Preferencje help
Polish version English version Język
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 14

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

Wyszukiwano:
w słowach kluczowych:  apolipoprotein
help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
1

Distribution of apolipoprotein E4 isoform in Alzheimer's disease in Poland

100%
Bratosiewicz-Zapart J., Kloszewska I., Sobow T., Liberski P. P.
Archivum Immunologiae et Therapiae Experimentalis
|
1997
|
tom 45
|
nr 2-3
2

Inhibition of serum amyloid A protein amyloid formation

72%
Sosnowska M., Jankowska E.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
The acute-phase protein serum amyloid A (SAA) is present in the bloodstream at the concentration below 1 µM under physiological conditions, but its level increases significantly during the acute-phase response following infection or inflammatory condition. A consequence of the long-term elevated SAA concentration is deposition of normally soluble serum amyloid A in the form of insoluble fibrils, impairing tissue structure and function. These deposits cause development of a secondary type amyloidosis, called amyloid A protein (AA) amyloidosis, which results in a death of thousands of people per annum around the world. The ability of SAA to form amyloids seems to be connected with the N-terminal portion of the molecule. The capacity of the synthetic peptides derived from the N-terminal sequence of human or mice SAA to form fibrils in vitro proves that the most amyloidogenic region is embedded within the protein’s first 15 amino acids. We decided therefore to use peptides consisting of 11–15 amino acids and the sequence derived from the N-terminus of the parent aggregating protein as a research tool for investigation of the molecular recognition and self-assembly mechanisms that promote the formation of SAA amyloid fibrils deposits. In this study, we tested the hypothesis that non-aggregating very short peptides derived from SAA sequence would interact with the analogous region in the protein molecule or its aggregation-prone N-terminal fragment, and block its assembly into oligomers and amyloid fibrils. We designed and synthesized a peptide with the sequence 1RSFFS5, derived from the human SAA primary structure, and then tested it as a potential inhibitor of the aggregation process of SAA protein. The hypothesis about the role of aromatic interactions in amyloid fibril formation led us to test another peptide: 17LVFF20, which is derived from the sequence of Aβ. We tested propensity of the N-terminal segment (1–15) of mice SAA for amyloid fibrils formation, incubating it either alone or together with the potential inhibitors. Thioflavin T (ThT) fluorescence test was used to detect amyloid fibrils formation. These tests confirmed that the designed peptides are able to diminish propensity of the aggregation-prone SAA peptides to form amyloid fibrils. There are currently no effective medical treatment of diseases associated with the systemic amyloidosis. We believe that results of the presented project open up new possibilities in designing compounds that are able to prevent formation of amyloid deposits and could be a starting point for the design of peptidomimetic molecules more suitable as potential drugs. The work was supported by grant NCN nr 2011/03/N/NZ5/01460 and grant BMN No 538-8440-1042-12.
3
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

ApoE genotype as risk factors for Alzheimer’s disease in the population of Lublin region, Poland

72%
Gustaw-Rothenberg K.
Journal of Pre-Clinical and Clinical Research
|
2008
|
tom 02
|
nr 2
4
Content available remote

Gender-related effect of cold water swimming on the seasonal changes in lipid profile, ApoB/ApoA-I ratio, and homocysteine concentration in cold water swimmers

72%
Checinska-Maciejewska Z., Miller-Kasprzak E., Checinska A., Korek E., Gibas-Dorna M., Adamczak-Ratajczak A., Bogdanski P., Krauss H.
Journal of Physiology and Pharmacology
|
2017
|
tom 68
|
nr 6
5

Distribution of apolipoprotein Al-containing lipoprotein subclasses in plasma of normolipidemic subjects

72%
Atmeh R. F., Kasasbeh A. Z., Abu Odeh M. R.
Acta Biochimica Polonica
|
2010
|
tom 57
|
nr 3
The distribution of apoA-I among apoA-I-containing lipoprotein (AI-Lp) subclasses in plasma was studied by immunoblotting utilizing agarose gel matrix incorporating anti-apoA-I as the transfer medium. Nine AI-Lp subclasses were detected in the plasma of normolipidemics, with relative molecular masses ranging from 70 000 to ≥ 354 000 and diameters from 7.12 to ≥ 11.6 nm. The mass distribution of AI-Lp subclasses was significantly different between males and females, and some subclasses increased gradually with age while others decreased. There was a significant strong positive correlation between subclass 1 (Mr 70 000-75 000) and subclass 3 (Mr 105 000-126 000) in all subjects and age groups. Analysis of similar AI-Lp or HDL subclasses reported in the literature showed variability in the sizes reported by various workers. This stresses the need for a unified classification of such subclasses, and this work contributes to this direction. The quantitative nature of the method used in this work compared with the semiquantitative approaches used earlier makes it a better method for the study of the quantitative changes of the subclasses in various physiological and pathological states. The method helps to generate ideas for in vitro and in vivo studies of apoA-I exchange among subclasses and in vivo kinetic studies. Conclusion. Plasma level of the AI-Lp subclasses varied quantitatively with age and gender, and strong correlations were detected between some subclasses. This work contributes to a better classification of AI-Lp subclasses according to their size. Comparison of the method used here with the methods reported in the literature revealed its advantages.
6

Molecular characterization of Polish patients with familial hypercholesterolemia: novel and recurrent LDLR mutations

72%
Chmara M., Wasag B., Zuk M., Kubalska J., Wegrzyn A., Bednarska-Makaruk M., Pronicka E., Wehr H., Defesche J. C., Rynkiewicz A., Limon J.
Journal of Applied Genetics
|
2010
|
tom 51
|
nr 1
95-106
Autosomal dominant hypercholesterolemia (ADH) is caused by mutations in the genes coding for the low-density lipoprotein receptor (LDLR), apolipoprotein B-100 (APOB), or proprotein convertase subtilisin/kexin type 9 (PCSK9). In this study, a molecular analysis of LDLR and APOB was performed in a group of 378 unrelated ADH patients, to explore the mutation spectrum that causes hypercholesterolemia in Poland. All patients were clinically diagnosed with ADH according to a uniform protocol and internationally accepted WHO criteria. Mutational analysis included all exons, exon-intron boundaries and the promoter sequence of the LDLR, and a fragment of exon 26 of APOB. Additionally, the MLPA technique was applied to detect rearrangements within LDLR. In total, 100 sequence variations were identified in 234 (62%) patients. Within LDLR, 40 novel and 59 previously described sequence variations were detected. Of the 99 LDLR sequence variations, 71 may be pathogenic mutations. The most frequent LDLR alteration was a point mutation p.G592E detected in 38 (10%) patients, followed by duplication of exons 4-8 found in 16 individuals (4.2%). Twenty-five cases (6.6%) demonstrated the p.R3527Q mutation of APOB. Our findings imply that major rearrangements of the LDLR gene as well as 2 point mutations (p.G592E in LDLR and p.R3527Q in APOB) are frequent causes of ADH in Poland. However, the heterogeneity of LDLR mutations detected in the studied group confirms the requirement for complex molecular studies of Polish ADH patients.
7

Impact of 75G/A apolipoprotein AI gene polymorphism on lipid profile in obese and non-obese men

72%
Wlodarczyk M., Wrzosek M., Nowicka G.
Żywienie Człowieka i Metabolizm
|
2014
|
tom 41
|
nr 2
Introduction: Obesity is a multifactorial disorder leading to disturbances in lipid metabolism and adverse plasma lipid profiles. 75G/A polymorphism in the apolipoprotein AI (apo AI) gene promoter has been shown to affect plasma HDL-cholesterol and apolipoprotein AI concentrations. However, the impact of this genetic variant on lipid profiles in obese subjects has not been well recognized. In the present study the relationship between 75G/A apo AI gene polymorphism (rs 670) and plasma lipids and apo AI concentrations in obese and non-obese males was assessed. Material and Methods: 114 men who were not taking lipid lowering drugs were examined: control group with body mass index (BMI) less than 25 (n = 34), overweight with BMI ranged 25-29 (n = 51) and obese subjects with BMI > 30 (n - 29). The 75G/A gene polymorphism of apo AI was determined by PCR-based method. Results: Higher serum HDL-cholesterol and apo AI concentrations in A allele carriers compared to GG homozygotes were observed in men with proper body mass (p = 0.037 and p = 0.056, respectively) and in overweight subjects (p = 0.0072 and p = 0.018, respectively) but not in obese men. Therefore, interaction may be suggested between 75G/A genetic variants in apo AI gene with obesity and its influence on plasma HDL-cholesterol and apo AI concentrations.
8
Content available remote

Bay x 1005 attenuates atherosclerosis in apoE-LDLR - double knockout mice

72%
Jawien J., Gajda M., Olszanecki R., Korbut R.
Journal of Physiology and Pharmacology
|
2007
|
tom 58
|
nr 3
Recently, we have shown that MK-886 - an inhibitor of five lipoxygenase activating protein (FLAP) inhibits atherosclerosis in apolipoprotein E / LDL receptor - double knockout mice. We, therefore, wanted to find out if other FLAP inhibitor - BAYx1005 given at a dose of 1.88 mg per 100 mg of body weight per day during 16 weeks, could also attenuate atherogenesis. In apoE/LDLR - DKO mouse model BAYx1005 inhibited atherogenesis, measured both by "en face" method (23.84 ± 2.7% vs. 15.16 ± 1.4%) and "cross-section" method (497236 ± 31516 µm2 vs. 278107 ± 21824 µm2). This is the first report that shows the effect of BAYx1005 on atherogenesis in gene-targeted mice.
9
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Evaluation of lipids, lipoproteins and apolipoproteins concentrations in cord blood serum of newborns from rural and urban environments

72%
Pac-Kozuchowska E.
Annals of Agricultural and Environmental Medicine
|
2007
|
tom 14
|
nr 1
The purpose of the present study was to check the infl uence of rural and urban environments on some of the parameters of lipids metabolism in the cord blood serum in healthy newborns, as well as the evaluation of the concentration of lipids, lipoproteins and apolipoproteins in the cord blood serum with relation to risk factors of atherosclerosis in the family of the studied newborns. The study included 75 newborns (37 from rural areas and 38 from urban areas). Newborns weight and length were recorded at birth. On the basis of the family history taken from the mothers, the atherosclerosis risk factors were established in the families of the studied newborns. In all of the studied newborns, concentration of triglycerides, total cholesterol and LDL, VLDL and HDL cholesterol as well as of apolipoproteins (apo-AI, apo-B) in the cord blood serum sampled soon after birth were performed. No statistically signifi cant differences between the mean levels of triglycerides, total cholesterol and cholesterol of fractions: LDL, VLDL, HDL and apolipoproteins (apo-AI, apo-B) in the cord blood serum in the newborns from rural and urban areas were found. However, when analysing the concentration of parameters of lipid metabolism in cord blood serum in newborns with regard to gender, higher concentrations of total cholesterol, LDL cholesterol and apo-AI in female newborns from rural areas, and higher HDL cholesterol and apo-AI in female newborns from urban regions were confi rmed. When analysing the concentration of lipids and lipoproteins in cord blood serum in newborns from families with risk factors confi rmed as compared to the families without that risk, both in the rural and urban regions no signifi cant differences were confi rmed. The studies have not proved any signifi cant differences between the levels of lipids, lipoproteins and apolipoproteins in the cord blood serum in newborns from rural and urban areas.
10

Association of serum triglyceride levels with APO CIII gene Sac I [SST I] polymorphism

72%
Wlodarczyk M., Nowicka G., Walczak A.
Żywienie Człowieka i Metabolizm
|
2007
|
tom 34
|
nr 6
Apolipoprotein CIII is a major protein component of chylomicrons and very low density lipoproteins (VLDL) and it is important in the regulation of triglyceride metabolism. Sst 1 polymorphism in the apolipoprotein CIII gene (APO CIII) has been recognized as a factor influencing levels of plasma triglycerides. We examined APO CIII Sac I (Sst I) variants and serum lipids profile in 175 subjects. DNA samples were analyzed by polymerase chain reaction (PCR) followed by Sac I (Sst I) digestion. The frequency of S2 allele was found to be three times higher among men with enhanced plasma triglyceride (TG) compared to men with normal TG levels (16,2% vs. 5,2%). Subjects with the S1S2 genotype compared to S1S1 homozygotes had higher plasma triglycerides and cholesterol levels (190 ± 155 mg/dl vs. 139 ± 90 mg/dl, p=0,035; 234 ± 60 mg/dl vs. 214 ± 37, p=0,04 respectively). These results indicate that a relationship between S2 allele of APO CIII gene and enhanced TG levels occur in studied population.
11

Differences between group X and group V secretory phospholipase A2 in lipolytic modification of lipoproteins

58%
Kamitani S., Yamada K., Yamamoto S., Ishimoto Y., Ono T., Saiga A., Hanasaki K.
Cellular and Molecular Biology Letters
|
2012
|
tom 17
|
nr 3
Secretory phospholipases A2 (sPLA2s) are a diverse family of low molecular mass enzymes (13–18 kDa) that hydrolyze the sn-2 fatty acid ester bond of glycerophospholipids to produce free fatty acids and lysophospholipids. We have previously shown that group X sPLA2 (sPLA2-X) had a strong hydrolyzing activity toward phosphatidylcholine in low-density lipoprotein (LDL) linked to the formation of lipid droplets in the cytoplasm of macrophages. Here, we show that group V sPLA2 (sPLA2-V) can also cause the lipolysis of LDL, but its action differs remarkably from that of sPLA2-X in several respects. Although sPLA2-V released almost the same amount of fatty acids from LDL, it released more linoleic acid and less arachidonic acid than sPLA2-X. In addition, the requirement of Ca2+ for the lipolysis of LDL was about 10-fold higher for sPLA2-V than sPLA2-X. In fact, the release of fatty acids from human serum was hardly detectable upon incubation with sPLA2-V in the presence of sodium citrate, which contrasted with the potent response to sPLA2-X. Moreover, sPLA2-X, but not sPLA2-V, was found to specifically interact with LDL among the serum proteins, as assessed by gel-filtration chromatography as well as sandwich enzyme-immunosorbent assay using anti-sPLA2-X and anti-apoB antibodies. Surface plasmon resonance studies have revealed that sPLA2-X can bind to LDL with high-affinity (Kd = 3.1 nM) in the presence of Ca2+. Selective interaction of sPLA2-X with LDL might be involved in the efficient hydrolysis of cell surface or intracellular phospholipids during foam cell formation.
12

Biological roles of liver X receptors in immune cells

58%
Pascual-Garcia M., Valledor A. F.
Archivum Immunologiae et Therapiae Experimentalis
|
2012
|
tom 60
|
nr 4
13

The origin and metabolism of a nascent pre-beta high density lipoprotein involved in cellular cholesterol efflux

58%
Wroblewska M.
Acta Biochimica Polonica
|
2011
|
tom 58
|
nr 3
 The pre-β HDL fraction constitutes a heterogeneous population of discoid nascent HDL particles. They transport from 1 to 25 % of total human plasma apo A-I. Pre-β HDL particles are generated de novo by interaction between ABCA1 transporters and monomolecular lipid-free apo A-I. Most probably, the binding of apo A-I to ABCA1 initiates the generation of the phospholipid-apo A-I complex which induces free cholesterol efflux. The lipid-poor nascent pre-β HDL particle associates with more lipids through exposure to the ABCG1 transporter and apo M. The maturation of pre-β HDL into the spherical α-HDL containing apo A-I is mediated by LCAT, which esterifies free cholesterol and thereby forms a hydrophobic core of the lipoprotein particle. LCAT is also a key factor in promoting the formation of the HDL particle containing apo A-I and apo A-II by fusion of the spherical α-HDL containing apo A-I and the nascent discoid HDL containing apo A-II. The plasma remodelling of mature HDL particles by lipid transfer proteins and hepatic lipase causes the dissociation of lipid-free/lipid-poor apo A-I, which can either interact with ABCA1 transporters and be incorporated back into pre-existing HDL particles, or eventually be catabolized in the kidney. The formation of pre-β HDL and the cycling of apo A-I between the pre-β and α-HDL particles are thought to be crucial mechanisms of reverse cholesterol transport and the expression of ABCA1 in macrophages may play a main role in the protection against atherosclerosis.
14

Apolipoproteins AI and B, and LpAI lipoprotein particles in normocholesterolemic and hypercholesterolemic subjects with documented coronary heart disease

58%
Jarosz A., Nowicka G.
Żywienie Człowieka i Metabolizm
|
2008
|
tom 35
|
nr 2
The relation between coronary heart disease risk and low density lipoprotein and high density lipoprotein cholesterol concentrations is well accepted. These parameters are widely used in coronary heart disease risk assessment. However, an evidence is accumulated that other lipoprotein related parameters may be useful in CHD risk prediction. The aim of the study was to assess differences in plasma levels of apolipoproteins AI and B, and apo AI containing lipoprotein subpopulations LpAI and LpAI/AII, between subjects with and without documented coronary heart disease but similar total cholesterol and LDL cholesterol levels. 233 subjects were studied. CHD patients were characterized by higher apo B levels than Control subjects with similar LDL cholesterol levels and these differences were visible in normocholesterolemic as well as in hypercholesterolemic subjects. Significantly lower levels of LpAI particles were noted in CHD patients. The drop in LpAI was significant even when no differences in HDL-cholesterol and apo AI concentration occurred. The presented data support the idea that measurements of apolipoprotein B and apo AI and especially LpAI particles levels may improve CHD risk assessment. These markers may be particularly useful in patients with no classical risk factors, patients with serum and LDL cholesterol levels in normal range.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.