The Experts below are selected from a list of 273 Experts worldwide ranked by ideXlab platform
R A Yokel - One of the best experts on this subject based on the ideXlab platform.
-
Aluminum Citrate uptake by immortalized brain endothelial cells: implications for its blood-brain barrier transport.
Brain research, 2002Co-Authors: R A Yokel, Marieangela Wilson, Wesley R Harris, Andrew P HalestrapAbstract:The objective was to further test the hypothesis that Aluminum (Al) Citrate transport across the blood-brain barrier is mediated by a monocarboxylate transporter (MCT). Speciation calculations showed that Al Citrates were the predominant Al species under the conditions employed. Al Citrate did not inhibit lactate uptake and was not taken up by the rat erythrocyte, suggesting it does not serve as an effective substrate for either MCT1 or the anion exchanger. Studies were conducted with b.End5 cells derived from mouse brain endothelial cells to identify the properties of the carrier(s) mediating Al Citrate transport. Western blot analysis of b.End5 cells showed expression of the transferrin receptor and MCT1, but not MCT2 or MCT4. Uptake of Al Citrate was approximately 70% faster than Citrate. Citrate and Al Citrate uptake were sodium independent. Citrate uptake increased at pH 6.9 compared to 7.4, whereas Al Citrate uptake did not. Al Citrate uptake was reduced by inhibitors of mitochondrial respiration and oxidative phosphorylation, suggesting ATP dependence, but not by ouabain, suggesting no role for Na/K-ATPase. Uptake was not affected by alpha-ketoglutarate or malonate, substrates for the dicarboxylate carrier. Many substrates and inhibitors of MCT1 and organic anion transporters reduced Al Citrate uptake into b.End5 cells. BSP and fluorescein, organic anion transporter substrates/inhibitors, inhibited Al Citrate uptake. We conclude that Al Citrate transport across the blood-brain barrier is carrier-mediated, involving either an uncharacterized MCT isoform expressed in the brain such as MCT7 or MCT8 and/or one of the many members of the organic anion transporting protein family, some of which are known to be expressed at the blood-brain barrier.
-
Aluminum Citrate uptake by immortalized brain endothelial cells: implications for its blood-brain barrier transport.
Brain Research, 2002Co-Authors: R A Yokel, Wesley R Harris, Marieangela C. Wilson, Andrew P HalestrapAbstract:Abstract The objective was to further test the hypothesis that Aluminum (Al) Citrate transport across the blood–brain barrier is mediated by a monocarboxylate transporter (MCT). Speciation calculations showed that Al Citrates were the predominant Al species under the conditions employed. Al Citrate did not inhibit lactate uptake and was not taken up by the rat erythrocyte, suggesting it does not serve as an effective substrate for either MCT1 or the anion exchanger. Studies were conducted with b.End5 cells derived from mouse brain endothelial cells to identify the properties of the carrier(s) mediating Al Citrate transport. Western blot analysis of b.End5 cells showed expression of the transferrin receptor and MCT1, but not MCT2 or MCT4. Uptake of Al Citrate was ∼70% faster than Citrate. Citrate and Al Citrate uptake were sodium independent. Citrate uptake increased at pH 6.9 compared to 7.4, whereas Al Citrate uptake did not. Al Citrate uptake was reduced by inhibitors of mitochondrial respiration and oxidative phosphorylation, suggesting ATP dependence, but not by ouabain, suggesting no role for Na/K-ATPase. Uptake was not affected by α-ketoglutarate or malonate, substrates for the dicarboxylate carrier. Many substrates and inhibitors of MCT1 and organic anion transporters reduced Al Citrate uptake into b.End5 cells. BSP and fluorescein, organic anion transporter substrates/inhibitors, inhibited Al Citrate uptake. We conclude that Al Citrate transport across the blood–brain barrier is carrier-mediated, involving either an uncharacterized MCT isoform expressed in the brain such as MCT7 or MCT8 and/or one of the many members of the organic anion transporting protein family, some of which are known to be expressed at the blood–brain barrier.
-
Research report Aluminum Citrate uptake by immortalized brain endothelial cells: implications for its blood-brain barrier transport
2002Co-Authors: R A Yokel, Wesley R Harris, Marieangela C. Wilson, Andrew P HalestrapAbstract:The objective was to further test the hypothesis that Aluminum (Al) Citrate transport across the blood-brain barrier is mediated by a monocarboxylate transporter (MCT). Speciation calculations showed that Al Citrates were the predominant Al species under the conditions employed. Al Citrate did not inhibit lactate uptake and was not taken up by the rat erythrocyte, suggesting it does not serve as an effective substrate for either MCT1 or the anion exchanger. Studies were conducted with b.End5 cells derived from mouse brain endothelial cells to identify the properties of the carrier(s) mediating Al Citrate transport. Western blot analysis of b.End5 cells showed expression of the transferrin receptor and MCT1, but not MCT2 or MCT4. Uptake of Al Citrate was |70% faster than Citrate. Citrate and Al Citrate uptake were sodium independent. Citrate uptake increased at pH 6.9 compared to 7.4, whereas Al Citrate uptake did not. Al Citrate uptake was reduced by inhibitors of mitochondrial respiration and oxidative phosphorylation, suggesting ATP dependence, but not by ouabain, suggesting no role for Na / K-ATPase. Uptake was not affected by a-ketoglutarate or malonate, substrates for the dicarboxylate carrier. Many substrates and inhibitors of MCT1 and organic anion transporters reduced Al Citrate uptake into b.End5 cells. BSP and fluorescein, organic anion transporter substrates / inhibitors, inhibited Al Citrate uptake. We conclude that Al Citrate transport across the blood-brain barrier is carrier-mediated, involving either an uncharacterized MCT isoform expressed in the brain such as MCT7 or MCT8 and / or one of the many members of the organic anion transporting protein family, some of which are known to be expressed at the blood-brain barrier. © 2002 Elsevier Science B.V. All rights reserved. Theme: Neurotransmitters, modulators, transporters, and receptors Topic: Uptake and transporters
-
Aluminum transport out of brain extracellular fluid is proton dependent and inhibited by mersalyl acid, suggesting mediation by the monocarboxylate transporter (MCT1).
Toxicology, 1998Co-Authors: D C Ackley, R A YokelAbstract:Blood brain barrier transport of Aluminum Citrate was assessed in rats by microdialysis of the jugular vein as well as the right and left frontal cortices. Previous studies (Allen et al., 1995. Evidence for energy-dependent transport of Aluminum out of brain extracellular fluid. Toxicology 92, 193-202; Ackley and Yokel, 1997. Aluminum Citrate is transported from brain into blood via the monocarboxylic acid transporter located at the blood-brain barrier. Toxicology 120, 89-97), and the current study, demonstrated that the steady-state brain-to-blood ratio of the unbound extracellular Aluminum immediately surrounding the microdialysis probe is less than 1, suggesting the presence of a process other than diffusion across the blood brain barrier. It was speculated that a monocarboxylate transporter at the blood brain barrier was maintaining this ratio at less than 1 (Ackley and Yokel, 1997). Monocarboxylate transporters are proton co-transporters. Decreasing extracellular pH (increasing proton availability) increases monocarboxylate transport. After alkalinizing the dialysate perfusing a brain microdialysis probe (to pH = 10.2), the steady-state Aluminum brain-to-blood ratio increased from 0.35 to 0.80. The addition of the proton ionophore, p-(trifluoromethoxy)phenylhydrazone (FCCP) (1 mM), to brain dialysate increased this ratio from 0.21 to 0.61. These increased ratios suggest that a proton-dependent process is removing Al from brain extracellular fluid. The monocarboxylate transporter is the only known proton-dependent transporter at the blood-brain barrier. There are two known isoforms of this transporter in the rodent, MCT1 and MCT2. Organomercurial thiol reagents, such as mersalyl acid, inhibit MCT1 but not MCT2. Mersalyl acid (50 mM) addition to brain dialysate increased the steady-state Aluminum brain-to-blood ratio from 0.19 to 0.87, suggesting that MCT1 is at least partially mediating the efflux of Aluminum from brain extracellular fluid.
-
Aluminum Citrate is transported from brain into blood via the monocarboxylic acid transporter located at the blood-brain barrier.
Toxicology, 1997Co-Authors: D C Ackley, R A YokelAbstract:Aluminum Citrate transport across the blood-brain barrier was assessed in rats by in vivo microdialysis. Microdialysis probes were implanted in the jugular vein as well as the left and right frontal cortex. It was demonstrated previously (Allen et al., 1995), in this study, that the steady-state Aluminum Citrate brain-to-blood-ratio (BBr) is less than 1, suggesting the presence of a process other than diffusion. The addition of 2,4-dinitrophenol (10 microM) to the dialysate perfusing a microdialysis probe in the brain increased the steady-state Aluminum Citrate brain-to-blood-ratio to a value (1.14) not significantly different from 1, suggesting the presence of an active transporter that is blocked by the metabolic inhibitor. The addition of valproic and pyruvic acid, as putative and known substrates for the monocarboxylic acid transporter, respectively, to brain dialysate (10 and 100 mM) had different outcomes. Valproic acid was ineffective at either concentration, whereas pyruvic acid (100 mM) significantly increased the Aluminum Citrate brain-to-blood-ratio from 0.19 to 0.31. Pyruvic acid (1 M in the dialysate) increased the Aluminum Citrate brain-to-blood-ratio to a value not different from unity, suggesting competition between Aluminum Citrate and pyruvic acid for transport. The only energy-dependent, pyruvic acid-inhibitable transporter is the monocarboxylic acid transporter. Theoretical, pharmacokinetic modeling suggests that the transporter producing an Aluminum Citrate brain-to-blood-ratio less than 1 is predominantly located at the blood-brain barrier, rather than at neuronal or glial cell membranes. We propose that the monocarboxylic acid transporter at the blood-brain barrier maintains a steady-state Aluminum Citrate brain-to-blood-ratio much less than 1.
Athanasios Salifoglou - One of the best experts on this subject based on the ideXlab platform.
-
A novel dinuclear species in the aqueous distribution of Aluminum in the presence of Citrate.
Inorganic chemistry, 2003Co-Authors: Maria Dakanali, Catherine P. Raptopoulou, Andrea Lakatos, Tamás Kiss, Aristidis Terzis, István Bányai, Athanasios SalifoglouAbstract:The chemistry of Aluminum was explored in the presence of the physiological ligand citric acid and in low-pH aqueous media. As a result, the first dinuclear Aluminum−Citrate complex (NH4)4[Al2(C6H4O7)(C6H5O7)2]·4H2O was isolated at low pH (∼3.5), and was characterized by FT-IR spectroscopy and X-ray crystallography. The structural analysis reveals the presence of a dinuclear assembly of two Aluminum ions octahedrally coordinated to three Citrate ligands of differing protonation state. The NMR solution behavior of this complex emphasizes its time-dependent transformation into a number of variable nature species, ultimately leading to the thermodynamically stable trinuclear species. It also establishes the participation of the dinuclear complex as a viable component of the aqueous Al(III)−Citrate speciation. The chemical and structural features of this novel low molecular mass species provide considerable insight into Citrate's ability, as a natural ligand, to influence the chemistry of Aluminum in a pH-dep...
-
Synthesis, Structural Characterization, and Solution Behavior of the First Mononuclear, Aqueous Aluminum Citrate Complex
Inorganic Chemistry, 1999Co-Authors: Manolis Matzapetakis, Catherine P. Raptopoulou, A. Terzis, Andrea Lakatos, Tamás Kiss, Athanasios SalifoglouAbstract:The significance of the interaction between Aluminum and Citrate in biological media is exemplified by the synthesis, isolation, structural characterization, and solution behavior of the first mononuclear Aluminum Citrate complex. The chemical and structural features of the low molecular weight Aluminum Citrate species characterized help gain insight into Citrate's ability, as a natural ligand, to enhance Aluminum's absorption and thus affect its accumulation and biotoxicity at biological sites.
Kenneth E Mcmartin - One of the best experts on this subject based on the ideXlab platform.
-
Aluminum Citrate blocks toxicity of calcium oxalate crystals by preventing binding with cell membrane phospholipids.
American journal of nephrology, 2013Co-Authors: Chungang Guo, Tammy R. Dugas, Clinton Scates, Maria Garcia-villarreal, Thomas Ticich, Kenneth E McmartinAbstract:Background/Aims: Renal damage from ethylene glycol and primary hyperoxaluria is linked to accumulation of calcium oxalate monohydrate (COM) crystals in the renal
-
Aluminum Citrate Prevents Renal Injury from Calcium Oxalate Crystal Deposition
Journal of the American Society of Nephrology : JASN, 2012Co-Authors: Lauren M. Besenhofer, Marie C. Cain, Cody L. Dunning, Kenneth E McmartinAbstract:Calcium oxalate monohydrate crystals are responsible for the kidney injury associated with exposure to ethylene glycol or severe hyperoxaluria. Current treatment strategies target the formation of calcium oxalate but not its interaction with kidney tissue. Because Aluminum Citrate blocks calcium oxalate binding and toxicity in human kidney cells, it may provide a different therapeutic approach to calcium oxalate-induced injury. Here, we tested the effects of Aluminum Citrate and sodium Citrate in a Wistar rat model of acute high-dose ethylene glycol exposure. Aluminum Citrate, but not sodium Citrate, attenuated increases in urea nitrogen, creatinine, and the ratio of kidney to body weight in ethylene glycol–treated rats. Compared with ethylene glycol alone, the addition of Aluminum Citrate significantly increased the urinary excretion of both crystalline calcium and crystalline oxalate and decreased the deposition of crystals in renal tissue. In vitro, Aluminum Citrate interacted directly with oxalate crystals to inhibit their uptake by proximal tubule cells. These results suggest that treating with Aluminum Citrate attenuates renal injury in rats with severe ethylene glycol toxicity, apparently by inhibiting calcium oxalate’s interaction with, and retention by, the kidney epithelium.
-
Aluminum Citrate inhibits cytotoxicity and aggregation of oxalate crystals.
Toxicology, 2006Co-Authors: Chungang Guo, Kenneth E McmartinAbstract:Calcium oxalate monohydrate (COM), which represents a major component of kidney stones, is an end metabolite of ethylene glycol. COM accumulation has been linked with acute renal toxicity in ethylene glycol poisoning. COM injures the kidney either by directly producing cytotoxicity to the kidney cells or by aggregating in the kidney lumen leading to the blockage of urine flow. The present studies were designed to examine whether Aluminum Citrate could reduce the toxicity of COM. Toxicity was determined in human proximal tubule cells by leakage of lactate dehydrogenase or uptake of ethidium homodimer and in erythrocytes by degree of hemolysis. Aluminum Citrate significantly inhibited the leakage of lactate dehydrogenase from human proximal tubule cells and protected against cell death from COM. The inhibitory effect of Aluminum Citrate was greater than that of other Citrate or Aluminum salts such as sodium Citrate, Aluminum chloride, calcium Citrate, ammonium Citrate or potassium Citrate. Aluminum Citrate significantly inhibited the aggregation of COM crystals in vitro and decreased red cell membrane damage from COM. Aluminum Citrate appeared to directly interact with COM, but not with the cell membrane. As such, Aluminum Citrate reduced the cytotoxicity by a physico-chemical interaction with the COM surface, and not by dissolving the COM crystals. These studies suggest that Aluminum Citrate may protect against tissue damage that occurs with high levels of oxalate accumulation, especially in ethylene glycol poisoning and possibly in hyperoxaluric states.
Andrew P Halestrap - One of the best experts on this subject based on the ideXlab platform.
-
Aluminum Citrate uptake by immortalized brain endothelial cells: implications for its blood-brain barrier transport.
Brain research, 2002Co-Authors: R A Yokel, Marieangela Wilson, Wesley R Harris, Andrew P HalestrapAbstract:The objective was to further test the hypothesis that Aluminum (Al) Citrate transport across the blood-brain barrier is mediated by a monocarboxylate transporter (MCT). Speciation calculations showed that Al Citrates were the predominant Al species under the conditions employed. Al Citrate did not inhibit lactate uptake and was not taken up by the rat erythrocyte, suggesting it does not serve as an effective substrate for either MCT1 or the anion exchanger. Studies were conducted with b.End5 cells derived from mouse brain endothelial cells to identify the properties of the carrier(s) mediating Al Citrate transport. Western blot analysis of b.End5 cells showed expression of the transferrin receptor and MCT1, but not MCT2 or MCT4. Uptake of Al Citrate was approximately 70% faster than Citrate. Citrate and Al Citrate uptake were sodium independent. Citrate uptake increased at pH 6.9 compared to 7.4, whereas Al Citrate uptake did not. Al Citrate uptake was reduced by inhibitors of mitochondrial respiration and oxidative phosphorylation, suggesting ATP dependence, but not by ouabain, suggesting no role for Na/K-ATPase. Uptake was not affected by alpha-ketoglutarate or malonate, substrates for the dicarboxylate carrier. Many substrates and inhibitors of MCT1 and organic anion transporters reduced Al Citrate uptake into b.End5 cells. BSP and fluorescein, organic anion transporter substrates/inhibitors, inhibited Al Citrate uptake. We conclude that Al Citrate transport across the blood-brain barrier is carrier-mediated, involving either an uncharacterized MCT isoform expressed in the brain such as MCT7 or MCT8 and/or one of the many members of the organic anion transporting protein family, some of which are known to be expressed at the blood-brain barrier.
-
Aluminum Citrate uptake by immortalized brain endothelial cells: implications for its blood-brain barrier transport.
Brain Research, 2002Co-Authors: R A Yokel, Wesley R Harris, Marieangela C. Wilson, Andrew P HalestrapAbstract:Abstract The objective was to further test the hypothesis that Aluminum (Al) Citrate transport across the blood–brain barrier is mediated by a monocarboxylate transporter (MCT). Speciation calculations showed that Al Citrates were the predominant Al species under the conditions employed. Al Citrate did not inhibit lactate uptake and was not taken up by the rat erythrocyte, suggesting it does not serve as an effective substrate for either MCT1 or the anion exchanger. Studies were conducted with b.End5 cells derived from mouse brain endothelial cells to identify the properties of the carrier(s) mediating Al Citrate transport. Western blot analysis of b.End5 cells showed expression of the transferrin receptor and MCT1, but not MCT2 or MCT4. Uptake of Al Citrate was ∼70% faster than Citrate. Citrate and Al Citrate uptake were sodium independent. Citrate uptake increased at pH 6.9 compared to 7.4, whereas Al Citrate uptake did not. Al Citrate uptake was reduced by inhibitors of mitochondrial respiration and oxidative phosphorylation, suggesting ATP dependence, but not by ouabain, suggesting no role for Na/K-ATPase. Uptake was not affected by α-ketoglutarate or malonate, substrates for the dicarboxylate carrier. Many substrates and inhibitors of MCT1 and organic anion transporters reduced Al Citrate uptake into b.End5 cells. BSP and fluorescein, organic anion transporter substrates/inhibitors, inhibited Al Citrate uptake. We conclude that Al Citrate transport across the blood–brain barrier is carrier-mediated, involving either an uncharacterized MCT isoform expressed in the brain such as MCT7 or MCT8 and/or one of the many members of the organic anion transporting protein family, some of which are known to be expressed at the blood–brain barrier.
-
Research report Aluminum Citrate uptake by immortalized brain endothelial cells: implications for its blood-brain barrier transport
2002Co-Authors: R A Yokel, Wesley R Harris, Marieangela C. Wilson, Andrew P HalestrapAbstract:The objective was to further test the hypothesis that Aluminum (Al) Citrate transport across the blood-brain barrier is mediated by a monocarboxylate transporter (MCT). Speciation calculations showed that Al Citrates were the predominant Al species under the conditions employed. Al Citrate did not inhibit lactate uptake and was not taken up by the rat erythrocyte, suggesting it does not serve as an effective substrate for either MCT1 or the anion exchanger. Studies were conducted with b.End5 cells derived from mouse brain endothelial cells to identify the properties of the carrier(s) mediating Al Citrate transport. Western blot analysis of b.End5 cells showed expression of the transferrin receptor and MCT1, but not MCT2 or MCT4. Uptake of Al Citrate was |70% faster than Citrate. Citrate and Al Citrate uptake were sodium independent. Citrate uptake increased at pH 6.9 compared to 7.4, whereas Al Citrate uptake did not. Al Citrate uptake was reduced by inhibitors of mitochondrial respiration and oxidative phosphorylation, suggesting ATP dependence, but not by ouabain, suggesting no role for Na / K-ATPase. Uptake was not affected by a-ketoglutarate or malonate, substrates for the dicarboxylate carrier. Many substrates and inhibitors of MCT1 and organic anion transporters reduced Al Citrate uptake into b.End5 cells. BSP and fluorescein, organic anion transporter substrates / inhibitors, inhibited Al Citrate uptake. We conclude that Al Citrate transport across the blood-brain barrier is carrier-mediated, involving either an uncharacterized MCT isoform expressed in the brain such as MCT7 or MCT8 and / or one of the many members of the organic anion transporting protein family, some of which are known to be expressed at the blood-brain barrier. © 2002 Elsevier Science B.V. All rights reserved. Theme: Neurotransmitters, modulators, transporters, and receptors Topic: Uptake and transporters
G.p. Willhite - One of the best experts on this subject based on the ideXlab platform.
-
Experimental Study of the Gelation Behavior of a Polyacrylamide/Aluminum Citrate Colloidal-Dispersion Gel System
SPE Journal, 1998Co-Authors: Raja Ranganathan, Robert Lewis, C.s. Mccool, D.w. Green, G.p. WillhiteAbstract:This paper (SPE 52503) was revised for publication from paper SPE 37220, first presented at the 1997 SPE International Symposium on Oilfield Chemistry held in Houston, 18-21 February. Original manuscript received for review 18 February 1997. Received manuscript revised 27 June 1998. Revised manuscript approved 5 August 1998. Summary The gelation behavior of a polyacrylamide/Aluminum Citrate colloidal-dispersion gel (CDG) system was investigated in sandpacks at frontal advance rates of 2 ft/D. A gelatinous mass formed where the gelant encountered a change in flow medium. Permeabilities of homogeneous media were reduced only by factors that were similar to those obtained with a polymer displacement alone. A laboratory investigation of a polyacrylamide/Aluminum Citrate CDG system was conducted to determine whether the system develops in-depth permeability modification in unconsolidated sandpacks. The study includes flow of the polymer and in-situ gelation behavior of the gelant in porous media and aggregate growth during the gelation reaction in beakers. Flow experiments were conducted in long unconsolidated sandpacks in which the gel solution was mixed in-line before injection. Injection rates were designed to provide adequate residence time for the gel solution to develop in-situ flow resistance during displacements based on bulk gel characterization tests. Residual resistance factors were determined following a static rest period in which the sandpack was left saturated with the injected gel solution. For comparison, apparent viscosity and residual resistance factors were also determined for the polymer flowing through unconsolidated sandpacks. Membrane dialysis was used to study the aggregate size distribution of the gel system at selected times after mixing. In-depth in-situ flow resistance did not develop when the gelling solution was injected into the sandpacks at frontal advance rates of 2 ft/D. Propagation through the sandpack was similar to a polymer solution. Flow resistance was characterized by the formation of a gelatinous filter cake, which formed when the injected solution encountered a change in flow medium, such as a screen placed at the ends to retain sand in place, the interface between the 50-mesh coarse sand layer at the inlet and the rest of the sandpack, and void spaces. Delaying injection by 2 hours after mixing in-line (to simulate field conditions) resulted in severe front-end stripping of gel aggregates. In all cases, residual resistance factors for the gel solution were similar to those obtained with a polymer displacement alone. Effluent fractions from gel solution displacements never developed a gel structure, and their viscosities were significantly lower than the injected solution. In the study of gel size distribution, aggregates were not detected at reaction times of 4 and 8 hours. P. 337
-
An Experimental Study of the In Situ Gelation Behavior of a Polyacrylamide/Aluminum Citrate "Colloidal Dispersion" Gel in a Porous Medium and its Aggregate Growth During Gelation Reaction
All Days, 1997Co-Authors: Raja Ranganathan, Don W. Green, Robert Lewis, C.s. Mccool, G.p. WillhiteAbstract:Abstract A laboratory investigation of a polyacrylamide / Aluminum Citrate "colloidal dispersion" gel system was conducted to determine whether the system develops in-depth permeability modification in unconsolidated sandpacks. The study includes flow of the polymer and in situ gelation behavior of the gelant in porous media and aggregate growth during the gelation reaction in beakers. Flow experiments were conducted in long unconsolidated sandpacks where the gel solution was mixed in-line prior to injection. Injection rates were designed to provide adequate residence time for the gel solution to develop in situ flow resistance during displacements based on bulk gel characterization tests. Residual resistance factors were determined following a static rest period where the sandpack was left saturated with the injected gel solution. For comparison, apparent viscosity and residual resistance factors were also determined for the polymer flowing through unconsolidated sandpacks. Membrane dialysis was used to study the aggregate size distribution of the gel system at selected times after mixing. In-depth in situ flow resistance did not develop when the gelling solution was injected into the sandpacks at frontal advance rates of 2 ft/day. Propagation through the sandpack was similar to a polymer solution. Flow resistance was characterized by the formation of a gelatinous "filter cake" which formed when the injected solution encountered a change in flow medium, such as a screen placed at the ends to retain sand in place, the interface between the 50-mesh coarse sand layer at the inlet and the rest of the sandpack, and void spaces. Delaying injection by two hours after mixing in-line (to simulate field conditions) resulted in severe front-end stripping of gel aggregates. In all cases, residual resistance factors for the gel solution were similar to those obtained with a polymer displacement alone. Effluent fractions from gel solution displacements never developed a gel structure, and their viscosities were significantly lower than the injected solution. In the study of gel size distribution, aggregates were not detected at reaction times up to twelve hours. Introduction Application of gelled polymer treatments can significantly improve the amount of oil recoverable by displacement in waterflooding and other enhanced recovery operations in heterogeneous reservoirs containing zones of high permeability. A major factor influencing the success of such treatments is the extent to which the gel solution can be propagated into the reservoir before onset of gelation and formation of an immobile gel structure. Simulation of waterfloods following gelled polymer treatments has shown that in-depth placement of gels has a significant role in the incremental oil recoveries. The use of a partially hydrolyzed polyacrylamide-Aluminum Citrate "colloidal dispersion" gel has been claimed to produce long-term in-depth permeability modification in certain reservoirs resulting in significant incremental oil recoveries, and has been the subject of an extensive investigation in our laboratory. The polyacrylamide-Aluminum Citrate colloidal dispersion gel system developed by TIORCO Inc., Englewood, CO consists of low concentrations of HiVis 350, a partially hydrolyzed polyacrylamide with a viscosity average molecular weight of 27 million, and TIORCO 677, a chelated Aluminum Citrate solution. Typical concentrations used in this system are 300 ppm polymer and 15 ppm Al3+. This system is reported to be slow forming, thus allowing for in-depth permeability treatment of oil reservoirs. P. 103^
-
Improving reservoir conformance using gelled polymer systems. Fourteenth quarterly report, January 1, 1996--March 31, 1996
1996Co-Authors: D.w. Green, G.p. WillhiteAbstract:The general objectives are to (1) to identify and develop gelled polymer systems which have potential to improve reservoir conformance of fluid displacement processes, (2) to determine the performance of these systems in bulk and in porous media, and (3) to develop methods to predict the capability of these systems to recover oil from petroleum reservoirs. This work focuses on three types of gel systems - an aqueous polysaccharide (KUSP1) system that gels as a function of pH, the chromium(III)-polyacrylamide system and the Aluminum Citrate-polyacrylamide system. Laboratory research is directed at the fundamental understanding of the physics and chemistry of the gelation process in bulk form and in porous media. This knowledge will be used to develop conceptual and mathematical models of the gelation process. Mathematical models will then be extended to predict the performance of gelled polymer treatments in oil reservoirs. Technical progress of Task III, mechanisms of in situ gelation is presented in this progress report.
-
Improving reservoir conformance using gelled polymer systems. Quarterly report, 1 October 1995--31 December 1995
1996Co-Authors: D.w. Green, G.p. Willhite, C. Buller, S. Mccool, Shapour Vossoughi, M. MichnickAbstract:The general objectives are to (1) to identify and develop gelled polymer systems which have potential to improve reservoir conformance of fluid displacement processes, (2) to determine the performance of these systems in bulk and in porous media, and (3) to develop methods to predict the capability of these systems to recover oil from petroleum reservoirs. This work focuses on three types of gel systems -- an aqueous polysaccharide (KUSPL) system that gels as a function of pH, the chromium(Ill)-polyacrylamide system and the Aluminum Citrate-polyacrylamide system. Laboratory research is directed at the fundamental understanding of the physics and chemistry of the gelation process in bulk form and in porous media. This knowledge will be used to develop conceptual and mathematical models of the gelation process. Mathematical models will then be extended to predict the performance of gelled polymer treatments in oil reservoirs. Work has progressed on the size measurement of aggregates that form in the polyacrylamide-Aluminum Citrate ``colloidal dispersion`` system. The results from this study and other work on the polyacrylamide-Aluminum Citrate system indicate that aggregates and/or structure in the system may not occur unless the system is subjected to a shear deformation. Further work is required to determine if aggregates develop and crow in the polyacrylamide-Aluminum Citrate system.
-
Improving reservoir conformance using gelled polymer systems. Eleventh quarterly report, April 1, 1995--June 30, 1995
1995Co-Authors: D.w. Green, G.p. Willhite, C. Buller, S. Mccool, Shapour Vossoughi, M. MichnickAbstract:The general objectives are to (1) to identify and develop gelled polymer systems which have potential to improve reservoir conformance of fluid displacement processes, (2) to determine the performance of these systems in bulk and in porous media, and (3) to develop methods to predict the capability of these systems to recover oil from petroleum reservoirs. This work focuses on three types of gel systems -- an aqueous polysaccharide (KUSP1) system that gels as a function of pH, the chromium(III)-polyacrylamide system and the Aluminum Citrate-polyacrylamide system. Laboratory research is directed at the fundamental understanding of the physics and chemistry of the gelation process in bulk form and in porous media. This knowledge will be used to develop conceptual and mathematical models of the gelation process. Mathematical models will then be extended to predict the performance of gelled polymer treatments in oil reservoirs. Technical progress is described for the following tasks: physical and chemical characterization of gel systems; mechanisms of in situ gelation; and mathematical modelling of the gel systems.