Academic literature on the topic 'Lipoproteins'
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Journal articles on the topic "Lipoproteins"
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Ozsavci, Derya, A. Nazli, O. Bingol Ozakpinar, G. Yanikkaya Demirel, B. Vanizor Kural, and A. Sener. "Native High-Density Lipoprotein and Melatonin Improve Platelet Response Induced by Glycated Lipoproteins." Folia Biologica 64, no. 4 (2018): 144–52. http://dx.doi.org/10.14712/fb2018064040144.
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Activated platelets and glycated lipoproteins are responsible for atherothrombosis in diabetics. Melatonin and native high-density lipoproteins are crucial in the preservation of pro/oxidant-antioxidant balance. The aim of the present study was to investigate the in vitro effects of native high-density lipoproteins and melatonin on altering the platelet response induced by glycated lipoproteins. Low-density lipoproteins and high-density lipoproteins were purified from plasma by ultracentrifugation and were glycated with glucose for three weeks. After incubation with or without melatonin/or native highdensity lipoproteins, low-density lipoproteins, glycated low-density lipoproteins/glycated high-density lipoproteins were added to ADP-induced platelets. Oxidative parameters, caspase-3/9 and nitric oxide levels were measured spectrophotometrically; CD62-P/ annexin-V expression was determined by flow cytometry. In glycated low-density lipoprotein/glycated high-density lipoprotein-treated groups, platelet malondialdehyde/ protein carbonyl, P-selectin, annexin-V, caspase-3/9 levels were increased (ranging from P < 0.001 to P < 0.01); glutathione and nitric oxide levels were reduced (ranging from P < 0.001 to P < 0.01). In glycated low-density lipoprotein/glycated high-density lipoprotein-treated groups, melatonin treatment reduced malondialdehyde, protein carbonyl, CD62-P, annexin-V and caspase-3/9 (P < 0.001, P < 0.01) levels and elevated nitric oxide (only glycated low-density lipoproteins). In glycated low-density lipoprotein/glycated high-density lipoprotein-treated groups, native high-density lipoprotein treatment reduced malondialdehyde, protein carbonyl, annexin-V, caspase-3/9 levels (P < 0.001, P < 0.01) and increased glutathione; nitric oxide levels (only with gly-HDL). Both melatonin and high-density lipoproteins should be regarded as novel promising mechanism-based potential therapeutic targets to prevent atherothrombosis in diabetics.
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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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Biggerstaff, Kyle D., and Joshua S. Wooten. "Understanding lipoproteins as transporters of cholesterol and other lipids." Advances in Physiology Education 28, no. 3 (September 2004): 105–6. http://dx.doi.org/10.1152/advan.00048.2003.
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A clear picture of lipoprotein metabolism is essential for understanding the pathophysiology of atherosclerosis. Many students are taught that low-density lipoprotein-cholesterol is “bad” and high-density lipoprotein-cholesterol is “good.” This misconception leads to students thinking that lipoproteins are types of cholesterol rather than transporters of lipid. Describing lipoproteins as particles that are composed of lipid and protein and illustrating the variation in particle density that is determined by the constantly changing lipid and protein composition clarifies the metabolic pathway and physiological function of lipoproteins as lipid transporters. Such a description will also suggest the critical role played by apolipoproteins in lipid transport. The clarification of lipoproteins as particles that change density will help students understand the nomenclature used to classify lipoproteins as well.
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Yousef, Malaz, Nadia Bou Chacra, Neal M. Davies, and Raimar Löbenberg. "Lipoproteins within the lymphatic system: Insights into health, disease, and therapeutic implications." Applied Chemical Engineering 6, no. 2 (September 4, 2023): 2202. http://dx.doi.org/10.24294/ace.v6i2.2202.
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This analysis of contemporary findings aims to enhance our understanding of lipoprotein biology within the lymphatic system and its relevance to human health and disease. It delves into the complex interrelationship between lipoproteins and the lymphatic system, encompassing their diverse classes and pivotal roles in the absorption and transport of drugs, vitamins, and xenobiotics. Lipoproteins consist of a hydrophobic core comprising non-polar lipids and a hydrophilic membrane composed of phospholipids, free cholesterol, and apolipoproteins. The lymphatic system collaborates with lipoproteins in the absorption and transport of dietary lipids. Simultaneously, it plays a vital role in the regulation of body fluid levels and acts as a formidable defense mechanism against infections. Lipoprotein classes encompass chylomicrons, chylomicron remnants, very low-density lipoproteins, intermediate density lipoproteins, low-density lipoproteins, high-density lipoproteins, and lipoprotein (a). Understanding the intricate relationship between lipoproteins and the lymphatic system holds immense implications for comprehending the underlying pathological processes of various diseases such as atherosclerosis, diabetes and obesity among others. By shedding light on the interplay between lipoproteins and the lymphatic system, this report underscores the significance of conducting research that contributes to the advancement of our knowledge in this field. Ultimately, such research paves the way for potential therapeutic interventions and novel strategies to address numerous disorders.
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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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Heeren, J., W. Weber, and U. Beisiegel. "Intracellular processing of endocytosed triglyceride-rich lipoproteins comprises both recycling and degradation." Journal of Cell Science 112, no. 3 (February 1, 1999): 349–59. http://dx.doi.org/10.1242/jcs.112.3.349.
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The current study was performed to investigate the intracellular fate of triglyceride-rich lipoproteins. Triglyceride-rich lipoproteins are responsible for the delivery of lipids to various tissues, however, their intracellular pathway has not yet been elucidated. Here radiolabeled triglyceride-rich lipoproteins, associated with lipoprotein lipase, were used for the quantitative evaluation of the intracellular metabolism. Pulse chase experiments showed that after 90 minutes approximately 60% of the labeled protein, mainly apoproteins E and C, was released intact into the medium, where it re-associates with lipoproteins. Apoprotein B, in contrast, was degraded, following the same pathway as the apoprotein B from low density lipoproteins. In kinetic experiments uptake and intracellular fate of triglyceride-rich lipoproteins was compared to that of transferrin and low density lipoproteins. These experiments revealed that apoproteins were retained inside the cell much longer than transferrin, and unlike low density lipoproteins were not degraded. Using immunofluorescence it was shown that apoprotein E and lipoprotein lipase follow a distinct route from the sorting compartment to the surface, which is clearly distinguishable from the perinuclear transferrin recycling compartment. In contrast, the fluorescence labeled lipids were delivered to lysosomal compartments. The data presented here show that surface proteins of triglyceride-rich lipoproteins, such as apoproteins E and C and lipoprotein lipase follow a recycling pathway, whereas lipids and high molecular mass core proteins are degraded.
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Karpe, F., A. S. Bickerton, L. Hodson, B. A. Fielding, G. D. Tan, and K. N. Frayn. "Removal of triacylglycerols from chylomicrons and VLDL by capillary beds: the basis of lipoprotein remnant formation." Biochemical Society Transactions 35, no. 3 (May 22, 2007): 472–76. http://dx.doi.org/10.1042/bst0350472.
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The triacylglycerol content of chylomicrons and VLDL (very-low-density lipoprotein) compete for the same lipolytic pathway in the capillary beds. Although chylomicron triacylglycerols appear to be the favoured substrate for lipoprotein lipase, VLDL particles compete in numbers. Methods to quantify the specific triacylglycerol removal from VLDL and chylomicrons may involve endogenous labelling of the triacylglycerol substrate with stable isotopes in combination with arteriovenous blood sampling in humans. Arteriovenous quantification of remnant lipoproteins suggests that adipose tissue with its high lipoprotein lipase activity is a principal site for generation of remnant lipoproteins. Under circumstances of reduced efficiency in the removal of triacylglycerols from lipoproteins, there is accumulation of remnant lipoproteins, which are potentially atherogenic.
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Levels, J. H. M., P. R. Abraham, A. van den Ende, and S. J. H. van Deventer. "Distribution and Kinetics of Lipoprotein-Bound Endotoxin." Infection and Immunity 69, no. 5 (May 1, 2001): 2821–28. http://dx.doi.org/10.1128/iai.69.5.2821-2828.2001.
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ABSTRACT Lipopolysaccharide (LPS), the major glycolipid component of gram-negative bacterial outer membranes, is a potent endotoxin responsible for pathophysiological symptoms characteristic of infection. The observation that the majority of LPS is found in association with plasma lipoproteins has prompted the suggestion that sequestering of LPS by lipid particles may form an integral part of a humoral detoxification mechanism. Previous studies on the biological properties of isolated lipoproteins used differential ultracentrifugation to separate the major subclasses. To preserve the integrity of the lipoproteins, we have analyzed the LPS distribution, specificity, binding capacity, and kinetics of binding to lipoproteins in human whole blood or plasma by using high-performance gel permeation chromatography and fluorescent LPS of three different chemotypes. The average distribution of O111:B4, J5, or Re595 LPS in whole blood from 10 human volunteers was 60% (±8%) high-density lipoprotein (HDL), 25% (±7%) low-density lipoprotein, and 12% (±5%) very low density lipoprotein. The saturation capacity of lipoproteins for all three LPS chemotypes was in excess of 200 μg/ml. Kinetic analysis however, revealed a strict chemotype dependence. The binding of Re595 or J5 LPS was essentially complete within 10 min, and subsequent redistribution among the lipoprotein subclasses occurred to attain similar distributions as O111:B4 LPS at 40 min. We conclude that under simulated physiological conditions, the binding of LPS to lipoproteins is highly specific, HDL has the highest binding capacity for LPS, the saturation capacity of lipoproteins for endotoxin far exceeds the LPS concentrations measured in clinical situations, and the kinetics of LPS association with lipoproteins display chemotype-dependent differences.
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Baumgärtner, Maja, Uwe Kärst, Birgit Gerstel, Martin Loessner, Jürgen Wehland, and Lothar Jänsch. "Inactivation of Lgt Allows Systematic Characterization of Lipoproteins from Listeria monocytogenes." Journal of Bacteriology 189, no. 2 (October 13, 2006): 313–24. http://dx.doi.org/10.1128/jb.00976-06.
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ABSTRACT Lipoprotein anchoring in bacteria is mediated by the prolipoprotein diacylglyceryl transferase (Lgt), which catalyzes the transfer of a diacylglyceryl moiety to the prospective N-terminal cysteine of the mature lipoprotein. Deletion of the lgt gene in the gram-positive pathogen Listeria monocytogenes (i) impairs intracellular growth of the bacterium in different eukaryotic cell lines and (ii) leads to increased release of lipoproteins into the culture supernatant. Comparative extracellular proteome analyses of the EGDe wild-type strain and the Δlgt mutant provided systematic insight into the relative expression of lipoproteins. Twenty-six of the 68 predicted lipoproteins were specifically released into the extracellular proteome of the Δlgt strain, and this proved that deletion of lgt is an excellent approach for experimental verification of listerial lipoproteins. Consequently, we generated Δlgt ΔprfA double mutants to detect lipoproteins belonging to the main virulence regulon that is controlled by PrfA. Overall, we identified three lipoproteins whose extracellular levels are regulated and one lipoprotein that is posttranslationally modified depending on PrfA. It is noteworthy that in contrast to previous studies of Escherichia coli, we unambiguously demonstrated that lipidation by Lgt is not a prerequisite for activity of the lipoprotein-specific signal peptidase II (Lsp) in Listeria.
Dissertations / Theses on the topic "Lipoproteins"
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Zago, Vanessa Helena de Souza 1984. "Efeitos do polimorfismo T-786C do gene da óxido nítrico sintase endotelial (eNOS) e/ou da atorvastatina sobre parâmetros do metabolismo lipídico em adultos assintmáticos." [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309030.
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Orientadores: Eliana Cotta de Faria, José Eduardo Tanus dos SantosDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: O óxido nítrico (NO) é produzido no endotélio vascular pela óxido nítrico sintase endotelial (eNOS), enzima regulada negativamente pela presença do polimorfismo T- 786C, levando à disfunção endotelial. A lipoproteína de alta densidade (HDL) têm funções anti-aterogênicas bem estabelecidas, incluindo mecanismos que aumentam a atividade da eNOS. As estatinas são fármacos que possuem, dentre seus efeitos pleiotrópicos, a melhora na função do endotélio e na composição da HDL. Dada a importância tanto da expressão quanto da atividade da eNOS para a função endotelial, bem como dos efeitos pleiotrópicos das estatinas sobre estas duas variáveis, avaliamos os parâmetros bioquímicos e a composição das sub-frações de HDL (HDL2 e HDL3) após uso de placebo e atorvastatina em uma amostra populacional de 30 indivíduos, divididos em dois grupos: 15 indivíduos portadores do polimorfismo T-786C do gene da eNOS (CC) e 15 não portadores (TT). Duzentos indivíduos foram genotipados, e pareamos conforme idade e IMC 15 indivíduos TT e 15 indivíduos CC, que receberam placebo e/ou atorvastatina na dose de 10mg/dia, por 14 dias. Os parâmetros séricos analisados foram determinados através de métodos bioquímicos enzimáticos, radiométricos, nefelométricos e microultracentrifugação. Mediu-se lípides, lipoproteínas, composição das sub-frações da HDL (HDL2 e HDL3), apolipoproteínas, atividade da proteína de transferência de colesteril éster, metabólitos do NO e proteína C reativa. Após o uso da estatina, como esperado, drásticos efeitos redutores foram observados tanto nos lípides, lipoproteínas, apolipoproteínas e de forma independente do polimorfismo, além da redução de ácidos graxos livres nos portadores do genótipo CC. Nas sub-frações a relação lípides/proteínas foi reduzida tanto em HDL2 quanto em HDL3.O aumento da atividade da CETP nos portadores foi corrigido pela estatina e os níveis de ácidos graxos livres reduziram-se de maneira polimorfismo-dependente, em oposição à redução observada do nitrito, que foi polimorfismo-independente. usPCR e Lp(a) não se modificaram. A atorvastatina pode ter atuado sobre o transporte reverso de colesterol através da redução da atividade da lipase hepática e aumento de atividade da PLTP. Foram observadas interações genótipo/tratamento limítrofes para CETP e Lp(a). Estes resultados sugerem que o tratamento com estatinas pode ser relevante na prevenção primária da aterosclerose em portadores do polimorfismo, independentemente de modificações lipídicas séricas. Portanto estes indivíduos se beneficiariam com o uso de estatinas através da modulação da atividade da CETP e redução da concentração de ácidos graxos livres.
Abstract: Nitric oxide (NO) is produced in the vascular endothelium by endothelial nitric oxide synthase (eNOS), an enzyme negatively regulated by the presence of the T-786C polymorphism, leading to endothelial dysfunction. High-density lipoproteins (HDL) have well-established anti-atherogenic functions, for example mechanisms that enhance eNOS activity. Statins are drugs that have pleiotropic effects, such as the improvement in endothelial function and beneficial composition of HDL. Taking into account both the activity of eNOS on endothelial function, and the validity of the pleiotropic effects of statins, we evaluated the biochemical parameters and the composition of subfractions of HDL (HDL2 and HDL3) after use of placebo and atorvastatin at a dose of 10mg/day for 14 days, in a population sample of 30 individuals divided into two genotype groups of the T-786C polymorphism of the eNOS gene: CC (carriers) or TT (non-carriers). Two hundred individuals were genotyped, and the selected groups paired by age and BMI. The serum parameters analyzed were determined using biochemical enzymatic, radiometric, nephelometric and microultracentrifugation methods. We measured lipids, lipoproteins, the composition of sub-fractions of HDL (HDL2 and HDL3), apolipoproteins, activity of cholesteryl ester transfer protein, NO metabolites and hsCRP. After statin, as expected, drastic effects were observed both in lipids, lipoproteins, apolipoproteins, independently of the polymorphism. In HDL sub-fractions the ratio lipid/protein was smaller in both HDL2 and HDL3. CETP activity and free fatty acids were reduced in a polymorphism-dependent manner, and the reduction of nitrite was polymorphism-independent. hsCRP did not change. Atorvastatin may have acted on the reverse cholesterol transport by reducing the activity of hepatic lipase, increased PLTP activity and reducing CETP. There was a genotype/drug interaction effect on CETP and Lp(a). These results suggest that statin treatment may be relevant for primary prevention of atherosclerosis in patients with the polymorphism, irrespective of serum lipid changes. These individuals would benefit from the use of statins because of reduction of CETP activity and free fatty acids.
Mestrado
Ciencias Biomedicas
Mestre em Ciências Médicas
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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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Parra, Eliane Soler 1981. "Comparação entre a atividade da proteína de transferência de colesterol esterificado e o tamanho da HDL na associação com a aterosclerose carotídea." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/313596.
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Orientadores: Andrei Carvalho Sposito, Eliana Cotta de FariaTexto em português e inglês
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: A lipoproteína de alta densidade (HDL) é um complexo heterogêneo e versátil de partículas com variações funcionais resultantes da integração de uma vasta gama de componentes, como apolipoproteínas, receptores, transportadores, enzimas e fosfolípides, com ações indiretas ou diretas sobre o seu metabolismo. Além disso, as concentrações plasmáticas do colesterol da HDL (HDL-C) e seu tamanho representam importantes fatores inversos ao desenvolvimento de doenças cardiovasculares, particularmente em indivíduos em prevenção primária. A proteína de transferência de colesterol esterificado (CETP) desempenha uma função importante no transporte reverso do colesterol (TRC) que é umas das principais funções antiaterogênicas da HDL. No entanto, a atividade da CETP é inversamente associada às concentrações de HDL-C e ao tamanho da partícula. Adicionalmente, HDL grande demonstra ser mais efetiva no efluxo do colesterol, parte integrante do TRC, comparada à partícula de HDL menor. Nesse contexto, o objetivo do estudo foi avaliar, em indivíduos livres de doença aterosclerótica manisfesta, a associação entre o tamanho da HDL e a redução da atividade da CETP induzida geneticamente com a carga aterosclerótica carotídea. Utilizamos para esse fim dois polimorfismos da CETP, TaqIB e I405V, que foram bem caracterizados funcionalmente e encontrados frequentemente na população. Assim, os objetivos desta tese foram: (i) investigar se a presença dos polimorfismos TaqIB e I405V do gene da CETP está associada às concentrações de HDL-C e à aterosclerose carotídea subclínica (n=207); (ii) pesquisar se, além das concentrações de HDL-C, o tamanho da partícula de HDL está associado à aterosclerose subclínica (n=284). Para estes estudos foram determinados os perfis lipídicos, lipoproteícos e apoproteícos, proteína C-reativa (PCR), anticorpos anti-LDL oxidada, atividades das proteínas CETP e de transferência de fosfolípides (PLTP), HDL2 e HDL3 e o diâmetro da HDL. Os polimorfismos TaqIB e I405V da CETP também foram detectados. A espessura da camada íntima-medial da artéria carótida comum (EIMc) foi mensurada por ultrassonografia. Na presença do menor alelo dos polimorfismos TaqIB e I405V da CETP, EIMc correlacionou-se inversamente com atividade da CETP e positivamente com atividade da PLTP e anticorpos anti-LDL oxidada. Na análise multivariada, a presença do menor alelo do polimorfismo TaqIB, mas não do I405V, foi associado a um aumento de 5,1 vezes de risco de maior EIMc. No entanto, a atividade da CETP não diferiu entre os grupos de presença e ausência do menor alelo do polimorfismo TaqIB. Com relação ao tamanho das partículas, HDL maiores foram associadas a menores EIMc e foram melhores indicadores de risco de aterosclerose carotídea subclínica comparadas às concentrações de HDL-C. Em conclusão, o aumento do tamanho da HDL tem associação independente com a carga aterosclerótica e, embora o polimorfismo TaqIB também se associe, sua interação parece ser independente da atividade da CETP
Abstract: High-density lipoproteins ( HDL ) are a group of heterogeneous and complex particles with versatile functional changes resulting from the integration of a wide range of components, such as apolipoproteins, receptors, transporters, enzymes and phospholipids with indirect or direct actions on your metabolism. In addition, plasma concentrations of HDL cholesterol (HDL -C) and its size are inversely related to the development of cardiovascular diseases, particularly in primary prevention in individuals. The cholesterol ester transfer protein (CETP) plays an important role in reverse cholesterol transport (RCT), which is one of the main functions of HDL. However, CETP activity is inversely related to HDL-C and particle size. Additionally, largest HDL particles have demonstrated a higher cholesterol efflux capacity. In this context, the aim of the study was to evaluate, in individuals free of manifest atherosclerotic disease, the association between the size of HDL and CETP activity genetically induced with carotid atherosclerosis burden. We used for this purpose, two polymorphisms of CETP TaqIB and I405V, which have been well characterized functionally and often found in the population. The objectives of this thesis were: (i) to investigate whether the presence of polymorphisms I405V and TaqIB of CETP gene is associated with HDL-C and subclinical carotid atherosclerosis (n= 207); (ii) to investigate if, in addition to HDL-C, the particle size of HDL is associated with atherosclerosis (n= 284). We determined lipid, lipoprotein profiles and apolipoprotein, C-reactive protein (CRP), antibodies against oxidized LDL, CETP and phospholipid transfer protein (PLTP) activities, HDL2 and HDL3 and HDL size. The TaqIB and I405V CETP polymorphisms were also analyzed. Common carotid artery intima-media thickness (cIMT) was measured using ultrasonography. In the presence of the minor alleles of the TaqIB and I405V polymorphisms of CETP, cIMT was inversely correlated with CETP activity and positively with PLTP activity and antibodies against oxidized LDL. In multivariate analysis, the presence of the minor allele of the TaqIB polymorphism, but not the I405V, was associated with a 5.1 times increased risk of higher cIMT. However, CETP activity did not differ between the presence and absence of minor allele groups of the TaqIB polymorphism. Regarding HDL size, increased HDL size was associated with lower cIMT and was better marker of risk of subclinical carotid atherosclerosis compared to HDL-C. In conclusion, increased size of HDL is independently associated with atherosclerotic and, although TaqIB polymorphism is also associated, its interaction seems to be independent of CETP activity
Doutorado
Clinica Medica
Doutora em Clínica Médica
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González, Muñoz Marta. "Estudi dels canvis en la distribució de les subclasses de lipoproteïnes i partícules romanents en diferents condicions associades a risc arterioscleròtic: més enllà del colesterol." Doctoral thesis, Universitat Rovira i Virgili, 2016. http://hdl.handle.net/10803/401823.
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Tot i els enormes avenços en el camp de la prevenció del risc cardiovascular, una part molt significativa del infarts de miocardi es donen en individus amb un perfil lipídic de rutina normal. L’anàlisi avançat per ressonància magnètica nuclear (RMN) que determina la mida i el número de les partícules lipoproteiques, i la determinació de les lipoproteïnes romanents (LRs), poden donar resposta a les restriccions metodològiques que presenten els paràmetres lipídics convencionals.
En aquest context vam plantejar l’estudi en pacients amb Lupus Eritematós Sistèmic (LES), i amb aquest anàlisi avançat donar resposta al seu alt risc arterioscleròtic tot i presentar un perfil lipídic convencional mínimament alterat. Per altra banda, en LES la prevalença d’arteriosclerosi subclínica en edats joves és major que en població general, és a dir que l’edat no té un impacte tant fort en el procés arterioscleròtic. Tant l’edat com l’índex de massa corporal són coneguts i importants factors de risc arterioscleròtic, però mai han estat estudiats des d’aquest punt de vista en una població amb absència de cap patologia crònica. Finalment, donat que el colesterol transportat per la fracció de lipoproteïnes romanents RLP ha estat considerada un factor independent de risc arterioscleròtic, és important conèixer les partícules que la composen.
La conclusió és que l’anàlisi avançat de lípids i lipoproteïnes permet veure que la mida i el número de lipoproteïnes, junt amb les LR aporten informació addicional a la obtinguda pels paràmetres lipídics convencionals, en l’efecte del LES, l’edat i l’índex de massa corporal sobre el procés patogènic de l’arteriosclerosi; i el que de manera general anomenem LRs no és un grup homogeni de partícules i caldria deixar de parlar-ne com a tal.A pesar de los enormes avances en el campo de la prevención del riesgo cardiovascular, una parte muy significativa de infartos de miocardio se dan en individuos con un perfil lipídico de rutina normal. El análisis avanzado por resonancia magnética nuclear (RMN) que determina el tamaño y el número de las partículas lipoproteicas, y la determinación de las lipoproteínas remanentes (LRs), pueden dar respuesta a las restricciones metodológicas que presentan los parámetros lipídicos convencionales. En este contexto planteamos el estudio en pacientes con Lupus Eritematoso Sistémico (LES), y con este análisis avanzado dar respuesta a su alto riesgo aterosclerótico a pesar de presentar un perfil lipídico convencional mínimamente alterado. Por otra parte, en LES la prevalencia de arteriosclerosis subclínica en edades jóvenes es mayor que en población general, es decir que la edad no tiene un impacto tan fuerte en el proceso aterosclerótico. Tanto la edad como el índice de masa corporal son conocidos e importantes factores de riesgo aterosclerótico, pero nunca han sido estudiados desde este punto de vista en una población con ausencia de patología crónica. Por último, dado que el colesterol transportado por la fracción de lipoproteínas remanentes RLP ha sido considerado un factor independiente de riesgo aterosclerótico, es importante conocer las partículas que la componen. La conclusión es que el análisis avanzado de lípidos y lipoproteínas permite ver que el tamaño y el número de lipoproteínas, junto con las LR aportan información adicional a la obtenida por los parámetros lipídicos convencionales, en el efecto del LES, la edad y el índice de masa corporal sobre el proceso patogénico de la arteriosclerosis; y lo que de manera general llamamos LRs no es un grupo homogéneo de partículas y se debería dejar de hablar como tal.
Despite huge advances in the field of cardiovascular risk prevention, a significant proportion of heart attacks occur in individuals with a normal routine lipid profile. Advanced analysis by nuclear magnetic resonance (NMR), which determines the size and number of lipoprotein particles, and the determination of remnant lipoproteins (RLs) can help solve the methodological constraints presented by conventional lipid parameters. In this context we considered the study with advanced analysis, in patients with systemic lupus erythematosus (SLE) to respond to its high-risk atherosclerotic despite presenting a conventional minimally altered lipid profile. Moreover, in LES the prevalence of subclinical atherosclerosis at younger ages is greater than in the general population, meaning that age does not have a strong impact on the atherosclerotic process. Both age and body mass index (BMI) are known and are important risk factors for the atherosclerotic process, but they have never been studied from this point of view, in a population with an absence of any chronic disease. Finally, given that cholesterol transported for the fraction of remnant lipoproteins RLP has been considered an independent risk factor for atherosclerosis, it is important to know the particles composition. The conclusion is that advanced analysis of lipids and lipoproteins allows us to prove that the size and number of lipoproteins, together with LR, provide additional information on the effect of LES, age and BMI, in the pathogenic process of atherosclerosis, from that which is obtained by conventional lipid parameters; and what it is generally called RLs is not an homogeneous group particle and therefore it should not be talked about as such.
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Mallol, Parera Roger. "Development and evaluation of a novel advanced lipoprotein test based on 2d diffusion orderen 1h nmr spectroscopy." Doctoral thesis, Universitat Rovira i Virgili, 2014. http://hdl.handle.net/10803/296439.
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La determinació de la mida i el nombre de lipoproteïnes utilitzant tests avançats de lipoproteïnes és d'un gran interès clínic ja que el nombre de partícules LDL s'ha posicionat com a millor predictor de risc cardiovascular que el colesterol LDL. Tanmateix, els tests avançats de lipoproteïnes actuals encara no s'han introduït en l'àmbit clínic en gran part per la falta d'una estandarització. En aquesta tesi presentem el test LipoScale, un nou test avançat de lipoproteïnes basat en espectroscopia de RMN de difusió 2D. Amb aquest test es pretén obtenir una millor caracterització de les lipoproteïnes plasmàtiques, tant el seu contingut lipídic com la seva mida i nombre de partícules, de manera que amb ell s'aconsegueixi una millor predicció del risc cardiovascular. Durant el desenvolupament del test s’han estudiat diferents patologies i cohorts dins del marc de les malalties metabòliques (les quals són un factor de risc de les malalties cardiovasculars). Entre les malalties estudiades destaquem la diabetis, la dislipèmia aterògena i la síndrome de l’ovari poliquístic (PCOS). A més, també s’han monitoritzat canvis en el perfil de les lipoproteïnes deguts a intervencions nutricionals i a l’exercici. La principal diferència entre la nostra aproximació i la dels mètodes actuals és que aquests últims utilitzen mètodes de RMN 1D estàndards, mentre que el nostre test està basat en l'ús de gradients de camps magnètic, els quals generen espectres 2D amb els que es pot obtenir informació directa i objectiva de la mida de les partícules lipoproteiques. Aquesta tesi ha generat diferents publicacions científiques així com també s'ha fet la sol•licitud d'una patent europea i s'ha creat una spin-off per comercialitzar el test.La determinación del tamaño y el número de lipoproteínas utilizando tests avanzados de lipoproteínas es de un gran interés clínico ya que el número de partículas LDL se ha posicionado como mejor predictor de riesgo cardiovascular que el colesterol LDL. Sin embargo, los tests avanzados de lipoproteínas actuales aún no se han introducido en el ámbito clínico en gran parte por la falta de una estandarización. En esta tesis presentamos el test LipoScale, un nuevo test avanzado de lipoproteínas basado en espectroscopía de RMN de difusión 2D. Con este test se pretende obtener una mejor caracterización de las lipoproteínas plasmáticas, tanto su contenido lipídico como su tamaño y número de partículas, por lo que con él se consiga una mejor predicción del riesgo cardiovascular. Durante el desarrollo del test se han estudiado diferentes patologías y cohortes dentro del marco de las enfermedades metabólicas (las cuales son un factor de riesgo de las enfermedades cardiovasculares). Entre las enfermedades estudiadas destacamos la diabetes, la dislipemia aterògena y el síndrome del ovario poliquístico (PCOS). Además, también se han monitorizado cambios en el perfil de las lipoproteínas debidos a intervenciones nutricionales y el ejercicio. La principal diferencia entre nuestra aproximación y la de los métodos actuales es que estos últimos utilizan métodos de RMN 1D estándar, mientras que nuestro test está basado en el uso de gradientes de campo magnético, los cuales generan espectros 2D con los que se puede obtener información directa y objetiva del tamaño de las partículas lipoproteicas. Esta tesis a generado diferentes publicaciones científicas así como también se ha hecho la solicitud de una patente europea y se ha creado una spin-off para comercializar el test.
Determination of lipoprotein particle size and particle number using advanced lipoprotein analyses is of particular interest since the LDL particle number has been shown to improve cardiovascular disease risk prediction. Advanced lipoprotein tests (ALT), however, are not yet routinely introduced in clinical practice partly due to the lack of standardization. This thesis presents the LipoScale test, a novel advanced lipoprotein test based on 2D diffusion-ordered 1H NMR spectroscopy. This test is to obtain a better characterization of plasma lipoproteins in terms of their lipid content, particle size and particle number that will allow a better assessment of cardiovascular risk. During the development of the test various diseases and cohorts were studied in the context of metabolic diseases (which are a risk factor for cardiovascular disease). Among the diseases studied we highlight diabetes, atherogenic dyslipidemia and polycystic ovary syndrome (PCOS). In addition, changes were also monitored in the lipoprotein profile due to nutritional interventions and exercise. The main difference between our approach and the current NMR methods is that the latter use standard 1D methods, whereas our test is based on the use of magnetic field gradients, which generate the 2D spectra that can be used to get direct and objective information on lipoprotein particle sizes. This thesis generated various scientific publications, includes an application for a European patent and a spin-off has been created to commercialize the test.
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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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Bassora, Fernanda Dutra Santiago 1982. "Modulação funcional e genica de lipides e lipoproteinas plasmaticos e da aterosclerose carotidea na hiperalfalipoproteinemia." [s.n.], 2007. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309023.
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Orientador: Eliana Cotta de FariaDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: Está bem estabelecida na literatura especializada a associação inversa entre as concentrações plasmáticas de colesterol das lipoproteínas de alta densidade (HDL-C) e a incidência de doença arterial coronariana (DAC). Além de propriedades anti-oxidante, anti-inflamatória e anti-trombótica, a HDL participa do transporte reverso de colesterol, via pela qual o colesterol é captado das lipoproteínas e das membranas células periféricas e transportado ao fígado para sua excreção na forma livre ou de ácidos biliares. A lipase hepática (LH) possui função crucial no transporte reverso do colesterol, por sua atividade lipolítica e pela função de ligante à lipoproteínas facilitando sua captação tissular. A proteína de transferência de ésteres de colesterol (CETP), e mesma importância metabólica, promove a troca de ésteres de colesterol por triglicérides entre a HDL e as lipoproteínas ricas em triglicérides. Mutações nos genes que codificam estas proteínas têm sido muito estudadas para se compreender a função destas no metabolismo lipídico. O modelo experimental da hiperalfalipoproteinemia tem sido utilizado no decorrer dos últimos anos com o intuito de elucidar os mecanismos de ação da HDL e das proteínas reguladoras do seu metabolismo. A hiperalfalipoproteinemia é caracterizada pelo aumento das concentrações de HDL-C e é causada principalmente por deficiências genética de CETP e/ou LH. Os objetivos desta dissertação foram o de se estabelecer à modulação da hiperalfalipoproteinemia sobre os parâmetros antropométricos, bioquímicos, moleculares (¿514C/T do gene da LH e I405V do gene da CETP) e radiológicos (espessura da camada íntima média de carótidas) em uma amostra populacional brasileira. O estudo foi conduzido em 291 voluntários de ambos os sexos, classificados como hiperalfalipoproteinemicos (Hiper-A), HDL-C =68mg/dL, ou controles, HDL-C<68 e =32 mg/dL, de acordo com o valor do percentil 90, obtido em um estudo prévio do Laboratório de Lípides a partir população normolipidêmica. Os polimorfismos LH-514C/T e CETP I405V foram identificados através de técnicas de reação em cadeia polimerase (PCR) e a espessura da camada íntima-média de carótidas (EIM) pela ultra-sonografia de alta resolução. Em um primeiro trabalho observou-se em um sub-grupo de 169 indivíduos, com a medida da EIM, que somente a idade foi correlacionada com a EIM na hiperalfalipoproteinemia, enquanto que em controles houve modulação positiva pela idade, sexo masculino, pressão arterial sistólica, e controversamente com relatos da literatura, com HDL-C. Apesar de Hiper-A possuir um perfil com maior número de fatores de risco cardiovasculares, a semelhança encontrada na EIM de carótidas, assim como, da freqüência de EIM maior que 1 mm poderia, em parte, ser explicada pela grande diferença de modulação entre os grupos apontando para um traço protetor contra a aterosclerose carotídea em hiperalfalipoproteinemia. A ateroproteção reduzida em controles, tanto em homens quanto em mulheres, está de acordo com a observada associação negativa neste grupo entre EIM e a CETP com possível presença de HDL com a composição química alterada (ricas em TG e pobres em ésteres de colesterol), e ocorreu possìvelmente no sub-grupo masculino, com perfil pró-aterogênico evidente. Em um segundo trabalho, no sub-grupo de 169 indivíduos, com a medida da EIM, foi avaliado o efeito do polimorfismo LH-514C/T sobre a espessura da camada íntima-média de carótidas na hiperalfalipoproteinemia. Não se observou nenhuma variação de EIM em ambos os grupos em função deste polimorfismo. Quando comparados os grupos, o genótipo CC do polimorfismo LH-514C/T mostrou apenas tendência a maior EIM de carótidas em hiperalfalipoproteinemia (p<0,09), mas a freqüência de EIM maior que 1 mm foi igual. Em um terceiro trabalho, em 282-291 indivíduos foram avaliadas as semelhanças de freqüências entre os polimorfismos LH-514C/T e CETP I405V na hiperalfalipoproteinemia e normolipidemia. Ambos apresentaram altas freqüências, similares entre grupos e entre o polimorfismo LH-514C/T, CC 39%, CT+TT 61%; e o polimorfismo CETP I405V: II 26%, IV+VV 74% e CTL: CC 40%, CT+TT 60%, II 43% e IV+VV 57%. Descrevemos o polimorfismo LH-514C/T na hiperalfalipoproteinemia os TT vs CC apresentaram cintura menor, concentrações mais baixas de colesterol plasmático (C), fosfolípides (FL), LDL-C, estimativa do tamanho da LDL (LDL-C/ApoB). O polimorfismo CETP I405V na hiperalfalipoproteinemia em VV vs II, mostrou alta pressão arterial sangüínea e menores concentrações plasmáticas de HDL2TG e HDL3TG. O genótipo IV teve maiores concentrações plasmáticas de ApoAI e pressão arterial diastólica quando comparado com o genótipo II. Em resumo esta dissertação aponta para efeitos ateroprotetores ou neutros da hiperalfalipoproteinemia em uma amostra de população brasileira sobre a aterosclerose carotídea, inclusive no polimorfismo LH -514C/T. Os polimorfismos LH-514C/T e CETP I405V foram muito semelhantes com relação aos lípides e lipoproteínas séricos, mas não às proteínas reguladoras, oferecendo modulação protetora na hiperalfalipoproteinemia
Abstract: There is an inverse relationship between plasma concentration of high-density lipoprotein (HDL-C) and the risk of coronary arterial disease (CAD). Beyond anti-oxidant, anti-inflammatory and anti-thrombotic properties, HDL plays a role on the reverse cholesterol transport, where cholesterol is taken from lipoproteins and peripheral cells to the liver for excretion. Hepatic lipase (HL) plays a key role in this process, by its lipolitic activities and ligand functions. Cholesterol ester transfer protein (CETP), of equal metabolic importance, facilitates the exchange of cholesterol ester and triglycerides between HDL and triglyceride rich-lipoproteins. Mutations and polymorphisms of these enzymes have being studied in order to evaluate its activity and metabolic consequences. Hyperalphalipoproteinemia (Hyper-A) has being used in the latest years with the purpose of evaluating the anti and pro-atherogenic mechanisms of HDL and of regulating proteins. The aim of this work was to establish the modulation of hyperalphalipoproteinemia in relation to controls on the anthropometric, biochemical, radiological and molecular manifestations. This study was conducted on 291 volunteers, classified as Hyper-A, HDL-C=68mg/dL and controls, HDL-C <68 e 32 mg/dL according to the percentile 90th, obtained from a local normolipidemic population study. We determined clinic data, lipid, lipoproteins and radiological parameters of volunteers. The HL-514C/T and CETP I405V polymorphism were determined by polymerase chain reaction methods. The carotid intima-media thickness measurements were performed high performance ultrasound. We showed in the first manuscript that although possessing a higher risk coronary vascular disease profile the similarity found in carotid could in part be explained by the striking differences in its modulation between the two groups, indicating a protective trait against carotid atherosclerosis in hyperalphalipoproteinemia. In the Hyper-A population, was only correlated with age, while in controls had a positive correlation with age, male sex, systolic blood pressure, and surprisingly with HDL-C. This dissociation between IMT and HDL-C could be accounted for by a small HDL particle number in CTL. In the manuscript 2, the ¿514C/T polymorphism did not contribute to variations in the carotid IMT and Hyper-A did not modulate the IMT variations, contrary to Rundek et al., (2002) who investigated the ¿514C/T polymorphism on variations in the carotid IMT in 87 stroke-free subjects suggested that CC genotypes had increase of carotid IMT, FMT and HALP. The HL-514C/T e CETP I405V polymorphisms, were no associate, were highly prevalent in the two groups but were not associated with HDL-C. In Hyper-A, LH-514C/T induced lower plasma cholesterol (C), phospholipids (PL), LDL-C and LDL size (LDL-C/ApoB). In Hyper-A CETP I405V decreased blood pressure, reduced TG in HDL subfractions 2 and 3 of (HDL2TG and HDL3TG) and increase ApoAI. The HL -514C/T polymorphism in Hyper-A the TT vs CC had lower waist hip-circumference, cholesterol (C) concentrations, phospholipids (PL), LDL-C and estimated size particle by LDL-C/ApoB. The genotype TT was different between 2 groups: in Hyper-A with relation the CTL, had lower HL, estimated size particle by TG/HDL-C and higher HDL2C, HDL3C, HDL3TG, ApoAI and C concentrations and had higher C, estimated size particle by LDL-C/ApoB, ApoAI, HDL2C, HDL3C and estimated size particle by TG/HDL-C. The CETP I405V polymorphism in Hyper-A, the VV vs II had higher Systolic Blood Pressure and lower HDL2TG e HDL3TG concentrations. The IV genotype had higher ApoAI concentration and Diastolic Blood Pressure. In Hyper A, the VV genotype had higher HDL2C, HDL3C, ApoAI, e TG concentrations and reduced concentration of VLDL- and estimated size particle of LDL by TG/HDL-C. In summary, this work indicates an athero-protector and neutral effect on the carotid atherosclerosis in Hyper-A between HL-514C/T and CETP I405V polymorphisms both modulated for plasma lipids more atheroprotective
Mestrado
Ciencias Basicas
Mestre em Clinica Medica
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Medeiros, Ricardo Miguel Pedroso. "Caracterização preliminar dos níveis de colesterol plasmático em canídeos em função do sexo, raça, idade e condição corporal." Master's thesis, Universidade Técnica de Lisboa. Faculdade de Medicina Veterinária, 2011. http://hdl.handle.net/10400.5/3580.
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Dissertação de Mestrado Integrado em Medicina VeterináriaEnvolvido em múltiplas funções da homeostasia do corpo, o colesterol, depois de absorvido no lúmen intestinal e processado nos enterócitos, entra na corrente sanguínea onde é transportado sob a forma de lipoproteínas as quais se classificam de acordo com a sua densidade, resultante da quantidade e do tipo de apoproteínas e de colesterol que as constituem, em quilomicras, lipoproteínas de muito baixa densidade (VLDL), lipoproteínas de densidade intermédia (IDL), lipoproteínas de baixa densidade (LDL) e lipoproteínas de alta densidade (HDL), sendo esta última a fracção predominante no cão. É sabido que os valores de colesterol e o perfil das lipoproteínas plasmáticas variam em função de um conjunto de factores intrínsecos e extrínsecos ao indivíduo. O presente estudo utilizou uma amostra de 20 indivíduos (n=20) da espécie Canis lupus familiaris, e teve por objectivos: 1) Caracterizar os indivíduos incluídos no estudo quanto ao sexo, raça, idade e condição corporal; 2) Determinar a relação entre os valores plasmáticos de COL e as variáveis consideradas em 1); 3) Determinar a relação entre os valores plasmáticos de HDL-C e as variáveis consideradas em 1); 4) Determinar a relação entre os valores plasmáticos de COL e HDL-C. Os resultados obtidos permitiram concluir que na amostra a média dos valores de COL foi de 223,20±85,54mg/dL, encontrando-se a maioria dos indivíduos (95%) numa situação de normocolesterolémia. Os indivíduos mais velhos, os mais obesos e as fêmeas inteiras, foram os que apresentaram os valores de COL mais elevados. Para o HDL-C, a média foi de 86,02±10,37mg/dL, tendo sido os valores mais elevados registados em fêmeas inteiras, e os mais baixos nos indivíduos obesos. Os testes estatísticos realizados não permitiram contudo excluir a hipótese nula da ausência de diferenças nos valores de COL e de HDL-C, considerando os parâmetros sexo, raça e condição corporal para ambos e ainda, para o HDL-C, o factor idade.
ABSTRACT - Preliminary characterization of plasmatic cholesterol values in dogs based on gender, age, breed and body condition - Playing a role in multiple functions of the body homeostasis, the cholesterol, after being absorbed at intestinal lumen and processed by the enterocyte, reaches bloodstream, where its transport is performed by lipoproteins, classified by their density, which result from its constitution in apoproteins and cholesterol, in chylomicrons, very-low density lipoproteins (VLDL), intermediate density lipoproteins (IDL), low-density lipoproteins (LDL) and high-density lipoproteins (HDL), being this last one the predominant fraction in the dog. It is well known that total cholesterol and the profile of plasmatic lipoproteins vary in function of a set of factors, intrinsic and extrinsic to the individuals. The present study used a sample of 20 individuals of Canis lupus familiaris specie, to achieve the following objectives: 1) characterize the individuals included according to their gender, breed, age and body condition; 2) determine a relation between the plasmatic values of COL and the variables considered at 1); 3) determine the existence or not of a relation between the plasmatic values of HDL-C and the variables considered at 1); 4) determine the existence or not of a relation between the plasmatic values of COL and HDL-C. The results showed that the mean of COL values of the sample was 223,20±85,54mg/dL, and the majority of the individuals (95%) were in a situation of normocolesterolemia. The older individuals, the more obese and intact females showed the highest COL values. Concerning the HDL-C, the mean was 86,02±10,37mg/dL, the highest values were seen in intact females, and the lowest values were found in obese individuals. Nevertheless, the statistical tests to whom the sample was submitted did not allowed to exclude the nule hypothesis of the absence of differences in the values of COL and HDL-C considering gender, breed and body condition for both and still, for HDL-C, the age.
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Lindbohm, Nina. "Sialic acid in lipoproteins : with special reference to low density lipoproteins." Helsinki : University of Helsinki, 2000. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/lindbohm/.
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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.
Books on the topic "Lipoproteins"
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Hendriks, Wilhelmina Leonie. Lipoprotein lipase-mediated interactions of lipoproteins with macrophages. [Leiden: University of Leiden, 1998.
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J, Albers John, and Segrest Jere P, eds. Plasma lipoproteins. Orlando, FL: Academic Press, 1986.
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M, Gotto Antonio, ed. Plasma lipoproteins. Amsterdam: Elsevier, 1987.
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Fruchart, J. C., and J. Shepherd, eds. Human Plasma Lipoproteins. Berlin, Boston: De Gruyter, 1989. http://dx.doi.org/10.1515/9783110873665.
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von Eckardstein, Arnold, and Dimitris Kardassis, eds. High Density Lipoproteins. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-09665-0.
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Malmendier, C. L., and P. Alaupovic, eds. Lipoproteins and Atherosclerosis. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-1268-0.
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Kontush, Anatol, and M. John Chapman. High-Density Lipoproteins. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118158678.
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Colloquium, Fondation de recherche sur l'athérosclérose de la communauté française de Belgique International. Lipoproteins and atherosclerosis. New York: Plenum Press, 1987.
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1945-, Fruchart J. C., and Shepherd J. 1944-, eds. Human plasma lipoproteins. Berlin: De Gruyter, 1989.
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1937-, Levy Robert I., ed. Lipoproteins and atherosclerosis. New York: Raven Press, 1988.
Find full textBook chapters on the topic "Lipoproteins"
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Liu, Ming-Lin, and Daniel J. Rader. "Lipoproteins." In Atherosclerosis, 1–14. Hoboken, NJ: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118828533.ch1.
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Hersberger, Martin, Lucia Rohrer, and Arnold von Eckardstein. "Lipoproteins." In Laboratory Guide to the Methods in Biochemical Genetics, 497–548. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-76698-8_25.
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Soffer, Daniel. "Lipoproteins." In Encyclopedia of Exercise Medicine in Health and Disease, 516–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_45.
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Gooch, Jan W. "Lipoproteins." In Encyclopedic Dictionary of Polymers, 905. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14131.
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Wang, Changmin, and Zhiwei Li. "Lipoproteins." In Clinical Molecular Diagnostics, 179–93. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-1037-0_14.
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Borén, Jan, and Marja-Riitta Taskinen. "Metabolism of Triglyceride-Rich Lipoproteins." In Prevention and Treatment of Atherosclerosis, 133–56. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/164_2021_520.
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AbstractTriglycerides are critical lipids as they provide an energy source that is both compact and efficient. Due to its hydrophobic nature triglyceride molecules can pack together densely and so be stored in adipose tissue. To be transported in the aqueous medium of plasma, triglycerides have to be incorporated into lipoprotein particles along with other components such as cholesterol, phospholipid and associated structural and regulatory apolipoproteins. Here we discuss the physiology of normal triglyceride metabolism, and how impaired metabolism induces hypertriglyceridemia and its pathogenic consequences including atherosclerosis. We also discuss established and novel therapies to reduce triglyceride-rich lipoproteins.
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Dewanjee, Mrinal K. "Radioiodinated Lipoproteins." In Radioiodination: Theory, Practice, and Biomedical Applications, 513–22. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3508-9_13.
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Kontush, Anatol, Mats Lindahl, Marie Lhomme, Laura Calabresi, M. John Chapman, and W. Sean Davidson. "Structure of HDL: Particle Subclasses and Molecular Components." In High Density Lipoproteins, 3–51. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09665-0_1.
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Riwanto, Meliana, Lucia Rohrer, Arnold von Eckardstein, and Ulf Landmesser. "Dysfunctional HDL: From Structure-Function-Relationships to Biomarkers." In High Density Lipoproteins, 337–66. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09665-0_10.
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Annema, Wijtske, Arnold von Eckardstein, and Petri T. Kovanen. "HDL and Atherothrombotic Vascular Disease." In High Density Lipoproteins, 369–403. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09665-0_11.
Full textConference papers on the topic "Lipoproteins"
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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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Wang, Jingying. "Lipoproteins and Atherosclerotic Cardiovascular Diseases." In International Conference on Health Big Data and Intelligent Healthcare. SCITEPRESS - Science and Technology Publications, 2022. http://dx.doi.org/10.5220/0011371300003438.
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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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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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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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Robbins, David L., John P. Nolan, James H. Jett, Richard A. Keller, and Larry A. Sklar. "Analysis of individual lipoproteins and liposomes." In BiOS '97, Part of Photonics West, edited by Gerald E. Cohn and Steven A. Soper. SPIE, 1997. http://dx.doi.org/10.1117/12.274353.
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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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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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Spak, MM, EC Cauza, KC Cauza, UH Hanusch-Enserer, AD Dunky, and KK Kostner. "THU0036 The effect of infliximab on plasma lipoproteins." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.833.
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Fujii, S., and T. Kariya. "PLATELET FUNCTION AND LIPOPROTEINS IN PATIENTS WITH HYPOTHYROIDISM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643474.
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Platelet function and serum lipoprotein levels were studied in ten patients (two males and eight females) with hypothyroidism. Platelet aggregation and ATP release were determined by Lumi-aggregometer using ADP , collagen and epinephrine as stimulants. Platelet factor 4 (PF4) and thromboxane B2 (TXB2) were determined by radioimmunoassay. High density lipoproteincholesterol (HDL-C) was determined by heparin-manga-nese method. HDL subfractions were separated by gradient gel electrophoresis (PAA 4/30). Apolipopro-teins were measured by single radial immunodiffusion. Platelet aggregation increased in those patients at stimulating by epinephrine. ATP release also increased at stimulating by epinephrine. PF4 increased at stimulating by epinephrine. TXB2 increased at stimu-lating--by ADP or epinephrine significantly (p<0.05), respectively. Platelet aggregation was not correlated with thyroid hormones or total cholesterol levels.But it had a positive correlation tendency with HDL-C or HDL2-C and a negative one with HDL3-C levels.These results suggested some relationships between platelet function and HDL metabolism in patients with hypothyroidism.
Reports on the topic "Lipoproteins"
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Harper, P. V. In vivo metabolism of I-123 labeled semisynthetic low density lipoproteins. Office of Scientific and Technical Information (OSTI), December 1990. http://dx.doi.org/10.2172/7185351.
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Yang, Lin, Yanzhu Liu, Trudy M. Forte, Jeffrey W. Chisholm, John S. Parks, and Neil S. Shachter. Cultured human astrocytes secrete large cholesteryl ester- andtriglyceride-rich lipoproteins along with endothelial lipase. Office of Scientific and Technical Information (OSTI), December 2003. http://dx.doi.org/10.2172/886608.
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Jakhar, Shailja. EXPLORING THE INTERACTION OF AMPHIPHILIC MYCOBACTERIAL LIPOARABINOMANNAN WITH LIPOPROTEINS: IMLICATIONS FOR BLOOD BASED DIAGNOSIS. Office of Scientific and Technical Information (OSTI), May 2021. http://dx.doi.org/10.2172/1784691.
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Harper, P. V. In vivo metabolism of I-123 labeled semisynthetic low density lipoproteins. Final technical report, September 28, 1988--September 27, 1990. Office of Scientific and Technical Information (OSTI), December 1990. http://dx.doi.org/10.2172/10172803.
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Ismaiel, Abdulrahman, Ayman Jaaouani, Daniel-Corneliu Leucuta, Stefan-Lucian Popa, and Dan-Lucian Dumitrascu. The Visceral Adiposity Index in Non-Alcoholic Fatty Liver Disease and Liver Fibrosis — Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2021. http://dx.doi.org/10.37766/inplasy2021.12.0056.
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Review question / Objective: The objective of the study was to compare the mean difference and AUROC of Visceral Adiposity Index (VAI) in NAFLD/NASH/liver fibrosis patients and controls in observational studies. Condition being studied: Nonalcoholic fatty liver disease (NAFLD) is a multi-system disease, being mainly a liver pathology involving excessive hepatic fat accumulation unrelated to alcohol consumption or other secondary causes of hepatic steatosis. It is an emerging cause of concern and increasing clinical burden, imposing a public health challenge. NAFLD is the most common chronic liver disease and is predicted to be the most common indication for a liver transplant in Western countries by 2030, owing to a prevalence of 25% worldwide. The visceral adiposity index (VAI) is a scoring system based on body mass index, triglycerides, high-density lipoproteins (HDLs), and waist circumferences (WCs).
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Yogev, David, Ricardo Rosenbusch, Sharon Levisohn, and Eitan Rapoport. Molecular Pathogenesis of Mycoplasma bovis and Mycoplasma agalactiae and its Application in Diagnosis and Control. United States Department of Agriculture, April 2000. http://dx.doi.org/10.32747/2000.7573073.bard.
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Mycoplasma bovis and M. agalactiae are two phylogenetically related mycoplasmas which cause economically significant diseases in their respective bovine or small ruminant hosts. These organisms cause persistent asymptomatic infections that can result in severe outbreaks upon introduction of carrier animals into susceptible herds. Little is known about the mechanisms underlying mycoplasma-host interaction, variation in virulence, or of the factors enabling avoidance of the host immune system. In recent years it has become apparent that the ability of pathogenic microorganisms to rapidly alter surface antigenic structures and to fine tune their antigenicity, a phenomena called antigenic variation, is one of the most effective strategies used to escape immune destruction and to establish chronic infections. Our discovery of a novel genetic system, mediating antigenic variation in M. bovis (vsp) as well as in M. agalactiae (avg) served as a starting point for our proposal which included the following objectives: (i) Molecular and functional characterization of the variable surface lipoproteins (Vsp) system of M. bovis and comparison with the Vsp-counterpart in M. agalactiae (ii) Determination of the role of Vsp proteins in the survival of M. bovis when confronted by host defense factors, (iii) Assessment of Vsp-based genetic and antigenic typing of M. bovis and M. agalactiae for epidemiology of infection and (iv) Improvement of diagnostic tests for M. bovis and M. agalactiae based on the vsp-and vsp-analogous systems. We have carried out an extensive molecular characterization of the vsp system and unravelled the precise molecular mechanism responsible for the generation of surface antigenic variation in M. bovis. Our data clearly demonstrated that the two pathogenic mycoplasma species possess large gene families encoding variable lipoprotein antigens that apparently play an important role in immune evasion and in pathogen-host interaction during infection. Phase variable production of these antigens was found to be mediated by a novel molecular mechanism utilizing double site-specific DNA inversions via an intermediate vsp configuration. Studies in model systems indicate that phase variation of VspA is relevant in interaction between M. bovis and macrophages or monocytes, a crucial stage in pathogenesis. Using an ELISA test with captured VspA as an antigen, phase variation was shown to occur in vivo and under field conditions. Genomic rearrangements in the avg gene family of M. agalactiae were shown to occur in vivo and may well have a role in evasion of host defences and establishment of chronic infection. An epidemiological study indicated that patterns of vsp-related antigenic variation diverge rapidly in an M. bovis infected herd. Marked divergence was also found with avg-based genomic typing of M. agalactiae in chronically infected sheep. However, avg-genomic fingerprints were found to be relatively homogeneous in different animals during acute stages of an outbreak of Contagious Agalactiae, and differ between unrelated outbreaks. These data support the concept of vsp-based genomic typing but indicate the necessity for further refinement of the methodology. The molecular knowledge on these surface antigens and their encoding genes provides the basis for generating specific recombinant tools and serological methods for serodiagnosis and epidemiological purposes. Utilization of these methods in the field may allow differentiating acutely infected herds from chronic herds and disease-free herds. In addition the highly immunogenic nature of these lipoproteins may facilitate the design of protective vaccine against mycoplasma infections.
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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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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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