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Biomedical subjects

Z Reiner

Publications and source records attributed to Z Reiner.

At least 37 records · Page 2Linked to original sources
PubMed1983

Effect of l-dopa on growth hormone, glucose, insulin, and cortisol response in obese subjects.

Plasma growth hormone, glucose, insulin and cortisol response to oral administration of L-dopa and in insulin-tolerance test were investigated in 18 obese subjects. The results were compared with the results obtained in 10 normal subjects. The obese subjects displayed a lack of growth hormone responsiveness to L-dopa and a diminished GH responsiveness to hypoglycemia. There was no significant difference in glucose response to hypoglycemia in normal and obese subjects. Obese subjects showed normal increments of plasma cortisol following induction of hypoglycemia although there was no consistent cortisol response after L-dopa administration. A blood glucose response following L-dopa administration was seen in most of normal subjects while no increment of blood glucose was noticed in obese subjects.

Adult↗
PubMed1982

[Electrocardiographic changes in chronic obstructive lung diseases].

Various patterns and frequency of electrocardiographic changes in patients with chronic obstructive lung disease (COLD), as well as their relationship to the degrees of air-flow obstruction, were investigated. Electrocardiograms and pulmonary function tests were analysed in 302 patients (230 men and 72 women) with COLD, and the results were compared with the results of the same examinations obtained in 86 healthy subjects (63 men and 23 women). The most common electrocardiographic patterns were: a) "P pulmonale", b) right axis' deviation of the P wave, and right axis' deviation of the QRS complex, c) inversion of the T waves in standard (II and III) and in the precordial leads (V1 to V4), d) the presence of a qR pattern with delayed R wave in V1 (V5R) (onset of intrinsicoid deflection more than 0,003 seconds) which was often associated with an incomplete right bundle branch block.--P pulmonale and inversion of the T waves in standard and precordial leads were considered as labile, reversible electrocardiographic changes which do not show any correlation with the severity of COLD. Deviations of the P wave and QRS complex to the right, significantly correlated with the degree of the air-flow obstruction (P less than 0,05) in patients with COLD, but the changes are not sure signs of chronic cor pulmonale. On the contrary, qR pattern with delayed R wave in V1 (V5R) (onset of intrinsicoid deflection more than 0,03 seconds), which was often associated with an incomplete right bundle branch block, was significantly correlated (P less than 0,001) with the degree of air-flow obstruction in patients with COLD and may be considered as highly suggestive for the diagnosis of chronic cor pulmonale.

Bundle-Branch Block↗
PubMed1979

Triglyceride-poor very low density lipoprotein in human serum.

The chemical and physical properties of very low density lipoproteins, isolated from the pool of the sera of 60 persons with high pre-beta and normal triglyceride and cholesterol concentrations, have been studied. These very low density lipoproteins, a designated as triglyceride-poor very low density lipoproteins, consist of 20.5% phospholipids, 30.8% free cholesterol, 15% cholesterol esters and 33.7% triglycerides. Their protein content consists of 54.5% apo B, 26% apo A, 11.5% apo E and only 8% apo C, so they differ from any serum lipoprotein described until now. Triglyceride-poor very low density lipoproteins consist of spherical particles 300-450 A in diameter as revealed by electron microscopy.

Cholesterol↗
PubMedDate not supplied

Influence of renal functional mass on the catabolism of endogenous gastrin in humans.

The influences of renal function and mass on the catabolism of serum gastrin were studied in 27 patients with hypertension caused by unilateral parenchymal renal disease (77.8%), renal artery stenosis (11.1%) and essential hypertension (11.1%). Blood for gastrin analysis was taken by catheterization from the aorta, inferior vena cava, renal veins and cubital vein. Separate renal functions were measured using radioisotope methods and the renal mass was also calculated. Significant differences (p < 0.001) in serum gastrin concentration between the aorta (29.5 +/- 6.7 pmol/l), inferior vena cava (23.4 +/- 5.8 pmol/l) and cubital vein (19.4 +/- 4.5 pmol/l) were found. Extrarenal gastrin extraction amounted to 12.5% and was considerably lower than renal gastrin extraction (20.5%). There was a significant positive correlation between renal gastrin extraction and renal blood flow or renal functional mass. Kidneys have an important, but not exclusive, role in the catabolism of endogenous gastrin in humans. In the catabolism of some, or at least some molecular forms of, gastrin, the capillary systems of extrarenal tissues have an important role.

Adult↗
PubMedDate not supplied

Changes in serum lipid and lipoprotein levels in postmenopausal patients with node-positive breast cancer treated with tamoxifen.

Tamoxifen has been used for a long time as an adjuvant hormonal treatment in breast cancer patients. We studied 62 newly diagnosed postmenopausal women, aged 50-79 years, with node-positive breast cancer and receiving adjuvant tamoxifen (20 mg per day). Total serum cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, VLDL-cholesterol, apo AI, apo AII, apo B and Lp(a) were determined before the surgery and 3, 6, 9, 12 and 24 months after starting tamoxifen treatment. Tamoxifen significantly reduced total serum cholesterol (6.13+/-1.20 mmol/L vs 5.21+/-1.05 mmol/L) (P <0.01), LDL-cholesterol (3.72+/-0.70 mmol/L vs 2.93+/-0.51) (P <0.01) and Lp(a) (0.11+/-0.07 g/L vs 0.02+/-0.01 g/L) (P < 0.01). There were no changes in triglycerides or HDL-cholesterol serum levels during tamoxifen treatment. The results indicate that an additional beneficial effect of adjuvant tamoxifen therapy may be that it decreases cardiovascular risk in such patients.

Aged↗
PubMedDate not supplied

[Presence of Chlamydia pneumoniae antibodies in patients with ischemic heart disease and acute myocardial infarct].

Numerous seroepidemiological studies that suggest an association of C. pneumoniae infection and atherosclerosis have been published in last decade. The aim of this study was to assess a prevalence of C. pneumoniae antibodies in population of Zagreb area, and to investigate possible differences in prevalence of antibodies in patients with atherosclerosis and healthy controls. Forty-seven patients with coronary artery disease or myocardial infarction and 54 controls without any previous history of atherosclerosis were enrolled in the study. Sera were examined by microimmunofluorescence test. Persons with IgA antibody titers > or = 1:32, and/or IgG antibody titers > or = 1:64 were considered as seropositive. We found 75% seropositive in a total number of subjects, although number of seropositive and higher titers of antibodies were found more often in patients with atherosclerosis compared to control group: 74.5% of IgA seropositive patients versus 33.3% seropositive in control group, and 89.4% of IgG seropositive patients compared to 63% seropositive controls. Chronic (persistent) infections with C. pneumoniae were noted in 74.5% of patients and 33.3% controls.

Adult↗
PubMedDate not supplied

[New information on the pathophysiology of atherosclerosis].

The past decade has witnessed enormous progress in our understanding of the nature of this process. The development of an atherosclerotic plaque is a complex process which begins with endothelial dysfunction, the trigger for which are factors such as hypercholesterolemia, smoking, hypertension, hyperhomocysteinemia and impaired glucose metabolism. This dysfunction includes increased endothelial permeability to lipoproteins and other plasma constituents, which is mediated by NO, PDGF, prostacyclin, angiotensin II and endothelin; up-regulation of endothelial adhesion molecules including VCAM-1, ICAM-1, and selectins and migration of leukocytes and monocytes-macrophages in the subendothelial space mediated by oxidized LDL, MCP-1, PDGF and MCSF. The next step includes smooth-muscle cells migration (stimulated by PDGF and TGF-beta), T-cell activation (mediated by TNF-alpha and IL-2), formation of foam-cells from macrophages (mediated by oxidized LDL, MCSF, TNF-alpha and IL-1) and platelet adherence and aggregation (stimulated by thromboxane A2, tissue factor etc). The smooth muscle cells form a fibrous cap which confers mechanical stability of the plaque and separates the lipid rich thrombogenic core from the lumen and circulating blood. Whether a plaque will remain intact and therefore stable or rupture and lead to thrombosis causing an acute coronary syndrome (MI, unstable angina pectoris) depends upon a number of factors, the most important of which is its composition. Plaque size plays only a minor role in determining risk of an acute coronary syndrome. Rupture of the fibrous cap occurs due to thinning of the cap caused by an influx and activation of macrophages which release metalloproteinases and other proteolytic enzymes (stimulated by inflammatory cells, particularly T-lymphocytes). These enzymes cause degradation of the fibrous tissue of the cap which can result in thrombous formation and occlusion of the artery. Stable plaques have a thick fibrous cap, a small lipid core, and few inflammatory cells. In contrast, vulnerable plaques have a high lipid content, numerous inflammatory cells, and a thin fibrous cap with reduced collagen and vascular smooth muscle cells in it. Although vulnerable plaques are believed to account for only a small number of all coronary atheromas, they are responsible for most acute coronary events.

Arteriosclerosis↗
PubMedDate not supplied

[Estrogens and risks for onset of atherosclerosis].

There are many evidences suggesting that estrogens prevent atherosclerosis and its consequences such as coronary heart disease (CHD) in women. The risk for CHD is less in premenopausal women when compared with age-matched men, but the protective effect of estrogens is lost with menopause. A part of this beneficial effect may be ascribed to the ability of estrogens to favorably alter the plasma lipoproteins profile, i.e. increase HDL and decrease LDL and Lp(a). However, the changes in the lipid profile do not fully account for the protective effect afforded by estrogens, indicating that other mechanisms are likely to be involved. One of these mechanisms may include estrogens ability to prevent oxidative modification of LDL. A number of animal and human studies strongly suggest also a direct effect on the vascular endothelium, decreasing the expression of adhesion molecules involved in monocyte adhesion such as VCAM-1. It seems that estrogens also cause by increasing the synthesis of NO a decrease in chemokines involved in monocyte migration into the subendothelial space (TNF alpha, IL-1 and MCP-1) and growth factors influencing the migration of smooth muscle cells (PDGF). They also decrease fibrinogen and homocysteine, and these substances when increased are considered independent risk factors for CHD. However, the results of the first randomised controlled trial of hormone replacement therapy (HRT) with estrogens concerning the CHD published recently differ from previous observational epidemiological studies in both primary and secondary intervention, which showed beneficial effect of HRT. The final answer about the effects of HRT on CHD is expected from several ongoing trials.

Animals↗
PubMedDate not supplied

[Pathophysiology of atherosclerosis. I. The morphology and developmental levels of atherosclerotic changes].

The authors present an up-to-date review on natural history of atherosclerosis. After a short introduction dealing with history of atherosclerosis research, data about morphology and pathology of the normal arterial wall are presented. Special attention is focused on structural differences of arteries in different body districts as well as vascular endothelium and smooth muscle cells and their role in atherogenesis. Pathogenetic mechanisms in the evolution of lesions and morphology of different types of atherosclerotic lesions based on cellular and metabolic changes are explained in details: early lesions such as gelatinous elevations-insudative lesions, fetty dots and streaks and microthrombi; advanced lesions such as fibromusculoelastic lesions, pearly-white fibrous atherosclerotic plaques and atheromatous plaques; and complicated lesions with calcifications, ulcerations, thrombosis and hemorrhage.

Arteriosclerosis↗
PubMedDate not supplied

[Pathophysiology of atherosclerosis. II. Etiopathogenic mechanisms and risk factors].

The authors present an up-to-date review on etiopathogenesis of atherosclerosis. Theories of etiology of atherosclerosis are described: response-to-injury hypothesis, lipid deposition hypothesis, lysosome hypothesis, encrustation hypothesis, mural thrombi hypothesis, monoclonal and clonal senescence hypothesis. The role of endothelial injury and platelet adhesion as well as smooth muscle cells proliferation due to these events, their growth control and the role of macrophages in atherogenesis are explained thoroughly. Special attention is focused on the interaction of arterial cells and lipoproteins at sites of vessel injury, lipid metabolism of the lesion and on synergy of arterial injury caused by various injury mechanisms and hypercholesterolemia in atherogenesis. Atherosclerotic risk factors and their impact on atherogenesis are discussed as well (e.g. hyperlipoproteinemia, hypertension, tobacco smoking, diabetes and abnormal glucose tolerance, gout, obesity, menopause and oral contraceptives, diminished physical activity, type A of personality behavior etc.). The possibilities of regression or reversal of ateromatous plaques are presented too.

Animals↗
PubMedDate not supplied

[Lipids and cardiovascular diseases].

There are many evidences suggesting a direct relationship of hyperlipoproteinemia, particularly hypercholesterolemia, and coronary heart disease. Therefore, in this paper an up-to-date review of lipoprotein metabolism, the biochemical basis of atherogenic hyperlipoproteinemia and current concepts of etiology and pathogenesis of atherosclerosis are presented. A detailed explanation is given to what extent and why will reduction of blood cholesterol levels reduce the prevalence and severity of coronary heart disease as well as under what circumstances and at what level of blood cholesterol should dietary or drug treatment be started. Since diet is the cornerstone of therapy for hyperlipoproteinemia instructions concerning dietary treatment are given in details. If diet alone proves insufficient, drugs should be added to the regimen. A detailed review of all major forms of drug therapy is also given together with dosage and adverse effects of all hypolipidemic agents used until now.

Cardiovascular Diseases↗
PubMedDate not supplied

Endocrine responses to head and neck surgery in men.

It has been well established that surgical stress leads to profound changes in endocrine function and metabolism. However, the endocrine response varies depending upon the type and the extent of surgery. As no data were available about the endocrine changes during and following major head and neck surgery, this study was performed. Plasma levels of adrenocorticotropin (ACTH), cortisol, thyroid-stimulating hormone (TSH), thyroxin (T4), triiodothyronine (T3), growth hormone (GH), prolactin (PRL), gonadotropins (LH and FSH), oestradiol and testosterone were determined in 17 patients one day before, immediately after, as well as 2 and 4 days after head and neck surgery. An increase in ACTH, cortisol, PRL and GH, and a decrease in plasma oestradiol and testosterone values occurred immediately after surgery. There was a slow fall in cortisol levels after surgery, but they remained elevated even on the fourth postoperative day, whereas GH values returned on the fourth day to the initial level. There were no changes in gonadotropins, TSH and T3, but T4 values were found to be increased on the second and fourth postoperative day. The prolonged cortisol stimulation which was not described by other researchers after other kinds of surgery might be caused by vagal stimulation during and/or after head and neck surgery. Increased needs after a major head and neck surgery could explain the increment of T4 values.

Adrenocorticotropic Hormone↗