Relevant bibliographies by topics / LDL transport

Academic literature on the topic 'LDL transport'

Author: Grafiati
Published: 14 March 2023

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Journal articles on the topic "LDL transport"

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Rutledge, J. C. "Temperature and hydrostatic pressure-dependent pathways of low-density lipoprotein transport across microvascular barrier." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 1 (January 1, 1992): H234—H245. http://dx.doi.org/10.1152/ajpheart.1992.262.1.h234.

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To further investigate the chemical and physical nature of low-density lipoprotein (LDL) transport pathways across intact microvessels, the effect of changes in temperature and microvessel hydrostatic pressure were measured in individually perfused postcapillary vessels within frog mesenteric vascular beds. LDL microvessel transport was measured at two microvessel temperature ranges (18-21 degrees C and 4-6 degrees C) and compared with transport of fluorescein, a small solute. Also, LDL transport was measured at a series of hydrostatic pressures (3-20 cmH2O) at microvessel temperatures of 18-21 degrees C and 4-6 degrees C to determine whether LDL transport was coupled to water flow, which would be evidence for hydraulic pathways of solute transport across the microvascular barrier. Quantitative fluorescence microscopy was employed to determine apparent solute permeability coefficients (Ps) under the various temperature and hydrostatic pressure conditions studied. The ratio of Ps fluorescein 18-21 degrees C/4-6 degrees C [1.6 +/- 0.3 (SD)] indicated that fluorescein was freely diffusible across the microvascular barrier through water-filled pathways as transport was inversely proportional to temperature-dependent changes in viscosity. The larger ratio for LDL (Ps LDL 18-21/4-6 degrees C = 9.5 +/- 8.1) than for fluorescein cannot be explained by LDL transport through fixed hydraulic pathways alone and suggests additional or alternate LDL transport mechanisms. In addition, Ps LDL increased as microvessel hydrostatic pressure increased at microvessel temperatures of 18-21 degrees C but not at 4-6 degrees C. Coupling of LDL transport to water flow at the high microvessel temperature range, but not at the low range, indicated the presence of a hydraulic transport pathway that was effectively absent when the microvessel was cooled. These results demonstrated a highly temperature and hydrostatic pressure-dependent LDL pathway that is consistent with a dynamic porous extracellular or transcellular mechanism of LDL transport.
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von Eckardstein, Arnold. "LDL Contributes to Reverse Cholesterol Transport." Circulation Research 127, no. 6 (August 28, 2020): 793–95. http://dx.doi.org/10.1161/circresaha.120.317721.

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Kakava, Sofia, Eveline Schlumpf, Grigorios Panteloglou, Flavia Tellenbach, Arnold von Eckardstein, and Jerome Robert. "Brain Endothelial Cells in Contrary to the Aortic Do Not Transport but Degrade Low-Density Lipoproteins via Both LDLR and ALK1." Cells 11, no. 19 (September 28, 2022): 3044. http://dx.doi.org/10.3390/cells11193044.

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The transport of low-density lipoprotein (LDL) through the endothelium is a key step in the development of atherosclerosis, but it is notorious that phenotypic differences exist between endothelial cells originating from different vascular beds. Endothelial cells forming the blood–brain barrier restrict paracellular and transcellular passage of plasma proteins. Here, we systematically compared brain versus aortic endothelial cells towards their interaction with LDL and the role of proteins known to regulate the uptake of LDL by endothelial cells. Both brain endothelial cells and aortic endothelial cells bind and internalize LDL. However, whereas aortic endothelial cells degrade very small amounts of LDL and transcytose the majority, brain endothelial cells degrade but do not transport LDL. Using RNA interference (siRNA), we found that the LDLR–clathrin pathway leads to LDL degradation in either endothelial cell type. Both loss- and gain-of-function experiments showed that ALK1, which promotes transcellular LDL transport in aortic endothelial cells, also limits LDL degradation in brain endothelial cells. SR-BI and caveolin-1, which promote LDL uptake and transport into aortic endothelial cells, limit neither binding nor association of LDL to brain endothelial cells. Together, these results indicate distinct LDL trafficking by brain microvascular endothelial cells and aortic endothelial cells.
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Cancel, Limary M., Andrew Fitting, and John M. Tarbell. "In vitro study of LDL transport under pressurized (convective) conditions." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 1 (July 2007): H126—H132. http://dx.doi.org/10.1152/ajpheart.01188.2006.

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It is difficult to assess the transport pathways that carry low-density lipoprotein (LDL) into the artery wall in vivo, and there has been no previous in vitro study that has examined transendothelial transport under physiologically relevant pressurized (convective) conditions. Therefore, we measured water, albumin, and LDL fluxes across bovine aortic endothelial cell (BAEC) monolayers in vitro and determined the relative contributions of vesicles, paracellular transport through “breaks” in the tight junction, and “leaky” junctions associated with dying or dividing cells. Our results show that leaky junctions are the dominant pathway for LDL transport (>90%) under convective conditions and that albumin also has a significant component of transport through leaky junctions (44%). Transcellular transport of LDL by receptor-mediated processes makes a minor contribution (<10%) to overall transport under convective conditions.
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Li, Xiaoyin, Xiao Liu, Peng Zhang, Chenglong Feng, Anqiang Sun, Hongyan Kang, Xiaoyan Deng, and Yubo Fan. "Numerical simulation of haemodynamics and low-density lipoprotein transport in the rabbit aorta and their correlation with atherosclerotic plaque thickness." Journal of The Royal Society Interface 14, no. 129 (April 2017): 20170140. http://dx.doi.org/10.1098/rsif.2017.0140.

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Two mechanisms of shear stress and mass transport have been recognized to play an important role in the development of localized atherosclerosis. However, their relationship and roles in atherogenesis are still obscure. It is necessary to investigate quantitatively the correlation among low-density lipoproteins (LDL) transport, haemodynamic parameters and plaque thickness. We simulated blood flow and LDL transport in rabbit aorta using computational fluid dynamics and evaluated plaque thickness in the aorta of a high-fat-diet rabbit. The numerical results show that regions with high luminal LDL concentration tend to have severely negative haemodynamic environments (HEs). However, for regions with moderately and slightly high luminal LDL concentration, the relationship between LDL concentration and the above haemodynamic indicators is not clear cut. Point-by-point correlation with experimental results indicates that severe atherosclerotic plaque corresponds to high LDL concentration and seriously negative HEs, less severe atherosclerotic plaque is related to either moderately high LDL concentration or moderately negative HEs, and there is almost no atherosclerotic plaque in regions with both low LDL concentration and positive HEs. In conclusion, LDL distribution is closely linked to blood flow transport, and the synergetic effects of luminal surface LDL concentration and wall shear stress-based haemodynamic indicators may determine plaque thickness.
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Liscum, L., R. M. Ruggiero, and J. R. Faust. "The intracellular transport of low density lipoprotein-derived cholesterol is defective in Niemann-Pick type C fibroblasts." Journal of Cell Biology 108, no. 5 (May 1, 1989): 1625–36. http://dx.doi.org/10.1083/jcb.108.5.1625.

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Niemann-Pick disease type C (NPC) is characterized by substantial intracellular accumulation of unesterified cholesterol. The accumulation of unesterified cholesterol in NPC fibroblasts cultured with low density lipoprotein (LDL) appears to result from the inability of LDL to stimulate cholesterol esterification in addition to impaired LDL-mediated downregulation of LDL receptor activity and cellular cholesterol synthesis. Although a defect in cholesterol transport in NPC cells has been inferred from previous studies, no experiments have been reported that measure the intracellular movement of LDL-cholesterol specifically. We have used four approaches to assess intracellular cholesterol transport in normal and NPC cells and have determined the following: (a) mevinolin-inhibited NPC cells are defective in using LDL-cholesterol for growth. However, exogenously added mevalonate restores cell growth equally in normal and NPC cells; (b) the transport of LDL-derived [3H]cholesterol to the plasma membrane is slower in NPC cells, while the rate of appearance of [3H]acetate-derived, endogenously synthesized [3H]cholesterol at the plasma membrane is the same for normal and NPC cells; (c) in NPC cells, LDL-derived [3H]cholesterol accumulates in lysosomes to higher levels than normal, resulting in defective movement to other cell membranes; and (d) incubation of cells with LDL causes an increase in cholesterol content of NPC lysosomes that is threefold greater than that observed in normal lysosomes. Our results indicate that a cholesterol transport defect exists in NPC that is specific for LDL-derived cholesterol.
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Pfisterer, Simon G., Johan Peränen, and Elina Ikonen. "LDL–cholesterol transport to the endoplasmic reticulum." Current Opinion in Lipidology 27, no. 3 (June 2016): 282–87. http://dx.doi.org/10.1097/mol.0000000000000292.

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Kang, Hongyan, Jiali Yang, Weichen Zhang, Jinyan Lu, Xuejiao Ma, Anqiang Sun, and Xiaoyan Deng. "Effect of endothelial glycocalyx on water and LDL transport through the rat abdominal aorta." American Journal of Physiology-Heart and Circulatory Physiology 320, no. 4 (April 1, 2021): H1724—H1737. http://dx.doi.org/10.1152/ajpheart.00861.2020.

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A 42% degradation of the endothelial glycocalyx by hyaluronidase of the isolated rat abdominal aorta facilitated water and LDL transport across the vessel wall, suggesting endothelial glycocalyx as a transport barrier. A 24-h shear exposure increased LDL mean maximum infiltration distance, and enhanced EC apoptosis, which could be both inhibited by hyaluronidase treatment, suggesting endothelial glycocalyx may also act as a mechanosensor of shear to regulate EC apoptosis, thus affecting leaky junctions and regulating LDL transport.
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Skeggs, Josephine W., and Richard E. Morton. "LDL and HDL enriched in triglyceride promote abnormal cholesterol transport." Journal of Lipid Research 43, no. 8 (August 2002): 1264–74. http://dx.doi.org/10.1194/jlr.m100431-jlr200.

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Hypertriglyceridemia induces multiple changes in lipoprotein composition. Here we investigate how one of these modifications, triglyceride (TG) enrichment, affects HDL and LDL function when this alteration occurs under conditions in which more polar components can naturally re-equilibrate. TG-enriched lipoproteins were produced by co-incubating VLDL, LDL, and HDL with cholesteryl ester (CE) transfer protein. The resulting 2.5-fold increase in TG/CE ratio did not measurably alter the apoprotein composition of LDL or HDL, or modify LDL size. HDL mean diameter increased slightly from 9.1 to 9.4 nm. Modified LDL was internalized by fibroblasts normally, but its protein was degraded much less efficiently. This likely reflects an aberrant apolipoprotein B (apoB) conformation, as suggested by its resistance to V8 protease digestion and altered LDL electrophoretic mobility. TG-enriched LDL ineffectively down-regulated cholesterol biosynthesis compared with control LDL at the same protein concentration, but was equivalent in sterol regulation when compared on a cholesterol basis. TG-enriched HDL promoted greater net cholesterol efflux from cholesterol-loaded J774 cells. However, cholesterol associated with TG-enriched HDL was inefficiently esterified by lecithin:cholesterol acyltransferase, and TG-enriched HDLs were poor donors of CE to HepG2 hepatocytes by selective uptake.We conclude that TG-enrichment, in the absence of other significant alterations in lipoprotein composition, is sufficient to alter both cholesterol delivery and removal mechanisms. Some of these abnormalities may contribute to increased coronary disease in hypertriglyceridemia.
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Jensen, Jan Skov, Bo Feldt-Rasmussen, Knut Borch-Johnsen, Kurt Svarre Jensen, and Børge Grønne Nordestgaard. "Increased Transvascular Lipoprotein Transport in Diabetes: Association with Albuminuria and Systolic Hypertension." Journal of Clinical Endocrinology & Metabolism 90, no. 8 (August 1, 2005): 4441–45. http://dx.doi.org/10.1210/jc.2004-2420.

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Abstract Context: Diabetes is associated with a highly increased risk of atherosclerosis, especially if hypertension or albuminuria is present. Objective: We hypothesized that the increased transvascular lipoprotein transport in diabetes may be further accelerated if hypertension or albuminuria is present, possibly explaining increased intimal lipoprotein accumulation and thus atherosclerosis. Design: The study was cross-sectional and was performed in 1999–2002. Setting: The study took place in the referral center. Patients: The patients included 60 with diabetes mellitus (27 with type 1 diabetes and 33 with type 2 diabetes) and 42 healthy controls. All were randomly recruited. Main Outcome Measure: We used an in vivo method for measurement of transvascular transport of low-density lipoprotein (LDL). Autologous 131I-LDL was reinjected iv, and the 1-h fractional escape rate was taken as an index of transvascular transport. Results: Transvascular LDL transport was 1.8 (1.6–2.0), 2.3 (2.0–2.6), and 2.6 (1.3–4.0)%/[h × (liter/m2)] in healthy controls, diabetic controls, and diabetes patients with systolic hypertension or albuminuria, respectively (P = 0.013; F = 4.5; df =2; ANOVA). These differences most likely were not caused by altered hepatic LDL receptor expression, glycosylation of LDL, small LDL size, or medicine use. Conclusions: Transvascular LDL transport is increased in patients with diabetes mellitus, especially if systolic hypertension or albuminuria is present. Accordingly, lipoprotein flux into the arterial wall could be increased in these patients, possibly explaining accelerated development of atherosclerosis.
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Dissertations / Theses on the topic "LDL transport"

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Weinert, Sönke. "Der interzelluläre Transport Lipid-geladener Lysosomen aus Makrophagen in glatte Gefäßmuskelzellen führt zur phänotypischen Veränderung der Gefäßmuskelzellen in einen schaumzellartigen Phänotyp." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-150397.

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AIMS: Macrophages (MPs) and vascular smooth muscle cells (VSMCs) closely interact within the growing atherosclerotic plaque. An in vitro co-culture model was established to study how MPs modulate VSMC behaviour. METHODS AND RESULTS: MPs were exposed to fluorescence-labelled-acetylated LDL (FL-acLDL) prior to co-culture with VSMCs. Fluorescence microscopy visualized first transport of FL-acLDL within 6 h after co-culture implementation. When MPs had been fed with FL-acLDL in complex with fluorescence-labelled cholesterol (FL-Chol), these complexes were also transferred during co-culture and resulted in cholesterol positive lipid droplet formation in VSMCs. When infected with a virus coding for a fusion protein of Rab5a and fluorescent protein reporter (FP) to mark early endosomes, no co-localization between Rab5a-FP and the transported FL-acLDL within VSMCs was detected implying a mechanism independent of phagocytosis. Next, expression of lysosome-associated membrane glycoprotein 1 (LAMP1)-FP, marking all lysosomes in VSMCs, revealed that the FL-acLDL was located in non-acidic lysosomes. MPs infected with virus encoding for LAMP1-FP prior to co-culture demonstrated that intact fluorescence-marked lysosomes were transported into the VSMC, instead. Xenogenic cell composition (rat VSMC, human MP) and subsequent quantitative RT-PCR with rat-specific primers rendered induction of genes typical for MPs and down-regulation of the cholesterol sensitive HMG-CoA reductase. CONCLUSION: Our results demonstrate that acLDL/cholesterol-loaded lysosomes are transported from MPs into VSMCs in vitro. Lysosomal transfer results in a phenotypic alteration of the VSMC towards a foam cell-like cell. This way VSMCs may lose their plaque stabilizing properties and rather contribute to plaque destabilization and rupture.
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Curmi, Patrick. "Transport des lipoproteines de basse densite dans la paroi arterielle. Role fonctionnel des recepteurs ldl, effets de l'hyperpression arterielle." Paris 11, 1991. http://www.theses.fr/1991PA112127.

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Le cholesterol des plaques d'atherosclerose provient des lipoproteines de basse densite (ldl) d'origine plasmatique. Dans cette these, apres avoir decrit l'histoire de la decouverte des ldl et de leur implication dans l'atherosclerose, nous avons etudie dans l'aorte thoracique isolee de lapin, le role: 1) des recepteurs ldl dans le transport et la degradation des ldl. 2) de l'hyperpression sur le transport et la distribution des ldl. Dans la premiere etude, en comparant le devenir de ldl normales (ldln) a celui de ldl methylees, qui perdent leur capacite a etre reconnues par les recepteurs ldl, nous avons demontre que les recepteurs ldl sont actifs dans la paroi arterielle, qu'ils participent a la degradation des ldl, la partie interne de l'artere etant cataboliquement plus active que la media externe. Cette activite catabolique des recepteurs ldl pourrait prevenir l'accumulation de ldl dans la paroi arterielle a l'origine du processus atherosclereux. Dans la deuxieme etude, nous avons montre que l'hyperpression transmurale provoque une accumulation de ldl tres importante dans les couches internes de la paroi arterielle due a l'action synergique d'une augmentation de la permeabilite endotheliale, d'une augmentation de la convection des ldl, et d'une compaction de la media. Ces effets pourraient representer un des mecanismes par lesquels l'hypertension accelere le processus atherosclereux
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Dachet, Christiane. "Mode d'action d'un médicament hypolipidémiant , le Probucol : transport et catabolisme des LDL, modifications des propriétés physico-chimiques des lipoprotéines plasmatiques." Paris 12, 1987. http://www.theses.fr/1987PA120055.

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Dachet, Christiane. "Mode d'action d'un médicament hypolipidémiant, le Probucol transport et catabolisme des LDL, modification des propriétés physico-chimiques des lipoprotéines plasmatiques /." Grenoble 2 : ANRT, 1987. http://catalogue.bnf.fr/ark:/12148/cb376042497.

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Morris, Evan Daniel. "The role of the low-density lipoprotein receptor in transport and metabolism of LDL through the wall of normal rabbit aorta in vivo. Estimation of model parameters from optimally designed dual-tracer experiments." Case Western Reserve University School of Graduate Studies / OhioLINK, 1991. http://rave.ohiolink.edu/etdc/view?acc_num=case1055528562.

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Jesionek, Katarzyna. "Proces transportu lipoprotein niskiej gęstości (LDL) w ścianach naczyń krwionośnych." Doctoral thesis, Katowice: Uniwersytet Śląski, 2017. http://hdl.handle.net/20.500.12128/5753.

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The accumulation of low density lipoproteins within the arterial wall is associated with process of atherogenesis. Moreover, it is commonly accepted, that the development of the atherosclerotic plaque is enhanced by the biomechanical factors, such as hypertension and low wall shear stress. In addition to medical experiments, computational simulations of the LDL transport in the vascular wall are an important tool in the study of atherosclerosis. Simulations of the LDL transport affected by that biomechanical factors can improve the understanding of mechanisms responsible for the atherogenesis. In this thesis the extended theoretical model of the LDL transport in the arterial wall is introduced. Proposed model for the first time take into account two mentioned biomechanical factors simultaneously. In this model arterial wall is considered as a medium composed of four homogeneous porous layers. The transport of macromolecules in such structure is described by the volume-averaged advectiondiffusion- reaction equation. The first part of the thesis contains biological and physical basis of the modeling. In this part the process of atherogenesis affected by biomechanical factors is presented. Then the transport processes in porous media are discussed. In the main part of this thesis the extended four layer model of the LDL transport in the arterial wall is presented. In this section, differences between proposed model and other models, known from literature are emphasized. Moreover, the procedure of transport parameters estimation is described in details. It is important because in literature there are some extremely different transport parameters sets for the LDL transport in the vessel wall. The most important part of this section is the description of methods, which allow to impose biomechanical factors to the modelling. In the next part of the thesis results obtained in the modeling are discussed. This section is divided into two main parts. In the first one the influence of biomechanical factors on one-dimensional LDL concentration profiles within the arterial wall is investigated. In the second part, the example of applying the proposed model to analysis of clinical data is presented. The CT based geometry of the right coronary artery was used in calculations. To sum up, in the thesis it has been shown that it is possible to accurate model the LDL transport with good agreement with experiments. It can be the first step for clinical usage of theoretical calculations of the LDL transport in the arterial wall. Moreover, the analysis of the influence of biomechanical factors on this transport has allowed us to draw conclusions about reasons of the LDL accumulation process in the vessel wall.
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Luvualo, Nginamau Engrácia Simão. "Recrutamento e seleção na Macon Transportes, LDA." Master's thesis, Instituto Superior de Economia e Gestão, 2016. http://hdl.handle.net/10400.5/12534.

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Mestrado em Gestão de Recursos Humanos
O presente Trabalho Final de Mestrado reflete no desenvolvimento de um estágio curricular, com duração de três meses na área de Recursos Humanos, departamento de Recrutamento e Seleção da empresa Macon Transportes Lda. O objetivo deste trabalho passa pela apresentação detalhada das atividades relacionadas com o processo de recrutamento e seleção desenvolvidas na empresa Macon. O desafio atual é a condução do processo de contratação que, na maioria das vezes é falho por falta de critérios e instrumentos adequados e que na maioria das vezes pode gerar grandes perdas financeiras e perda de tempo. Desta feita, a primeira parte do relatório é dedicado ao enquadramento teórico, seguindo-se uma breve apresentação da instituição (MACON Transportes, Lda.), na terceira parte, foram apresentadas e detalhadas as atividades realizadas ao longo do estágio, e subsequentemente na quarta foram pormenorizadas as atividades desenvolvidas na empresa no período do estágio e por fim, foram elaboradas as discussões e conclusões e apresentadas as limitações e sugestões. O objetivo final do relatório de estágio é descrever as funções exercidas e as tarefas efetuadas, explicitando a relação entre a formação obtida ao longo do curso de mestrado e a sua aplicação no trabalho na empresa.
This present Masters Degree Final Work, reflects the development of an curricular internship, with a duration of three months in Human Resources area, department of Recruitment and selection of Macon Transport Lda company. The objective of this work goes through the detailed presentation of activities related to the procedure for recruitment and selection developed in Macon Company. . The current challenge is to leading the hiring process that most of the times it´s flawed for lack of criteria and instrument that in most of the times can cause great financial and time losses. By this, the first part of the report is dedicated to the theoretical framework, followed by a brief presentation of the institution (MACON Transportes, Lda.), in the third part, we were presented and detailed the activities carried out throughout the internship, and subsequently in the fourth they were detailed the activities developed at the company at internship period and finally were prepared the discussions and conclusions and brought the limitations and suggestions. The ultimate goal of internship report is to describe the functions exercised and performed tasks, explaining the relation between the training obtained along master course and its application at work in the company
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Yang, Xiao. "Green Hub Location-Routing Problem for LTL transport." Thesis, Nantes, 2018. http://www.theses.fr/2018NANT4034/document.

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Le problème de localisation de hubs et tournées combinées (Hub Location-Routing Problem, HLRP), concerne la conception d’un réseau de transport performant entre de nombreuses origines (fournisseurs) et destinations (clients). Ce système est basé sur la localisation de plates formes (hubs) permettant de concentrer les flux et l’organisation de tournées pour la collecte des marchandises des fournisseurs et la distribution vers les clients. Nous étudions le cas spécifique du HLRP à capacités et allocations uniques (CSAHLRP) et de processus de tournées de collecte et distribution séparés. Nous proposons un modèle de programmation linéaire mixte (MILP) et un Algorithme Mémétique (MA) pour ce problème en vue de la minimisation du coût total du réseau de transport. De plus, nous étendons le modèle MILP pour le cas bi-objectif afin de minimiser à la fois le coût total et les émissions de CO2 du transport. Notre algorithme Mémétique (MA) et adapté et combiné à un algorithme génétique de tri non-dominé élitiste rapide (NSGAII) afin de déterminer des approximations du front de Pareto. Enfin, nous proposons une procédure en deux phases pour résoudre le HLRP mono objectif, comportant la résolution du problème de localisation des hubs (HLP) suivi pour chaque hub de la résolution de deux problèmes de tournées relatifs à la collecte et la livraison. Notre modèle MILP mono objectif est décomposé et notre MA est adapté pour résoudre le problème suivant ces deux étapes. Un ensemble d’instances de différents tailles et caractéristiques a été développée afin de conduire des expérimentations et de valider nos approches de résolution de ces différents problèmes
We study the Hub Location-Routing Problem (HLRP) aiming at the design of an efficient freight transportation network for LTL (less-than-truck) transport between many origins (suppliers) and destinations (clients). Such a network relies on the location of consolidation hubs, the organization of routings for the collection/distribution of freight from suppliers to hubs and from hubs to clients, as well as direct shipment of consolidated freight between hubs. We focus on the Capacitated Single Allocation Hub Location-Routing Problem (CSAHLRP) in the case of distinct collection and delivery processes. We propose mixed integer linear programming (MILP) model and a Memetic Algorithm (MA) to solve the problem for minimizing the total cost of the network. Then we extend the model into a bi-objective model for minimizing both the total cost and CO2 emissions of transport. A modified memetic algorithm (MA) combined with a fast elitist non-dominated sorting genetic algorithm (NSGAII) is developed to capture the trade-off between minimizing total cost and CO2 emissions and exhibit approximations of the Pareto front. At last, a two step procedure is proposed to solve the single-objective HLRP based on a hub location problem (HLP) and two distinct vehicle routing problems for suppliers and clients allocated to each hub by the first step. Our single objective MILP model is decomposed accordingly and our MA is adapted to solve the HLRP following these two steps. A data base of instances of different sizes and characteristics has been developed in order to conduct extensive experiments for solving all these problems using the different solution techniques and validate our approaches
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Mebrahtu, Fanuel M. "Transport and extraction of Au(lll) using thiourea ligands." Thesis, Stellenbosch : Stellenbosch University, 2004. http://hdl.handle.net/10019.1/50206.

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Thesis (MSc)--Stellenbosch University, 2004.
ENGLISH ABSTRACT: A series of di- and mono-substituted acyl(aroyl) thioureas were examined for the extraction and transportation of Au(III). Two-phase metal ion extraction experiments were employed to investigate the extraction behaviour of these ligands. The effect of varying ligand concentration on the extraction trend of these ligands was investigated. The results show that the different substituent groups on the benzoyl ring can affect the extraction pattern of the metal. Furthermore, the alkyl substituents on the thiourea moiety and varying the ligand concentration have an influence on the percentage of metal ion extracted. With the exception of the H2L2(N,N-di-propyl-N'- benzoylthiourea ) ligand the di-alkyl substituted thioureas were more efficient for the metal ion extraction than the mono-alkyl ligands. In almost all the experimental set ups there was reduction of the Au(lIl) to Au(l) and Au(O) but it was more pronounced with HL3 (N,N-di-(2-hydroxyethyl)-N'-benzoylthiourea). Transport experiments were also conducted, the experimental set up for transportation was a concentric type cell involving a 3-phase system - 2 aqueous phases ( source and receiving phase) separated by a chloroform membrane incorporating the ligand. The transport results however only gave a satisfactory result of about 5% of gold transported by the HL1 (N,N-dibutyl-N'-benzoylthiourea). All other ligands attempted resulted in metal ion being present in the organic phase, but no metal ion present in the receiving phase. To help drive the transport of the metal ion to the receiving phase CN-, S203 2- and perchloric acid were incorporated into the receiving phase. The transport results were not enhanced with these substances being present in the aqueous receiving phase. The aqueous source and receiving phases were analyzed by flame atomic absorption spectroscopy (FAAS). Finally the N,N-diethyl-N'-camphanoylthiourea (HL10) ligand and its complex with Au(l) were synthesised. Single crystals of the complex were grown for X-ray crystallography and the crystal and molecular structure of the complex was determined. The complex crystallizes in the monoclinic space group P21. The cell parameters are a = 10.7356(7)A b = 16.3443(11)A c = 10.9268(7)A f3 = 103.1450(10t , and final R-factor of 1.76%. The coordination sphere around Au(l) shows a nearly linear arrangement of sulphur and chloride.
AFRIKAANSE OPSOMMING: In hierdie proefskrif is In aantal mono- en di-gesubstitueerde asiel(ariel) thioureums ondersoek vir die transportasie en ekstraksie van Au(III). Twee-fase metaalioon vloeistof-vloeistof ekstraksie eksperimente is gebruik om die ekstraksie patroon van hierdie ligande te ondersoek. Die effek van verskillende ligand konsentrasies op die ekstraksie neiging van hierdie ligande is ondersoek. Resultate toon dat die verskillende substituente op die benziel ring die ekstraksie patroon van die metaalioon beïnvloed. Verder, is gevind dat die alkiel substituente op die thioureum saam met varierende ligand konsentrasies geensins die metaalioon ekstraksie beïnvloed nie. Met die uitsondering van H2L2 (N,N-dipropiel-N'-benzielthioureum) is die di-alkiel gesubstitueerde ligande meer effektief vir metaalioon ekstraksie in vergelyking met die mono-alkiel ligande. In baie van die eksperimente is In reduksie van Au(llI) na Au(l) en Au(O) gesien en dit is baie duidelik met ligand HL3 (N,N-di(2- hidroksie-etiel)N'-benzielthioureum). Alle waterige fases is ge-analiseer met gebruik van Atoomabsorpsie Spektroskopie (AAS). Transportasie eksperimente is ook uitgevoer met gebruik van In drie-fase selsisteem. Twee waterige fases (bron- en ontvang-fase) is geskei met die chloroform membraan fase wat die ligande bevat. Hierdie eksperimente het net In 5% Au(lll) transportasie getoon met HL1(N,N-dibutiel-N'-benzielthioureum). Daar was geen transportasie van Au(lIl) met enige van die ander ligande. Analise van die twee waterige fases het getoon dat die metaalioon eindelik goed ge-ekstraeer is en is teenwoordig in die membraan fase. Om die transportasie van Au(lIl) aan te spoor, is CN-, s2ol- en perchloorsuur in die ontvang-fase geinkorporeer. Die resultate was geensins beïnvloed nie. N,N-di-etiel-N'-kamfonielthioureum (HL10)ligande en die kompleks daarvan met Au(l) is ook gesintetiseer. Enkel-kristalle van die kompleks is verkry en X-straal kristallografiese analiese is onderneem. Hierdie kompleks kristalliseer in die monokliniese ruimtegroep P21,met a =10.7356(7)Á, b=16.3443(11)Á, c=10.9268(7)Á en ~=103.1450(10t. Die finale R-faktor is 1.76%. Die koordinasie om Au(l) toon In liniêre geometrie met swael en chloor.
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Wirbeleit, Frank. "Arsenic diffusivity study by comparison of post-Surface and post-implant diffusion in silicon with Local Density Diffusion (LDD-) model approximation." Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-186124.

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The LDD model was first applied to Arsenic concentration profiles determined in surface diffusion experiments by Yoshida and Arai [1]. The new method presented is based on a mathematical convolution with a delta-function-like concentration profile. By comparing the LDD approximation of post-surface diffusion with post-implant diffusion experiments, the same LDD model parameter r is found to hold for both experimental arrangements. This work found that post-implant diffusivity is concentration dependant and this might indicate an anomalous diffusion mechanism for Arsenic.
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Books on the topic "LDL transport"

1

Farḥāt, Raymūn. al- Mawsūʻah al-qanūnīyah lil-naql al-jawwī wa-al-baḥrī wa-al-barrī =: Encyclopédie juridique des transports aériens, maritimes et terrestres. Bayrūt: [s.n.], 1987.

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İslâm Konferansı Teşkilatı Üye Ülkeler Ulaştırma Bakanları Toplantısı (1st 1987 Istanbul, Turkey). İslâm Konferansı Teşkilatı Üye Ülkeler Ulaştırma Bakanları 1. Toplantısı =: Al-Ijtimāʻ al-Wizārī al-Awwal lil-Naql wa-al-Muwāṣalāt lil-Duwal al-Aʻḍāʼ fī Munaẓẓamat al-Muʼtamar al-Islāmī = The First Meeting of the Ministers of Transport of the OIC Member Countries. İstanbul: D.B. Deniz Nakliyat, 1987.

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Wiklund, Olov, and Jan Borén. Pathogenesis of atherosclerosis: lipid metabolism. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0011.

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Lipids are carried in plasma as microparticles, lipoproteins, composed of a core of hydrophobic lipids and a surface of amphipathic lipids. In addition, the particles carry proteins (i.e. apolipoproteins). The proteins have key functions in the metabolism as receptor ligands, enzymes or activators. Lipoproteins are classified based on density into: chylomicrons, VLDL, IDL, LDL, and HDL. Retention of apoB-containing lipoproteins (LDL, IDL, and VLDL) in the arterial intima is the initiating event in the development of atherosclerosis. Retention is mediated by binding of apoB to structural proteoglycans in the intima. Increased plasma concentration of apoB-containing lipoproteins is the main risk factor for atherosclerotic cardiovascular disease (CVD) and the causative role of LDL has been demonstrated in several studies. Lp(a) is a subclass of LDL and elevated Lp(a) is an independent risk-factor, primarily genetically mediated. Genetic data support that high Lp(a) causes atherosclerosis. Elevated triglycerides in plasma are associated with increased risk for CVD. Whether triglycerides directly induce atherogenesis is still unclear, but current data strongly support that remnant particles from triglyceride-rich lipoproteins are causal. HDL are lipoproteins that have been considered to be important for reversed cholesterol transport. Low HDL is a strong risk-factor for CVD. However, the causative role of HDL is debated and intervention studies to raise HDL have not been successful. Reduction of LDL is the main target for prevention and treatment, using drugs that inhibit the enzyme HMG-CoA reductase, i.e. statins. Other drugs for LDL reduction and to modify other lipoproteins may further reduce risk, and new therapeutic targets are explored.
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Sada, Nagisa, and Tsuyoshi Inoue. Lactate Dehydrogenase. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0029.

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Glucose is transported into neurons and used as an energy source. It is also transported into astrocytes, a type of glial cell, and converted to lactate, which is then released to neurons and used as another energy source. The latter is called the astrocyte-neuron lactate shuttle. Although the lactate shuttle is a metabolic pathway, it also plays important roles in neuronal activities and brain functions. We recently reported that this metabolic pathway is involved in the antiepileptic effects of the ketogenic diet. Lactate dehydrogenase (LDH) is a metabolic enzyme that mediates the lactate shuttle, and its inhibition hyperpolarizes neurons and suppresses seizures. This enzyme is also a molecular target of stiripentol, a clinically used antiepileptic drug for Dravet syndrome. This review provides an overview of electrical regulation by the astrocyte-neuron lactate shuttle, and then introduces LDH as a metabolic target against epilepsy.
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Quigley, Conor. Completing the Internal Market of the European Community: 1993 Legislation, Transport, Customs, and Travel, 1993 Basic Work and 1993 Supplements/Lsl (Transport, Customs and Travel , Vol 1-2). Graham & Trotman, 1993.

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Book chapters on the topic "LDL transport"

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Hori, Hitoshi, Yoshijiro Nazumi, and Yoshihiro Uto. "Boron Tracedrug Design for Neutron Dynamic Therapeutics for LDL." In Oxygen Transport to Tissue XXXV, 385–89. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7411-1_51.

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Habenicht, Andreas J. R., Peter Salbach, and Uwe Janßen-Timmen. "LDL Receptor-Dependent Polyunsaturated Fatty Acid Transport and Metabolism." In Cellular Metabolism of the Arterial Wall and Central Nervous System, 167–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84949-7_11.

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Sakellarios, A. I., D. I. Fotiadis, and L. K. Michalis. "Finite Element Modeling of LDL Transport in Carotid Artery Bifurcations." In IFMBE Proceedings, 1967–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-89208-3_469.

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de Loor, A., and S. Kenjereš. "Towards Numerical Simulations of Atherosclerosis: Modelling of Low-Density-Lipoprotein (LDL) Transport through Multi-Layered Arterial Wall." In IFMBE Proceedings, 2158–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-29305-4_566.

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Curmi, Patrick A., Lucienne Juan, and Alain Tedgui. "Effect of the Transmural Pressure on LDL and Albumin Transport and Distribution Across the Intact Arterial Wall." In Biofluid Mechanics, 217–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-52338-0_27.

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Carpenter, Harry J., Mergen H. Ghayesh, Anthony C. Zander, and Peter J. Psaltis. "Effect of Nonlinear Blood Viscosity on LDL Transport and Fluid-Structure Interaction Biomechanics of a Multi-stenosis Left Circumflex Coronary Artery." In NODYCON Conference Proceedings Series, 39–48. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-81162-4_4.

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Balachandar, R., C. Polatel, B. S. Hyun, K. Yu, C. L. Lin, W. Yue, and V. C. Patel. "LDV, PIV and Les Investigation of Flow Over a Fixed Dune." In Sedimentation and Sediment Transport, 171–78. Dordrecht: Springer Netherlands, 2003. http://dx.doi.org/10.1007/978-94-017-0347-5_27.

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Ferreira, Rui M. L. "Turbulent Flow Hydrodynamics and Sediment Transport: Laboratory Research with LDA and PIV." In Experimental Methods in Hydraulic Research, 67–111. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-17475-9_4.

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Qu, Z. Y., Q. L. Yu, and H. J. H. Brouwers. "Effect of LDH Nano-Flakes on the Mechanical and Transport Properties of Lightweight Concrete." In RILEM Bookseries, 3–16. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90236-4_1.

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Liu, X., Y. B. Fan, and X. Y. Deng. "Effect of the Endothelial Glycocalyx Layer on the Transport of LDLs in the Artery." In IFMBE Proceedings, 406–9. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-14515-5_104.

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Conference papers on the topic "LDL transport"

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Cancel, L. M., and J. M. Tarbell. "The role of apoptosis in LDL transport through endothelial cell monolayers." In 2007 IEEE 33rd Annual Northeast Bioengineering Conference. IEEE, 2007. http://dx.doi.org/10.1109/nebc.2007.4413343.

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Cancel, L. M., F. Piraino, and J. M. Tarbell. "The role of apoptosis in LDL transport through endothelial cell monolayers." In 2010 36th Annual Northeast Bioengineering Conference. IEEE, 2010. http://dx.doi.org/10.1109/nebc.2010.5458234.

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Filipovic, Nenad, Mirko Rosic, Irena Tanaskovic, Oberdan Parodi, and Dimitris Fotiadis. "Computer simulation and experimental analysis of LDL transport in the arteries." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6090031.

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Ilea, Mihai, Marius Turnea, Calin Corciova, and Mariana Rotariu. "AN E-LEARNING TOOL FOR MATHEMATICAL MODEL OF CHOLESTEROL HOMEOSTASIS DEPENDING ON DIET AND AGES." In eLSE 2020. University Publishing House, 2020. http://dx.doi.org/10.12753/2066-026x-20-200.

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The human health has many important aspects and the cholesterol regulation is one of them. The low-density lipoproteins cholesterol (LDL-C) transports plasma cholesterol (about 60%) and it is responsible by its depositing on arteries for atherosclerotic process, increasing the probability of cardiovascular events. High-density lipoproteins (HDL) can reduce this process by transport about 30% of plasma cholesterol. The balance is modified in the process of aging and depend also of other factors as diet, and physical exercises. An educational tool is proposing that use basically two mathematical models: (1) a simple one by two compartment model proposed by Wona & Hrydziuszko that include an dietary term, and (2) a more complex one that include the mechanism of simulation of aging proposed by Mc Auley. The values of parameters for both models are taken from literature and the user can modify them in order to test and simulated the models. The diet is modeled in the first model as an additive variable, and other variable are deduced from stability analysis and are assumed based on heuristic trials. In the second model, the mechanism of aging is simulated empirically (because the complete mechanism is not known yet) by increasing the LDL-C values and decreasing the number of hepatic LDL receptors (HLDLR) by decreasing the parameter that represents rate of synthesis. The tool has a library with selected curves for (HDL-C) and (LDL-C) from different countries of the world by age and sex extracted from literature. In the future development, this information will be used to model and analytic additive function for (LDL-C) curve by fitting of parameters with experimental one in system of differential equations that models the cholesterol homeostasis.
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Piraino, Francesco, Limary M. Cancel, Alberto Redaelli, and John M. Tarbell. "Effect of Simvastatin on the Apoptosis and Permeability of Endothelial Cell Monolayers." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206588.

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Atherosclerosis is a chronic inflammatory response in the walls of arteries promoted by plasma proteins that carry cholesterol and triglycerides. The initiating event in atherosclerosis is the transport of low density lipoprotein (LDL) into the subendothelial space.
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Dabagh, Mahsa, Payman Jalali, and Kambiz Vafai. "The Effect of Hypertension on the Transport of LDL Across the Deformable Arterial Wall." In POROUS MEDIA AND ITS APPLICATIONS IN SCIENCE, ENGINEERING, AND INDUSTRY: 3rd International Conference. AIP, 2010. http://dx.doi.org/10.1063/1.3453811.

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Imai, Yohsuke, Kodai Sato, Takuji Ishikawa, and Takami Yamaguchi. "Effects of Arterial Geometry on Inflow Rate Into Cerebral Aneurysms on Curved Arteries." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176556.

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Pathobiological studies have demonstrated that atherosclerotic lesions have been found on the wall of saccular cerebral aneurysms [1]. We propose a hypothesis that some of these aneurysms are prevented from rupturing due to the atherosclerotic lesions. It has been presented that mass transport of biochemical species such as LDL and ATP, has some important roles in the development of atherosclerosis. A variety of Computational Fluid Dynamics (CFD) studies of the mass transport has been performed for arteries [2, 3], few studies have however, done for aneurysms.
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SAKELLARIOS, A. I., M. I. PAPAFAKLIS, C. V. BOURANTAS, L. K. MICHALIS, and D. I. FOTIADIS. "PREDICTION OF ATHEROSCLEROTIC PLAQUE FORMATION BASED ON LDL TRANSPORT FOR A 3D PATIENT SPECIFIC CORONARY ARTERY WITH DEFORMABLE WALLS." In Proceedings of the 9th International Workshop on Mathematical Methods in Scattering Theory and Biomedical Engineering. WORLD SCIENTIFIC, 2010. http://dx.doi.org/10.1142/9789814322034_0012.

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Sakellarios, Antonis I., Panagiotis K. Siogkas, Lambros S. Athanasiou, Themis P. Exarchos, Michail I. Papafaklis, Christos V. Bourantas, Katerina K. Naka, et al. "Three-dimensional modeling of oxidized-LDL accumulation and HDL mass transport in a coronary artery: A proof-of-concept study for predicting the region of atherosclerotic plaque development." In 2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2013. http://dx.doi.org/10.1109/embc.2013.6610550.

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Anderson, O. A., L. Soroka, and J. W. Kwan. "Studies of bright beam transport by the LBL MFE group." In High-brightness beams for advanced accelerator applications. AIP, 1992. http://dx.doi.org/10.1063/1.42149.

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