The Experts below are selected from a list of 267 Experts worldwide ranked by ideXlab platform
Kraemer D. Luks - One of the best experts on this subject based on the ideXlab platform.
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Extending a classical EOS correlation to represent solid–Fluid Phase equilibria
Fluid Phase Equilibria, 2006Co-Authors: Kimberly E. Carter, Kraemer D. LuksAbstract:Abstract A strategy is presented for describing all the solid–Fluid Phase equilibria of a binary mixture, by combining a classical equation-of-state with a general mathematical artifice for the fugacity of the solid Phase. As a case study, the strategy is applied to predict the solid–Fluid Phase equilibria of the binary mixture methane + carbon dioxide using the Soave–Redlich–Kwong equation-of-state to represent all real and hypothetical Fluid Phases. A system stability criterion is used to identify the slg locus, which is the intersection of the sl and sg equilibrium regions.
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Patterns of solid–Fluid Phase equilibria: II. Interplay with Fluid Phase criticality and stability
Fluid Phase Equilibria, 2000Co-Authors: Joseph A. Labadie, D.c. Garcia, Kraemer D. LuksAbstract:Abstract In an earlier paper, the van der Waals equation of state was used in combination with a common mathematical artifice for the solid-Phase fugacity function to map out the slg loci for a model binary homologous series of solvent+solute mixtures as a function of the solute's parametric characterization. The computations suggested new possibilities for solid–Fluid Phase equilibrium topography, heretofore not reported in the literature. To provide a better understanding of these computations, the authors have computed and mapped out the critical point loci, concurrently applying Phase and system stability analysis. These new computations, which confirm the earlier solid–Fluid computations, provide a detailed picture of how the solid–Fluid topography for this particular series of model mixtures evolves as solvent–solute parametric differences increase.
Howard S Kruth - One of the best experts on this subject based on the ideXlab platform.
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Interleukin 10 promotes macrophage uptake of HDL and LDL by stimulating Fluid-Phase endocytosis
Biochimica et biophysica acta. Molecular and cell biology of lipids, 2019Co-Authors: Diego Lucero, Howard S Kruth, Promotto Islam, Lita A. Freeman, Xueting Jin, Milton Pryor, Jingrong Tang, Alan T. RemaleyAbstract:Abstract Objective Highly elevated plasma levels of interleukin-10 (IL-10) are causally associated with “Disappearing HDL Syndrome” and low plasma LDL-cholesterol, but the underlying mechanism is poorly understood. Fluid-Phase endocytosis, a process highly dependent on actin dynamics, enables cells to internalize relatively high amounts of extracellular Fluids and solutes. We sought to investigate whether IL-10 induces lipoprotein uptake by Fluid-Phase endocytosis in macrophages. Methods and results Macrophages (RAW264.7, Kupffer and human) were incubated with vehicle (PBS) or IL-10 (20 ng/ml) for 7 days. Uptake of HDL, LDL, and/or Fluid-Phase endocytosis probes (albumin-Alexa680®, 70 kDa FITC-Dextran and Lucifer Yellow, LY) was evaluated by FACS. Intracellular cofilin and phosphorylated cofilin (p-cofilin) levels were determined by immunoblotting. Macrophage uptake of lipoproteins and probes was non-saturable and increased after IL-10 incubation (p Conclusions Interleukin-10 induces the uptake of HDL and LDL by Fluid-Phase endocytosis by increasing actin-filament rearrangement in macrophages, thus providing a plausible mechanism contributing to “Disappearing HDL Syndrome”.
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measurement of aortic cell Fluid Phase pinocytosis in vivo by flow cytometry
Journal of Vascular Research, 2017Co-Authors: Joshua J Anzinger, Clovis S Palmer, Pradeep K Dagur, Manoj Kumar Barthwal, Howard S KruthAbstract:Objective: Fluid-Phase pinocytosis is a receptor-independent mechanism of endocytosis that occurs in all mammalian cells and may be a mechanism for the uptake of LDL by macrophages. As there are currently no methods for the measurement of Fluid-Phase pinocytosis by individual aortic cells in vivo, we sought to identify a suitable method. Methods: ApoE-/- mice were retro-orbitally injected with AngioSPARK fluorescent nanoparticles specifically designed to not interact with cells. After 24 h, mice were sacrificed, and the aortas were isolated and then digested to analyze aortic cell uptake of AngioSPARK by flow cytometry. Results: CD11b-expressing aortic macrophages from mice injected with AngioSPARK showed high levels of Fluid-Phase pinocytosis compared to aortic cells not expressing CD11b (4,393.7 vs. 408.3 mean fluorescence intensity [MFI], respectively). Conclusion: This new technique allows for the measurement of Fluid-Phase pinocytosis by aortic cells in vivo, making it possible to examine the cell-signaling molecules and drugs that affect this process. Published by S. Karger AG, Basel
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Fluid Phase pinocytosis of ldl by macrophages a novel target to reduce macrophage cholesterol accumulation in atherosclerotic lesions
Current Pharmaceutical Design, 2013Co-Authors: Howard S KruthAbstract:Circulating low-density lipoprotein (LDL) that enters the blood vessel wall is the main source of cholesterol that accumulates within atherosclerotic plaques. Much of the deposited cholesterol accumulates within plaque macrophages converting these macrophages into cholesterol-rich foamy looking cells. Cholesterol accumulation in macrophages contributes to cholesterol retention within the vessel wall, and promotes vessel wall inflammation and thrombogenicity. Thus, how macrophages accumulate cholesterol and become foam cells has been the subject of intense investigation. It is generally believed that macrophages accumulate cholesterol only through scavenger receptor-mediated uptake of modified LDL. However, an alternative mechanism for macrophage foam cell formation that does not depend on LDL modification or macrophage receptors has been elucidated. By this alternative mechanism, macrophages show receptor-independent uptake of unmodified native LDL that is mediated by Fluid-Phase pinocytosis. In receptor-independent, Fluid-Phase pinocytosis, macrophages take up LDL as part of the Fluid that they ingest during micropinocytosis within small vesicles called micropinosomes, and by macropinocytosis within larger vacuoles called macropinosomes. This produces cholesterol accumulation in macrophages to levels characteristic of macrophage foam cells in atherosclerotic plaques. Fluid-Phase pinocytosis of LDL is a plausible mechanism that can explain how macrophages accumulate cholesterol and become disease-causing foam cells. Fluid-Phase pinocytosis of LDL is a relevant pathway to target for modulating macrophage cholesterol accumulation in atherosclerosis. Recent studies show that phosphoinositide 3-kinase (PI3K), liver X receptors (LXRs), the macrophage colony-stimulating factor (M-CSF) receptor, and protein kinase C (PKC) mediate macrophage macropinocytosis of LDL, and thus, these may be relevant targets to inhibit macrophage cholesterol accumulation in atherosclerosis.
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murine bone marrow derived macrophages differentiated with gm csf become foam cells by pi3kγ dependent Fluid Phase pinocytosis of native ldl
Journal of Lipid Research, 2012Co-Authors: Joshua J Anzinger, Manoj Kumar Barthwal, Janet Chang, Thomas Bohnacker, Matthias P Wymann, Qing Xu, Howard S KruthAbstract:Accumulation of cholesterol by macrophage uptake of LDL is a key event in the formation of atherosclerotic plaques. Previous research has shown that granulocyte-macrophage colony-stimulating factor (GM-CSF) is present in atherosclerotic plaques and promotes aortic lipid accumulation. However, it has not been determined whether murine GM-CSF-differentiated macrophages take up LDL to become foam cells. GM-CSF-differentiated macrophages from LDL receptor-null mice were incubated with LDL, resulting in massive macrophage cholesterol accumulation. Incubation of LDL receptor-null or wild-type macrophages with increasing concentrations of ¹²?I-LDL showed nonsaturable macrophage LDL uptake that was linearly related to the amount of LDL added, indicating that LDL uptake was mediated by Fluid-Phase pinocytosis. Previous studies suggest that phosphoinositide 3-kinases (PI3K) mediate macrophage Fluid-Phase pinocytosis, although the isoform mediating this process has not been determined. Because PI3K? is known to promote aortic lipid accumulation, we investigated its role in mediating macrophage Fluid-Phase pinocytosis of LDL. Wild-type macrophages incubated with LDL and the PI3K? inhibitor AS605240 or PI3K?-null macrophages incubated with LDL showed an ?50% reduction in LDL uptake and cholesterol accumulation compared with wild-type macrophages incubated with LDL only. These results show that GM-CSF-differentiated murine macrophages become foam cells by Fluid-Phase pinocytosis of LDL and identify PI3K? as contributing to this process.
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fluorescent pegylated nanoparticles demonstrate Fluid Phase pinocytosis by macrophages in mouse atherosclerotic lesions
Journal of Clinical Investigation, 2009Co-Authors: Chiara Buono, Joshua J Anzinger, Marcelo Amar, Howard S KruthAbstract:The uptake of lipoproteins by macrophages is a critical step in the development of atherosclerotic lesions. Cultured monocyte-derived macrophages take up large amounts of native LDL by receptor-independent Fluid-Phase pinocytosis, either constitutively or in response to specific activating stimuli, depending on the macrophage phenotype. We therefore sought to determine whether Fluid-Phase pinocytosis occurs in vivo in macrophages in atherosclerotic lesions. We demonstrated that fluorescent pegylated nanoparticles similar in size to LDL (specifically nontargeted Qtracker quantum dot and AngioSPARK nanoparticles) can serve as models of LDL uptake by Fluid-Phase pinocytosis in cultured human monocyte–derived macrophages and mouse bone marrow–derived macrophages. Using fluorescence microscopy, we showed that atherosclerosis-prone Apoe-knockout mice injected with these nanoparticles displayed massive accumulation of the nanoparticles within CD68+ macrophages, including lipid-containing foam cells, in atherosclerotic lesions in the aortic arch. Similar results were obtained when atherosclerotic mouse aortas were cultured with nanoparticles in vitro. These results show that macrophages within atherosclerotic lesions can take up LDL-sized nanoparticles by Fluid-Phase pinocytosis and indicate that Fluid-Phase pinocytosis of LDL is a mechanism for macrophage foam cell formation in vivo.
Keith E Gubbins - One of the best experts on this subject based on the ideXlab platform.
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Molecular simulation of Fluid Phase equilibria
Pure and Applied Chemistry, 1993Co-Authors: Keith E GubbinsAbstract:Recent advances in direct and indirect methods of molecular simulation for studying Fluid Phase equilibria are reviewed. The emphasis is on Phase equilibria for Fluids of nonspherical molecules, including ionic Fluids, aqueous mixtures, hydrocarbons and chain molecules.
Wolfgang Arlt - One of the best experts on this subject based on the ideXlab platform.
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Modeling of solid/Fluid Phase equilibria in multicomponent systems at high pressure
Chemical Engineering & Technology, 2001Co-Authors: Matthias Seiler, J. Groß, B. Bungert, Gabriele Sadowski, Wolfgang ArltAbstract:A model is derived which enables the calculation of solid/Fluid Phase equilibria in multicomponent systems over the entire pressure range. The model requires only generally available caloric data of the pure solids. The non-ideality of the Fluid Phase is described using the SAFT equation of state. The model is verified on experimental Phase equilibrium data of binary and ternary n-alkane mixtures as well as on the system naphthalene-CO 2 .
Eric Jakobsson - One of the best experts on this subject based on the ideXlab platform.
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incorporation of surface tension into molecular dynamics simulation of an interface a Fluid Phase lipid bilayer membrane
Biophysical Journal, 1995Co-Authors: See Wing Chiu, M Clark, V Balaji, Shankar Subramaniam, H L Scott, Eric JakobssonAbstract:In this paper we report on the molecular dynamics simulation of a Fluid Phase hydrated dimyristoylphosphatidylcholine bilayer. The initial configuration of the lipid was the x-ray crystal structure. A distinctive feature of this simulation is that, upon heating the system, the Fluid Phase emerged from parameters, initial conditions, and boundary conditions determined independently of the collective properties of the Fluid Phase. The initial conditions did not include chain disorder characteristic of the Fluid Phase. The partial charges on the lipids were determined by ab initio self-consistent field calculations and required no adjustment to produce a Fluid Phase. The boundary conditions were constant pressure and temperature. Thus the membrane was not explicitly required to assume an area/phospholipid molecule thought to be characteristic of the Fluid Phase, as is the case in constant volume simulations. Normal to the membrane plane, the pressure was 1 atmosphere, corresponding to the normal laboratory situation. Parallel to the membrane plane a negative pressure of -100 atmospheres was applied, derived from the measured surface tension of a monolayer at an air-water interface. The measured features of the computed membrane are generally in close agreement with experiment. Our results confirm the concept that, for appropriately matched temperature and surface pressure, a monolayer is a close approximation to one-half of a bilayer. Our results suggest that the surface area per phospholipid molecule for Fluid phosphatidylcholine bilayer membranes is smaller than has generally been assumed in computational studies at constant volume. Our results confirm that the basis of the measured dipole potential is primarily water orientations and also suggest the presence of potential barriers for the movement of positive charges across the water-headgroup interfacial region of the phospholipid.