Bibliografías temáticas / LDLrKO

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Literatura académica sobre el tema "LDLrKO"

Autor: Grafiati
Publicado: 1 de febrero de 2025
Última modificación: 31 de julio de 2025

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Artículos de revistas sobre el tema "LDLrKO"

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Dupasquier, Chantal M. C., Elena Dibrov, Annette L. Kneesh, et al. "Dietary flaxseed inhibits atherosclerosis in the LDL receptor-deficient mouse in part through antiproliferative and anti-inflammatory actions." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 4 (2007): H2394—H2402. http://dx.doi.org/10.1152/ajpheart.01104.2006.

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Dietary flaxseed has been shown to have potent antiatherogenic effects in rabbits. The purpose of the present study was to investigate the antiatherogenic capacity of flaxseed in an animal model that more closely represents the human atherosclerotic condition, the LDL receptor-deficient mouse (LDLrKO), and to identify the cellular mechanisms for these effects. LDLrKO mice were administered a regular diet (RG), a 10% flaxseed-supplemented diet (FX), or an atherogenic diet containing 2% cholesterol alone (CH) or supplemented with 10% flaxseed (CF), 5% flaxseed (CF5), 1% flaxseed (CF1), or 5% coc
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Forrest, Lolita M., Elena Boudyguina, Martha D. Wilson, and John S. Parks. "Echium oil reduces atherosclerosis in apoB100-only LDLrKO mice." Atherosclerosis 220, no. 1 (2012): 118–21. http://dx.doi.org/10.1016/j.atherosclerosis.2011.10.025.

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Cao, Qiang, Xin Cui, Rui Wu та ін. "Myeloid Deletion of α1AMPK Exacerbates Atherosclerosis in LDL Receptor Knockout (LDLRKO) Mice". Diabetes 65, № 6 (2016): 1565–76. http://dx.doi.org/10.2337/db15-0917.

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Bi, Xin, Xuewei Zhu, MyNgan Duong, et al. "Liver ABCA1 Deletion in LDLrKO Mice Does Not Impair Macrophage Reverse Cholesterol Transport or Exacerbate Atherogenesis." Arteriosclerosis, Thrombosis, and Vascular Biology 33, no. 10 (2013): 2288–96. http://dx.doi.org/10.1161/atvbaha.112.301110.

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Baumgartner, Roland, Felipe B. Casagrande, Randi B. Mikkelsen, et al. "Disruption of GPR35 Signaling in Bone Marrow-Derived Cells Does Not Influence Vascular Inflammation and Atherosclerosis in Hyperlipidemic Mice." Metabolites 11, no. 7 (2021): 411. http://dx.doi.org/10.3390/metabo11070411.

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G-protein-coupled receptor-35 (GPR35) has been identified as a receptor for the tryptophan metabolite kynurenic acid (KynA) and suggested to modulate macrophage polarization in metabolic tissues. Whether GPR35 can influence vascular inflammation and atherosclerosis has however never been tested. Lethally irradiated LdlrKO mice were randomized to receive GPR35KO or wild type (WT) bone marrow transplants and fed a high cholesterol diet for eight weeks to develop atherosclerosis. GPR35KO and WT chimeric mice presented no difference in the size of atherosclerotic lesions in the aortic arch (2.37 ±
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Schaftenaar, Frank, Jacob Amersfoort, Hidde Douna, et al. "Vaccination with ApoB100 Derived HLA-A2 Restricted CD8 T Cell Epitopes Did Not Reduce Atherosclerosis in Male LDLrKO hApoB100tg HLA-A2tg Mice." Atherosclerosis Supplements 32 (June 2018): 100–101. http://dx.doi.org/10.1016/j.atherosclerosissup.2018.04.307.

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Jasiecki, Jacek, Monika Targońska, Anna Janaszak-Jasiecka, et al. "Novel Tools for Comprehensive Functional Analysis of LDLR (Low-Density Lipoprotein Receptor) Variants." International Journal of Molecular Sciences 24, no. 14 (2023): 11435. http://dx.doi.org/10.3390/ijms241411435.

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Familial hypercholesterolemia (FH) is an autosomal-dominant disorder caused mainly by substitutions in the low-density lipoprotein receptor (LDLR) gene, leading to an increased risk of premature cardiovascular diseases. Tremendous advances in sequencing techniques have resulted in the discovery of more than 3000 variants of the LDLR gene, but not all of them are clinically relevant. Therefore, functional studies of selected variants are needed for their proper classification. Here, a single-cell, kinetic, fluorescent LDL uptake assay was applied for the functional analysis of LDLR variants in
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Strøm, Thea Bismo, Katrine Bjune, Luís Teixeira da Costa, and Trond P. Leren. "Strategies to prevent cleavage of the linker region between ligand-binding repeats 4 and 5 of the LDL receptor." Human Molecular Genetics 28, no. 22 (2019): 3734–41. http://dx.doi.org/10.1093/hmg/ddz164.

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Abstract A main strategy for lowering plasma low-density lipoprotein (LDL) cholesterol levels is to increase the number of cell-surface LDL receptors (LDLRs). This can be achieved by increasing the synthesis or preventing the degradation of the LDLR. One mechanism by which an LDLR becomes non-functional is enzymatic cleavage within the 10 residue linker region between ligand-binding repeats 4 and 5. The cleaved LDLR has only three ligand-binding repeats and is unable to bind LDL. In this study, we have performed cell culture experiments to identify strategies to prevent this cleavage. As a par
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Persson, Lena, Cecilia Gälman, Bo Angelin, and Mats Rudling. "Importance of Proprotein Convertase Subtilisin/Kexin Type 9 in the Hormonal and Dietary Regulation of Rat Liver Low-Density Lipoprotein Receptors." Endocrinology 150, no. 3 (2008): 1140–46. http://dx.doi.org/10.1210/en.2008-1281.

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Hormonal or dietary challenge can stimulate hepatic low-density lipoprotein receptor (LDLR) expression through posttranscriptional mechanisms. We here tested whether such observations may be due to regulation of proprotein convertase subtilisin/kexin type 9 (PCSK9). Treatment with glucagon resulted in a 2-fold increase in hepatic LDLR protein expression, whereas its mRNA levels were reduced; this occurred simultaneously with a 70% reduction in PCSK9 expression. Insulin treatment resulted in responses opposite to those seen by treatment with glucagon. Furthermore, high-dose ethinylestradiol tre
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Kim, Meewhi, and Ilya Bezprozvanny. "Differences in Recycling of Apolipoprotein E3 and E4—LDL Receptor Complexes—A Mechanistic Hypothesis." International Journal of Molecular Sciences 22, no. 9 (2021): 5030. http://dx.doi.org/10.3390/ijms22095030.

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Apolipoprotein E (ApoE) is a protein that plays an important role in the transport of fatty acids and cholesterol and in cellular signaling. On the surface of the cells, ApoE lipoparticles bind to low density lipoprotein receptors (LDLR) that mediate the uptake of the lipids and downstream signaling events. There are three alleles of the human ApoE gene. Presence of ApoE4 allele is a major risk factor for developing Alzheimer’s disease (AD) and other disorders late in life, but the mechanisms responsible for biological differences between different ApoE isoforms are not well understood. We her
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Tesis sobre el tema "LDLrKO"

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Henry, Doriane. "Etude du lien entre la MASLD et l'athérosclérose : implication du récepteur nucléaire PPARα". Electronic Thesis or Diss., Université de Lille (2022-....), 2024. http://www.theses.fr/2024ULILS053.

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Selon l’Organisation Mondiale de la Santé (OMS), les maladies cardiovasculaires (MCV) représentent la première cause de mortalité dans le monde. La prévalence augmentée de la maladie hépatique stéatosique associée à un dysfonctionnement métabolique (MASLD) et sa relation étroite avec le syndrome métabolique laissent suggérer un rôle du foie dans le développement de ces MCV. Cependant, le lien entre MASLD et MCV reste encore peu clair. Dans ce contexte, grâce à l’utilisation d’un modèle murin adapté et de différents outils moléculaires développés au laboratoire, j’ai pu réaliser mes travaux de
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Wanschel, Amarylis Claudine Bonito Azeredo. "Biodisponibilidade cardiovascular do oxdo nitrico em camundongos LDLr-/-." [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314780.

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Orientador: Marta Helena Krieger<br>Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia<br>Made available in DSpace on 2018-08-15T17:17:07Z (GMT). No. of bitstreams: 1 Wanschel_AmarylisClaudineBonitoAzeredo_D.pdf: 3059995 bytes, checksum: afbb018ffe3bb06b61c7420a0fa4664f (MD5) Previous issue date: 2010<br>Resumo: O objetivo deste trabalho foi avaliar a biodisponibilidade do óxido nítrico (NOo) nas disfunções cardiovasculares, especificamente na hipertrofia ventricular esquerda e na aterosclerose. Para tanto, realizamos dois estudos em camundongos deficientes do recept
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Nguyen, My-Anh. "Characterization of PCSK9-mediated LDLR Degradation in Hepatic and Fibroblast Cells." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/26114.

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The discovery that proprotein convertase subtilisin/kexin type 9 (PCSK9) mediates degradation of low-density lipoprotein receptors (LDLR) indicates a critical role in LDL metabolism. PCSK9 is a secreted protein that binds to the epidermal growth factor-like (EGF)-A domain of LDLR and directs the receptor for degradation in lysosomes by an unknown mechanism. A gain-of-function mutation, D374Y, increases binding to LDLR EGF-A >10-fold and is associated with a severe form of hypercholesterolemia in humans. Similar to previous studies, data obtained in my project has established that PCSK9 was ca
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Wanschel, Amarylis Claudine Bonito Azeredo. "Aterogenese em femeas LDLr-/- : efeito da S-nitroso-N-acetilcisteina (SNAC)." [s.n.], 2006. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314556.

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Orientador: Marta Helena Krieger<br>Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia<br>Made available in DSpace on 2018-08-07T20:20:15Z (GMT). No. of bitstreams: 1 Wanschel_AmarylisClaudineBonitoAzeredo_M.pdf: 1512032 bytes, checksum: 92d5d4fda32e196e08b7ee261c365152 (MD5) Previous issue date: 2006<br>Resumo: A incidência de riscos de doença aterosclerótica cardiovascular é maior em homens do que em mulheres na fase reprodutiva, essa diferença diminui quando diminui a produção de estrógenos após a menopausa. Uma série de estudos sugere que essa diferença em
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Vasconcelos, Karina Alves da Silva. "Identificação de mutações no gene do receptor da lipoproteína de baixa densidade (LDLR) em pacientes com hipercolesterolemia familiar." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/17/17138/tde-02122015-101322/.

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Hipercolesterolemia familiar (HF) é uma doença autossômica dominante, caracterizada por elevados níveis plasmáticos da lipoproteína de baixa densidade (LDL), desenvolvimento de xantoma tendíneo e arco corneal, além do aumento do risco de doença coronariana e acidente vascular cerebral prematuros. Frequentemente subdiagnosticada, estima-se que apenas 10% dos 400.000 indivíduos com HF no Brasil têm conhecimento da própria doença; afetando, desta forma, a qualidade e a expetativa de vida dos pacientes. Mutações no gene do receptor da LDL (LDLR) são consideradas as alterações genéticas mais freque
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Beehler, Kaitlyn. "MiR-1908 Is a Cholesterol Responsive MicroRNA Implicated In Cholesterol Regulation." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/40422.

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Leveraging miRNA-Seq data and the 1000 Genomes imputed genotypes, we identified rs174561-C as a strong miRQTL for circulating miRNA-1908-5p (P=4.8x10-31) which has an inverse relationship with circulating LDL-C, fasting glucose and A1c. Here I investigated the molecular mechanism(s) linking miR1908-5p to cholesterol metabolism. First, by overexpression experiments in HuH-7 cells demonstrate that the presence of the C allele, associated with lower LDL-C levels, significantly increases miR-1908-5p by 2.15-fold relative to the T allele. Further experiments revealed that 72-hour cholesterol deplet
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Scholtz, C. L. (Charlotte Latitia). "Molecular investigation into regulatory regions of the LDLR gene involved in lipoprotein metabolism." Thesis, Stellenbosch : Stellenbosch University, 2001. http://hdl.handle.net/10019.1/52345.

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Thesis (PhD) -- University of Stellenbosch, 2001.<br>ENGLISH ABSTRACT: The advent of the new millennium saw the complete sequencing of the entire human genome. Only approximately 30 000 genes, much less than was initially predicted, have been identified to be responsible for the genetic diversity in humans. This discovery has prompted a shift in the approach to disease research, since one gene can be involved in numerous diseases. This phenomenon seems to be especially true for the low-density lipoprotein receptor (LDLR) gene. Various substances beside sterols can induce transcription of
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Leitch, Eilidh Kathryn. "Identification and development of novel cyclic peptide inhibitors of IDOL mediated LDLR degradation." Thesis, University of Southampton, 2017. https://eprints.soton.ac.uk/417920/.

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Cholesterol is an essential component of the plasma membrane however if present in excess, free cholesterol is toxic to cells and can lead to complications such as atherosclerosis, and ultimately cardiovascular disease. The low density lipoprotein receptor binds and internalises circulating plasma cholesterol, present in low density lipoprotein molecules. The low density lipoprotein receptor has two main transcriptional regulators: liver X receptors and sterol regulatory element binding proteins and post-transcriptional regulators, namely the E3-ubiquitin ligase IDOL, which binds and ubiquitin
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Werutsky, Carlos Alberto. "As bases moleculares das hipercolesterolemias familiares no Brasil: o Rio Grande do Sul." Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/17/17138/tde-01082007-105409/.

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A hipercolesterolemia familiar (HF) é uma doença autossômica dominante causada por mutações no gene do receptor de LDL (LDLR) (cromossomo 19p13.1 - p13.3), que alteram parcialmente ou totalmente a função do LDLR. A HF é também uma das doenças genéticas mais comuns com freqüências estimadas de heterozigotos e homozigotos de 1/500 e 1/1.000.000, respectivamente. Manifesta-se com altos níveis de LDL colesterol, arco corneal, xantomas tendíneos e sintomas prematuros de doença coronariana.. A grande heterogeneidade observada na manifestação clínica desta doença pode ser explicada, ao menos parcialm
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Lin, Jennifer W. "Techniques for identifying long-range residue correlations in the fifth binding module of LDLR." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/36808.

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Thesis (M. Eng.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2006.<br>Includes bibliographical references (p. 87-90).<br>The study of correlations between residues in distal regions of a protein structure may provide insights into the mechanism of protein folding. Such long-range correlations may exist between distant residues that are conserved by evolution or physically related by motion. Two computational approaches, one involving hidden Markov models (HMMs) and the other applying molecular dynamics (MD), were implemented to identify a compr
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Libros sobre el tema "LDLrKO"

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Cicmil, Svetlana. Organisational behaviour and change in the context of total quality principles: The LDLR case study. Leicester Business School, De Montfort University, 1995.

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High Cholesterol: Education for Patients and the Public. Exon Publications, 2025. https://doi.org/10.36255/high-cholesterol.

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High cholesterol is a common health condition that increases the risk of heart disease, stroke, and other cardiovascular problems. This article provides a comprehensive guide on high cholesterol, including its causes, symptoms, diagnosis, treatment, and long-term management. It begins with an explanation of what cholesterol is and how excessive levels can harm the body. The article highlights the widespread prevalence of high cholesterol, noting how lifestyle choices and genetic factors, including mutations in the LDLR, APOB, and PCSK9 genes, play a role in cholesterol regulation. The symptoms
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Capítulos de libros sobre el tema "LDLrKO"

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Arroyo, E., C. Asperilla, L. Prieto, M. Herrera, and J. M. Ruiz de la Cuesta. "Frequency Multivariate Analysis of LDLR, GYPA, HBGG, D7S8 and GC in 12 Different Populations." In 16th Congress of the International Society for Forensic Haemogenetics (Internationale Gesellschaft für forensische Hämogenetik e.V.), Santiago de Compostela, 12–16 September 1995. Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80029-0_145.

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Varma, S., A. D. McIntyre, and R. A. Hegele. "Atypical Presentation and Treatment Response in a Child with Familial Hypercholesterolemia Having a Novel LDLR Mutation." In JIMD Reports. Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/8904_2016_29.

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Hara, M., A. Kido, K. Saito, et al. "Allele Frequency Distribution of Five Loci (LDLR, GYPA, HBGG, D7S8 and GC) in a Japanese Population." In 16th Congress of the International Society for Forensic Haemogenetics (Internationale Gesellschaft für forensische Hämogenetik e.V.), Santiago de Compostela, 12–16 September 1995. Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80029-0_164.

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Miścicka-Śliwka, D., K. Śliwka, A. Syroczyńska, T. Grzybowski, B. Baranowska, and J. A. Berent. "Allele Frequencies of D1S80, LDLR, GYPA, D7S8, GC, HBGG and SE 33 in Polish Population Sample." In 16th Congress of the International Society for Forensic Haemogenetics (Internationale Gesellschaft für forensische Hämogenetik e.V.), Santiago de Compostela, 12–16 September 1995. Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80029-0_177.

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Tagliabracci, Adriano, Loredana Buscemi, Nicola Cucurachi, Roberto Mencarelli, Raffaele Giorgetti, and Santo Davide Ferrara. "A Population Study of 5 PCR Genetic Markers, LDLR, GYPA, HBGG, D7S8 and Gc, in Italy." In 16th Congress of the International Society for Forensic Haemogenetics (Internationale Gesellschaft für forensische Hämogenetik e.V.), Santiago de Compostela, 12–16 September 1995. Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80029-0_196.

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Masliah, Eliezer, and Brian Spencer. "Applications of ApoB LDLR-Binding Domain Approach for the Development of CNS-Penetrating Peptides for Alzheimer’s Disease." In Methods in Molecular Biology. Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2806-4_21.

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Crespillo, M., J. A. Luque, P. García, E. Ramírez, R. M. Fernández, and J. L. Valverde. "Population Study for the HLA-DQA1, LDLR, GYPA, HBGG, D7S8 and GC Loci in North-East of Spain." In 16th Congress of the International Society for Forensic Haemogenetics (Internationale Gesellschaft für forensische Hämogenetik e.V.), Santiago de Compostela, 12–16 September 1995. Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80029-0_153.

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Herrera, M., C. Asperilla, M. A. Aumente, L. Prieto, E. Arroyo, and J. M. Ruiz de la Cuesta. "Frequency Data on the Loci LDLR, GYPA, HBGG, D7S8 and GC in a population resident in Madrid (Spain)." In 16th Congress of the International Society for Forensic Haemogenetics (Internationale Gesellschaft für forensische Hämogenetik e.V.), Santiago de Compostela, 12–16 September 1995. Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80029-0_165.

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García, O., P. Martín, C. Albarrán, and A. Alonso. "Allele frequencies of HLA-DQA1, LDLR, GYPA, HBGG, D7S8 and GC in the resident population of the Basque Country." In Acta Medicinæ Legalis Vol. XLIV 1994. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79523-7_11.

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Castillo, M. I., M. Paredes, C. Peñuela, I. Bustos, M. Jimenez, and A. Galindo. "Determination of the Allele and Genotype Frequencies of Loci HLA-DQA1, LDLR, GYPA, HBGG, D7S8 and GC in Bogota-Colombia." In 16th Congress of the International Society for Forensic Haemogenetics (Internationale Gesellschaft für forensische Hämogenetik e.V.), Santiago de Compostela, 12–16 September 1995. Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80029-0_149.

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Actas de conferencias sobre el tema "LDLrKO"

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Kong, Jeremy, and Alessio Lomuscio. "Model Checking Multi-Agent Systems against LDLK Specifications." In Twenty-Sixth International Joint Conference on Artificial Intelligence. International Joint Conferences on Artificial Intelligence Organization, 2017. http://dx.doi.org/10.24963/ijcai.2017/158.

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We define the logic LDLK, a formalism for specifying multi-agent systems. LDLK extends LDL with epistemic modalities, including common knowledge, for reasoning about the evolution of knowledge states of the agents in the system. We study the complexity of verifying a multi-agent system against LDLK specifications and show this to be in PSPACE. We give an algorithm for the practical verification of multi-agent systems specified in LDLK. We show that the model checking algorithm, based on alternating-automata and nFA, is amenable to symbolic implementation on OBDDs. We introduce MCMAS LDLK , an
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Ly, Kévin, Anna Kwiatkowska, Sophie Routhier, et al. "Development of Peptide Inhibitors Disrupting PCSK9-LDLR Protein-Protein Interactions." In The Twenty-Third American and the Sixth International Peptide Symposium. Prompt Scientific Publishing, 2013. http://dx.doi.org/10.17952/23aps.2013.110.

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Larrea Sebal, Asier, Unai Galicia Garcia, Shifa Jebari Benslaiman, et al. "MLb-LDLr: LDLaren hartzaile aldaeren eragina aurresateko ikasketa automatikoko eredua." In IV. Ikergazte. Nazioarteko ikerketa euskaraz. UEU arg, 2021. http://dx.doi.org/10.26876/ikergazte.iv.04.01.

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Gao, Ya, Wenhui Zhang, and Xue-Yang Zhu. "Multi-Agent Automata and Its Application to LDLK Satisfiability Checking." In 2021 IEEE 21st International Conference on Software Quality, Reliability and Security (QRS). IEEE, 2021. http://dx.doi.org/10.1109/qrs54544.2021.00111.

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ПОЛЯКОВА, Е. А., Е. С. ЯКИМЕНКО, А. Д. ПЕРЕЛЯЕВ, М. Д. БУШУЕВА та А. В. МАЗИНГ. "МУТАЦИЯ В ГЕНЕ LDLR (ГЕТЕРОЗИГОТА) У ПАЦИЕНТКИ С МУЛЬТИФОКАЛЬНЫМ АТЕРОСКЛЕРОЗОМ". У ОЖИРЕНИЕ, САХАРНЫЙ ДИАБЕТ И КОМОРБИДНЫЕ ЗАБОЛЕВАНИЯ. Медиапапир, 2024. http://dx.doi.org/10.52565/9785001104315_102.

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Khuu, MP, K. Kiouptsi, G. Pontarollo, et al. "Gut microbiota promotes arterial thrombus formation in hyperlipidemic Ldlr-/- mouse model." In GTH Congress 2023 – 67th Annual Meeting of the Society of Thrombosis and Haemostasis Research – The patient as a benchmark. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0042-1760466.

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Tworowska, Izabela, Leo G. Flores II, Rafal Zielinski, et al. "Abstract LB-A16: Imaging of glioblastoma using LDLR-based targeted delivery system." In Abstracts: AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; October 26-30, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1535-7163.targ-19-lb-a16.

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Etxebarria Gallego, Aitor. "Hiperkolesterolemia familiarra: LDLR, APOB eta PCSK9-en mutazioen balioztapen funtzionala diagnostiko zehatz baterako." In I. Ikergazte. Nazioarteko ikerketa euskaraz. UEU arg, 2015. http://dx.doi.org/10.26876/ikergazte.i.104.

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Hoi, Yiemeng, Mark Van Doormaal, Yu-Qing Zhou, Xiaoli Zhang, R. Mark Henkelman, and David A. Steinman. "Degree of Retrograde Flow and Its Effect on Local Hemodynamics and Plaque Distribution in an Aortic Regurgitation Murine Model of Atherosclerosis." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53161.

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Previously, Zhou et al. [1] presented a novel mouse model of aortic valve regurgitation (AR) to explore the effect of altered hemodynamics on atherogenesis. In these ldlr−/− mice with AR, extensive atherosclerotic plaque was found along the naturally lesion-free descending thoracic (DTAo) and abdominal aorta (AbAo), with distinct spatial distributions suggestive of a strong local hemodynamic influence (Fig. 1, top). Doppler ultrasound measurement showed that both DTAo and AbAo of the AR mice experienced an oscillatory flow pattern induced by the diastolic retrograde flow, as opposed to the con
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Мешков, А. Н., А. И. Ершова, А. В. Киселева та ін. "Спектр вариантов в генах LDLR, APOB и PCSK9 у российских пациентов с семейной гиперхолестеринемией". У Вычислительная биология и искусственный интеллект для персонализированной медицины. Федеральное государственное бюджетное учреждение «Национальный медицинский исследовательский центр эндокринологии» Министерства здравоохранения Российской Федерации, 2021. http://dx.doi.org/10.14341/cbaipm-2021-21.

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