8031–42. http://dx.doi.org/10.1039/c4sm00743c.

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Dissertations / Theses on the topic "Osmotic cell swelling"

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Hall, James Anthony. "Swelling-activated transport of diverse solutes in mammalian cells." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320647.

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Befroy, Douglas Eugene. "Osmotic shock : modulation of contractile function, pH←i and ischaemic damage in the perfused guinea-pig heart." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326024.

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Deng, Wu. "ROLE OF ENDOTHELIN-1 IN THE REGULATION OF THE SWELLING-ACTIVATED Cl- CURRENT IN ATRIAL MYOCYTES." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/12.

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Swelling-activated Cl- current (ICl,swell) is an outwardly rectifying Cl- current that influences cardiac electric activities and acts as a potential effector of mechanoelectrical feedback that antagonizes the effects of stretch-activated cation channels. Persistent activation of ICl,swell has been observed in multiple models of cardiovascular diseases. Previously we showed that angiotensin II (AngII) signaling and reactive oxygen species (ROS) produced by NADPH oxidase (NOX) are involved in the activation of ICl, swell by both beta1-integrin stretch and osmotic swelling. Because endothelin-1 (ET-1) is a potential downstream mediator of AngII and ETA receptor blockade abrogates AngII-induced ROS generation, we studied how ET-1 signaling regulates ICl,swell and the relationship between AngII and ET-1 signaling. Under isosmotic conditions, ET-1 elicited an outwardly rectifying Cl- current that was fully blocked by the highly selective ICl,swell inhibitor DCPIB and by osmotic shrinkage. Selective ETA blockade (BQ123), but not ETB blockade (BQ788), fully suppressed the ET-1-induced current. ET-1-induced ICl,swell was abolished by blockade of EGFR kinase (AG1478) and PI-3K inhibitors (LY294002 and wortmannin), which also suppress beta1-integrin stretch- and swelling-induced ICl,swell. ET-1-induced ICl,swell was abrogated by ebselen, a membrane-permeant glutathione peroxidase mimetic that dismutates H2O2 to H2O, suggesting that ROS were required intermediates in ET-1-induced activation of ICl,swell. Both NOX and mitochondria are important sources of ROS in cardiomyocytes. Blocking NOX with apocynin or mitochondrial complex I with rotenone both completely suppressed ET-1-induced ROS generation and activation of ICl,swell, indicating that ROS from both NOX and mitochondria were required to activate ICl,swell, and complete block by inhibitors of either ROS source suggests mitochondrial and NOX must act in series rather than in parallel. ICl,swell elicited by antimycin A, which stimulates superoxide production by mitochondrial complex III, was insensitive to NOX inhibitor apocynin and the NOX fusion peptide inhibitor gp91ds-tat. Activation of ICl,swell induced by diazoxide, which stimulates mitochondrial ROS production by opening mitochondrial KATP channels, was not affected by gp91ds-tat. These data suggests that mitochondrial ROS is downstream from NOX in the regulation of ICl,swell. Mitochondrial ROS production that is enhanced by NOX ROS is likely to be responsible for the activation of ICl,swell by ET-1. In order to determine the role of ERK in the proposed signaling pathway that regulates ICl,swell, we examined the effect of ERK inhibitors (PD 98059 and U0216) on the activation of ICl,swell elicited by ET-1, EGF, and H2O2. ERK inhibitors partially blocked ET-1-induced ICl,swell but fully inhibited activation of ICl,swell in response to EGF. However, ERK inhibitors did not affect ICl,swell elicited by exogenous H2O2. We also established the the relationship of ET-1 to AngII and osmotic swelling in the regulation of ET-1 ICl,swell. ETA blockade abolished ICl,swell elicited by both AngII and osmotic swelling, whereas AT1 blockade did not effect ET-1-induced ICl,swell, suggesting that ET-1 signaling is downstream from AngII and osmotic swelling. HL-1 cell is a murine atrial cell line that retain phenotypic characteristics of adult cardiomyocytes. We showed that osmotic swelling and ET-1 turned on DCPIB-sensitive outwardly rectifying Cl- current in HL-1 cells with both physiological and symmetrical Cl- gradients. The swelling-induced current was suppressed by gp91ds-tat and rotenone but insensitive to apocynin. Blockade of ETA receptor (BQ123) and NOX (gp91ds-tat) completely inhibited ET-1-induced ICl,swell in HL-1 cells. These data indicate that ICl,swell is present in HL-1 cell and regulated by similar mechanisms as in native cells. Finally, we confirmed the production of ROS by ET-1 signaling by flow cytometry of HL-1 cells using the nominally H2O2-selective fluorescent probe C H2DCFDA-AM. Exposure to ET-1 increased ROS production, as did H2O2, a positive control. ET-1-induced ROS production was fully suppressed by both gp91ds-tat and rotenone. HL-1 cell ROS production also was stimulated by the mitochondrial complex III inhibitor antimycin A, and antimycin A-induced ROS production was blocked by rotenone but not by gp91ds-tat. These data suggest that ET-1 ETA receptor signaling elicits ICl,swell by sequentially stimulating ROS production by NOX and mitochondria. ETA receptor signaling is down stream from AngII in the osmotic swelling-induced activation of ICl,swell and is upstream from EGFR kinase and PI-3K. Endothelin signaling is likely to be an important means of activating ROS production and ICl,swell in a variety of cardiovascular diseases.
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Wen-ChenShih and 施玟甄. "Osmotic swelling induces the differential cytoskeleton remodeling between normal and cancer cells." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/10413534112883880270.

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碩士
國立成功大學
藥理學研究所
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Hypotonicity-induced cell swelling is characterized by a modulation of cytoskeletal architecture and activation of membrane ion transport, which result in regulatory volume decrease. Little is known about the possible signal differences involved in volume-regulated cytoskeletal dynamics between normal and cancer cells. By the models of ovarian and cervical cancer, my thesis aims to elucidate the dynamics of F-actin and actin-associated proteins in osmotic swelling of normal and cancer cells. In response to hypotonicity, ovarian and cervical cancer cells swelled and an obvious alteration in cellular architecture occurred. The actin cytoskeleton was remodeled to counteract cell swelling, which consisted of the reduction of the ventral stress fibers and the formation of cortical actin and F-actin patches at the cell border. In the isotonic condition, ezrin, a member of ERM family, mainly distributed in the cytosol. Hypotonicity induced the recruitment of ezrin as well as phospho-FAK Tyr397 to F-actin-enriched membrane protrusions. The converse alterations for actin network and ezrin recruitment were observed in parallel with surface area changes. Interestingly, hypotonicity-induced the interaction of F-actin, ezrin, and phospho-FAK Tyr397 was inhibited by the ERK1/ERK2 inhibitor (50 μM PD98059). These data indicate that hypotonicity-activated MAPK pathway (ERK1/ERK2) is involved the interaction between F-actin, ezrin, and phospho-FAK Tyr397. In contrast, normal epithelial cells of cervix and ovary showed poor adjustment of surface area change, no obvious F-actin remodeling, and no active focal adhesions in response to hypotonicity. Thus, this study demonstrates hypotonicity induces the different osmo-sensitive cytoskeletal remodeling between normal and cancer cells.
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Book chapters on the topic "Osmotic cell swelling"

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Janmey, Paul A., C. Casey Cunningham, George F. Oster, and Thomas P. Stossel. "Cytoskeletal Networks and Osmotic Pressure in Relation to Cell Structure and Motility." In Mechanics of Swelling, 333–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84619-9_17.

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Evans, Evan. "Osmotic Swelling-Pressurization-Rupture of Isolated Cells and Disjoining of Cell Aggregates in Soft Tissues." In Mechanics of Swelling, 293–313. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84619-9_15.

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Dong, C., J. You, S. Aznavoorian, D. Savarese, and L. A. Liotta. "Actin Polymerization and Gel Osmotic Swelling in Tumor Cell Pseudopod Formation." In Cell Mechanics and Cellular Engineering, 515–33. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4613-8425-0_28.

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Boersma, L., Yongsheng Feng, and Xiaomei Li. "Osmotic Adjustment in Plant Cells Exposed to Drought and Temperature Stress: Can a Cause and Effect Hypothesis be Formulated and Tested?" In Mechanics of Swelling, 143–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84619-9_6.

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Ayee, Manuela A. A., and Irena Levitan. "Membrane Stiffening in Osmotic Swelling." In Cell Volume Regulation, 97–123. Elsevier, 2018. http://dx.doi.org/10.1016/bs.ctm.2018.07.003.

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Chao, Pei-Chuan, Mettupalayam Sivaselvan, and Frederick Sachs. "Cytoskeletal Contribution to Cell Stiffness Due to Osmotic Swelling; Extending the Donnan Equilibrium." In Cell Volume Regulation, 83–96. Elsevier, 2018. http://dx.doi.org/10.1016/bs.ctm.2018.07.002.

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Maynard Smith, John, and Eors Szathmary. "The origin of eukaryotes." In The Major Transitions in Evolution. Oxford University Press, 1997. http://dx.doi.org/10.1093/oso/9780198502944.003.0012.

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The basic structures of a bacterial and a eukaryotic cell are shown in Fig. 8.1. The differences whose origins call for an explanation are as follows: • The bacterial cell has a rigid outer cell wall, usually made of the peptidoglycan, murein. In eukaryotes, the rigid cell wall is not universal, and cell shape is maintained primarily by an internal cytoskeleton of filaments and microtubules. • Eukaryotic cells have a complex system of internal membranes, including the nuclear envelope, endoplasmic reticulum and lysosomes. • Bacteria have a single circular chromosome, attached to the rigid outer cell wall. In eukaryotes, linear chromosomes are contained within a nuclear envelope, which separates transcription from translation: communication between nucleus and cytoplasm is via pores in the nuclear envelope. • Eukaryotes have a complex cytoskeleton. The actomyosin system powers cell division, phagocytosis, amoeboid motion and the overall contractility to resist osmotic swelling. Microtubules and the associated motor proteins (kinesin, dynein and dynamin) ensure the accurate segregation of chromosomes in mitosis, ciliary motility and the movement of transport vesicles. Intermediate filaments form the structural basis for the association of the endomembranes and nuclear-pore complexes with the chromatin to form the nuclear envelope, while other intermediate filaments help to anchor the nucleus in the cytoplasm. One crucial difference between prokaryotes and most eukaryotes has been omitted from Fig. 8.1: this is the presence of mitochondria, and, in plants and algae, of chloroplasts. The reason for the omission is that, on the scenario for eukaryote origins that seems to us most plausible, these intracellular organelles originated later in time than the structures shown in the figure. The differences between these cell types justifies the recognition of two empires of life (above the kingdom level): Bacteria and Eukaryota (Cavalier-Smith, 199la; Table 8.1). (It is interesting that this taxonomic rank was recognized by Linnaeus.) Within each of the empires, there are two major categories: Bacteria consist of the kingdoms Eubacteria and Archaebacteria, and Eukaryota are divided into the superkingdoms Archaezoa and Metakaryota. The justification for these divisions is as follows. The Archaebacteria, in contrast to the Eubacteria, never have murein cell walls, and their single cell membrane contains isoprenoidal ether rather than acyl ester lipids.
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Conference papers on the topic "Osmotic cell swelling"

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Powell, Tracy A., Rouzbeh Amini, Alina Oltean, Vincent A. Barnett, Kevin D. Dorfman, Yoav Segal, and Victor H. Barocas. "Elasticity of the Lens Capsule as Measured by Osmotic Swelling." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19487.

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Basement membranes are planar extracellular matrices ubiquitous within tissues and serve roles in the organization, support and regulation of resident cell populations. The ocular lens capsule is experimentally accessible accounting for its wide use as a model in studies of basement membrane mechanics [1–3]. Optical tracking of passive osmotic swelling, unlike previously employed methods of determining the elasticity of the lens capsule, involves minimal manipulation of the lens, which is desirable when using smaller animal models, such as the mouse.
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Bian, Liming, Terri Ann N. Kelly, Eric G. Lima, Gerard A. Ateshian, and Clark T. Hung. "Finite Element Modeling of Osmotic Swelling in Tissue-Engineered Cartilage." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192368.

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Proteoglycans and Type II collagen represent the two major biochemical constituents of articular cartilage. Collagen fibrils in cartilage resist the swelling pressure that arises from the fixed charges of the glycosaminoglycans (GAGs), and together they give rise to the tissue’s unique load bearing properties. As articular cartilage exhibits a poor intrinsic healing capacity, there is significant research in the development of cell-based therapies for cartilage repair. In some of our tissue engineering studies, we have observed a phenomenon where chondrocyte-seeded hydrogel constructs display cracking in their central regions after significant GAG content has been elaborated in culture. A theoretical analysis was performed to gain greater insights into the potential role that the spatial distribution of proteoglycan and collagen may play in this observed response.
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Oungoulian, Sevan R., Kelvin Chan, Jason Barritt, Casey A. McDonald, Alan B. Copperman, David Elad, and Gerard A. Ateshian. "Influence of Zona Pellucida Area Expansion Stiffness on the Passive Response of Oocytes to Osmotic Loading." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53826.

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The zona pellucida (ZP) is a thick glycoprotein shell surrounding the mammalian egg cell (oocyte) that regulates spermatozoa access during fertilization and protects the zygote during early embryonic development [1]. Hardening of the zona pellucida over the cell fertilization cycle is a well-recognized phenomenon and has been investigated using contact methods to measure shear and bending elasticity from indentation and micropipette aspiration [2, 3]. However, the area elasticity of the ZP, which provides resistance to cell swelling under variable osmotic environments, has not yet been reported. A recently devised theoretical model [4] suggests that the ZP area expansion modulus may be determined through non-contact hypo-osmotic loading of the oocyte. If successful, this method may be suited for implementation by practicing fertility health professionals during routine manipulation.
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Hulme, Paul, Simon Chi, Dominic Young, John Matyas, and Neil A. Duncan. "Enzymatic Digestion Technique Influences Regulatory Volume Decrease of Isolated Bovine Chondrocytes." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32671.

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Cell volume regulation has been observed in almost all cell types examined to date. When cells are exposed to hypotonic solutions a quick increase in volume is followed by a more gradual return, termed regulatory volume decrease (RVD). The mechanism associated with RVD depends upon cell type and species, but in bovine chondrocytes the non-selective osmolyte channels are mainly responsible [1]. In a chondrocyte, volume control is critical for the maintenance of metabolism, and biosynthesis. Volume fluctuations can be due to changes in hydrostatic pressure, fluid flows, deformation, and extracellular matrix (ECM) hydration. Alterations in hydration can occur during static loading of articular cartilage or during the early stages of osteoarthritis [1], which have been correlated with changes in cellular metabolism. The swelling behaviour of chondrocytes, and the mechanism by which they sense and respond to changes in their physico-chemical environment, are not well understood [1]. To investigate the effects of osmotic environment on chondrocyte behaviour it is often beneficial to isolate cells from the ECM, which can be achieved by a variety of techniques. To investigate the effect of isolation technique on the swelling behaviour of bovine chondrocytes, two enzymatic digestion techniques were chosen for this study.
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Frojmovic, Mony M., Truman Wong, Jane Wylie, and J. G. White. "PLATELET EXTERNAL SURFACE MEMBRANE IS OSMOTICALLY DOUBLED IRRESPECTIVE OF SIZE OR SPECIES (HUMAN/BOVINE): DYNAMICS AND MEMBRANE SOURCES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643905.

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Osmotic swelling can double the external plasma membrane surface area of human platelets independently of size, proposed to recruit the open surface-connected canalicular system ((SCCS) (Thrombos. Res. Suppl. VI: 119, 1986). As bovine (B) platelets have been reported to lack SCCS, we compared osmotic swelling for B and human (H) cells. Addition of water to piatelet-rich-plasma (10-90% v/v) caused sequential shape change and osmotic spherocyte (OS) formation, analyzed for size and surface area changes from time-dependent phase-contrast videomicroscopic images. Selected samples were fixed and stained with tannic acid prior to osmic acid fixation for visualization of open SCCS by transmission electron microscopy. B platelets required 3-4x less water dilution of PRP than H platelets, with significant OS forming at 20% water addition. Continued water dilution converted 50% of platelets to OS, with maximally stable swelling and no significant lysis for bovine OS up to 60% dilution. Electron micrographs of unactivated discocytes (D) and of optimally-swollen OS showed open SCCS in human D not detectable in any of the swollen platelets, though granules, mitochondria and a small number of vesicles and vacuoles persisted; no evidence for any open SCCS was found for bovine D or OS, though the OS otherwise appeared similar to H-0S. Geometric measurements of D and nonlysed OS showed a stable, maximal 2.1±0.1 fold increase in external plasma membrane surface area with osmotic swelling, identical for different-sized H platelets (mean volume = 2.8-6.8 f1) or for B platelets (3.6 f1 ). B platelets show equal or greater sensitivity for ADP-induced activation as H platelets, with 2-fold slower maximal rates of recruitment in early aggregation. As osmotic swelling appears to primarily externalize SCCS in H platelets, the identical relative amounts of internal membrane externalized for B platelets is hypothesized to arise from an osmotically more labile, “closed”, and structurally simpler SCCS or from a distinct membrane source tnan in H platelets.
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Huyghe, J. M., C. J. M. Jongeneelen, F. Kraaijeveld, and Y. Schroeder. "3D Finite Strains in Bovine Annulus Fibrosus Tissue." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176508.

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Abstract:
Intervertebral disc tissue consists of a fluid-filled extra-cellular matrix, in which living cells are sparsely dispersed. The mechanical function is highly dependent on the composition of the extra-cellular matrix, which primary consists of collagen fibrils and negatively charged proteoglycans. Due to the fixed charges of the proteoglycans (PG’s), the cation concentration inside the tissue is higher than physiological. This excess of ion particles leads to an osmotic pressure difference, which causes swelling of the tissue [1]. Because the intervertebral disc is gripped between two vertebrae, the swelling is constrained in vivo, resulting in a intradiscal pressure of 0.1 to 0.2 MPa in supine position. It has been shown that the osmotic pressure inside cartilaginous tissues is much higher than would be expected based on its FCD [2]. This is because part of the water in the tissue is absorbed by the collagen fibers. The proteoglycan molecules, because of their large size, are excluded from this intra-fibrillar space. This means that their effective concentrations are much higher in the extra-fibrillar space than if they were distributed uniformly throughout the entire matrix. Hence, the effective fixed charge density is higher than if computed from total tissue water content. A recent study demonstrates that intrafibrillar water increases osmolarity within the annulus fibrosus substantially [3]. On the other hand, Wognum et al. [4] showed by means of a physical and a numerical model of the disc that high osmolarity within the disc has a protective effect against crack propagation within the disc. Hence, the decrease in osmolarity associated with degeneration may be an explanation of (1) the growing number of cracks observed in the degenerating disc as well as (2) the poor correlation between external loading and crack propagation [5]. The purpose of the present study is to test the hypothesis of Wognum et al. [4] through direct observation of the deformation of annulus fibrosus tissue around discontinuities within its collagen network.
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