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Biomedical subjects

M Kellner

Publications and source records attributed to M Kellner.

At least 55 records · Page 3Linked to original sources
PubMed1994

Endocrine characterization of the new dopamine autoreceptor agonist roxindole.

Roxindole (5-Hydroxy-3-(4-phenyl-1,2,3,6-tetrahydropyridil-(1)-butyl)-indol) is a newly developed compound with a high dopamine autoreceptor agonistic potency at D2 receptors. Evaluation of roxindole for clinical purposes in psychiatric patients revealed that the substance has contrary to expectation merely negligible antipsychotic but considerable antidepressive effects. Interestingly it is nearly devoid of any side effects. To further characterize the endocrine effects, 1 mg roxindole was applied at 09:00 to 6 male volunteers and the effects compared to placebo. From 08:00 to 13:00 blood samples were drawn every 30 min. No effect on adrenocorticotropin and cortisol secretion was observed, neither mean plasma concentrations nor area values differed significantly. 90 min after roxindole administration an enhanced release of growth hormone could be observed, comparison of mean hormonal concentration revealed statistical significance (p < 0.05). Also the area values differed significantly (roxindole vs. placebo mean +/- SD 18.1 +/- 17.1 vs. 7.7 +/- 8.0 micrograms x h/l; p < 0.05). After roxindole also a pronounced reduction of prolactin plasma levels from 5.3 +/- 1.4 micrograms/l to 1.1 +/- 0.4 microgram/l within 150 min could be observed. Mean plasma concentrations (p < 0.05) and area values differed significantly (roxindole vs. placebo mean +/- SD 14.8 +/- 13.5 vs. 34.4 +/- 18.1; p < 0.05). Roxindole had no effect on blood pressure parameters and heart rate. The major findings of the present exploratory study are, that roxindole has potent effects on the facilitation of growth hormone secretion and the inhibition of prolactin release. Both findings are complementary and point also to interesting postsynaptic dopamine receptor agonistic effects.

Adrenocorticotropic Hormone↗
PubMed1993

Transfer of genetic information from the mycoparasite Parasitella parasitica to its host Absidia glauca.

The infection of the model organism Absidia glauca by P. parasitica is accompanied by the fusion of both mycelia. By two lines of evidence we were able to show that this process is associated with the transfer of genes. First, auxotrophically labelled A. glauca mutants are efficiently complemented as a consequence of transfer of the parasite's genetic material. Second, for a plasmid-coded dominant marker (neomycin resistance), which is expressed in either organism, we proved the presence of plasmid DNA in recombinant recipients by molecular analysis at the DNA level. We propose the term para-recombinants for describing recombinant inter-generic chimaerae, which are generated as a consequence of mycoparasitism.

DNA, Fungal↗
PubMed1993

Oligomycin F, a new immunosuppressive homologue of oligomycin A.

Oligomycin F, a new homologue of oligomycin A (1), was isolated from a Streptomyces species and structure 2 was deduced by NMR methods. Compound 2 is highly active against plant pathogenic fungi and is an extremely potent suppressive agent for various immunological systems.

Animals↗
PubMed1992

Atrial natriuretic factor inhibits the CRH-stimulated secretion of ACTH and cortisol in man.

Corticotrophic secretion of ACTH is stimulated by corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP), and suppressed by glucocorticoids. In vitro and preclinical studies suggest that atrial natriuretic factor (ANF) may be a peptidergic inhibitor of pituitary-adrenocortical activity. The aim of this study was to elucidate a possible role of ANF as a modulator of ACTH release in humans. A bolus injection of 100 micrograms human CRH (hCRH) during a 30 min intravenous infusion of 5 micrograms/min human alpha atrial natriuretic factor (h alpha ANF) was administered at 19:00 to six healthy male volunteers. In comparison to saline, a blunted CRH-stimulated secretion of ACTH (mean maximum plasma level +/- SD 45 min after hCRH: saline 46.2 +/- 14.2 pg/ml, h alpha ANF 34.6 +/- 13.8 pg/ml, p-value = 0.007) and a delayed rise (10 min) in cortisol were detected. The maximum plasma cortisol levels remained nearly unchanged between saline and h alpha ANF administration (mean maximum plasma level +/- SD 60 min after hCRH: saline 182 +/- 26 ng/ml, h alpha ANF 166 +/- 54 ng/ml). No effects of h alpha ANF on basal cortisol levels were observed; in contrast, basal ACTH plasma levels were slightly reduced. Basal blood pressure and heart rate remained unaffected. In the control experiment, infusion of 3 IU AVP in the same experimental paradigm increased basal and stimulated ACTH and cortisol levels significantly in comparison to saline. These observations suggest that intravenously administered haANF inhibits the CRH-stimulated release of ACTH in man.

Adrenocorticotropic Hormone↗
PubMed1991

Glycosylation of alpha 1-acid glycoprotein in relation to duration of disease in acute and chronic infection and inflammation.

Microheterogeneity of acute phase proteins frequently differs in acute and chronic types of inflammation. However, it is unknown whether these changes depend on the duration of the inflammation in a given disease. We therefore investigated the microheterogeneity of alpha 1-acid glycoprotein (AGP) in sera from patients with acute and chronic bacterial infection in comparison to rheumatoid arthritis and ankylosing spondylitis. In acute bacterial infection Con A-reactivity of AGP was significantly elevated. By contrast, AGP in chronic bacterial infection showed the same glycosylation pattern as rheumatoid arthritis and ankylosing spondylitis being characterized by a decreased reactivity to Con A. Serial measurements in individual patients with bacterial infections showed a transition from the initially elevated to decreased reactivity to Con A as the disease became chronic.

Acute Disease↗
PubMed1988

Copper storage disease of the liver and chronic dietary copper intoxication in two further German infants mimicking Indian childhood cirrhosis.

A severe copper storage disease of the liver with micronodular cirrhosis resembling Indian childhood cirrhosis (ICC) was found in two siblings of a German family leading to death in one infant at the age of 13 months. The fatal outcome correlated with severe ballooning of hepatocytes and excessive formation of Mallory bodies. The copper content of the liver was 698 micrograms per gramme wet weight (control 5 micrograms) in the living patient and 2154 micrograms per gramme dry weight (controls 39, 54 micrograms) in the dead infant. In both cases copper was stored not only in hepatocytes but also to a high degree in mesenchymal cells. Chronic contamination of drinking water supplied from a well via copper pipes could be verified as the cause of copper intoxication, lending further support to ICC as an environmental, acquired disorder. Accumulation of exogenic copper already very early in infancy appears most important for the development of the disease, as both the parents and one child not exposed to copper intoxication during the first 9 months of its life are clinically healthy.

Chemical and Drug Induced Liver Injury↗
PubMed1984

Ribosomal RNA structure in the diploid and phylogenetically polyploid amphibian species Hyla and Odontophrynus.

Ribosomal RNA of the diploid amphibian species Hyla chrysoscelis and Odontophrynus americanus is structurally modified by hidden breaks. Phylogenetically polyploid related species like the tetraploid Hyla versicolor, the tetraploid Odontophrynus americanus and the octoploid Ceratophrys ornata do not show hidden breaks in ribosomal RNA. Structural modifications of rRNA molecules in diploid amphibians has no detectable effect on the ribosomal activity in vitro.

Amphibians↗
PubMed1979

[Prostaglandin E1. Emergency therapy in infants with preductal coarctation of the aorta (author's transl)].

Three infants with preductal coartation, tubular hypoplasia of the aortic arch, and VSD were treated with Prostaglandin E1 (PGE1)-infusion to dilate the ductus arteriosus Botalli. Before PGE1-therapy the infants were treated with Furosemide and Digitalis, but they remained oliguric or anuric. During PGE1-infusion the pressure in the descending aorta rose and urine output increased significantly. Obviously the blood flow into the descending aorta via the ductus arteriosus was improved during PGE1-infusion. In all three cases surgery was successfull after PGE1-therapy. Before PGE1-therapy of preductal coarctation the diagnosis should be clear and also classical therapy with Furosemide and Digitalis should be tried.

Aortic Coarctation↗
PubMed1978

[Prostaglandin E1 therapy in infants with cyanotic congenital heart malformations: hemodynamic and angiographic findings (author's transl)].

During emergency cardiac catheterization, the mechanism of action of prostaglandin E1 (PG-E1) was studied in 7 newborn infants with cyanotic congenital heart malformations and decreased pulmonary blood flow. The main effects upon hemodynamics were an increase of pulmonary blood flow and a decrease of systemic blood flow. At the same time systemic blood pressure decreased slightly and a rise in systemic vascular resistance was calculated. An aortogram before and 15--20 minutes after the infusion of Pg-E1 was started, demonstrated a marked increase of the pulmonary blood flow and a dilation of the ductus arteriosus. Together with these hemodynamic effects the arterial and central venous oxygen saturation rose. In one infant with severe Tetralogy of Fallot, the ductus had already closed and could not be reopened by PgE1. In this infant PG-E1-Infusion had no effect upon arterial oxygen saturation. From these observations it can be concluded that dilation of the ductus is responsible for the rise in arterial oxygen saturation. 3the different indications for therapy with PG-E1 in the neonate are discussed.

Cardiac Catheterization↗
PubMed1978

[Effect of prostaglandin E1 on the hemodynamics in newborn infants with pulmonary atresia (author's transl)].

The effect of prostaglandin E1 (PGE1) on the haemodynamics during cardiac catheterisation was studied in 6 newborn infants with pulmonary atresia and ductus-dependent pulmonary perfusion. In 4 patients with initial arterial O2-saturations between 24% and 45% pulmonary blood flow increased from a mean value of 1.0 to 4.5 1/min/m2, 15--20 minutes after the infusion of PGE1 was started. At the same time the systemic blood flow decreased markedly, the systemic blood pressure varied only slightly, and a marked increase in systemic vascular resistance was calculated. In one further patient with a relatively high initial arterial O2 saturation the pulmonary blood flow increased only minimally, whereas in the remainder patient with low initial arterial oxygen saturation there was no change after PGE1 during the investigation.

Blood Pressure↗
PubMed1977

[Prostaglandin E1: effect on blood gases in infants with cyanotic congenital heart disease (author's transl)].

15 infants with cyanotic congenital heart disease (pulmonary atresia, Ebstein-Syndrom) were treated with Prostaglandin E1. During treatment there was a significant rise of PO2 and SO2 in the arterial, capillary and central venous blood. There was a minor rise of pH and HCO3; the arterial pCO2 fell slightly. We used PGE1-therapy as pretreatment before the heart operation, so that the critical babies go to the operation well oxygenated and in a better state. The side effects we observed (tachypnoe, tachycardia, hyperpyrexia, augmented urine output, erythemas, apnoic spells) seemed less important than the great advantage of a better oxygenation of these hypoxic babies.

Bicarbonates↗