PubMed Health⌕ Search

Biomedical subjects

H Heine

Publications and source records attributed to H Heine.

At least 19 recordsLinked to original sources
PubMed1992

Modulation of endotoxin-induced monokine release in human monocytes by lipid A partial structures that inhibit binding of 125I-lipopolysaccharide.

We have previously shown that the synthetic tetraacyl precursor Ia (compound 406, LA-14-PP, or lipid IVa) was not able to induce the production of tumor necrosis factor, interleukin-1, and interleukin-6 in human monocytes but strongly antagonized lipopolysaccharide (LPS)-induced formation of these monokines. This inhibition was detectable at the level of mRNA production. To achieve a better understanding of molecular basis of this inhibition, we investigated whether lipid A precursor Ia (LA-14-PP), Escherichia coli-type lipid A (LA-15-PP), Chromobacterium violaceum-type lipid A (LA-22-PP), and synthetic lipid A partial structures and analogs (LA-23-PP, LA-24-PP, and PE-4) were able to influence the binding of 125I-LPS to human monocytes and compared this inhibitory activity with the agonistic and antagonistic action in the induction of monokines in human monocytes. 125I-LPS (20 ng per well) was added to human monocytes in the presence or absence of unlabeled rough Re mutant-derived LPS (Re-LPS) or lipid A compounds, and specific LPS binding was determined after 7 h. This binding was found to be dependent on CD14 as shown by the use of an anti-CD14 monoclonal antibody. Compound LA-14-PP was found to inhibit the binding of 125I-LPS to the cells in a similar dose-response to that of unlabeled LPS. This shows that the inhibitory capacity on LPS binding does not correlate with the monokine-inducing capacity because Re-LPS is active in inducing tumor necrosis factor, interleukin-1, and interleukin-6, while LA-14-PP is not. The strong capacity of LA-14-PP to inhibit 125I-LPS binding, however, correlates with the strong inhibitory capacity of this compound on LPS-induced monokine production. Compounds LA-15-PP, LA-23-PP, and LA-24-PP were active in the inhibition of 125I-LPS binding but were 5- to 10-fold weaker than Re-LPS and LA-14-PP. Of all lipid A structures tested, compound LA-22-PP expressed the weakest inhibitory capacity on LPS binding. These compounds showed again that the activity of binding inhibition does not correlate with the monokine-inducing capacity. We assume that the inhibitory effects of lipid A partial structures on LPS-induced monokine production have their origin in a competitive inhibition between LPS and the lipid A partial structures for the same binding site on the cell membrane.

Antigens, CD↗
PubMed1992

Biological activity of synthetic phosphonooxyethyl analogs of lipid A and lipid A partial structures.

We investigated the biological activity of four new synthetic analogs of lipid A, termed PE-1, PE-2, PE-3, and PE-4. All compounds contain an alpha-oxyethyl-linked (-O-CH2-CH2-) phosphoryl group in position 1 of the reducing glucosaminyl residue (GlcN I) of lipid A. PE-1 is a hexaacylated analog of Escherichia coli lipid A (compound 506). PE-2 differs from PE-1 in carrying two myristic acid residues at GlcN I. PE-3 has the same acylation pattern as PE-2, but GlcN I is present in the beta anomeric form. Finally, PE-4 represents an analog of tetraacyl precursor Ia (compound 406). Structure-activity relationships of these compounds were determined by measuring their capacity to induce tumor necrosis factor alpha, interleukin 1, and interleukin 6 release by human mononuclear cells and to cause mitogenicity of murine spleen cells. The results show that replacement of the glycosidic phosphoryl residue by a phosphonooxyethyl group had no substantial effect on the biological activity of compounds. However, the anomeric configuration of GlcN I was found to be of great biological relevance, as, in general, the alpha anomer (PE-2) expressed high activity, and the beta anomer (PE-3) expressed low mediator-inducing and mitogenic activity. The absence of the 3-hydroxyl groups within the acyl residues at GlcN I in PE-2 was found to only slightly affect the induction of monokines in human mononuclear cells compared with that of PE-1 or lipid A (506). These stable 1-phosphonooxyethyl analogs of lipid A may be candidates in the development of immunomodulators for the treatment of systemic endotoxicosis.

Animals↗
PubMed1990

[15N tracer technical studies of protein metabolism in arteriosclerosis patients].

The incorporation of the stable isotope 15N in plasma proteins and blood cells after oral application of 3 g 15NH4Cl (95 At% 15N) per 70 kg body weight was followed up in 11 patients with ischemic heart disease or peripheral arteriosclerosis and in 7 healthy control subjects. Preliminary results indicate that the turnover of plasma protein, especially fibrin, is elevated in patients with arteriosclerosis. Investigations of platelets intimate a decreased turnover of platelet protein in patients with arteriosclerosis as compared to control subjects. Possible reasons for these alterations are discussed.

Arteriosclerosis↗
PubMed1990

[Assessment of prognosis in acute myocardial infarct after reaching the maximum enzyme activity].

A new method is described for estimation of the prognosis of acute myocardial infarction progress due to temporary decrease in the isoenzymes, i.e. malic dehydrogenase (MDH), aspartate aminotransferase (ASAT), lactic dehydrogenase (LDH), and the decrease in the creatine kinase (CK). It is shown that the time of enzymatic activity is an essential factor. If 120 hours of decrease in enzymatic activity of MDH, LDH, and CK are exceeded, the prognosis of the myocardial infarction deteriorates dramatically.

Aged↗
PubMed1990

Extreme decrease of linoleic acid in renal medulla from rats after a diet supplemented with cod liver oil.

Spontaneously hypertensive (SHR) and normotensive rats were fed a diet supplemented with linseed oil or cod liver oil for 22 weeks. The most remarkable finding was an extreme fall of linoleic acid in lipids from renal medulla after cod liver oil supplementation. In free fatty acids (FFA) eicosatrienoic acid (C2): 3n-9) appeared increased as a sign of essential fatty acid (EFA) deficiency.

Animals↗
PubMed1990

Combined Doppler and M-mode analysis of diastolic filling behaviour in arterial hypertension with and without left ventricular hypertrophy.

The authors analysed Doppler and M-mode derived diastolic parameters of left ventricular filling in patients with arterial hypertension with and without left ventricular hypertrophy (LVH) and with hypertrophic nonobstructive cardiomyopathy (HNCM). In hypertrophied hearts they demonstrated that the transmitral flow during rapid filling phase was significantly reduced. The lower early diastolic flow is compensated by an augmentation of atrial systole. Diastolic filling anomalies are the consequence of an impaired ventricular relaxation due to LVH as could been proved by the M-mode derived retraction constant Te. Diastolic filling anomalies significantly depend on the extent of left ventricular hypertrophy. Impaired diastolic function was found in hypertensive patients without LVH. In this case, diastolic disorders indicate an early involvement of the heart in the hypertensive process.

Adult↗
PubMed1990

[Prognosis assessment of acute myocardial infarction on the basis of temporal changes of isoenzyme activities].

A new method is described for determining the prognosis of acute myocardial infarction (AMI) progress due to temporal increase in the isoenzyme, i.e. malic dehydrogenase (MDH), aspartate aminotransferase (ASAT), lactic dehydrogenase (LDH), and the increase in the creatine kinase (CK). It is shown that the time of enzymatic activity is an essential factor. If 25 hours of increase in enzymatic activity of MDH and CK are exceeded, AMI deteriorates dramatically.

Adult↗
PubMed1989

[Anticoagulants and inhibitors of thrombocyte function in the long-term treatment of arteriosclerosis].

Oral anticoagulants are suitable for the delay of progression of arteriosclerosis. The therapeutic effect is bound to the stability of the hypocoagulation with values of the thromboplastin time between 15 to 20%. There is a high risk of thrombosis after discontinuation of the therapy. Of the inhibitors of thrombocyte function acetyl salicylic acid preparations are antithrombotically effective. The controversies of dosage high (= 1,500 mg/d) or low (= 20-30 mg/d) are opposed by the concept of the individual dosage via the ASA-test.

Adult↗
PubMed1989

[Immunomodulation by leukocytolysis. On the significance of lectin-polysaccharide complexes].

Polymorphonuclear granulocytes (PMNs) are thought to function only as phagocytes. The ability of PMNs for a physiologically lysis has not been noticed so far. Therefore, PMNs are not only a clamp between the specific and unspecific immune system but an important regulator of the homoeostasis. All immune modifiers therapeutically used seem to stimulate the physiologically lysis of PMNs. This has been shown with mistletoe lectins. Most remarkable are findings that show lectins bound to polysaccharides drastically rise the ability of PMNs to undergo lysis.

Adenocarcinoma, Scirrhous↗
PubMed1989

Individually controlled aspirin in the long-term treatment of patients with chronic arterial diseases.

A simple method of measuring the biological effect of acetylsalicylic acid (ASA), based on the determination of the disaggregation rate (DR) of platelet aggregation induced by adenosine diphosphate (ADP), is described. The DR was found to correlate with the inhibition of the production of malondialdehyde (MDA) by platelets (r = 0.66, P less than 0.001). Therefore, the DR was used for laboratory monitoring of the ASA effect. The study included 63 arteriosclerotic patients--patients with ischemic heart disease (IHD), peripheral arterial disease (PAD), or cerebrovascular insufficiency (CVI) -- who were analyzed before treatment and after receiving ASA in an individually controlled dosage. Before treatment the authors found an increased level of MDA and a longer euglobulin clot lysis time in patients when compared with healthy volunteers (n = 16). Extremely different doses of ASA were required to normalize initially elevated MDA levels in patients. Normalization of the MDA level corresponds to a DR of at least 50% (in comparison with 0-13% without treatment). When judging the ASA dose individually from the 50% DR, the authors demonstrated that there were no differences in the levels of cyclooxygenase- and lipoxygenase-derived eicosanoids between healthy volunteers (n = 16) and arteriosclerotic patients receiving 100-250 mg (n = 18), 500 mg (n = 17), or 750-1500 mg ASA per day (n = 6). Thus, their results support the idea of using individually controlled ASA as the most promising way of resolving the "aspirin dilemma" and provide a simple and reproducible method of measuring the biological effect of ASA.

Adenosine Diphosphate↗
PubMed1989

[Influencing the fibrinolytic activity by antithrombotics in patients with atherosclerosis].

In 106 atherosclerotic patients receiving an anticoagulant therapy and 91 patients receiving acetylsalicylic acid, fibrinogen and fibrin degradation products were determined as well as euglobulin lysis before and after venous occlusion. Platelet function data and thromboxane (TXB2) were also determined. Since "moderate" anticoagulant therapy with thromboplastin time values 26-40% results in deteriorated fibrinolysis data, anticoagulant therapy is strictly to remain within the therapeutic range of 15-20% up to 25% thromboplastin time at maximum. Treatment with acetylsalicylic acid proved useful on condition that the required dose was determined individually. This type of treatment will then be able to reduce the thromboxane level and positively influence the fibrinolytic potential.

Anticoagulants↗
PubMed1989

[Functional morphology of pulp tissue].

As compared with mesenchyme no genuine defense cells are developed in the tissue of the dental pulp and the nervous tissue. This is a further hint for the common development from ectoderm. The three dimensional meshwork of pulpa fibroblasts ("mesectoderm") is structured by elongated cell processes connected with each other by a variety of special cell junctions ("electronic cell coupling"). Metabolites from the microcirculation and neuropeptides from vegetative axons influence the activity of fibroblasts synthetizing groundsubstance. The meshwork of the groundsubstance has exclusion effects concerning molecules with a distinct molecular weight and charge. Thus a primitive defense system is established. With this the role of a newly described cell type of the dental pulp, the "lymphocytic pericyte" is discussed. Because of the poor capacity of the pulpa tissue for immunological reactions pathologically disorders may easily become chronically spreading their antigenic components throughout the body.

Adult↗
PubMed1989

[Is there a structural principle of the myocardium?].

Up to now neither by macroscopical nor histological findings a structural principle of the myocardium could be found. The tremendous complexity in the various courses of myocardium fibres and connective tissue as well as the pump diagram of the heart as a functional reference of all heart actions point to aspects of the heart function as a determined chaos. This could be demonstrated by a simple structural principle of the myocardium namely the myocardium fibres and connective tissue strands are arranged in the form of intermeshed hyperboloids. These could be of interest in the construction of artificial hearts. These new insights in form and function of the myocardium allow to discuss in a new way normal and pathological functions of the heart and to develop new therapeutical approaches.

Animals↗
PubMed1987

Life stress and hypertension.

Based on psycho-physiological, clinical and epidemiological studies, essential arterial hypertension is considered to be a consequence of an inadequate 'person-environment fit', objectively, subjectively or both. Besides genetic predisposition, salt intake, obesity and physical inactivity, psychological factors--among them 'hyper-reactivity' of the sympathetic nervous system, predisposing behaviour patterns and stressful life-events--should be taken into account in reaching a better understanding of the causes, prediction and prevention of hypertension. It was demonstrated that a maladaptation in various functional systems, even to minor psycho-emotional stress, is an important pathogenetic link between environment, objectively defined stressors and blood pressure regulation from the earliest phases of the disease. Implications for further research and behavioural interventions, together with other lifestyle-related factors, are discussed for improving the population-based health care in cardiovascular disease in the G.D.R.

Adolescent↗
PubMed1986

Different changes of n-6 and n-3 fatty acids in adipose tissue from spontaneously hypertensive (SHR) and normotensive rats after diets supplemented with linolenic or eicosapentaenoic acids.

In spontaneously hypertensive (SHR) and normotensive rats of the Wistar-Kyoto (WKY) and Wistar-Schönwalde (WSCHOE) strain, diets supplemented with n-3 fatty acids of different chain length (alpha-linolenic acid, LNA--C 18:3, n-3 with linseed oil and eicosapentaenoic acid, EPA--C 20:5, n-3 with cod liver oil) were fed over a period of 22 weeks. After the LNA-rich diet, among the long-chain n-3 fatty acids EPA in epididymal adipose tissue remained unchanged, whereas docosapentaenoic (DPA) and docosahexaenoic acids (DHA) fell. The n-6 fatty acids linoleic (LA) and arachidonic acid (AA) both appeared decreased. After the EPA-rich diet, all n-3 fatty acids, i.e. not only EPA, DPA and DHA, but also LNA were augmented when compared with controls fed commercially available pellets. Among the n-6 fatty acids LA was extremely depressed, whereas AA appeared increased. The p/s-ratio was elevated after the LNA-rich diet, but decreased after the EPA-rich diet. The data indicate a differential effect of dietary n-3 fatty acids of different chain length on the supply of other n-3 fatty acids, of LA and AA as well as on the p/s-ratio in adipose tissue of rats. Blood pressure was not influenced by either diet in either SHR or in both normotensive strains of rats.

Adipose Tissue↗