Biomedical subjects

J Hybenova

Publications and source records attributed to J Hybenova.

2 recordsLinked to original sources

PubMed1999

[Endothelial dysfunction and lipid profiles: analysis of the EDO Study].

On the basis of experimental as well as clinical observations, endothelial dysfunction is (defined as impaired or absent endothelium-dependent relaxation) considered to be an important factor in the atherogenesis. Serum lipids abnormalities have been accepted as an epidemiological risk factor of atherosclerosis. In vitro, experimental as well as epidemiological studies revealed the fact, that lipoprotein oxidation plays an important role in atherogenesis. Recently invented non-invasive methods to test and measure the endothelial function in vivo opened the opportunity to study the influence of different serum lipids on the endothelial function directly. Therefore, we decided to employ this non-invasive method for studying the endothelial function and observe the influence of various levels of plasma lipids and lipoprotein oxidation on the endothelial function of arteries in middle-aged men, since they are the most endangered part of population. In our study we used a method of measuring the diameter of a. radialis by high-resolution ultrasound (Sonoline 450, Siemens, Japan) and further mathematical and statistical analysis of functional as well as relative vasodilation reserve followed these measurements. Blood samples were taken within 24 hours of ultrasonography to study serum lipids (total cholesterol, HDL, triglycerides) and parameters of oxidation/antioxidation (superoxid dismutase--SOD, malondialdehyde--MDA). Sixty men, 25-45 years old, from an area of basically the same level of pollution were examined. We found a negative correlation between FVDR and TCH (p = 0.01), FVDR and Tg (p = 0.002) and FVDR a TCH/HDL (p = 0.015). Positive correlation exists (p < 0.001) between TCH, Tg levels and TCH/HDL ratio and MDA level in all cases. Analysing further data from the EDO Study, we can conclude, that increased plasma lipids are more likely to be oxidized, which, in turn, is the probable reason of endothelium-dependent vasodilation impairment.

Adult↗

PubMed1999

[Is PLA1/A2 gene polymorphism of platelet membrane glycoprotein IIIa a risk factor for myocardial infarct?].

BACKGROUND: The PlA1/A2 polymorphism of the human platelet membrane glycoprotein IIIa gene cause T-->C transition in the exon ii (position 1565) resulting in the leucine-->proline substitution in amino-acid sequence. This polymorphism was shown to be associated with increased risk of myocardial infarction (MI). AIM: To test genetic parameters of the PlA1/A2 polymorphism in our population and to assess the relation between mutant PlA2 allele and MI. METHODS: DNA was isolated from peripheral blood, collected from 40 patients with MI and with present risk factors (hypertension, hypercholesterolaemia, diabetes, obesity, smoking...), 33 patients with MI without risk factors, 34 controls with equivalent average age to both groups of the MI-patients, 58 control probands without MI in their family history and 33 healthy controls randomly recruited. After PCR amplification the resulting 267 bp fragment was digested with the restriction endonuclease NciI and subfragments were separated electrophoretically in 12% polyacrylamide gel. RESULTS: The frequency of the PlA2 allele was 0.121 in patients with MI without risk factors, 0.205 in patients with present risk factors, 0.162 in controls of the equivalent average age to the MI-patients, 0.172 in controls without MI in their family history and 0.20 in healthy controls randomly recruited. Genotype frequencies were in all groups in genetic equilibrium. Although the groups differed significantly (p < 0.01) in serum concentrations of total cholesterol, HDL-cholesterol, LDL-cholesterol, apolipoprotein A-1, apolipoprotein B and malondialdehyde, no significant differences in the serum concentrations of these metabolites between A1/A1, A1/A2 and A2/A2 genotypes were observed. CONCLUSIONS: PLA1/A2 polymorphism is associated with MI, however not as a dominant risk factor, but as a part of environmentally influencable multigene system. There is no relation between genotypes of the PLA1/A2 polymorphism and the lipoproteins plasma concentrations. (Tab. 4, Ref. 17.)

Adult↗