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Biomedical subjects

H Bukowska

Publications and source records attributed to H Bukowska.

15 recordsLinked to original sources
PubMed2001

Homocysteine, fibrinogen, and lipoprotein(a) levels are simultaneously reduced in patients with chronic renal failure treated with folic acid, pyridoxine, and cyanocobalamin.

Ischemic heart disease and other complications of atherosclerosis are the usual cause of death in patients with chronic renal failure. Important factors associated with early onset of atherosclerosis in these patients are hyperhomocysteinemia, hyperfibrinogenemia, and elevated levels of lipoprotein(a) (Lp(a)). Folic acid (15 mg/d), pyridoxine (150 mg/d), and cyanocobalamin (1 mg/wk) were administered for 4 weeks in 21 patients receiving dialysis, and a simultaneous, statistically significant reduction in the concentration of homocysteine, fibrinogen, and Lp(a) was found. A positive correlation between decreasing homocysteine and fibrinogen levels was also noted. The parameters studied approached presupplementation values 6 months after vitamins were discontinued. The results suggest that vitamin supplementation has a favorable effect on risk factors of atherosclerosis in patients with renal failure and that interactions may exist between homocysteine, fibrinogen, and Lp(a).

Adult↗
PubMed2001

[Reduction of the plasma LDL-cholesterol level among young healthy men as a result of the change from butter to soft margarine in the unbalanced diet].

The aim of the study was to evaluate the level of lipid profile on 83 healthy males consuming soft type margarine instead of butter, in their unbalanced diet. For this purpose double blind, cross-over methodology was applied. After stabilization period of consuming the diet, the whole sample was randomly divided into two subgroups (A n--37; B n--46). First group was consuming 15 g of the butter twice a day (30 g in total) and the second identically packed soft type margarine (also twice a day 15 g; 30 g in total) containing high level (33.3 g/100 g) of polyunsaturated fatty acids. After four weeks, the diet of subgroups was mutually exchanged--group consuming margarine consumed butter and the opposite. The feeding pattern of both groups was monitored with the aid of FOOD 2 computer programme. The group under investigation consisted of healthy males at the age 23.3 +/- 2.5, BMI 24.4 +/- 3.9 kg/m2; WHR 0.82 + -0.06 and normal blood pressure. Exchange of butter into soft margarine caused the increase of P/S ratio from 0.30 to 0.78 in their diet. Both investigated groups shoved average decrease of 10.7% of blood cholesterol content (in group A 13.8%), LDL cholesterol of about 9.8% and triglycerides ca 12.7% (higher decrease in group B--16.7%). Both groups while on margarine diet shoved small decrease of HDL cholesterol (3.9%). It can not be the matter of serious concern due to average HDL content in both groups was ca 52 mg/dl (ca 1.4 mmol/l)--it means considerably excessive the limited risk (35 mg/dl; 0.90 mmol/l). Application of the margarine diet in group A caused the decrease the ratios of total cholesterol to HDL cholesterol from 3.84 into 3.52; whereas in group B from 4.15 into 3.75. It was also concluded, that the low trans isomer margarine show no effect on lipoprotein Lp(a). Back to the diet with butter after 4 weeks carry down the beneficial effects of diet with margarine on lipid profile. The results indicate that for lipid profile the consumption of soft margarine was more beneficial than butter, even for unbalanced diet.

Adult↗
PubMed2000

Ibuprofen inhibits adhesiveness of monocytes to endothelium and reduces cellular oxidative stress in smokers and non-smokers.

BACKGROUND: Cigarette smoking is a major risk factor in atherosclerosis and a useful model from which to study chronic inflammation. We compared monocyte function, lipid profiles and inflammatory markers in smokers and non-smokers, before and after oral ibuprofen intake. The adhesion of freshly isolated monocytes to native and tumour necrosis factor alpha (TNFalpha) stimulated human umbilical vein endothelial cells (HUVEC), as well as superoxide anion (O2-) levels and hydrogen peroxide (H2O2) production in resting and phorbol myristate acetate (PMA) stimulated monocytes were determined. MATERIALS AND METHODS: A group of nine smokers without any other coronary risk factor was compared with an age-matched group of 9 non-smokers. Tests were performed before and after a two-week course of oral ibuprofen (600 mg day-1). RESULTS: In smokers before ibuprofen, monocyte adhesion to native and TNFalpha-stimulated HUVEC was increased (P < 0001 and P < 0.01, respectively), and so were O2- levels in native and PMA-stimulated monocytes (P < 0.01 and P < 0.001, respectively). Ibuprofen reduced the adhesion of monocytes to native and stimulated HUVEC (P < 0.001) and O2- generation by resting and PMA-stimulated cells (P < 0.01) in both groups. H2O2 production by resting and PMA-stimulated monocytes was reduced in smokers and non-smokers (P < 0.01). Interestingly, ibuprofen increased HDL cholesterol levels in smokers (P < 0.01) and non-smokers (P < 0.001), and reduced the level of triglycerides in smokers (P < 0.05). CONCLUSION: Oral administration of ibuprofen reduced the adhesion of monocytes to HUVEC, suppressed oxidative stress and increased HDL cholesterol levels in smokers and non-smokers.

Adult↗
PubMed1999

Ibuprofen protects low density lipoproteins against oxidative modification.

Oxidative modification of LDL by vascular cells has been proposed as the mechanism by which LDL become atherogenic. The effect of ibuprofen on LDL modification by copper ions, monocytes and endothelial cells was studied by measuring lipid peroxidation products. Ibuprofen inhibited LDL oxidation in a dose-dependent manner over a concentration range of 0.1 to 2.0 mM. Ibuprofen (2 mM, 100 microg/ml LDL) reduced the amount of lipid peroxides formed during 2 and 6 h incubation in the presence of copper ions by 52 and 28%, respectively. Weak free radical scavenging activity of ibuprofen was observed in the DPPH test. The protective effect of ibuprofen was more marked when oxidation was induced by monocytes or endothelial cells. Ibuprofen (1 mM, 100 microg/ml LDL) reduced the amount of lipid peroxides generated in LDL during monocyte-mediated oxidation by 40%. HUVEC-mediated oxidation of LDL in the absence and presence of Cu2+ was reduced by 32 and 39%, respectively. More lipid peroxides appeared when endothelial cells were stimulated by IL-1beta or TNFalpha and the inhibitory effect of ibuprofen in this case was more pronounced. Ibuprofen (1 mM, 100 microg/ml LDL) reduced the amount of lipid peroxides formed during incubation of LDL with IL-1beta-stimulated HUVEC by 43%. The figures in the absence and presence of Cu2+ for HUVEC stimulated with TNFalpha were 56 and 59%, respectively. To assess the possibility that ibuprofen acts by lowering the production rate of reactive oxygen species, the intracellular concentration of H2O2 was measured. Ibuprofen (1 mM) reduced intracellular production of hydrogen peroxide in PMA-stimulated mononuclear cells by 69%. When HUVEC were stimulated by IL-1beta or TNFalpha the reduction was 62% and 66%, respectively.

Antioxidants↗
PubMed1998

Antioxidant status of children with steroid-sensitive nephrotic syndrome.

Eighteen children with steroid-sensitive nephrotic syndrome (SSNS) were studied. The control group comprised 20 healthy children. The following indirect parameters of reactive oxygen species activity were determined in nephrotic patients during four stages of the disease (full relapse before prednisone administration, disappearance of proteinuria, prednisone cessation, unmaintained remission): plasma malondialdehyde (MDA) levels, copper/zinc superoxide dismutase (CuZn SOD) activity and glutathione peroxidase (GPX) activity in erythrocytes, reduced glutathione (GSH) and vitamin C levels in whole blood, and vitamin E level in serum. Increased MDA levels, reduced vitamin C levels, and enhanced CuZn SOD activity were found in relapse. GSH concentration was high during all four stages. Vitamin E level was also increased, parallel to the pattern of serum lipids. GPX activity remained low during the proteinuria stage and in remission. We conclude that the majority of abnormal findings can be attributed to the hyperlipidemia of NS. Low GPX activity may be a factor limiting the antioxidant capacity in NS. The present study is inconclusive regarding the role of free radicals in the proteinuria of NS.

Adolescent↗
PubMed1998

[Determination of the usefulness of selected biochemical parameters for assessing the advanced atheromatous changes in human coronary arteries].

It is generally accepted that atherosclerosis is a dynamic process in which many factors of lipid, hemostatic or other nature play their negative and positive roles. The purpose of the study was to determine the relationship between the atheromatous changes in coronary arteries being assessed angiographically and the lipid and hemostatic risk factors, as well as to select biochemical parameters, which would be helpful for prognosing the degree of intensity with regard to atheromatous changes in coronary arteries. Studies of lipid parameters and hemostasis system were performed in 31 men with atherosclerosis of coronary vessels being angiographically estimated. The degree of intensity concerning the atheromatous changes was defined in a point scale according to Gensini based on the magnitude of coronary artery stenosis and its localization in respect of significance for myocardial function. The studied patients were divided into two groups, which differed by the degree of the intensity of atheromatous changes in coronary arteries: group I--men with mild (M-CAD, score < 32) n = 15, group II--men with severe atherosclerotic changes (S-CAD, score > or = 32) n = 16. The characteristics of both groups are given in table 1. All patients were on nitrates, salicylates, beta-blockers and calcium channel blockers. No antilipemics or anticoagulants were administered. The following biochemical parameters were determined in all men: cholesterol-Ch; triglycerides-TG; phospholipids-PL; apolipoproteins: Apo A, Apo A-I, Apo B; lipoproteins: VLDL, LDL, HDL and their lipids and proteins components; lipoprotein (a)-Lp(a); fibrinogen-Fb; euglobulin lysis time-ELT; inhibitor tissue plasminogen activator PAI-1; antithrombin III--AT III; spontaneous platelet aggregation-SPA, platelet factor 4-PF 4 and glucose. Table 2 lists the lipid parameters in serum and lipoprotein fractions. The levels for apolipoproteins A, A-I, B, lipoprotein (a), hemostatic parameters and glucose are given in table 3. Tables 4 and 5 present the results of multiple regression analysis for severity of atherosclerotic changes (score--dependent variable y) lipid and hemostatic parameters and glucose (independent variables x) in both groups. Prognostic variables necessary for the best fit in the model of relationship studied have been selected. Independent variables x are listed in descending order according to the absolute value of b*x. On the basis of the performed statistical analysis of the results of studies it has been ascertained that the biochemical parameters differentiating the patients with regard to the intensity of atheromatous changes are the coefficients: LDL-Ch/HDL-Ch and Apo B/Apo A ratio, LDL-PL, Fb and ELT whose values were higher as well as HDL-Apo A-I whose value was lower in the group of men with more severe atherosclerotic changes in coronary arteries (S-CAD). The stepwise multivariate analysis indicates that the most profound prognostic significance in risk of coronary atherosclerosis is claimed successively by: glucose, LDL-PL, HDL-Apo A-I, AT III, Fb, ELT, PAI-1, SPA, Lp(a), Apo B and PF 4. The results of the accomplished studies point out that the above-mentioned lipid, hemostatic parameters and glucose may be helpful in prognosing the severity of coronary atherosclerosis.

Adult↗
PubMed1996

[Evaluation of lipoprotein (a) and fibrinogen levels in men after premature myocardial infarction and in their sons].

Lipoprotein (a) and fibrinogen admittedly are independent risk factors of coronary heart disease. Since Lp (a) has been shown to inhibit plasminogen binding to endothelial cells and to fibrin monomers, this led to the speculation that high Lp (a) levels in plasma could interfere with fibrinolysis. Therefore the aim of our work was to estimate the lipoprotein (a) and fibrinogen levels and to find correlation between lipoprotein (a) and fibrinogen levels at the men after a myocardial infarction and also at their sons. We examined 33 men of age 31-57 after a myocardial infarction and their 18 sons 4-14 years old. The control group consisted of 40 men of age 18-57 and their 19 sons 5-14 years old. The Lp (a) was determined with electroimmunodiffusion method and fibrinogen by Clauss method. The fibrinogen level in the examined group was found to be statistically significantly higher (338 mg/dl) than in the control group (313 mg/dl). There was no correlation between Lp(a) and fibrinogen concentration. In the group of sons of patients mean fibrinogen and Lp (a) levels were similar to those of the control group. However there was a negative correlation between the fibrinogen and the triglycerides concentration in sons of patients but not in the control group. The results seem to confirm the significance of fibrinogen as a risk factor for the development of the coronary heart disease.

Adolescent↗