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Biomedical subjects

A F De Schaepdryver

Publications and source records attributed to A F De Schaepdryver.

At least 19 recordsLinked to original sources
PubMed1993

[Knowledge of the human body. At the 450th anniversary of the first edition of Andreas Vesalius' life work. "De Humani Coporis Fabrica Libri Septem"].

As an introduction to the symposium we pay attention successively: firstly, to the "Magister divinus", to Andreas Vesalius' personality, according to the testimony of his pupil Fallopius; secondly, to his ingenious lifework, the "De Humani Corporis Fabrica", according to the opinion of Sir William Osler, "the greatest medical book ever written", finally, to the historical evolution leading to the Vesalian way of thinking and working. All this proves that Vesalius' work is a fundamental turning point in the development of medicine as well as in the evolution of scientific practice in a general sense. It is also one of the highlights in the construction of mankind's intellectual patrimony.

Anatomy↗
PubMed1992

[Clinical pharmacology: current status and perspectives].

In view of the ever increasing complexity of individualized pharmacotherapy, the study of new and potent drugs in man and the misuse and abuse of drugs, WHO-Study Group reports and a recent enquiry in Belgium, France and W. Germany stress that the development of clinical pharmacology is an absolute necessity for patients, physicians, health authorities, the pharmaceutical industry and society at large. It seems this development could be optimally achieved by setting up, within Services of General Medicine or Internal Medicine of University Hospitals and large Public Hospitals, autonomous Units of Clinical Pharmacology with the responsibility to take an active part: a) at the service level: 1) in patient care, either directly in general medical services or drug problem oriented consultations, or indirectly through consultative functions and pharmacotherapeutic conferences; 2) in drug monitoring services, management of cases of overdose, drug information, drug utilization surveys, pharmaco-epidemiology, ethical committees, formulary committees, drug regulatory agencies and studies of Phase I, II and III; b) at the teaching level: 1) in courses of clinical pharmacology sui generis, to undergraduates, in close collaboration with the University Department of Pharmacology; 2) at the postgraduate level, as a specialty in se, and as part of the training in medical specialties and at the level of continuing education of general practitioners and specialists; c) at the research level: 1) in clinical pharmacokinetic studies, with special attention to interindividual variability and genetic factors, to drug concentration/effect studies, to drug interactions, and in pharmacodynamic studies, in view of the development of new approaches in the study of drug-receptor interactions; 2) in the design, realization and evaluation of Phase I, II and III studies, clinical trials and multicenter drug studies.

Belgium↗
PubMed1986

In-vitro study of the enkephalinergic hypothesis for non-adrenergic, non-cholinergic innervation in the cat stomach.

It has been suggested that enkephalins are involved in the gastric relaxation induced by stimulation of the non-adrenergic, non-cholinergic vagal fibres in the cat stomach. Experiments were therefore performed on strips of cat stomach. With longitudinal and circular gastric fundus and corpus strips from reserpinized cats, non-adrenergic, non-cholinergic relaxatory responses could be elicited by transmural electrical stimulation in Tyrode solution containing atropine and 5-hydroxytryptamine. Morphine, leu-enkephalin and met-enkephalin did not influence the tone of the strips or the relaxation evoked by stimulation at 8 Hz, and neither did the opioid antagonist, naloxone. These results do not support the enkephalinergic hypothesis for the non-adrenergic, non-cholinergic vagal fibres in the cat stomach.

Animals↗
PubMed1984

Release of dopamine, noradrenaline and dopamine B-hydroxylase from mouse neuroblastoma.

The murine C1300 neuroblastoma tumor was found to secrete dopamine, noradrenaline and dopamine B-hydroxylase into the circulation of tumor-bearing A/J mice. The plasma levels of dopamine, noradrenaline and dopamine B-hydroxylase increased with the size of the tumor, and the increase in noradrenaline paralleled the increase in dopamine B-hydroxylase (r = 0.86). The vesicular storage of dopamine and noradrenaline in the tumor was evidenced by a decrease of the tissue content of dopamine and noradrenaline 24 hours after the administration of reserpine (5 micrograms/g) respectively to 17.6% and 7.8% of control values. A similar observation could be made for the levels of dopamine and noradrenaline in the plasma of reserpinized C1300 mice. The total activity of dopamine B-hydroxylase in the tumor and in plasma was unaffected by the reserpine treatment. Chronic administration of 6-hydroxydopamine (100 micrograms/g for 8 days) had no effect on the tissue contents of dopamine, noradrenaline or dopamine B-hydroxylase. The release of catecholamines and dopamine B-hydroxylase from the C1300 neuroblastoma was studied in vitro on superfused tumor slices. Stimulation of these slices with 56 mM KC1 or with 5.10(-5) M tyramine failed to induce the release of endogenous dopamine, noradrenaline or dopamine B-hydroxylase above the basal outflow levels. These results are suggestive for a non-exocytotic release of catecholamines and dopamine B-hydroxylase from the neuroblastoma tumor.

Animals↗
PubMed1982

Multiple molecular forms of dopamine beta-hydroxylase in the C1300 mouse neuroblastoma tumor and in the serum of tumor-bearing mice.

The distribution of the enzymatic activity of dopamine beta-hydroxylase (DBH) in linear sucrose gradients was studied for a soluble fraction of the C1300 mouse neuroblastoma tumor, for the serum of tumor-bearing A/J mice, and for adrenal tissue and serum of control mice. In controls (adrenal gland and serum of A/J mice), about 75% of the DBH activity was associated with a high-molecular-weight form, denoted as DBHA, with an apparent sedimentation coefficient of 11.3 S. About 25% of the DBH activity was attributable to a slower-sedimenting species (7.1 S), denoted as DBHB. In tumor supernatants and in the serum of tumor-bearing mice, about 55% of the DBH activity was present as the 7.1 S species (DBHB), while only 35% was recovered as the high-molecular-weight form (DBHA). Approximately 5% of the activity could be attributed to a separate form, with a sedimentation coefficient of about 4.5 S. This form is designated DBHC. The ratio DBHB/DBHA is significantly higher in tumor tissue and in serum of tumor-bearing mice than in controls. The three enzymically active forms of DBH in the C1300 tumor are considered to represent the tetrameric (DBHA), dimeric (DBHB), and monomeric (DBHC) forms of the enzyme.

Animals↗
PubMed1980

Immunohistochemical evidence for a plasma membrane localization of dopamine-beta-hydroxylase in the mouse neuroblastoma.

Dopamine-beta-hydroxylase (D beta H), a glycoprotein enzyme which converts dopamine into noradrenaline, was purified from C1300 mouse neuroblastoma and used to raise antibodies in rabbits. Using an indirect immunofluorescence technique the cellular localization of D beta H in C1300 mouse neuroblastoma was compared with that of the superior cervical ganglion. C1300 neuroblastoma D beta H was found to be predominantly localized in the plasma membrane, in contrast to its intracellular localization in the superior cervical ganglion of A/J mice. At least part of the enzyme was found to be associated with the external side of the plasma membrane.

Animals↗
PubMed1979

The effects of beta-adrenoceptor blockade on renin, angiotensin, aldosterone and catecholamines at rest and during exercise.

1 beta-adrenoceptor blockade with metoprolol provoked, both at rest and during exercise, a decrease of 'active' renin and angiotensin II together with an increase of 'inactive' renin and unchanged 'total' renin. The significant exercise-provoked increases in angiotensin II, plasma renin activity and 'active', 'inactive' and 'total' renin when on placebo, were reduced by metoprolol. 2 No significant change in serum sodium and potassium and in plasma aldosterone was found during beta-adrenoceptor blockade at rest. During exercise plasma aldosterone dropped significantly without any change in serum sodium or potassium. 3 Plasma noradrenaline increased significantly at rest on metoprolol. The increase in plasma noradrenaline and adrenaline during exercise was similar on placebo and on metoprolol.

Adult↗