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Biomedical subjects

L Romics

Publications and source records attributed to L Romics.

At least 55 records · Page 3Linked to original sources
PubMed1996

Lipoprotein(a) concentration and phenotypes in primary biliary cirrhosis.

We studied a selected group of 39 female patients suffering from primary biliary cirrhosis (PBC). This disease is characterized by typical lipoprotein alterations and elevated concentrations of serum cholesterol. Despite the increased concentration of atherogenic lipoproteins, enhanced atherogenesis is not characteristic of PBC. Serum total cholesterol, triglycerides, HDL2 and HDL3-cholesterol concentrations were measured by enzymatic methods or in combination with precipitation procedures. Apolipoproteins were determined by using immunonephelometric methods. ELISA sandwich method was used for lipoprotein(a) determinations. Apoprotein(a) phenotyping (isoforms) was performed by Western blotting with specific antibodies. The concentrations of serum lipids, lipoproteins and apoproteins (AI, AII and B) were found in the range of earlier investigations. The serum lipoprotein(a) concentration did not differ between the PBC patients and control subjects (10.0/0.1-54/, median 2.55 vs. 11.5/0-75/, median 5.2 mg/dl). In the advanced stages of PBC we found a higher number of patients with low lipoprotein concentration (lower than 1 mg/dl). In patients with shorter durations and milder histological alterations high HDL2 cholesterol subfractions has been detected (stage I = 0.42 +/- 0.18, stage II = 0.53 +/- 0.29 and stage III = 0.62 +/- 0.41 vs. stage IV = 0.26 +/- 0.15 mmol/l, P < 0.05). Despite the elevation of atherogenic lipoproteins, high HDL2-cholesterol and normal lipoprotein(a) concentrations may be one of the reasons why patients with advanced PBC are not placed at increased risk for atherosclerosis.

Adult↗
PubMed1995

[Effect of pancreas transplantation on triglyceride metabolism].

Transplantation of pancreatic gland with systemic venous drainage of the graft causes elevated plasma levels of insulin. To examine lipid metabolism triglyceride clearance capacity, lipolytic enzymes, plasma lipids and lipoproteins were quantified in pancreas-kidney transplant recipients and compared them to lipid parameters of healthy controls and those of patients who had received only kidney transplants. Eleven pancreas-kidney transplant recipients with type I diabetes, 9 non-diabetic kidney transplant recipients as controls for the effects of immunosuppressive medication, and 11 healthy controls were studied. In pancreas-kidney transplant recipients fasting cholesterol, non-HDL cholesterol, triglyceride levels were found 5.5 (+/- 1.0), 3.4 (+/- 0.78) and 1.06 (+/- 0.29) respectively and expressed in mmol/L (mean +/- SE). The results were statistically not different from those of healthy controls. In contrast, non-diabetic kidney transplant recipients cholesterol, non-HDL cholesterol and triglyceride levels were increased to 6.1 (+/- 0.81) (p < 0.05), 4.6 (+/- 1.1) (p < 0.05) and 2.34 (+/- 1.53) mmol/L (p < 0.05). HDL cholesterol averaged 2.08 (+/- 0.36) in pancreas-kidney transplant recipients, clearly higher than that of kidney transplant recipients 1.53 (+/- 0.39) mmol/L (p > 0.01), or of controls 1.61 (+/- 0.37) mmol/L (p < 0.05). In pancreas-kidney transplant recipients postprandial lipaemia was the lowest and lipase activity was the highest compared both to kidney transplant recipients (p < 0.001, p < 0.05) and controls (p < 0.01, p < 0.05). This excellent triglyceride clearing capacity appears to be the result of a high activity of lipoprotein lipase, which, can be explained by the peripheral hyperinsulinaemia.

Endopeptidases↗
PubMed1995

[Molecular genetic markers of Alzheimer dementia].

Alzheimer's dementia (AD) is a progressive neurodegenerative disease which is one of the most common forms of dementia in the above 65 years old age group. Diagnosis is based upon evaluation of cognitive skills, elimination of other dementia associated diseases and on cranial CT examination. However, definitive diagnosis is proved only by neurohistological findings. The etiology of the disease is unknown and effective treatment is not available. Intensive research into the pathomechanism of the disease revealed a connection between increased frequency of apolipoprotein E4 allele and later onset of AD. The aim of the author's research was to characterize apolipoprotein E polymorphisms in AD patients and to examine immunological factors which could play an important role in the development of the disease such as the polymorphism of complement and lipoprotein(a) [Lp(a)] alleles previously had not been investigated. 35 AD patients (26 female, 9 male) were examined (mean age 66.4 years +/- 8.7 SD). 18 of these patients showed late onset of the disease. The E4 allele was significantly more frequent in both early and late onset groups compared to controls (0.29 vs. 0.14 and 0.33 vs 0.09). The high frequency of apo E4 found in the early onset group in this study differs from other international data. Serum lipid, lipoproteins, Lp(a) concentrations and Lp(a) phenotype distribution showed no significant difference compared to controls. Furthermore, it was found that the frequency of complement C4AQ0 (null) and Bf F alleles was higher in the late onset AD group compared to controls (0.35 vs 0.139 and 0.305 vs. 0.225) suggesting an active involvement of the complement system in the pathogenesis of this disease.

Age Factors↗
PubMed1995

High lipoprotein(a) levels with predominance of high molecular weight apo(a) isoforms in patients with pulmonary embolism.

Lipoprotein(a) (Lp(a)) may interact with the cellular components and protein co-factors of fibrinolysis. To evaluate the effect of Lp(a) in thromboembolic diseases of the venous system, we measured serum levels and the isoform distribution of apo(a) in 25 patients with pulmonary embolism (18 men, 7 women, aged 21-77 years). The control group was adjusted for sex and age (P = 0.189). Serum Lp(a) concentration was significantly higher in the study group (median: 9.3 vs. 4.3 mg dL-1). As the distribution of high and low molecular weight subtypes of apo(a) did not show any differences (P = 0.127) between the two groups, the elevated Lp(a) levels in patients with pulmonary embolism could not be attributed to the investigated kringle-4 polymorphism of the apo(a) gene and therefore other genetic or non-genetic implications are indicated.

Adult↗
PubMed1995

Microangiopathy in primary hyperlipoproteinemia.

The microvascular basement membrane thickness were investigated by electron microscope within skeletal muscle of 17 untreated patients with primary hyperlipoproteinemia. The average of minimal basement membrane thickness of hyperlipidemic patients were significantly different (p < 0.001) from that of the controls (127 +/- 44.6 nm vs 39.9 +/- 12.4 nm). In conclusion, hyperlipoproteinemia without diabetes mellitus might contribute to the damage of the capillary vessel wall.

Adult↗
PubMed1994

[Effect of lovastatin on serum lipids and lipoproteins. Hungarian multicenter, open-label study].

The authors studied the effects of lovastatin on the parameters of serum and lipoprotein lipids in an open multicenter trial. 160 patients with hypercholesterolemia participated in the study, 151 of whom completed the trial. After a 4 week period of dietary measures, the patients were treated with lovastatin for 12 weeks while combining standard lipid lowering diet. The initial dose of the drug was 20 mg, this was increased until serum cholesterol level decreased under 5.2 mmol/l, or to a maximal daily dose of 80 mg. By the end of the 12th week, serum cholesterol level was reduced by an average of 33% (p < 0.001), LDL-cholesterol by an average of 45% (p < 0.001), serum triglyceride concentration by an average of 22% (p < 0.001) and HDL-cholesterol increased by an average of 13% (p < 0.001). Lovastatin showed a very good safety profile, therapy had to be cancelled due to the occurrence of adverse events only in 4 cases.

Adult↗
PubMed1993

Plasma lipoprotein (a) concentration and phenotypes in diabetes mellitus.

Patients with Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes mellitus are at increased risk of developing atherosclerotic vascular diseases. A variety of lipoprotein abnormalities have been described as being associated with this increased risk. In this study, apo(a) isoform frequencies and lipoprotein(a) [Lp(a)] concentrations were determined in Type 1 and Type 2 diabetic patients in order to investigate a possible contribution of Lp(a) to the increased risk for atherosclerosis in diabetes. No significant differences in plasma Lp(a) concentrations were found in two ethnically different populations (Austrians from the province of Tyrol and Hungarians from Budapest) in either type of diabetes when compared to respective control groups (91 Type 1 and 112 Type 2 diabetic patients vs 202 control subjects in the Hungarian study and 44 Type 1 diabetic and 44 Type 2 diabetic vs 125 control subjects in the Austrian study). There were also no significant apo(a) isoform frequency differences between both patient groups and control subjects in the two study groups. These data, obtained from two large ethnically different populations, provide no evidence of a contribution of Lp(a) to the increased risk for atherosclerosis in diabetes.

Adult↗
PubMed1992

[The effect of low density lipoprotein (LDL) on NO formation and on arginase activity in mouse peritoneal macrophages].

A large body of the evidence is available to the causative relationship between the elevated blood plasma concentrations of LDL and the atherogenesis. The oxid-LDL (modified LDL) is internalized more rapidly by the macrophages, and there is now substantial evidence that the modified LDL is actually present in atherosclerotic lesions. Recently it has been proved that the endothel cells and monocyta/macrophages generate nitric oxide (NO) from arginine, and that the LDL inhibits the formation of NO in endothel cells. The authors found that the human LDL in vitro exerts an inhibitory effect on the formation of NO in murine PED (peritoneal exudate cells) and synchronously severalfold increasing of the arginase activity in the culture media. Both effects of LDL proved to be dose dependent and the oxid-LDL has been found to be more effective. The increased activity of arginase provides a very likely explanation for the reducing of NO production in macrophage treated by LDL. The reducing or blocking of NO-formation causes a local vasocontraction which induces clinical symptoms.

Animals↗
PubMed1992

[Relationship between platelet hyperactivation and dyslipoproteinemia in diabetic nephropathy].

The relationship between the secundaer hyperlipidaemia and pathological platelet activation was examined in 40 insulin-treated diabetic patients without nephropathy and 21 with nephropathy. Diabetic nephropathy was recorded with the measurements of serum creatinine, serum beta 2-microglobulin, and urine albumin excretion. Haemostasis and lipoprotein metabolism were characterized with determination of platelet aggregation, plasma beta thromboglobulin, thromboxane-B2, serum triglyceride, HDL and LDL cholesterol concentration, respectively. In the normalbuminuric group serum triglyceride and thromboxane-B2 positively correlated. In the nephropathic group serum cholesterol and beta thromboglobulin, as well as LDL and beta thromboglobulin, finally, LDL and thromboxane-B2 showed significant positive correlation. In diabetic patients without nephropathy platelet aggregate ratio was in positive correlation with the serum triglyceride, while the ED50-S elevated with the increase of serum cholesterol and LDL. The nephropathic group exhibited no such parallelisms. However, there were significant correlations of LDL with serum creatinine in both groups of diabetic patients. Our results seem to indicate that the increase of LDL could be associated with the change of LDL structure. Interactions of modified LDL and the platelet membrane might contribute to the platelet hyperactivation both in the nephropathy-free and nephropathic cases.

Diabetes Mellitus, Type 1↗
PubMed1992

[The role of endogenous free radicals of nitric oxide (NO)].

The role of endothelium in vasodilatation has only emerged in the last ten years. It was observed that many endogenous substances from endothelial cells triggered the release of a substance which was named endothelium-derived relaxing factor (EDRF). Later has been showed that NO accounted for most if not all of the biological activity of EDRF. The endothelial synthesis of NO originates from L-arginine and could be blocked by the methyl analogue (e.g. NG-mono-methyl-L-arginine). Beside endothelial cells NO could be identified in several mammalian tissues including brain, hepatocytes, lung and macrophages. NO mediated the control of vascular tone and blood pressure via vascular smooth muscle cells which exert relaxation and constriction of blood vessels. It is considered NO represents signal for the guanylate cyclase system which regulates the intracellular concentration of Ca2+ ions. It is well known that the concentration of Ca2+ ions play discern direct role in the relaxation and contraction of smooth muscle, respectively.

Endothelium↗
PubMed1992

Platelet function in male diabetics with and without macrovascular complications.

Changes of platelet aggregation in relation to macroangiopathy and to some of its risk factors were observed in microangiopathy-free, well-controlled type 1 diabetic males. Platelet aggregate ratio was generally lower in patients (n = 77) than in age-matched healthy subjects (n = 48). In the absence of cigarette smoking, hypertension, obesity and hypercholesterolemia (n = 25) in vitro platelet hyperaggregation was found induced with epinephrine, collagen or arachidonic acid, and to a lesser degree with ADP. There was no change in the presence of at least one risk factor in addition to diabetes (n = 29), but there was a further significant increase in platelet aggregation when overt coronary, cerebral or peripheral artery disease was present (n = 23).

Adenosine Diphosphate↗
PubMed1992

The effect of azathioprine, cyclosporine A and insulin on the in vitro lymphocyte-mediated cytotoxicity in type I diabetic patients.

Previously both specific and nonspecific immune reactions have been reported in patients with type I diabetes mellitus. In this study the effect of various immunosuppressive drugs and insulin was studied on in vitro lymphocyte-mediated cytotoxicity in 20 type I diabetic patients. Twenty sex- and age-matched healthy subjects served as controls. Human pancreas-extract (300 micrograms/ml protein)-coated, 51-Chromium labeled chicken erythrocytes were used as target cells and separated T-lymphocytes as effector cells with and without azathioprine 50 micrograms/50 microliters (Wellcome), Cyclosporine A 5 ng/50 microliters (Sandoz) and MC Actrapid insulin 0.1 IU/50 microliters (Novo). The degree of cytotoxicity was expressed with cytotoxic capacity: the number of maximal killed target cells. Simultaneously islet cell antibodies (ICA) in sera and the number of activated T-lymphocytes were assessed. Significant lymphocyte-mediated cytotoxicity was observed in the majority of type I diabetic patients (18/20), while no cytotoxicity was found in the control cases. The cytotoxicity decreased in all 16 patients using azathioprine or insulin, independently of ICA and HLA-DR positivity. The number of killed target cells was lowered considerably by Cyclosporine A in all 18 patients having cytotoxicity against pancreas-extract. Our observations reveal that Cyclosporine A proved to be the most effective immunosuppressive agent in vitro. It decreases not only the leucocyte migration inhibition as previously observed, but also the lymphocyte-mediated cytotoxicity, which represents the late stage of cellular immune reactions against pancreatic tissue.

Adolescent↗
PubMed1992

Elevated levels of plasma and urine beta-thromboglobulin or thromboxane-B2 as markers of real platelet hyperactivation in diabetic nephropathy.

Serum creatinine, immunoreactive serum and urine beta 2-microglobulin, plasma and urine thromboglobulin, plasma thromboxane-B2 levels and daily protein excretion were determined in 61 insulin-treated diabetic patients, comparing the different patient groups (complication free, nephropathy without and with azotaemia) with control subjects. In the groups of diabetic patients, plasma and urine beta-thromboglobulin (BTG) and plasma thromboxane-B2 levels were higher than in the controls. There was a significant positive correlation between urine BTG and beta 2-microglobulin in the group without complication, and between the plasma BTG and beta 2-microglobulin, and plasma BTG and thromboxane levels in the diabetic group with azotaemia. In contrast to some previous assumptions, the increased level of plasma BTG reflects a real platelet hyperactivation in patients with diabetic nephropathy. At the same time, urine BTG also increases. Determination of urine BTG is more simple with less possibility of methodological error.

Adult↗