scholarly journals The role of cell swelling in the stimulation of glycogen synthesis by insulin

1992 ◽  
Vol 282 (3) ◽  
pp. 789-796 ◽  
Author(s):  
M al-Habori ◽  
M Peak ◽  
T H Thomas ◽  
L Agius
Keyword(s):  
Cell Volume ◽  
Glycogen Synthesis ◽  
Metabolic Effects ◽  
Cell Swelling ◽  
Free Medium ◽  
K Uptake ◽  
Osmotic Swelling ◽  
Cation Content ◽  
Secondary Mechanism ◽  
Stimulation Of

In hepatocyte cultures, insulin stimulates cellular accumulation of K+, partly (approximately 20%) by net replacement of cell Na+, but largely (approximately 80%) by increasing the cell K++Na+ content, with a consequent increase in cell volume. An increase in cation content occurred within 5 min of exposure to insulin and was not secondary to metabolic changes. Insulin also increased the cation content, by increasing the Na+ content, in a K(+)-free medium or when K+ uptake was inhibited with 1 mM-ouabain. However, insulin did not increase the cation content in a Na(+)-free medium. The stimulation of glycogen synthesis by insulin, like the increase in cation content, was blocked in a Na(+)-free medium, but not when K+ uptake was inhibited. Hypo-osmotic swelling restored the stimulation of glycogen synthesis in a Na(+)-free medium, indicating that the lack of effect of insulin in the iso-osmotic Na(+)-free medium was not due to a direct requirement for Na+ for glycogen synthesis, but to a secondary mechanism, dependent on Na+ entry, that can be mimicked by hypo-osmotic swelling. Quinine increased cell volume further and caused a further increase in glycogen synthesis. The hypothesis that cellular uptake of K+ may be part of the mechanism by which insulin controls metabolism was discounted, because inhibition of K+ uptake does not block the metabolic effects of insulin [Czech (1977) Annu. Rev. Biochem. 46, 359-384]. The present results support the hypothesis that an increase in cell cation content, and thereby cell volume, rather than K+ uptake, is part of the mechanism by which insulin stimulates glycogen synthesis in hepatocytes.

scholarly journals Regulation of glycogen synthesis and glycolysis by insulin, pH and cell volume. Interactions between swelling and alkalinization in mediating the effects of insulin

1992 ◽  
Vol 282 (3) ◽  
pp. 797-805 ◽  
Author(s):  
M Peak ◽  
M al-Habori ◽  
L Agius
Keyword(s):  
Cell Volume ◽  
Glycogen Synthesis ◽  
Potassium Acetate ◽  
Cell Swelling ◽  
Osmotic Swelling ◽  
Cation Content ◽  
Alkaline Conditions ◽  
Inhibition Of Glycolysis ◽  
Free Media ◽  
Stimulation Of

The effects of changes in cell volume and pH on glycogen synthesis and glycolysis and their control by insulin were investigated in hepatocyte cultures. 1. Cell acidification, by increasing [CO2] from 2.5% to 5%, inhibited glycolysis and stimulated glycogen synthesis. The inhibition of glycolysis was also observed in Na(+)-free media and when K+ uptake was inhibited, but the stimulation of glycogen synthesis was abolished under these conditions, suggesting that it is secondary to ionic or volume changes. Alkalinization had converse effects on glycolysis and glycogen synthesis. 2. In HCO3(-)-containing media, replacement of NaCl with sodium acetate or potassium acetate, like acidification with CO2, inhibited glycolysis and stimulated glycogen synthesis. The latter correlated with an increase in cation content. Amiloride, an inhibitor of Na+/H+ exchange, inhibited both the increase in cation content and the stimulation of glycogen synthesis, suggesting that the latter is secondary to cell swelling. 3. Hypo-osmotic swelling increased glycogen synthesis in HCO3(-)-containing media, in both the absence and the presence of Na+ and at both 2.5% and 5% CO2, but it increased glycolysis in the presence of Na+ and at 2.5%, but not at 5%, CO2. In HCO3(-)-free media, during acidification and swelling, glycogen synthesis correlated with pH and not with cell volume, indicating that inhibition by acidification over-rides stimulation by swelling. 4. Stimulation of glycolysis by insulin was not additive with stimulation by alkalinization. The stimulation of glycogen synthesis by insulin was partially suppressed under alkaline conditions; it was markedly suppressed in isosmolar Na(+)-free media and restored by hypo-osmotic swelling. In hypo-osmolar Na(+)-free media insulin prevented the decrease in glycogen synthesis with decreasing [HCO3-], suggesting that it counteracts inhibition by acidification. 5. It is concluded that glycogen synthesis and glycolysis are both stimulated by cell swelling and inhibited by acidification, under certain conditions, but glycolysis is more sensitive to inhibition by acidification and glycogen synthesis to stimulation by swelling. Consequently, simultaneous swelling and acidification is associated with inhibition of glycolysis and stimulation of glycogen synthesis. Stimuli that cause swelling and alkalinization activate both glycogen synthesis and glycolysis, alkalinization being more important in control of glycolysis and swelling in control of glycogen synthesis. Both cell swelling and alkalinization are components of the mechanism by which insulin controls glycogen synthesis and glycolysis.

Mechanism of potassium uptake in neuropile glial cells in the central nervous system of the leech

1990 ◽  
Vol 63 (5) ◽  
pp. 1089-1097 ◽  
Author(s):  
W. A. Wuttke
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cell Volume ◽  
Normal Saline ◽  
Cell Swelling ◽  
Equilibrium Potential ◽  
K Uptake ◽  
The Central Nervous System ◽  
The Mean ◽  
K Concentration

1. Ion-selective double-barreled microelectrodes (ISME) were used to measure intracellular K+ (aKi), Na+ (aNai), and Cl- (aCli) activities of neuropile glial (NG) cells in the central nervous system of the medicinal leech Hirudo medicinalis. Ion fluxes were induced by an increase in extracellular K+ concentration [( K+]o) and analyzed to elucidate the ionic mechanism of the K+ uptake occurring under such conditions. 2. In addition, the K+ concentration of the extracellular space of the nerve cell body region (NCBR) and the neuropile (N) was measured with neutral carrier K(+)-ISME. In normal saline (4 mM K+), a concentration of 4.2 mM was measured in both extracellular spaces. No differences between the K+ concentration of the bathing fluid and the extracellular spaces were found at higher (i.e., 10 and 40 mM) K+ concentrations. 3. In normal saline, the mean membrane potential (Em) was -68 mV, and the mean aKi, aNai, and aCli were found to be 77, 10, and 7 mM, respectively. The corresponding equilibrium potentials were -81, 56, and -66 mV. The chloride equilibrium potential (ECl) was similar to Em, and it is concluded that chloride is passively distributed across the NG cell membrane. 4. When [K+]o was transiently increased 10-fold (i.e., to 40 mM), aKi and a Cli increased transiently by 22 and 25 mM, respectively, and the membrane depolarized to -28 mV, which was similar to both K+ equilibrium potential (EK) and ECl. The KCl uptake was accompanied by a transient decrease in aNai to 5 mM. 5. After incubation for at least 1 h in Na(+)-free saline, NG cells accumulated K+ in the absence of extracellular Na+ to levels similar to those observed in the presence of Na+. Therefore the uptake of K+ was not dependent on external--and probably also internal--Na+. 6. Changes in cell volume induced by the increase in [K+]o were estimated by loading NG cells with choline and monitoring its intracellular concentration with Corning-K(+)-ISME. In saline containing 40 mM K+, NG cell volume increased to approximately 150% of its volume in normal saline. 7. It is concluded that the mechanism of K+ uptake in NG cells is by passive KCl and water influx, which causes cell swelling.

scholarly journals Cell volume and bile acid excretion

1992 ◽  
Vol 288 (2) ◽  
pp. 681-689 ◽  
Author(s):  
D Häussinger ◽  
C Hallbrucker ◽  
N Saha ◽  
F Lang ◽  
W Gerok
Keyword(s):  
Amino Acids ◽  
Cell Volume ◽  
Liver Cell ◽  
Bile Flow ◽  
Cell Swelling ◽  
Isolated Perfused Rat Liver ◽  
Cell Shrinkage ◽  
Volume Changes ◽  
Close Relationship ◽  
Stimulation Of

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.

Effects of apical membrane Cl(-)-formate exchange on cell volume in rabbit proximal tubule

1990 ◽  
Vol 258 (3) ◽  
pp. F530-F536 ◽  
Author(s):  
L. Schild ◽  
P. S. Aronson ◽  
G. Giebisch
Keyword(s):  
Proximal Tubule ◽  
Cell Volume ◽  
Apical Membrane ◽  
Cell Swelling ◽  
Volume Changes ◽  
Proximal Tubule Cells ◽  
Volume Increase ◽  
Tubule Lumen ◽  
Stimulation Of

We used real-time recordings of cell volume changes to test for the role of the Cl(-)-formate exchanger in mediating NaCl entry across the apical membrane of rabbit proximal tubule cells. In the absence of extracellular Cl-, 0.5 and 5 mM formate in the tubule lumen induced an increase in cell volume of 1 and 9%, respectively. Formate-induced cell swelling was reduced by alkalinizing the tubule lumen or by addition of luminal amiloride (2 mM), indicating that the increase in cell volume results from the intracellular accumulation of Na-formate via nonionic diffusion of formic acid in parallel with Na(+)-H+ exchange. The cell volume increase induced by 0.5 mM formate was potentiated (from 1 to 4%) by Cl-, as expected for a formate-mediated stimulation of NaCl uptake via parallel Cl(-)-formate exchange and Na(+)-H+ exchange across the apical membrane. By contrast, the cell volume increase induced by 5 mM formate was attenuated (from 9 to 4%) by Cl-. The attenuating effect of Cl- on formate-induced cell swelling required the operation of the apical membrane Cl(-)-formate exchanger. The effect of 1:1 Cl(-)-formate exchange to attenuate formate-induced cell swelling can be explained if the cell possesses a volume-activated anion exit pathway, most likely at the basolateral cell membrane, that is capable of mediating the efflux of Cl- but not formate from the cell.

scholarly journals Volume-sensitive K transport in human erythrocytes.

1986 ◽  
Vol 88 (6) ◽  
pp. 719-738 ◽  
Author(s):  
D Kaji
Keyword(s):  
Cell Volume ◽  
Human Erythrocytes ◽  
Cell Swelling ◽  
K Channel ◽  
K Uptake ◽  
Transport Pathway ◽  
Free Media ◽  
K Transport ◽  
Hypotonic Swelling ◽  
External K

Studies have been carried out on human erythrocytes to examine the alterations of K transport induced by swelling or shrinking the cells by osmotic and isosmotic methods. Hypotonic swelling of erythrocytes (relative cell volume, 1.20) resulted in a striking, four- to fivefold augmentation in the ouabain-resistant K influx over the value obtained at a normal cell volume. Shrinking the cells in hypertonic media resulted in a small but statistically significant reduction in K influx. Three different methods of varying cell volume gave similar results. These include the addition of sucrose and of NaCl to hypotonic media and the isosmotic (nystatin) method. The major fraction of the K influx in swollen cells is specific in its requirement for Cl or Br and is not supported by thiocyanate, iodide, nitrate, methylsulfate, or acetate. Bumetanide (0.1 mM), MK-196 (0.2 mM), and piretanide (1 mM) are poorly effective in suppressing K uptake in swollen cells, but at higher concentrations, bumetanide (1 mM) inhibits 80% of the Cl-dependent K influx in swollen cells. The bumetanide concentration required to inhibit 50% of the Cl-dependent K influx is 0.17 mM. The volume-sensitive K influx is independent of both extracellular and intracellular Na, so that the (Na + K + 2Cl) cotransport pathway is not a likely mediator of the volume-sensitive K transport. A variety of inhibitors of the Ca-activated K channel are ineffective in suppressing swelling-induced K influx. Like K uptake, the efflux of K is also enhanced by cell swelling. Swelling-activated K efflux is Cl dependent, is independent of extracellular and intracellular Na, and is observed with both hypotonic and isosmotic methods of cell swelling. The activation of K efflux by cell swelling is observed in K-free media, which suggests that the volume-sensitive K transport pathway is capable of net K efflux. The addition of external K to hypotonic media resulted in an increase in K efflux compared with the efflux in K-free media, and this increase was probably due to K/K exchange. Thus, hypotonic or isosmotic swelling of human erythrocytes results in the activation of a ouabain-resistant, Cl-dependent, Na-independent transport pathway that is capable of mediating both net K efflux and K/K exchange.

scholarly journals Relationship between cell volume and ion transport in the early distal tubule of the Amphiuma kidney.

1985 ◽  
Vol 86 (1) ◽  
pp. 31-58 ◽  
Author(s):  
W B Guggino ◽  
H Oberleithner ◽  
G Giebisch
Keyword(s):  
Cell Membrane ◽  
Cell Volume ◽  
Cell Membranes ◽  
Apical Cell ◽  
Distal Tubule ◽  
Cell Swelling ◽  
Osmotic Swelling ◽  
Apical Cell Membrane ◽  
Basolateral Cell Membrane ◽  
Tubule Cells

The roles of apical and basolateral transport mechanisms in the regulation of cell volume and the hydraulic water permeabilities (Lp) of the individual cell membranes of the Amphiuma early distal tubule (diluting segment) were evaluated using video and optical techniques as well as conventional and Cl-sensitive microelectrodes. The Lp of the apical cell membrane calculated per square centimeter of tubule is less than 3% that of the basolateral cell membrane. Calculated per square centimeter of membrane, the Lp of the apical cell membrane is less than 40% that of the basolateral cell membrane. Thus, two factors are responsible for the asymmetry in the Lp of the early distal tubule: an intrinsic difference in the Lp per square centimeter of membrane area, and a difference in the surface areas of the apical and basolateral cell membranes. Early distal tubule cells do not regulate volume after a reduction in bath osmolality. This cell swelling occurs without a change in the intracellular Cl content or the basolateral cell membrane potential. In contrast, reducing the osmolality of the basolateral solution in the presence of luminal furosemide diminishes the magnitude of the increase in cell volume to a value below that predicted from the change in osmolality. This osmotic swelling is associated with a reduction in the intracellular Cl content. Hence, early distal tubule cells can lose solute in response to osmotic swelling, but only after the apical Na/K/Cl transporter is blocked. Inhibition of basolateral Na/K ATPase with ouabain results in severe cell swelling. This swelling in response to ouabain can be inhibited by the prior application of furosemide, which suggests that the swelling is due to the continued entry of solutes, primarily through the apical cotransport pathway.

Physiology and pathophysiology of Na+/H+exchange and Na+-K+-2Cl−cotransport in the heart, brain, and blood

2006 ◽  
Vol 291 (1) ◽  
pp. R1-R25 ◽  
Author(s):  
S. F. Pedersen ◽  
M. E. O'Donnell ◽  
S. E. Anderson ◽  
P. M. Cala
Keyword(s):  
Cell Volume ◽  
Cell Function ◽  
Cell Damage ◽  
Cellular Responses ◽  
Exercise Stress ◽  
Cell Swelling ◽  
Cell Shrinkage ◽  
Comprehensive Overview ◽  
Wide Range ◽  
Stimulation Of

Maintenance of a stable cell volume and intracellular pH is critical for normal cell function. Arguably, two of the most important ion transporters involved in these processes are the Na+/H+exchanger isoform 1 (NHE1) and Na+-K+-2Cl−cotransporter isoform 1 (NKCC1). Both NHE1 and NKCC1 are stimulated by cell shrinkage and by numerous other stimuli, including a wide range of hormones and growth factors, and for NHE1, intracellular acidification. Both transporters can be important regulators of cell volume, yet their activity also, directly or indirectly, affects the intracellular concentrations of Na+, Ca2+, Cl−, K+, and H+. Conversely, when either transporter responds to a stimulus other than cell shrinkage and when the driving force is directed to promote Na+entry, one consequence may be cell swelling. Thus stimulation of NHE1 and/or NKCC1 by a deviation from homeostasis of a given parameter may regulate that parameter at the expense of compromising others, a coupling that may contribute to irreversible cell damage in a number of pathophysiological conditions. This review addresses the roles of NHE1 and NKCC1 in the cellular responses to physiological and pathophysiological stress. The aim is to provide a comprehensive overview of the mechanisms and consequences of stress-induced stimulation of these transporters with focus on the heart, brain, and blood. The physiological stressors reviewed are metabolic/exercise stress, osmotic stress, and mechanical stress, conditions in which NHE1 and NKCC1 play important physiological roles. With respect to pathophysiology, the focus is on ischemia and severe hypoxia where the roles of NHE1 and NKCC1 have been widely studied yet remain controversial and incompletely elucidated.

Regulation of vascular endothelial cell volume by Na-K-2Cl cotransport

1992 ◽  
Vol 262 (2) ◽  
pp. C436-C444 ◽  
Author(s):  
W. C. O'Neill ◽  
J. D. Klein
Keyword(s):  
Endothelial Cells ◽  
Cell Volume ◽  
Vascular Endothelial Cell ◽  
Cell Swelling ◽  
Hypertonic Medium ◽  
Aortic Endothelial Cells ◽  
Endothelial Integrity ◽  
Stimulation Of ◽  
In Cells ◽  
Aortic Endothelial

The relationship between cell volume and Na-K-2Cl cotransport was studied in cultured bovine aortic endothelial cells. Hypertonic cell shrinkage increased bumetanide-sensitive, Na- or Cl-dependent K influx without altering bumetanide-insensitive influx. Greater stimulation of cotransport was observed in cells shrunken isosmotically either by preincubation in K-free and Na-free medium or by preincubation in hypotonic medium. Cell swelling, produced by preincubation in isotonic high-K medium, inhibited bumetanide-sensitive K influx. Simultaneous measurements of [3H]bumetanide binding and K influx revealed an increased number of binding sites without an increased influx per binding site in shrunken cells. Bumetanide did not alter the volume or ion content of cells in isotonic or hypertonic medium, indicating that no net influx of ions occurs through cotransport under these conditions. In isosmotically shrunken cells, there was greater stimulation of bumetanide-sensitive influx than of bumetanide-sensitive efflux, resulting in net bumetanide-sensitive influx. Rapid recovery of cell K, Na, and water occurred over 10-20 min and was inhibited by bumetanide or by the removal of external Na or Cl. These data demonstrate that Na-K-2Cl cotransport in aortic endothelial cells is regulated by cell volume, possibly through changes in the number of functional cotransporters, and mediates a brisk regulatory volume increase in isosmotically shrunken cells. Although thermodynamically favored, no net influx occurs through Na-K-2Cl cotransport in cells of normal volume or in hypertonically shrunken cells. This suggests additional regulation of cotransport, perhaps through trans-inhibition by intracellular Cl. Regulation of cell volume by Na-K-2Cl cotransport may be important in maintaining endothelial integrity.

scholarly journals Myosin light chain kinase and Src control membrane dynamics in volume recovery from cell swelling

2011 ◽  
Vol 22 (5) ◽  
pp. 634-650 ◽  
Author(s):  
Elisabeth T. Barfod ◽  
Ann L. Moore ◽  
Benjamin G. Van de Graaf ◽  
Steven D. Lidofsky
Keyword(s):  
Cell Volume ◽  
Light Chain ◽  
Myosin Light Chain Kinase ◽  
Myosin Light Chain ◽  
Myosin Ii ◽  
Membrane Dynamics ◽  
Cell Swelling ◽  
Membrane Turnover ◽  
Osmotic Swelling ◽  
Volume Recovery

 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.

scholarly journals Mitogenic and Metabolic Effects of Type I IGF Receptor Overexpression in Insulin Receptor-Deficient Hepatocytes

Endocrinology ◽  
2001 ◽  
Vol 142 (8) ◽  
pp. 3354-3360 ◽  
Author(s):  
Jane J. Kim ◽  
Byung-Chul Park ◽  
Yoshiaki Kido ◽  
Domenico Accili
Keyword(s):  
Cell Proliferation ◽  
Insulin Receptor ◽  
Glycogen Synthesis ◽  
Insulin Receptors ◽  
Metabolic Effects ◽  
Insulin Receptor Substrate ◽  
Type I ◽  
Wild Type ◽  
Igf I ◽  
Stimulation Of

Abstract We have previously shown that hepatocytes lacking insulin receptors (Ir−/−) fail to mediate metabolic responses, such as stimulation of glycogen synthesis, while retaining the ability to proliferate in response to IGFs. In this study we have asked whether overexpression of type I IGF receptors would rescue the metabolic response of Ir−/− hepatocytes. After IGF-I stimulation, insulin receptor substrate-1 and -2 phosphorylation and PI3K activity were restored to levels similar to or greater than those seen in wild-type cells. Rates of cell proliferation in response to IGF-I increased approximately 2-fold, whereas glycogen synthesis was restored to wild-type levels, but was comparatively smaller than that elicited by overexpression of insulin receptors. In summary, overexpression of IGF-I receptors in Ir−/− hepatocytes normalized insulin receptor substrate-2 phosphorylation and glycogen synthesis to wild-type levels, whereas it increased cell proliferation above wild-type levels. Moreover, stimulation of glycogen synthesis was submaximal compared with the effect of insulin receptor overexpression. We conclude that IGF-I receptors are more efficiently coupled to cell proliferation than insulin receptors, but are less potent than insulin receptors in stimulating glycogen synthesis. The data are consistent with the possibility that there exist intrinsic signaling differences between insulin and IGF-I receptors.

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