Relevant bibliographies by topics / Lipoprotein A

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  2. Dissertations / Theses
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  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'Lipoprotein A'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 March 2023

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Journal articles on the topic "Lipoprotein A"

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Myers, D. E., W. N. Huang, and R. G. Larkins. "Lipoprotein-induced prostacyclin production in endothelial cells and effects of lipoprotein modification." American Journal of Physiology-Cell Physiology 271, no. 5 (November 1, 1996): C1504—C1511. http://dx.doi.org/10.1152/ajpcell.1996.271.5.c1504.

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Although lipoprotein modification has been implicated in atherogenesis, the effect of modified forms of lipoproteins on vascular cell function has not been fully resolved. We have investigated lipoprotein-induced prostaglandin production by macrovascular endothelial cells. This study delineates early responses of endothelial cells after exposure to native and modified forms of the lipoproteins. Modification of lipoproteins by oxidation or glycation significantly affected the capacity of lipoproteins to induce prostacyclin (PGI2) production by bovine aortic endothelial cells (BAEC). Modified low-density lipoprotein (LDL) increased PGI2 production in the short term (up to 24 h), but oxidized LDL caused an inhibition of PGI2-producing capacity in longer term incubations (48-72 h). Glycated (Glc) high-density lipoprotein 3 (HDL3) caused higher production of PGI2 in the short term (4-24 h) but reached similar levels as HDL3 over time. Glycation of high-density lipoprotein 2 had no effect on the PGI2-producing capacity of the lipoprotein. Thus modification of the lipoproteins affects their potential to induce PGI2 production in endothelial cells, and this may have an influence on vascular function in disease states such as diabetes and atherosclerosis. Although the changes appear to contradict data from long-term in vivo studies, these results from in vitro studies may reflect the situation in very early lesion development. GlcLDL, while causing an increase in endothelial cell PGI2 production, may be involved in compromised endothelial function, since GlcLDL is prone to oxidation.
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De Sanctis, Juan B., Isaac Blanca, and Nicholas E. Bianco. "Effects of Different Lipoproteins on the Proliferative Response of Interleukin-2-Activated T Lymphocytes and Large Granular Lymphocytes." Clinical Science 89, no. 5 (November 1, 1995): 511–19. http://dx.doi.org/10.1042/cs0890511.

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1. T lymphocytes and large granular lymphocytes internalized chylomicrons, very low-density lipoprotein, low-density lipoprotein, high-density lipoprotein and acetyl modified low-density lipoprotein through different receptors as assessed by flow cytometry. The observed internalization ranged from 8% to 20%. 2. All lipoproteins induced proliferative responses in T lymphocytes and large granular lymphocytes at optimum concentrations (40 μg of protein/ml for all lipoproteins except high-density lipoprotein). Chylomicrons, very low-density lipoprotein and low-density lipoprotein increased T-lymphocyte proliferative response by fourfold while inducing respectively a seven-, nine- and sevenfold increment in large granular lymphocytes. Similarly, high-density lipoprotein and acetyl modified low-density lipoprotein respectively induced a nine- and sevenfold increment in T cells and a 17- and eightfold increment in large granular lymphocyte proliferative response. 3. Both cell types internalized more lipoprotein when they were stimulated with interleukin 2. Chylomicrons and low-density lipoprotein internalization was increased threefold and very low-density lipoprotein internalization twofold, while high-density lipoprotein internalization was unchanged in both cell types. Acetyl modified low-density lipoprotein internalization was fourfold higher in large granular lymphocytes only. 4. The proliferative response of interleukin-2 stimulated cells was different from that of unstimulated cells. Chylomicrons and very low-density lipoprotein induced a sixfold increment in T-cell proliferative response but only a fourfold increment in large granular lymphocytes. Low-density lipoprotein and acetyl modified low-density lipoprotein induced respectively a sevenfold and eightfold increment in T cells and a eightfold and threefold increment in large granular lymphocyte proliferative response. Highdensity lipoprotein did not affect T-lymphocyte proliferative response while inducing a twofold increase in large granular lymphocytes. 5. Lipoproteins are important in the proliferative response of unstimulated and interleukin-2-stimulated cells.
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Yasmin, Raheela, Aashi Ahmed, Ambreen Javed, Maleha Asim, Rabbia Shabbir, Shahida Mushtaq, and Faiza Irshad. "The Effect of Blood Sugar Fasting Levels on Diabetic Dyslipidemia." Pakistan Journal of Medical and Health Sciences 16, no. 4 (April 26, 2022): 360–61. http://dx.doi.org/10.53350/pjmhs22164360.

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Background: Diabetic dyslipidemia is a group of lipoprotein defects described by raised triglycerides, elevated low density lipoprotein and reduced levels of high density lipoprotein. Objective: To assess the effect of blood sugar fasting levels on individual lipoproteins. Study design: Cross-sectional study Place and duration of study: Fauji Foundation Hospital Rawalpindi & POF Hospital Wah Cantt from 1st February 2014 to 31st July 2014. Methodology: Fifty patients with age from 30 to 70 years were enrolled. Patients' body mass index was calculated. Serum cholesterol, high density lipoprotein and triglyceride levels were estimated by enzymatic colorimetric kit. Low density lipoprotein was calculated by Friedewald equation. Results: The mean blood sugar fasting level was 204.050±87.0755. The P-value of low density lipoproteins to blood sugar fasting and cholesterol to high density lipoprotein ratio blood sugar fasting were significant i.e. 0.03 and<0.001 respectively. Conclusion: Dyslipidemia worsened with uncontrolled blood sugar fasting. Elevated low density lipoprotein and cholesterol to high density lipoprotein ratio was observed. Keywords: Blood sugar fasting, Type 2 diabetes mellitus (T2DM), Cardiovascular system (CVS), Dyslipidemia, high density lipoprotein (HDL)
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Huang, Haibin, Mingqun Lin, Xueqi Wang, Takane Kikuchi, Heather Mottaz, Angela Norbeck, and Yasuko Rikihisa. "Proteomic Analysis of and Immune Responses to Ehrlichia chaffeensis Lipoproteins." Infection and Immunity 76, no. 8 (May 19, 2008): 3405–14. http://dx.doi.org/10.1128/iai.00056-08.

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ABSTRACT Ehrlichia chaffeensis is an obligately intracellular gram-negative bacterium and is the etiologic agent of human monocytic ehrlichiosis (HME). Although E. chaffeensis induces the generation of several cytokines and chemokines by leukocytes, E. chaffeensis lacks lipopolysaccharide and peptidoglycan. Bioinfomatic analysis of the E. chaffeensis genome, however, predicted genes encoding 15 lipoproteins and 3 posttranslational lipoprotein-processing enzymes. The present study showed that by use of multidimensional liquid chromatography followed by tandem mass spectrometry, all predicted lipoproteins as well as lipoprotein-processing enzymes were expressed by E. chaffeensis cultured in the human promyelocytic leukemia cell line HL-60. Consistent with this observation, a signal peptidase II inhibitor, globomycin, was found to inhibit E. chaffeensis infection and lipoprotein processing in HL-60 cell culture. To study in vivo E. chaffeensis lipoprotein expression and host immune responses to E. chaffeensis lipoproteins, 13 E. chaffeensis lipoprotein genes were cloned into a mammalian expression vector. When the DNA constructs were inoculated into naïve dogs, or when dogs were infected with E. chaffeensis, the animals developed delayed-type hypersensitivity reactions at cutaneous sites of the DNA construct deposition and serum antibodies to these lipoproteins. This is the first demonstration of lipoprotein expression and elicitation of immune responses by a member of the order Rickettsiales. Multiple lipoproteins expressed by E. chaffeensis in vitro and in vivo may play key roles in pathogenesis and immune responses in HME.
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Giesecke, Yvonne, Samuel Soete, Katarzyna MacKinnon, Thanasis Tsiaras, Madeline Ward, Mohammed Althobaiti, Tamas Suveges, James E. Lucocq, Stephen J. McKenna, and John M. Lucocq. "Developing Electron Microscopy Tools for Profiling Plasma Lipoproteins Using Methyl Cellulose Embedment, Machine Learning and Immunodetection of Apolipoprotein B and Apolipoprotein(a)." International Journal of Molecular Sciences 21, no. 17 (September 2, 2020): 6373. http://dx.doi.org/10.3390/ijms21176373.

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Plasma lipoproteins are important carriers of cholesterol and have been linked strongly to cardiovascular disease (CVD). Our study aimed to achieve fine-grained measurements of lipoprotein subpopulations such as low-density lipoprotein (LDL), lipoprotein(a) (Lp(a), or remnant lipoproteins (RLP) using electron microscopy combined with machine learning tools from microliter samples of human plasma. In the reported method, lipoproteins were absorbed onto electron microscopy (EM) support films from diluted plasma and embedded in thin films of methyl cellulose (MC) containing mixed metal stains, providing intense edge contrast. The results show that LPs have a continuous frequency distribution of sizes, extending from LDL (> 15 nm) to intermediate density lipoprotein (IDL) and very low-density lipoproteins (VLDL). Furthermore, mixed metal staining produces striking “positive” contrast of specific antibodies attached to lipoproteins providing quantitative data on apolipoprotein(a)-positive Lp(a) or apolipoprotein B (ApoB)-positive particles. To enable automatic particle characterization, we also demonstrated efficient segmentation of lipoprotein particles using deep learning software characterized by a Mask Region-based Convolutional Neural Networks (R-CNN) architecture with transfer learning. In future, EM and machine learning could be combined with microarray deposition and automated imaging for higher throughput quantitation of lipoproteins associated with CVD risk.
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Faria, Eliana Cotta de, Adriana Celeste Gebrin, Wilson Nadruz Júnior, and Lucia Nassi Castilho. "Phospholipid transfer protein activity in two cholestatic patients." Sao Paulo Medical Journal 122, no. 4 (2004): 175–77. http://dx.doi.org/10.1590/s1516-31802004000400009.

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CONTEXT: Plasma phospholipid transfer protein mediates the transfer of phospholipids from triglyceride-rich lipoproteins, very low density lipoproteins and low density lipoproteins to high density lipoproteins, a process that is also efficient between high density lipoprotein particles. It promotes a net movement of phospholipids, thereby generating small lipid-poor apolipoprotein AI that contains particles and subfractions that are good acceptors for cell cholesterol efflux. CASE REPORT: We measured the activity of plasma phospholipid transfer protein in two cholestatic patients, assuming that changes in activity would occur in serum that was positive for lipoprotein X. Both patients presented severe hypercholesterolemia, high levels of low density lipoprotein cholesterol and, in one case, low levels of high density lipoprotein cholesterol and high levels of phospholipid serum. The phospholipid transfer activity was close to the lower limit of the reference interval. To our knowledge, this is the first time such results have been presented. We propose that phospholipid transfer protein activity becomes reduced under cholestasis conditions because of changes in the chemical composition of high density lipoproteins, such as an increase in phospholipids content. Also, lipoprotein X, which is rich in phospholipids, could compete with high density lipoproteins as a substrate for phospholipid transfer protein.
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Renee Ruhaak, L., Arnoud van der Laarse, and Christa M. Cobbaert. "Apolipoprotein profiling as a personalized approach to the diagnosis and treatment of dyslipidaemia." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 56, no. 3 (March 19, 2019): 338–56. http://dx.doi.org/10.1177/0004563219827620.

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An elevated low-density lipoprotein cholesterol concentration is a classical risk factor for cardiovascular disease. This has led to pharmacotherapy in patients with atherosclerotic heart disease or high heart disease risk with statins to reduce serum low-density lipoprotein cholesterol. Even in patients in whom the target levels of low-density lipoprotein cholesterol are reached, there remains a significant residual cardiovascular risk; this is due, in part, to a focus on low-density lipoprotein cholesterol alone and neglect of other important aspects of lipoprotein metabolism. A more refined lipoprotein analysis will provide additional information on the accumulation of very low-density lipoproteins, intermediate density lipoproteins, chylomicrons, chylomicron-remnants and Lp(a) concentrations. Instead of measuring the cholesterol and triglyceride content of the lipoproteins, measurement of their apolipoproteins (apos) is more informative. Apos are either specific for a particular lipoprotein or for a group of lipoproteins. In particular measurement of apos in atherogenic particles is more biologically meaningful than the measurement of the cholesterol concentration contained in these particles. Applying apo profiling will not only improve characterization of the lipoprotein abnormality, but will also improve definition of therapeutic targets. Apo profiling aligns with the concept of precision medicine by which an individual patient is not treated as ‘average’ patient by the average (dose of) therapy. This concept of precision medicine fits the unmet clinical need for stratified cardiovascular medicine. The requirements for clinical application of proteomics, including apo profiling, can now be met using robust mass spectrometry technology which offers desirable analytical performance and standardization.
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Dodds, P. F., A. Lopez-Johnston, V. A. Welch, and M. I. Gurr. "The effects of chemically modifying serum apolipoproteins on their ability to activate lipoprotein lipase." Biochemical Journal 242, no. 2 (March 1, 1987): 471–78. http://dx.doi.org/10.1042/bj2420471.

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Lipoprotein lipase activity was measured in an acetone-dried-powder preparation from rat epididymal adipose tissue using pig serum or pig serum lipoprotein, which had been chemically modified, as activator. Modification of acidic amino acids of lipoproteins with NN-dimethyl-1,3-diamine resulted in a complete loss of ability to activate lipoprotein lipase. Modification of 34% of lipoprotein arginine groups with cyclohexanedione resulted in the loss of 75% of the activation of lipoprotein lipase; approx. 42% of the original activity was recovered after reversal of the modification. This effect was dependent on the cyclohexanedione concentration. Modification of 48% of lipoprotein lysine groups with malonaldehyde decreased the maximum activation by 20%, but three times as much lipoprotein was required to achieve this. Non-enzymic glycosylation of lipoprotein with glucose, under a variety of conditions resulting in up to 28 nmol of glucose/mg of protein, had no effect upon the ability to activate lipoprotein lipase. In contrast non-enzymic sialylation resulted in a time-dependent loss of up to 60% of ability to activate lipoprotein lipase. Reductive methylation and acetoacetylation of serum did not affect the ability to activate lipoprotein lipase. The results are compared to the effects of similar modifications to low density lipoproteins on receptor-mediated endocytosis.
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Öörni, Katariina, Satu Lehti, Peter Sjövall, and Petri T. Kovanen. "Triglyceride-Rich Lipoproteins as a Source of Proinflammatory Lipids in the Arterial Wall." Current Medicinal Chemistry 26, no. 9 (May 21, 2019): 1701–10. http://dx.doi.org/10.2174/0929867325666180530094819.

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Apolipoprotein B –containing lipoproteins include triglyceride-rich lipoproteins (chylomicrons and their remnants, and very low-density lipoproteins and their remnants) and cholesterol-rich low-density lipoprotein particles. Of these, lipoproteins having sizes below 70-80 nm may enter the arterial wall, where they accumulate and induce the formation of atherosclerotic lesions. The processes that lead to accumulation of lipoprotein-derived lipids in the arterial wall have been largely studied with a focus on the low-density lipoprotein particles. However, recent observational and genetic studies have discovered that the triglyceriderich lipoproteins and their remnants are linked with cardiovascular disease risk. In this review, we describe the potential mechanisms by which the triglyceride-rich remnant lipoproteins can contribute to the development of atherosclerotic lesions, and highlight the differences in the atherogenicity between low-density lipoproteins and the remnant lipoproteins.
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Niu, You-Guo, and Rhys D. Evans. "Metabolism of very-low-density lipoprotein and chylomicrons by streptozotocin-induced diabetic rat heart: effects of diabetes and lipoprotein preference." American Journal of Physiology-Endocrinology and Metabolism 295, no. 5 (November 2008): E1106—E1116. http://dx.doi.org/10.1152/ajpendo.90260.2008.

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Very-low-density lipoprotein (VLDL) and chylomicrons (CM) are major sources of fatty acid supply to the heart, but little is known about their metabolism in diabetic myocardium. To investigate this, working hearts isolated from control rats and diabetic rats 2 wk following streptozotocin (STZ) injection were perfused with control and diabetic lipoproteins. Analysis of the diabetic lipoproteins showed that both VLDL and CM were altered compared with control lipoproteins; both were smaller and had different apolipoprotein composition. Heparin-releasable lipoprotein lipase (HR-LPL) activity was increased in STZ-induced diabetic hearts, but tissue residual LPL activity was decreased; moreover, diabetic lipoproteins stimulated HR-LPL activity in both diabetic and control hearts. Diabetic hearts oxidized lipoprotein-triacylglycerol (TAG) to a significantly greater extent than controls (>80% compared with deposition as tissue lipid), and the oxidation rate of exogenous lipoprotein-TAG was increased significantly in diabetic hearts regardless of TAG source. Significantly increased intracardiomyocyte TAG accumulation was found in diabetic hearts, although cardiac mechanical function was not inhibited, suggesting that lipotoxicity precedes impaired cardiac performance. Glucose oxidation was significantly decreased in diabetic hearts; additionally, however, diabetic lipoproteins decreased glucose oxidation in diabetic and control hearts. These results demonstrate increased TAG-rich lipoprotein metabolism concomitant with decreased glucose oxidation in type 1 diabetic hearts, and the alterations in cardiac lipoprotein metabolism may be due to the properties of diabetic TAG-rich lipoproteins as well as the diabetic state of the myocardium. These changes were not related to cardiomyopathy at this early stage of diabetes.
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Dissertations / Theses on the topic "Lipoprotein A"

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Kohn, Meifania Monica. "Lipoprotein ontology: a formal representation of Lipoproteins." Thesis, Curtin University, 2013. http://hdl.handle.net/20.500.11937/1827.

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Lipoproteins serve as a mode of transport for the uptake, storage and metabolism of lipids. Dysregulation in lipoprotein metabolism, known as dyslipidaemia, is strongly correlated to various diseases such as cardiovascular disease. Lipoprotein Ontology provides a formal representation of lipoprotein concepts and relationships that can be used to support the intelligent retrieval of information, faciliate collaboration between research groups, and provide the basis for the development of tools for the diagnosis and treatment of dyslipidaemia.
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Soran, Handrean. "Glycation of Lipoproteins and the Role High Density Lipoprotein and Paraoxonase -1." Thesis, University of Manchester, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.532197.

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Espinosa, Garcia Irma Leticia. "Differential density lipoprotein profiling for the characterization of Lipoprotein(a)." Texas A&M University, 2006. http://hdl.handle.net/1969.1/4359.

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Lipoprotein(a) (Lp(a)) has been described as an emerging risk factor for cardiovascular disease. The complexity of the Lp(a) molecule sets a challenge for the determination of the risk it represents for the cardiovascular system. The objective of the present study was to develop a rapid method for the separation, purification, density measurement, and characterization of Lp(a) from serum using a procedure that is isoform independent. The objective was met by linking ultracentrifugation with affinity separations for the specific separation of Lp(a) from other lipoproteins. The mean density distribution of Lp(a) was determined by a differential density lipoprotein profile (DDLP). For DDLP, the lipoprotein density distribution of a serum sample with elevated Lp(a) levels was determined by ultracentrifugation using NaBiEDTA complex as a density gradient. Lp(a) was removed from a second aliquot of the same serum sample by carbohydrate affinity using wheat germ agglutinin (WGA). WGA was demonstrated to have high specificity for Lp(a) in serum. The Lp(a)-depleted sample was ultracentrifuged to obtain a lipoprotein density distribution in the absence of Lp(a). A DDLP was obtained after subtracting the Lp(a)-depleted lipoprotein density profile from the untreated lipoprotein density profile. DDLP gives relevant information of the lipoproteins in serum such as density, Lp(a) isoform, and subclass characteristics. Lp(a) was quantitatively removed from serum with a recovery efficiency of more than 80%. Lp(a) was purified by ultracentrifugation. Lp(a) obtained in this way retained its inherent density and immunoreactivity. Lp(a) was further characterized by gel electrophoresis and Western blot as well as by capillary electrophoresis. Capillary electrophoresis demonstrated to be a powerful analytical technique for the characterization of Lp(a) and apoprotein(a) isoforms. The major outcome of this research was the effectiveness of using affinity separations coupled with density ultracentrifugation for the isolation of pure Lp(a) from serum and its isoform characterization based on density and electromobility. The methodology developed and described here are relevant in a clinical setting for the analysis of Lp(a).
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Hacquebard, Mirjam Rebecca. "Alpha-tocopherol acquisition by plasma lipoproteins and changes in lipoprotein profile after cardiac surgery." Doctoral thesis, Universite Libre de Bruxelles, 2008. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/216586.

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Alpha-tocopherol, the most abundant form of vitamin E in man, is transported in the circulation by plasma lipoproteins. It plays important roles, not only in preventing lipid peroxidation, but also in modulating several cell functions such as cell signaling and gene expression. While chylomicrons transport dietary alpha-tocopherol after intestinal absorption, LDL and HDL are the major carriers of alpha-tocopherol in fasting plasma and largely contribute to its delivery to cells and tissues. Exchanges of alpha-tocopherol occur between plasma lipoproteins. In addition, alpha-tocopherol transfers have also been observed, in both directions, between plasma lipoproteins and artificial chylomicrons such as intravenous lipid emulsion particles used in parenteral nutrition. In acute conditions, intravenous supply of vitamin E via lipid emulsions, which bypasses the intestinal tract, may offer some advantages over oral administration to rapidly increase alpha-tocopherol plasma concentration. However, many questions remain unanswered regarding kinetics and factors facilitating vitamin E exchanges between lipid emulsions and plasma lipoproteins. The first part of this work aimed at characterizing alpha-tocopherol transfers between alpha-tocopherol rich emulsion particles and plasma lipoproteins as well as the potential for plasma proteins to modulate such transfers. An in vitro model of incubation was used in which emulsion triglyceride concentration was relatively low and lipoprotein levels comparable to those commonly found in the circulation. Results indicate a high capacity for LDL and HDL to acquire extra-amounts of alpha-tocopherol by rapid mass transfers from alpha-tocopherol-rich emulsion particles. Data further shows that, at a fixed alpha-tocopherol concentration provided by emulsion particles, the limiting factor for alpha-tocopherol enrichment is not the capacity of plasma lipoproteins to accommodate extra-amounts of alpha-tocopherol but the facilitating effect of plasma proteins on alpha-tocopherol transfer, the duration of the incubation and possibly the competition between different acceptor particles. Two lipid transfer proteins, PLTP and CETP, appear to largely mediate facilitation of alpha-tocopherol transfer; however, other plasma proteins may be involved. Data further shows that alpha-tocopherol enriched LDL and HDL can readily transfer newly acquired alpha-tocopherol to cells, without any regulation by plasma proteins.

Short-term prophylactic vitamin E supplementation has been suggested to be beneficial in some patients in acute conditions who present reduced plasma vitamin E concentrations in association with important changes in plasma lipids and severe oxidative stress. However, it was not clear whether low plasma vitamin E concentration in critically ill patients is related to changes in the composition of plasma lipoproteins or to a decrease in the number of alpha-tocopherol carriers. In the second part of this work, two clinical studies were conducted to analyze changes of lipoprotein concentration and composition in relation to inflammatory reaction and oxidative stress in selected subgroups of critically ill patients, namely patients undergoing cardiac surgery with different procedures. Important changes in LDL and HDL lipid content were observed, some of which contrast with previous observations made in critically ill septic patients. The reduced plasma level of alpha-tocopherol measured after cardiac surgery is entirely due to a reduced number of circulating LDL and HDL particles. Data suggests that such reduced number in alpha-tocopherol carriers post-surgery may impede the delivery of alpha-tocopherol to cells in conditions of increased requirements due to oxidative stress. Avoidance of extracorporeal circulation during cardiac surgery does not reduce inflammation-related changes in plasma lipids but largely prevents oxidative stress. This data on changes occurring in plasma lipoproteins may help to better define strategies against pro-inflammatory changes or oxidative stress. If further studies would confirm a clinical benefit with evidence-based rationale, alpha-tocopherol enriched lipid emulsions may be used to guarantee a sufficient alpha-tocopherol supply in acute conditions associated with fewer alpha-tocopherol transporters and increased requirements due to high risk of oxidative tissue injury.


Doctorat en Sciences biomédicales et pharmaceutiques
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Ma, Feng. "Clinical Assessment of Anti-Atherogenic Function of HighDensity Lipoprotein (HDL)." Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS583.

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Il a été bien établi chez l’Homme qu'il existe une forte association entre les faibles concentrations plasmatiques de cholestérol associé aux lipoprotéines de haute densité (HDL-C) et le risque accru de maladie cardiovasculaire (MCV). Augmenter le taux de HDL-C a donc été proposé comme stratégie thérapeutique visant à réduire le risque de MCV. En effet, les HDL présentent de multiples fonctions athéroprotectrices, notamment la capacité d’efflux du cholestérol, ainsi que des activités antioxydantes, anti-inflammatoires, vasodilatatrices, cytoprotectrices, anti-infectieuses et anti- thrombotiques. Cependant, des essais cliniques à grande échelle ont révélé que l'augmentation du HDL-C induite par un médicament ne réduisait pas nécessairement le risque CV. En outre, des études de randomisation mendélienne ont montré que des concentrations faibles de HDL-C déterminées génétiquement ne se traduisaient pas toujours par un risque accru de MCV. Récemment, plusieurs études épidémiologiques à grande échelle ont mis en évidence une dépendance en forme de U entre la maladie cardiovasculaire et les taux de HDL-C, établissant un lien entre un taux de HDL-C extrêmement élevé et un risque CV élevé. Afin de surmonter les limites du HDL-C en tant que facteur de risque CV, le concept de fonctionnalité des lipoprotéines HDL a été étudié, ce qui a permis de développer un test permettant la mesure de la capacité des HDL à faire de l’efflux de cholestérol comme approche de prédiction du risque. Cependant, ce concept révèle plusieurs faiblesses, telles que la préservation de l'efflux de cholestérol tissulaire chez les patients ayant un taux de HDL-C bas d'origine génétique. Dans la circulation, le métabolisme des HDL est intimement lié à celui des triglycérides (TG) par divers facteurs, notamment des enzymes, telles que la lipoprotéine lipase (LPL), et des protéines de transfert lipidique, telles que la protéine de transfert d'esters de cholestérol (CETP). La contribution des niveaux circulants de TG au risque élevé de MCV a été établie dans des modèles multivariés. On pense que les lipoprotéines riches en triglycérides (TGRL) contribuent à l'athérosclérose via leurs particules résiduelles produites lors de la lipolyse des TGRL par la LPL. Des études antérieures ont montré que les HDL sont capables d'empêcher l'accumulation de ces particules residuelles de TGRL dans la paroi artérielle. Il a donc été proposé que le faible taux de HDL-C représente un biomarqueur de niveaux élevés de résidus de TGRL générés par la lipolyse. On ignore actuellement si cette association peut expliquer la relation en forme de U entre le risque CV et le taux de HDL-C. En outre, les mécanismes sous-jacents à l'association entre le HDL-C, les résidus de TG et les MCV restent obscurs. Dans la présente étude, nous proposons une hypothèse selon laquelle les HDL circulants peuvent se charger en lipides, tels que le cholestérol libre (FC) et le phospholipide (PL), et des protéines provenants de la surface des résidus des TGRL générés au cours de la lipolyse médiée par la LPL, puis les transporter vers le foie dans un processus appelé le transport inverse des résidus (RRT). Nous suggérons en outre que les modifications de la RRT sous-tendent les relations entre HDL-C et MCV. Pour évaluer cette hypothèse, nous avons conçu un nouveau test in vitro évaluant les transferts lipidiques des TGRL aux HDL au cours de la lipolyse et l'avons appliqué à plusieurs populations de sujets présentant des taux plasmatiques de HDL-C différents. Les mécanismes de transfert de lipides de surface vers les HDL ont également été étudiés. Nous avons observé que les HDL, isolés par ultracentrifugation ou par déplétion plasmatique de l'apolipoprotéine B, acquéraient des lipides de surface, y compris FC et PL, des TGRL lors d'une lipolyse induite par le LPL à 37 ° C, en fonction du temps, comme l'a révélé la photométrie [...]
It has been well established that there is a strong association between low concentrations of high-density lipoprotein-cholesterol (HDL-C) in human plasma and the risk of cardiovascular disease (CVD). Raising HDL-C level was therefore proposed as a therapeutic strategy to decrease CV risk. Indeed, HDL displays multiple atheroprotective functions, including cholesterol efflux capacity as well as antioxidative, anti-inflammatory, vasodilatory, cytoprotective, anti-infectious and anti-thrombotic activities. However, large-scale clinical trials revealed that drug-induced HDL-C raising did not necessarily reduce CV risk. Furthermore, Mendelian randomization studies reported that genetically determined low HDL-C concentrations did not always translate to increased risk of CVD. Recently, a U-shape dependence between CV disease and HDL-C levels was observed in several large-scale epidemiological studies, linking extremely high HDL-C to elevated CV risk. To overcome the limitations of HDL-C as a CV risk factor, a concept of HDL functionality was developed which resulted in the development of the measurement of cholesterol efflux capacity of HDL as a risk-predicting approach. However, this concept reveals several weaknesses, such as, preservation of tissue cholesterol efflux in patients with genetically low HDL-C. In the circulation, HDL metabolism is intimately linked to that of triglyceride (TG) by various factors, including enzymes, such as lipoprotein lipase (LPL), and lipid transfer proteins, such as cholesteryl ester transfer protein (CETP). The contribution of circulating TG levels to the elevated risk of CVD was established in multivariate models. Triglyceride-rich lipoproteins (TGRLs) are thought to contribute to atherosclerosis via their remnant particles produced during lipolysis of TGRLs by LPL. Earlier studies showed that HDL is capable of preventing TGRL remnants from accumulation in the arterial wall. Low HDL-C was therefore proposed to represent a biomarker of elevated levels of TGRL remnants generated by the lipolysis. It is presently unknown whether this association can account for the U-shape relationship between CV risk and HDL-C. In addition, mechanisms underlying the association between HDL-C, TG remnants and CVD remain obscure. In the present study, we propose a hypothesis that in the circulation HDL can acquire lipids, such as free cholesterol (FC) and phospholipid (PL), and proteins from TGRL surface remnants generated during LPL-mediated lipolysis, and subsequently transport them to the liver in a process termed reverse remnant transport (RRT). We further suggest that RRT alterations underlie the relationships between HDL-C and CVD. To assess this hypothesis, we designed a novel in vitro assay evaluating lipid transfers from TGRL to HDL during lipolysis and applied it to several populations of subjects greatly differing in plasma HDL-C levels; mechanisms of surface lipid transfer to HDL were also studied. We observed that HDL, isolated by ultracentrifugation or by apolipoprotein B depletion of plasma, acquired surface lipids, including FC and PL, from TGRL upon LPL-induced lipolysis at 37°C in a time-dependent fashion as revealed by photometry [...]
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Ooi, Esther M. M. "Regulation of lipoprotein transport in the metabolic syndrome : impact of statin therapy." University of Western Australia. School of Medicine and Pharmacology, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0125.

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[Truncated abstract] The metabolic syndrome is characterized by cardiovascular risk factors including dyslipidemia, insulin resistance, visceral obesity, hypertension and diabetes. The dyslipidemia of the metabolic syndrome includes elevated plasma triglyceride and apolipoprotein (apo) B levels, accumulation of small, dense low-density lipoprotein (LDL) particles and low high-density lipoprotein (HDL) cholesterol concentration. However, the precise mechanisms for this dyslipoproteinemia, specifically low plasma HDL cholesterol, are not well understood. This thesis therefore, focuses on HDL, its structure, function and metabolism. However, lipoprotein metabolism is a complex interconnected system, which includes forward and reverse cholesterol transport pathways. Hence, this thesis also examines and discusses the metabolism of apoB-containing lipoproteins. This thesis tests the general hypothesis that apolipoprotein kinetics are altered in the metabolic syndrome, and that lipid regulating therapies can improve these kinetic abnormalities. The aims were first, to compare and establish the clinical, metabolic and kinetic differences between metabolic syndrome and lean subjects; and second, to determine the regulatory effects of statin therapy, specifically, rosuvastatin on lipoprotein transport in the metabolic syndrome. Five observation statements were derived from the general hypothesis and examined in the studies described below. The findings are presented separately as a series of original publications. Study 1 Twelve men with the metabolic syndrome and ten lean men were studied in a case-control setting. ... These findings explain the HDL raising effects of rosuvastatin in the metabolic syndrome. Collectively, these studies suggest that the dyslipidemia of the metabolic syndrome results from increased production rates of VLDL and LDL particles, reduced fractional catabolic rates of these lipoproteins, together with accelerated catabolism of HDL particles. Treatment with rosuvastatin increases the catabolic rates of all apoB-containing lipoproteins and at a higher dose, decreases LDL apoB production. These effects are consistent with inhibition of cholesterol synthesis leading to an upregulation of LDL receptors. Rosuvastatin decreases the fractional catabolism of HDL particles. The effects of rosuvastatin on HDL kinetics may be related to a reduction in triglyceride concentration and cholesterol ester transfer protein activity. These findings are consistent with the general hypothesis that apolipoprotein kinetics are altered in the metabolic syndrome, and that statin therapy improves these kinetic abnormalities.
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Gordon, Scott M. "The role of high density lipoprotein compositional and functional heterogeneity in metabolic disease." University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1353100684.

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Toledo, Júnior Alceu de Oliveira. "MARCADORES BIOQUÍMICOS NAS DISLIPIDEMIAS E NO RISCO CARDIOVASCULAR: ANÁLISE COMPARATIVA À FÓRMULA DE MARTIN." Universidade Estadual de Ponta Grossa, 2018. http://tede2.uepg.br/jspui/handle/prefix/2712.

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Submitted by Angela Maria de Oliveira (amolivei@uepg.br) on 2018-12-19T13:31:11Z No. of bitstreams: 2 license_rdf: 811 bytes, checksum: e39d27027a6cc9cb039ad269a5db8e34 (MD5) Alceu de Oliveira Toledo Junior.pdf: 3822777 bytes, checksum: 8621dbda843628c32379a4d6c54e0ac2 (MD5)
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Este estudo tem como objetivo avaliar comparativamente perfis de marcadores bioquímicos que melhor caracterizem e/ou associem-se às dislipidemias, na modalidade diagnóstica por ampliar a estratificação do risco cardiovascular ou no seu monitoramento para melhor condução. Para isso avaliamos o perfil lipídico composto por colesterol total, triglicérides, colesterol da lipoproteína de alta densidade e da lipoproteína de baixa densidade; esta com a fórmula de Martin, e ainda o colesterol em conteúdo que não faz parte das lipoproteínas de alta densidade, correlacionando-os com os marcadores: lipoproteína a, apoproteína B e colesterol da lipoproteína de baixa densidade; com uso do método homogêneo. Foram selecionados 1012 pacientes, segmentados por faixas etárias, sexo e condição de uso ou não de inibidores de produção hepática do colesterol. Para ampliar o poder dessa análise agrupada os exames realizados foram separados em subgrupos, considerando-se valores obtidos e metodologias utilizadas; correlacionando-se os resultados. A pesquisa foi realizada com variáveis qualitativas e quantitativas, procedendo-se ao uso de testes estatísticos não paramétricos para sua compreensão, distribuição e análise agrupada. Nossos resultados mostraram evidências que o risco cardiovascular não se associa apenas ao colesterol da lipoproteína de baixa densidade obtido pela fórmula de Martin, mas a outras variáveis, sob associação às seguintes análises comparativas: que o uso da apoproteína B amplia o diagnóstico de inclusão das dislipidemias em 43% usando valores referenciais sexo-independentes e com uma nova faixa de monitoramento em 84 mg/dL. Que o colesterol da lipoproteína de baixa densidade obtido pelo método homogêneo apresenta discordância analítica em +3,5% e tendo estratificação diagnóstica 48% superior. E que a lipoproteína a apresenta-se superior a 30 mg/dL em 26% dos pacientes, porém com prevalência e segmentação específicas nas mulheres entre 51 a 60 anos, sendo necessária sua análise numa aparente discordância, superior a 10 mg/dL, quando da comparação de resultados entre a fórmula de Martin e o método homogêneo.
This study aims to comparatively evaluate the profiles of biochemical markers that best characterize and / or associate with dyslipidemias, in the diagnostic modality by increasing the stratification of cardiovascular risk or its monitoring for better conduction. For this, we evaluated the lipid profile composed of total cholesterol, triglycerides, high density lipoprotein cholesterol and low density lipoprotein; and the cholesterol in non-high density lipoprotein content, correlating them with the markers: lipoprotein A, apoprotein B and low density lipoprotein cholesterol; using the homogeneous method. A total of 1012 patients were selected, segmented by age, sex and condition of use or inhibition of hepatic cholesterol production. In order to increase the power of this group analysis the exams were separated into subgroups, considering the obtained values and methodologies used; correlating the results. The research was carried out with qualitative and quantitative variables, using nonparametric statistical tests for their comprehension, distribution and grouped analysis. Our results showed evidence that cardiovascular risk is not only associated with the low density lipoprotein cholesterol obtained by Martin's formula, but other variables, in association with the following comparative analyzes: that the use of apoprotein B expands the diagnosis of inclusion of dyslipidemias in 43 % using genderindependent baseline values and with a new monitoring range of 84 mg/dL. That the low density lipoprotein cholesterol obtained by the homogeneous method presents an analytical disagreement at + 3.5% and having a 48% higher diagnostic stratification. In addition, lipoprotein a levels were higher than 30 mg/dL in 26% of the patients, but with a specific prevalence and segmentation in women between the ages of 51 and 60 years, with an apparent disagreement of more than 10 mg/dL when of the comparison of results between the Martin formula and the homogeneous method.
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Sledziecka, Anna Katarzyna. "Covalent lipoprotein(a) assembly : characterization of oxidase activity responsible for catalyzing covalent lipoprotein(a)." Kingston, Ont. : [s.n.], 2008. http://hdl.handle.net/1974/1596.

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Gabel, Brent R. "Analysis of lipoprotein(a) assembly." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ35960.pdf.

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Books on the topic "Lipoprotein A"

1

Jayme, Borensztajn, ed. Lipoprotein lipase. Chicago: Evener Publishers, 1987.

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Hendriks, Wilhelmina Leonie. Lipoprotein lipase-mediated interactions of lipoproteins with macrophages. [Leiden: University of Leiden, 1998.

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Ordovas, Jose M. Lipoprotein Protocols. New Jersey: Humana Press, 1998. http://dx.doi.org/10.1385/1592595820.

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A, Converse Carolyn, and Skinner E. Roy, eds. Lipoprotein analysis. Oxford [England]: IRL Press at Oxford University Press, 1992.

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1924-, Scanu Angelo M., ed. Lipoprotein (a). San Diego: Academic Press, 1990.

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James, Shepherd, ed. Lipoprotein metabolism. London: Baillie re, 1987.

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M, Ordovas J., ed. Lipoprotein protocols. Totowa, NJ: Humana Press, 1998.

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Kostner, Karam, Gerhard M. Kostner, and Peter P. Toth, eds. Lipoprotein(a). Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-24575-6.

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Angel, Aubie, and Jiri Frohlich, eds. Lipoprotein Deficiency Syndromes. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-1262-8.

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International Conference on Lipoprotein Deficiency Syndromes (1985 Vancouver, B.C.). Lipoprotein deficiency syndromes. New York: Plenum Press, 1986.

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Book chapters on the topic "Lipoprotein A"

1

Bährle-Rapp, Marina. "Lipoprotein." In Springer Lexikon Kosmetik und Körperpflege, 325. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-71095-0_6064.

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Harlapur, Manjunath, and Daichi Shimbo. "Lipoprotein." In Encyclopedia of Behavioral Medicine, 1299–300. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_1276.

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Malik, Jamil A., Theresa A. Morgan, Falk Kiefer, Mustafa Al’Absi, Anna C. Phillips, Patricia Cristine Heyn, Katherine S. Hall, et al. "Lipoprotein." In Encyclopedia of Behavioral Medicine, 1168–69. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_1276.

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Harlapur, Manjunath, and Daichi Shimbo. "Lipoprotein." In Encyclopedia of Behavioral Medicine, 1–2. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4614-6439-6_1276-2.

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Fruchart, J. C., and G. Luc. "Lipoprotein Oxidation." In Lipid-Soluble Antioxidants: Biochemistry and Clinical Applications, 553–66. Basel: Birkhäuser Basel, 1992. http://dx.doi.org/10.1007/978-3-0348-7432-8_43.

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Nallamshetty, Shriram, Jorge Plutzky, and Jorge Plutzky. "Lipoprotein Disorders." In MGH Cardiology Board Review, 105–19. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-4483-0_6.

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Sorrentino, Matthew J. "Lipoprotein(a)." In Hyperlipidemia in Primary Care, 173–79. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60327-502-6_10.

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Rader, Daniel J., and Sumeet A. Khetarpal. "Lipoprotein Physiology." In Dyslipidemias, 1–12. Totowa, NJ: Humana Press, 2015. http://dx.doi.org/10.1007/978-1-60761-424-1_1.

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Enkhmaa, Byambaa, Erdembileg Anuurad, Wei Zhang, and Lars Berglund. "Lipoprotein(a)." In Dyslipidemias, 25–55. Totowa, NJ: Humana Press, 2015. http://dx.doi.org/10.1007/978-1-60761-424-1_3.

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Bock, H. H., P. May, and J. Herz. "Lipoprotein Transport." In Transgenic Models in Pharmacology, 397–421. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18934-0_14.

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Conference papers on the topic "Lipoprotein A"

1

Koller, E., and F. Koller. "LIPOPROTEIN BINDING TOHUMAN PLATELETS IS LOCATED AT GPIIb/IIIa COMPLEX." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643702.

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Human Platelets possess specific binding sites for low density lipoproteins (LDL) and high density lipoproteins(HDL)(1). Binding of both classes of plasma lipoproteins, though competitive, has been shown by several groups to facilitate platelet activation.Isolated washed platelets occasionally aggregate upon addition of high concentrations of LDL even in the absence of known platelet activators. The proteins responsible for this binding have been visualized by ligand blotting (2). Both types of ligand specifically bind to two glycoproteins with molecular weights of 135 and 115 kD, respectively. The conditions of binding to these two proteins, however, markedly differ from those known for other lipoprotein receptors.Following extensive purification, these two species are still present at concentrations relative to each other that depend markedly on the conditions of purification. The purified, solubilized receptor was tested under various conditions, including in the absence and presence of calcium, after disulfide-reduction, and following chymotrypsin digestion. In parallel experiments, the same preparations were tested with respect to binding of fibrinogen, different lectins, and thealloantibody anti-PlAI . The results strongly support the assumption, that the two protein bands associated with lipoprotein binding are constituents of the GP-IIb/IIIa complex.These first results may have greatimplications for our understanding ofthe mechanism by which lipoproteins facilitate platelet stimulation.
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FATHIL, Noor Mahdi. "EFFECT OF THE ENERGY DRINK (TIGER) ON THE PARAMETERS OF LIPID PROFILEIN THE FEMALE ALBINO MICE." In III.International Scientific Congress of Pure,Appliedand Technological Sciences. Rimar Academy, 2021. http://dx.doi.org/10.47832/minarcongress3-5.

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The aim of research is to clarify effect of an energy drink (Tiger) on Lipid profile physiological parameters in female mice for a period of four weeks. Adults female mice were used in research and divide to two groups. The first group is the control group that give distilled water (D.w.) for four weeks and the second group was treated group with tiger concentration dose 1.5 ml/mg for period of four weeks. After the end of the dosing period, sacrifices animals and the blood samples are collected without anticoagulant, and blood serum is obtained and kept at− 20 °C for biochemical tests. The research was seen that there was the significant increase (p<0.05) in a cholesterol and the highdensity lipoproteins, with a significant decrease (p< 0.05) in value of triglycerides and a very low-density lipoprotein(VLDL), a Low density lipoprotein (LDL) was showed non –significant (P≥0.05) in the dosed group as compare as the control group. Key words: Energy Drink (Tiger ), Cholesterol(CHO), Triglycerides (TG), HighDensity Lipoprotein (HDL), Very Low-Density Lipoprotein (VLDL), The (LDL) Low-Density Lipoprotein.
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Damirchi, Behzad, Amir Rouhollahi, Salman Sohrabi, and Seyyed Mahdi Nemati Mehr. "Modeling and Stability Analysis of Truncated High Density Lipoprotein (HDL) System Using Martini Coarse Grain Technique." In ASME 2013 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/imece2013-64808.

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Lipoproteins are biochemical compounds containing both proteins and lipids. These particles carry chemicals like cholesterol and triglycerides that are not soluble in aqueous solutions. This paper presents modeling of lipoprotein system using coarse grain molecular dynamics technique and stability analysis of this system in a water solution like blood. A high density lipoprotein (HDL) that consists of two annular monomers is modeled. Also there are lipid bilayers located in center of the rings, so the whole HDL and lipid bilayers are called lipoprotein system. First, all atom model is provided and then coarse-grain model is obtained using MARTINI technique. Modeling of the system in all atom and coarse-grain is performed by VMD and simulation is executed by NAMD. System is simulated for 400ns with time step of 20fs in NPT ensemble. System temperature assumed similar to normal human body temperature. Finally the structure shape and stability of system were considered and results were analyzed.
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Hubbard, A. R., and C. A. Jennings. "TISSUE FACTOR-FACTOR VII INHIBITION REQUIRES FACTOR Xa AND PLASMA LIPOPROTEINS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643291.

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Tissue factor rapidly loses procoagulant activity when incubated with defibrmated normal plasma and calcium ions. Inhibition is apparently directed against the tissue factor-Factor VII complex (TF-EVII) and requires Factor Xa and a component(s) found in A1 (OH)3-adsorbed plasma (AP). We have developed a two stage assay for the inhibitor which involves first, the incubation of a TF-FVII complex with test material in the presence of Factor Xa, followed by the amidolytic assay of residual TF-EVII activity.Our studies have indicated that the component of AP responsible for this effect is lipoprotein. Incubation of AP with antiserum to apo-lipoprotein B (apo B) reduced the inhibitory activity by 73%, whereas antisera to antithrombin III and a2-macroglobulin had no effect. Inhibition by AP does not appear to be caused by an artefact of adsorption, since the inhibitory-capacity of AP was 59% of normal, defibrinated plasma. This correlated well with the apo B antigen in AP, which was 64% of normal. Moreover, the dose/response lines of AP and normal plasma were parallel, suggesting that the inhibitor assay is not affected by the presence of normal levels of coagulation factors.Purified lipoprotein-rich fractions prepared from AP using density gradient ultracentrifugation all contained inhibitory activity. Incubation of these fractions with anti-apo B greatly reduced the inhibition by the very low density and low density lipoprotein-rich fractions (VLDL and LDL) but had essentially no effect on the high density lipoprotein-rich fractions (HDL). Incubation of LDL with Factor Xa produced an inhibitory component which eluted together with the apo B antigen during gel filtration. Inhibition appears to require the interaction of Factor Xa with plasma lipoproteins, particularly LDL. The product of this interaction is then able to bind and inhibit the TF EVII complex. The requirement of Factor Xa in order for inhibition to be expressed is indicative of a feedback anticoagulant response which may have physiological significance.
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Palvinskaya, Tatsiana, Christopher Lenox, MaryEllen Antkowiak, Elianne Burg, Anne E. Dixon, Michael B. Fessler, Matthew Poynter, and Benjamin T. Suratt. "Low Density Lipoprotein Activate Neutrophils." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4349.

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Ittrich, H., O. Bruns, A. Bartelt, K. Peldschus, M. Kaul, G. Adam, and J. Heeren. "In-vivo MR imaging of lipoprotein distribution and metabolism using spio-labeled lipoproteins at 3T." In 2013 International Workshop on Magnetic Particle Imaging (IWMPI). IEEE, 2013. http://dx.doi.org/10.1109/iwmpi.2013.6528361.

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Kuemmerle, Nancy Benton, Leslie E. Lupien, Nicole C. Smits, Wilson L. Davis, and William B. Kinlaw. "Abstract 5607: Lipoprotein lipase binds to the surface of cancer cells and facilitates uptake of lipoproteins." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5607.

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Chen, Meifania, and Maja Hadzic. "Towards a methodology for Lipoprotein Ontology." In 2010 IEEE 23rd International Symposium on Computer-Based Medical Systems (CBMS). IEEE, 2010. http://dx.doi.org/10.1109/cbms.2010.6042680.

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Prabhu, Anmiv S., Alejandro Moraga, Michael Cecchini, Rafael Mulero, Stephen Olsen, Young I. Cho, and Min Jun Kim. "Synthetic Nanoscale Architectures for Lipoprotein Separation." In ASME 2008 International Mechanical Engineering Congress and Exposition. ASMEDC, 2008. http://dx.doi.org/10.1115/imece2008-66535.

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Current low density lipoprotein (LDL) apheresis procedures are expensive and time consuming. We report here a novel technique to detect and separate nanoparticles using solid state nanopores. Our technique relies on the resistive pulse phenomenon used in coulter counters. We used a 150nm diameter nanopore to detect nanoparticles that closely resembled HDL and LDL in terms of their size and surface charge. Statistical analysis of the translocation data revealed that our setup preferentially allowed the particles resembling HDL to pass thorough while restricting the translocation of the particles that resembled LDL.
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Wang, Min S., and Scott M. Reed. "Electrophoretic mobility of lipoprotein nanoparticle mimics." In 2011 IEEE 11th International Conference on Nanotechnology (IEEE-NANO). IEEE, 2011. http://dx.doi.org/10.1109/nano.2011.6144448.

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Reports on the topic "Lipoprotein A"

1

Kahl, S. B. Low density lipoprotein development and evaluation. Office of Scientific and Technical Information (OSTI), November 1995. http://dx.doi.org/10.2172/421327.

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Hinshaw, Jerald C. Synthesis of Lipoprotein Immunostimulants for Treating Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada434134.

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Hinshaw, Jerald C. Synthesis of Lipoprotein Immunostimulants for Treating Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2004. http://dx.doi.org/10.21236/ada423265.

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Rubin, E. M., and A. S. Plump. The use of transgenic animals to study lipoprotein metabolism. Office of Scientific and Technical Information (OSTI), December 1993. http://dx.doi.org/10.2172/102282.

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Hung, Hsuan-Yu, Hui-Hsiung Lai, Hui-Chuan Lin, and Chung-Yu Chen. Impact of interferon-free antivirus therapy on lipid profiles in patients with chronic hepatitis C: A network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0055.

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Review question / Objective: P: ("Hepatitis C"[Mesh] AND "Hepacivirus"[Mesh] AND "Hepatitis C, Chronic”[Mesh]) I: (direct acting antiviral OR asunaprevir OR boceprevir OR daclatasvir OR dasabuvir OR elbasvir OR glecaprevir OR grazoprevir OR ledipasvir OR ombitasvir OR paritaprevir OR pibrentasvir OR simeprevir OR sofosbuvir OR telaprevir OR velpatasvir OR voxilaprevir) C: placebo O: ( "Cholesterol, VLDL"[Mesh] OR "Cholesterol, LDL"[Mesh] OR "Cholesterol, HDL"[Mesh] OR "Dyslipidemias"[Mesh] OR "lipoprotein cholesterol ester, human" [Supplementary Concept] OR "lipoprotein cholesterol" [Supplementary Concept] ) OR ((lipoprotein cholesterol) OR ("lipidemia") OR (lipid metabolism) OR (lipid)). Information sources: We conducted a comprehensive literature search of PubMed, Cochrane Library, Embase, and Ovid MEDLINE electronic databases from their inception to May 20, 2022.
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Lacko, Andras G. High Density Lipoprotein Complexes as Delivery Vehicles for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada416984.

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Lacko, Andras G. High Density Lipoprotein Complexes as Delivery Vehicles for Breast Cancer Chemotherapy. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada408103.

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Zhang, Wei-Yang. Studies on the Formation of Murein-Bound Lipoprotein in Escherichia coli. Fort Belvoir, VA: Defense Technical Information Center, April 1992. http://dx.doi.org/10.21236/ad1011159.

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Krauss, R. M., and D. M. Dreon. Low density lipoprotein subclasses and response to a low-fat diet in healthy men. Office of Scientific and Technical Information (OSTI), November 1994. http://dx.doi.org/10.2172/41265.

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Chen, Jiankun, Yingming Gu, Lihong Yin, Minyi He, Na Liu, Yue Lu, Changcai Xie, Jiqiang Li, and Yu Chen. Network meta-analysis of curative efficacy of different acupuncture methods on obesity combined with insulin resistance. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0075.

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Review question / Objective: Population：Patients diagnosed as obesity with insulin resistance. Obesity reference: Consensus of experts on the Prevention and treatment of adult obesity in China in 2011 and Consensus of Chinese experts on medical nutrition therapy for overweight/obesity in 2016 were developed by the Obesity Group of Chinese Society of Endocrinology(CSE); BMI≥28. IR reference: According to the Expert opinions on insulin resistance evaluation published by Chinese Diabetes Society, HOMA-IR≥2.68 is regarded as the standard for the diagnosis of IR. Regardless of age, gender and course of disease. Patients diagnosed as obesity with insulin resistance. Intervention：Any kind of acupuncture, moxibustion, acupuncture+moxibustion, warm acupuncture, electropuncture, auricular point, acupoint application and acupoint catgut embedding. Comparison：Other acupuncture treatments, Drug therapy or blank control. Outcome：Primary outcomes: ①Fasting blood-glucose (FBG); ②Fasting serum insulin (FINS); ③Homeostasis model assessment-IR (HOMA-IR); ④Body Mass Index (BMI). Secondary outcomes: ①Waistline; ②Waist-hip ratio;③Triglyceride (TG); ④Total cholesterol (TC); ⑤High-density lipoprotein (HDL); ⑥Low-density lipoprotein (LDL). Study: Randomized controlled trials (RCTs) of different acupuncture methods in the treatment on obesity with insulin resistance, blind method and language are not limited. Randomized controlled trials (RCTs).
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