Dissertations / Theses: 'Apolipoprotein B-100'

1

Mahala, Bonginkosi. "Familial Defective binding apolipoprotein B-100 the Cape Town Experience." Master's thesis, University of Cape Town, 2009. http://hdl.handle.net/11427/3421.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Wang, Xingyu. "An immunochemical analysis of human apolipoprotein B-100 structure-function relationships." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ32458.pdf.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Rubinsztein, David Chaim. "Monogenic hypercholesterolemia in South Africans : familial hypercholesterolemia in Indians and familial defective apolipoprotein B-100." Doctoral thesis, University of Cape Town, 1993. http://hdl.handle.net/11427/27142.

Full text

Abstract:

LDL-receptor mutations and familial defective apolipoprotein B-100 (codon 3500) (FOB), the known causes of monogenic hypercholesterolemia (MH), have similar clinical features. The nature of the mutations responsible for MH in South Africans of Indian origin was previously unknown. Similarly, the mutations in the LDL-receptor gene of a South African Black FH homozygote had also not been characterised. The aim of this thesis was to identify and analyse the LDL-receptor mutations in the Indian homozygotes NS, D, AV and AA and in the Black homozygote JL. In addition, the possible importance of FOB as a cause of MH in South Africans was also assessed. The patient NS was characterized as having two "Null" LDL-receptor alleles. His skin fibroblasts expressed no detectable LDL-receptor protein and very low levels of LDL-receptor mRNA of approximately normal size. Since NS' s LDLreceptor promoter sequence was normal, his alleles are likely to harbour exonic point mutations or minor rearrangements that cause premature stop codons. The patient D was found to be a heteroallelic homozygote. Two new point mutations in the LDL receptor, Asp₆₉ -Tyr and Glu₁₁₉-Lys, were identified. D's fibroblasts expressed about 30% of the normal surf ace complement of receptors that bound LDL poorly. This low number could at least be partially explained by their decreased stability. These mutations were not identified in any other Indian FH or hypercholesterolemic patients. Patients AV and AA were both shown to be homoallelic homozygotes for the Pro₆₆₄ -Leu mutation. This mutation was identified in 4 unrelated Muslim families of Gujerati origin suggesting that the mutation arose from this area in India. Contrary to previous reports (Knight et al. 1990, Soutar et al. 1989), neither LOL nor β-VLDL binding were shown to be affected by this mutation. These mutant receptors were rapidly degraded. Thus the disease FH in these subjects is presumably due to the low steady-state level of mature receptors that are functionally normal but exhibit accelerated turnover. The Pedi FH homozygote, JL, expressed very few LOL receptors due to decreased receptor synthesis associated with low mRNA levels and not due to enhanced degradation. One of JL's LOL receptor alleles has a 3 b.p. deletion in repeat 1 of the promoter (G. Zuilani, H. Hobbs and L.F. de Waal, personal communication). The nature of the defect in his other allele is unknown. The importance of FOB as a cause of monogenic hypercholesterolemia in the South African Indian, "Coloured" and Afrikaner populations was determined by screening hypercholesterolemic subjects with or without xanthomata. The absence of FOB in such patients, in whom the relevant common or founder South African mutations were excluded, suggested that this disorder was rarer in these groups than in North America and Europe. FOB was identified in two different families of mixed British and Afrikaner ancestry. One family contained individuals who were heterozygous for the FOB mutation, as well as the FH Afrikaner-1 and the FH Afrikaner-2 LOL-receptor mutations. In addition, 4 compound heterozygotes, who had both FOB and the FH Afrikaner-1 mutation and one individual whu inherited all 3 defects, were identified. This family allowed us to characterise the compound heterozygotes with one mutant LOLreceptor allele and FOB as having a condition that was probably intermediate in severity between the FH heterozygote and homozygote states.

APA, Harvard, Vancouver, ISO, and other styles

4

Alberty, Deborah J. "A study of time and temperature variables affecting apolipoprotein B-100 on iodipamide ethyl ester particles /." Online version of thesis, 1993. http://hdl.handle.net/1850/11252.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Bamji-Mirza, Michelle. "Defining an Intracellular Role of Hepatic Lipase in the Formation of Very Low Density Lipoproteins and High Density Lipoproteins." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20134.

Full text

Abstract:

Hepatic lipase (HL) plays a pivotal role in the catabolism of apolipoprotein (apo)B-containing lipoproteins and high density lipoprotein (HDL) particles through its reported catalytic and non-catalytic extracellular functions. The current study tested the hypothesis that HL expression might impair formation and secretion of hepatic derived very low density lipoproteins (VLDL) and apoA-I (nascent HDL). Stable or transient expression of human HL (hHL) in McA-RH7777 cells resulted in decreased incorporation of [3H]glycerol into cell-associated and secreted (VLDL-associated) 3H-triacylglcyerol (TAG) relative to control cells. Stable expression of catalytically-inactive hHL (hHLSG) also resulted in decreased secretion of VLDL-associated 3H-TAG whereas cell-associated 3H-TAG levels were unchanged. Expression of hHL or hHLSG increased cell-associated 35S-apoB100 with relatively no change in secreted 35S-apoB100. Importantly, hHL or hHLSG expression resulted in reduced 3H-TAG associated with the microsomal lumen lipid droplets (LLD), and increased relative expression of ApoB and genes involved in lipogenesis and fatty acyl oxidation. Transient expression of hHL in HL-null primary hepatocytes, mediated by adenoviral gene transfer, resulted in decreased steady-state levels of cell-associated and secreted apoA-I and reduced rates of synthesis and secretion of 35S-apoA-I. HL-null hepatocytes exhibited increased levels of secreted 35S-apoA-I relative to wildtype hepatocytes while cell-associated 35S-apoA-I levels were normal. Transient expression of a hHL chimera (hHLmt), in which the C-terminus of hHL was replaced with mouse HL sequences, exerted an inhibitory effect on apoA-I production similar to that of hHL even though hHLmt was secreted less effectively than hHL with impaired exit from the endoplasmic reticulum (ER) as compared with hHL. In contrast, stable expression of hHL in McA-RH7777 cells resulted in a dose-dependent increase in cell-associated and secreted 35S-apoA-I levels. These studies demonstrate that hHL has an intracellular (but non-catalytic) role in reducing the content of the LLD and ultimately the buoyancy of secreted VLDL particles, and that the N-terminal sequences of ER-residing hHL directly or indirectly modulates the production and secretion of apoA-I (nascent HDL) from hepatocytes.

APA, Harvard, Vancouver, ISO, and other styles

6

Vauhkonen, Matti. "Surface structure of human low density lipoproteins carbohydrate structure of apolipoprotein B-100 and properties of the surface lipid layer /." Helsinki : Finnish Society of Sciences and Letters, 1990. http://catalog.hathitrust.org/api/volumes/oclc/22137261.html.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Brinkmann, Jan Ole [Verfasser]. "Vessel function of the atherosclerotic low-density-lipoprotein-receptor-deficient apolipoprotein-B-100-only mouse / Jan Ole Brinkmann." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2008. http://d-nb.info/102325784X/34.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Delporte, Cédric. "Etude des modifications de l'apolipoprotéine B-100 induites par la myéloperoxydase à l'aide de la chromatographie liquide couplée à la spectrométrie de masse." Doctoral thesis, Universite Libre de Bruxelles, 2012. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209655.

Full text

Abstract:

Les maladies cardiovasculaires constituent la première cause de décès dans le monde et l’athérosclérose est le premier facteur causal de ces maladies. Parmi les multiples facteurs de risque athéromateux, un facteur est souvent décrit :la modification des lipoprotéines de basse densité (LDLs). Bien que le phénomène d’athérogénèse ne soit pas encore complètement résolu, il est actuellement admis que les LDLs natives passent la paroi vasculaire et s’accumulent au niveau sous-endothélial où elles sont oxydées et endocytées par les macrophages. Une théorie plus récente indique que les LDLs peuvent être également modifiées dans la circulation.

Néanmoins, le processus par lequel ces lipoprotéines sont modifiées reste hautement controversé. Depuis quelques années, le modèle de modification des LDLs par la myéloperoxydase est apparu comme un modèle physiopathologique contrairement au modèle longuement utilisé de l’oxydation des LDLs par le cuivre. La myéloperoxydase est une enzyme présente dans les granules primaires des neutrophiles mais qui lors d’inflammations chroniques, comme dans l’athérosclérose, peut se retrouver dans le milieu extracellulaire et former un oxydant puissant qui attaque les protéines, les lipides ou les acides nucléiques. Les LDLs modifiées par la myéloperoxydase ne sont plus reconnues par le récepteur membranaire spécifique pour les LDLs. De plus, très peu d’études ont décrit à ce jour les modifications apportées par la myéloperoxydase aux LDLs.

Dans ce contexte, nous avons étudié la spécificité de la myéloperoxydase à modifier les LDLs. Dans ce modèle, la partie protéique de la lipoprotéine est majoritairement touchée. C’est pourquoi nous avons développé et optimisé des méthodes d’analyse par spectrométrie de masse de l’apolipoprotéine B-100, la seule protéine de la LDL. De plus, l’activité de la myéloperoxydase à la surface des LDLs a également été investiguée.

Les résultats de ce travail montrent que la myéloperoxydase s’attaque de manière spécifique aux LDLs et que le modèle chimique utilisant de l’acide hypochloreux pour mimer l’action de la myéloperoxydase n’est pas parfait. Enfin, nous avons également observé des changements dans l’activité enzymatique lorsque la myéloperoxydase est adsorbée à la surface des LDLs.

Doctorat en Sciences biomédicales et pharmaceutiques
info:eu-repo/semantics/nonPublished

APA, Harvard, Vancouver, ISO, and other styles

9

Cummings, Michael Hunter. "Application of a stable isotope mass-spectrometry method to examine the regulation of very-low-density lipoprotein apolipoprotein B-100 in physiological and pathological states." Thesis, St George's, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307608.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Mero-Matikainen, Niina. "Postprandial metabolism of HLD and apolipoproteins B-48 and B-100." Helsinki : University of Helsinki, 1999. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/mero-matikainen/.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Majd, Zouher. "Metabolisme in vivo des lipoproteines humaines contenant l'apolipoproteine b100 : mise au point et applications du marquage endogene par la leucine deuteree." Lille 2, 1995. http://www.theses.fr/1995LIL2P265.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

BARRETO, NETO Augusto Cesar. "Síndrome metabólica e concentrações de apolipoproteínas a-i e b-100 em adolescentes com excesso de peso." Universidade Federal de Pernambuco, 2012. https://repositorio.ufpe.br/handle/123456789/12967.

Full text

Abstract:

Submitted by Susimery Vila Nova (susimery.silva@ufpe.br) on 2015-04-10T19:05:06Z No. of bitstreams: 2 AA_TESE_AUGUSTO BARRETO_24_FINAL.pdf: 7044027 bytes, checksum: b32212b7e2af41f68cadfffb8f3eb892 (MD5) license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5)
Made available in DSpace on 2015-04-10T19:05:06Z (GMT). No. of bitstreams: 2 AA_TESE_AUGUSTO BARRETO_24_FINAL.pdf: 7044027 bytes, checksum: b32212b7e2af41f68cadfffb8f3eb892 (MD5) license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) Previous issue date: 2012
A Síndrome Metabólica (MetS) é uma desordem complexa representada por um conjunto de fatores de risco cardiovasculares, usualmente relacionados à deposição central de gordura. Existem importantes lacunas no que se refere ao grau da ocorrência da MetS em adolescentes, bem como sobre a contribuição de marcadores aterogênicos, a exemplo das apolipoproteínas A-I (APOA-I) e B100 (APOB-100) nessa síndrome. Este estudo tem como objetivos estimar as prevalência de excesso de peso e da MetS em adolescentes escolares, analisar e caracterizar as concentrações de apolipoproteínas A-I e B-100 em escolares com ou sem MetS. Foram desenvolvidos 2 estudos de corte transversal, sequenciais, envolvendo a mesma população de escolares de 10 a 19 anos de ambos os sexos, regularmente matriculados na rede pública e privada de ensino do município de Vitória de Santo Antão-PE. O primeiro corte rastreou o excesso de peso em 2.866 escolares e o segundo corte, a MetS naqueles escolares que apresentaram excesso de peso no primeiro screening. Para avaliação do perfil das apolipoproteínas nos escolares diagnosticados com MetS, foi constituído um grupo controle, selecionado entre os escolares que não apresentaram MetS. Esse pareamento permitiu estabelecer um parâmetro de comparação mais apropriado para avaliação das eventuais flutuações na distribuição das apolipoproteínas na MetS. A amostra foi do tipo poli-etapas, selecionando-se as unidades amostrais elementares por partilha proporcional. A obesidade foi avaliada pelo índice de massa corporal, circunferência da cintura, razão cintura e estatura e circunferência do pescoço. A MetS foi definida pelas recomendações da National Cholesterol Education Program Adult Treatment Panel III (2001) e da International Diabetes Federation (2007), e o risco cardiovascular pela razão das concentrações de apolipoproteínas A-I e B-100. Na análise dos dados foram empregadas técnicas estatísticas descritivas e multivariadas. A prevalência de excesso de peso analisada pelo índice de massa corporal foi de 17,8% (IC95%:16,4-19,2) e a de obesidade abdominal foi de 4,2% (IC95%:3,5-5) para a circunferência da cintura e de 11,4% (IC95%:10,2-11,5) quando da razão da circunferência da cintura e estatura e 30,1% (IC95%:28,4-31,8) para circunferência do pescoço. A razão APOB-100/APOA-I elevada esteve presente em 35,5% (IC95%: 29,5-41,8) e a MetS foi identificada em 14,5% (IC95%: 10,4-19,5) e 18,5% (IC95%: 14-29) dos adolescentes com excesso de peso de acordo com os critérios do IDF(2007) e NCEP/ATP-III (2001), respectivamente. As medianas da razão APOB-100/APOA-I foram significativamente mais elevadas entre os adolescentes com a MetS (p<0,001). A análise de regressão de Poisson ajustada mostrou como fatores de risco independentes, para o excesso de peso dos adolescentes, as mães com escolaridade igual ou superior a 9 anos de estudo (RP= 1,27 IC95% 1,06-1,53), adolescentes pertencentes à classe social mais elevada (RP= 2,06 IC95% 1,59-2,67) e o uso de televisão em dias de semana acima de 3h/dia (RP= 1,3 IC95% 1,07-1,60). Já para elevada razão da APOB-100/APOAI os fatores de risco independentes foram o baixo HDL-c (RP=1,77 IC95% 1,2-2,6) e o elevado LDL-c (RP=3,28 IC95% 2,4-4,5). Conclusão: A elevada prevalência de excesso de peso impõe a adoção de estratégias de prevenção e controle, sobretudo aquelas focalizadas na redução à exposição aos fatores de risco, visando o efetivo combate à pandemia da obesidade em adolescentes. A elevação do HDL-c e redução do LDL-c podem reduzir o risco global de doenças cardiometabólicas em adolescentes. Uma razão APOB-100/APOA-I elevada pode constituir uma característica importante da MetS em adolescentes e pode proporcionar um mecanismo adicional para explicar o aumento do risco cardiovascular em indivíduos com esta síndrome.

APA, Harvard, Vancouver, ISO, and other styles

13

Pirani, Parisa. "Surface-Engineered Magnetic Nanoparticles for Sample Preparation and Analysis of Proteins and Peptides." ScholarWorks@UNO, 2015. http://scholarworks.uno.edu/td/2012.

Full text

Abstract:

Sample preparation as an essential step in mass spectrometry-based analysis, plays a critical role in proteomics studies. Magnetic nanoparticles (MNPs) have been widely used in protein and peptide sample preparation due to their magnetic properties, biocompatibility, easy synthesis and surface functionalization. MNPs loaded with analyte or analyte modification reagent can be easily separated from the reaction medium by an externally applied magnetic field. The small size of MNPs provides high analyte loading and extraction capacity. Additionally, MNP can be decorated with different functional groups to achieve selective modification or extraction of analyte. In this study we have utilized silica coated iron oxide magnetic nanoparticles (Fe3O4@SiO2 MNPs) for protein and peptide sample preparation. Fluorescence-based methods were utilized for quantitative and qualitative characterization of N-hydrosucccinimidyl (NHS) ester groups on the surface of Fe3O4@SiO2 MNPs. Fluorophore Dansylcadaverine was conjugated to NHS ester functional groups. Fluorometric measurement of cleaved dansylcadaveine was employed to determine the number of NHS ester groups per MNPs that was found to be 2.6 × 102 and 3.4 × 103for 20 nm and 100 nm Fe3O4@SiO2 MNPrespectively. The efficiency of labeling native bovine serum albumin (BSA) by NHS ester coated Fe3O4@SiO2 MNPs was also explored in terms of maximizing the number of MNPs conjugated per BSA molecule or maximizing the number of BSA molecules conjugated per each MNP. Lysine residues of apolipoprotein B-100 (apoB-100) on the surface of intact human low density lipoprotein (LDL) were labeled by NHS ester modified Fe3O4@SiO2 MNPs in aqueous solvents at room temperature. The MNP labeledapoB-100 was treated by SDS to remove lipids and then digested using trypsin. Tryptic peptides were eluted from MNPs by cleaving disulfide linkage between labeled peptides and MNPs. LC-MS/MS analysis found 28 peptides containing labeled lysine residues. These lysine residues should be on the solvent exposed surface of LDL since the large size of MNPs prevents contact of the labeling reagent to those lysines embedded inside the structure of LDL. TCEP- immobilized Fe3O4@SiO2MNPs were fabricated and utilized for reduction of disulfide bonds in bovine pancreas insulin and two different cyclic peptides. Disulfide bonds were efficiently cleaved at room temperature in both organic and aqueous solvents confirmed by LC-MS/MS analysis of reduced/alkylated protein and peptides. Disulfide reduction and alkylation reactions was performed in one step and the reducing agent was simply separated from peptide and protein solution by magnetic separation.

APA, Harvard, Vancouver, ISO, and other styles

14

Ginon, Isabelle. "La deficience familiale en apolipoproteine b-100 : une nouvelle forme d'hypercholesterolemie familiale : etude clinique et genetique de 11 familles." Lyon 1, 1993. http://www.theses.fr/1993LYO1M245.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Duvillard, Laurence. "Étude cinétique par isotopie stable des apolipoprotéines A-I, A-II et B-100 chez des patients diabétiques non insulinodépendants, sous antidiabétiques oraux et après mise en route d'une insulinothérapie." Dijon, 1999. http://www.theses.fr/1999DIJOMU12.

Full text

Abstract:

Nous avons étudié la cinétique des apolipoprotéines B-100, A-I et A-II chez des sujets porteurs d'un diabète non insulinodépendant mal équilibré, en utilisant la L-[1-13C]leucine comme traceur, et la spectrométrie de masse isotopique par combustion pour mesurer l'enrichissement en traceur des protéines. Chez ces patients, la concentration plasmatique de l'apoB-100 des VLDL, des IDL est augmentée et la concentration de l'apoB-100 des LDL normale. La production de l'apoB-100 des VLDL est augmentée et le taux de catabolisme de l'apoB-100 et des VLDL , des IDL et des LDL ralenti. Par ailleurs, la concentration de l'apoA-I des HDL est diminuée en rapport avec un catabolisme très accéléré et une production modérément augmentée. Le métabolisme de l'apolipoprotéine A-II des HDL n'est pas modifié de manière significative. Nous avons ensuite étudié l'eefet d'une insulinothérapie de 2 mois sur les anomalies métaboliques précédemment mises en évidence. L'insulinothérapie permet de diminuer la concentration de l'apoB-100 des VLDL en accélérant son catabolisme. Le catabolisme de l'apoB-100 des VLDL des IDL est également augmanté et celui de l'apoB-100 des LDL normalisé. En revenche, l'insulinothérapie ne permet pas de corriger les anomalies métaboliques de l'apoA-I. Les modifications du métabolisme de l'apoB-100 observées au cours du diabète non insulinodépendant sont potentiellement athérogènes parce que la concentration de l'apoB-100 des VLDL et des IDL est augmentée et parce que le temps de résidence des VLDL, des IDL et des LDL est prolongé. En corrigeant partiellement ces anomalies, l'insulinothérapie est susceptible de diminuer le développement des lésions athéromateuses chez ces patients

APA, Harvard, Vancouver, ISO, and other styles

16

Ansari, Basir Sahar. "Role of miRNAs in Translational Control of Human Apolipoprotein B-100 mRNA." Thesis, 2013. http://hdl.handle.net/1807/42671.

Full text

Abstract:

Apolipoprotein B (apoB) is a key structural and functional protein of lipoproteins and is synthesized constitutively in the liver. This study investigated the role of microRNAs (miRNAs) in translational control of apolipoprotein B (apoB) mRNA and protein synthesis. Using bioinformatic analysis, I identified two specific miRNAs namely, miR-544 and miR-1202 with potential to interact with 3’ and 5’ UTR of apoB, respectively. Using HepG2 cells as the model system, the effects of transfection of exogenous miRNAs and inhibition of endogenous miRNAs were assessed on the expression of apoB mRNA and protein synthesis, as well as apoB mRNA traffic into cytoplasmic P-bodies. miR-544 induced a significant reduction in apoB mRNA expression and protein synthesis while increasing the co-localization of apoB mRNA into P-bodies. In contrast, transfection of miR-1202 increased apoB mRNA expression and protein synthesis. In summary, these data demonstrate that specific miRNAs are involved in translational control of apoB mRNA.

APA, Harvard, Vancouver, ISO, and other styles

17

Soufi, Muhidien [Verfasser]. "Funktionelle Charakterisierung neu identifizierter Defekte des LDL-Rezeptors und von Apolipoprotein B-100 / vorgelegt von Muhidien Soufi." 2008. http://d-nb.info/989711838/34.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Khandan, Negin. "Adsorption av Low Density Lipoprotein (LDL) till modifierade agaros matriser." Thesis, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:hkr:diva-15418.

Full text

Abstract:

Individer med homozygot familjär hyperkolesterolemi(FH), har höga halter av Low Density Lipoprotein (LDL) vilket leder till ökad risk för kardiovaskulära sjukdomar. Behandling av dessa individer kan göras med extrakorporal elimination av LDL med hjälp av specifika reningskolonner. Syftet med studien var att utvärdera några agarosmodifierade adsorbenter för denna applikation. Adsorbenterna, modifierad polyakrylat (DALI), agaros (Zetaros), direkt sulfateradZetarose och taurin immobiliserad Zetarose, inkuberades med humant plasma spädd med PBS, och en volyms förhållande mellan matris och plasman på 1:5. Inkubering utfördes i rumstemperatur under 60 min med kontinuerlig blandning i rotator. Efter inkubation centrifugerades proverna och LDL bestämdes i såväl supernatant som pellet. Totalmängd adsorberade proteiner analyserades också i eluat från erhållen pellet. LDL bestämdes indirekt med hjälp av Friedewaldsformel (LDL = totalkolesterol (TC) –highdensitylipoprotein (HDL) - (0,45 x Triglycerider(TG)). TC och TG bestämdes enzymatiskt medan HDL kvantifierades som TC efter utfällning av LDL med dextransulfat. Resultaten visar tydligt att DALI har god adsorptionsförmåga.Dock uppvisar de modifierade Zetaroserna begränsad adsorptionskapacitet för LDL. Vid desorption av adsorbenterna visar SDS en bättre elueringsförmåga än NaCl relaterad till protein, vilket tyder hydrofoba proteiner. Metodiken som används i studien är lämplig för vidare studier av andra adsorbenter som förväntas användas i kliniska applikationer för elimination av LDL hos FH patienter.
Individuals that suffer from homozygote Familiar Hyperkolesterolemia (FH), has increased amounts of Low Density Lipoproteins (LDL) which leads to a higher risk of cardiovascular diseases. Treatment of these individuals can be achieved by extracorporeal elimination of LDL using specific columns. The aim of this study was to evaluate different agarose-modified adsorbents ability to adsorb LDL from human plasma. The adsorbents (DALI, Zetarose, sulphonated Zetarose and taurine immobilized onto Zetarose) were incubated for 60 minutes with human plasma diluted with PBS, in a ratio of 1:5 between the matrix and the plasma during rotation with a rotator. After incubation the samples were centrifuged and the LDL content was determined in both the supernatant and the pellet. The amount proteins adsorbed were assayed by eluting the pellets. LDL was determined indirectly using Friedwalds equation; LDL= Total cholesterol (TC) - High density lipoprotein (HDL)-(0,45x Triglycerides (TG). The values of TC and TG in the sample were determined enzymatically, whilst HDL was quantified as TC after LDL-precipitation by dextran sulfate. The results clearly show that DALI has good adsorption capacity, but none of the modified Zetaroses shows any capacity to absorb LDL from human plasma. Desorption of the adsorbents using SDS gave higher amounts of eluated protein compared to NaCl elution, indicating hydrofobic proteins. However, the methods used in this study could be used to evaluate new adsorbents for LDL-elimination applications in patients with chronic hyperlipemia.

APA, Harvard, Vancouver, ISO, and other styles

19

Smutova, Viktorija. "Neuraminidases as triggers of atherosclerosis." Thèse, 2017. http://hdl.handle.net/1866/20244.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

TENG, YEN-NI, and 鄧燕妮. "Human Genetic Diseases Part I：Mucopolysaccharidosis Type I：Mutational Analysis of the IDUA Gene in Two Chinese Patients Part II：Familial Defective Apolipoprotein B-100：a Study of Hyperlipidemia Type II Patients in Taiwan." Thesis, 2000. http://ndltd.ncl.edu.tw/handle/9x2zg6.

Full text

Abstract:

博士
國立臺灣師範大學
生物研究所
88
The purpose of this study is to investigate two human genetic disorders, mainly autosomal recessive - mucopolysaccharidosis type I (MPS I) and autosomal dominant - familial defective apolipoprotein (apo) B-100 (FDB), at molecular level in Taiwan. In the study of MPS I, DNA screening for α-L-iduronidase (IDUA) gene mutations for two Chinese MPS I patients was performed by polymerase chain reaction (PCR), single-strand conformation polymorphism (SSCP), and DNA sequencing analysis. The D4 patient has 1447del27 (Ser453→Arg in addition to in frame deletion of codons 454-462) in one allele and 1474ins15 (in frame insertion of 5 unrelated amino acids at codon 463) in the other allele. Patient L5 also has heterozygous mutations; the maternal allele has L346R (T to G transversion in codon 346) and the paternal allele has 388-3c>g (C to G transversion at position -3 of the 3'' splice site of intron 2). Expression of recombinant IDUA cDNA containing 1447del27 or 1474ins15 mutation showed traced amounts of α-L-iduronidase activity (0.1 %, 0.3 %) compared to that of normal cDNA upon transfection into COS-7 cells. By northern blot analysis, 24 % 1447del27 mRNA and 49 % 1474ins15 mRNA were detected. The IDUA protein produced by 1447del27 and 1474ins15 mutations was beyond the detection by IDUA polyclonal antibody. The data suggest that the 1447del27 and 1474ins15 mutations result in the severe Hurler phenotype of the D4 patient. In transfected COS-7 cells, L346R showed no appreciable α-L-iduronidase activity (0.4 % of normal activity), although it did not cause apparent reduction in IDUA mRNA or protein level. The 388-3c>g mutation caused a significant decrease in the level of IDUA mRNA. In about 4 % time, the mutation caused the cells to use a cryptic CAG sequence 58 bp upstream from the 3'' splice site and lead to insertion of 58 intronic nucleotides. IDUA cDNA containing mutated acceptor splice site showed low efficiency of splicing in expression study. The results provide further support for the importance of cytosine at -3 position in RNA processing. In the study of FDB, the apo B gene segment around codon 3500 was screened by heteroduplex analysis, single strand conformation polymorphism (SSCP) analysis and DNA sequencing analysis in a total of 373 hyperlipidemic individuals. Two single-base mutations were detected. One mutation, ACA3528→ACG change, resulted in degenerate codon with no amino acid substitution. The other mutation, CGG3500→CAG mutation, resulted in an Arg3500→Gln substitution (R3500Q). The prevalence of heterozygote in this selected population was 0.3 % (95 % confidence interval, 0.01-1.5 %) for the R3500Q mutation, and 2.4 % (95 % confidence interval, 1.1-4.5 %) for the previously described R3500W mutation. The results suggest that R3500Q mutation is not a significant factor contributing to moderate hypercholesterolemia in Chinese (P = 0.027). Family studies of the R3500Q carrier revealed an extra two individuals heterozygous for the mutation, and both of them were hypercholesterolemic. An analysis of the R3500Q allele using 6 diallelic markers and the 3''HVR marker revealed a haplotype which was the same as that reported in a Chinese American but differed from that reported in a Chinese Canadian. The data support limited multiple recurrent origins for R3500Q in Chinese population.

APA, Harvard, Vancouver, ISO, and other styles

21

Sattler, Alexander M. [Verfasser]. "In-vivo-Kinetik der Apolipoproteine B-100 und A-I bei Patienten mit Hyperlipidämie unter dem Einfluss des Lipidsenkers Lifibrol / vorgelegt von Alexander Markus Sattler." 2003. http://d-nb.info/972805605/34.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Dissertations / Theses on the topic 'Apolipoprotein B-100'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles