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Biomedical subjects

C van der Meer

Publications and source records attributed to C van der Meer.

At least 37 records · Page 2Linked to original sources
PubMed1981

Value of serum calcitonin estimation in clinical oncology.

In 132 consecutive patients with carcinoma of various organs, a higher serum immunoreactive calcitonin (ICT) concentration (median level 50 pg/ml) was found than in 68 normal subjects (median level 20 pg/ml). The incidence of hypercalcitoninaemia was 40%. All 9 patients with primary liver-cell carcinoma were hypercalcitoninaemic. On the other hand, none of the 7 patients with a carcinoma of the breast had raised ICT levels. In bronchogenic cancer a relationship between ICT and cell type was found, with a predominance of high ICT in patients with oatcell and other undifferentiated types, whereas in squamous-cell carcinomas and adenocarcinomas of the lung hypercalcitoninaemia was relatively rare. When we divided all our patients according to differentiation of the tumour cell, it was found that the lower the degree of differentiation, the higher the ICT concentration, whereas opposite results were observed for CEA. When ICT and CEA were estimated concurrently, we found at least one marker increased in 70% of our patients. Our results demonstrate that patients with metastases in the liver have more frequently and increased ICT. In addition, we conclude that lifespan can be expected to be lower in patients with high ICT levels. In a longitudinal study of 46 patients, there was a positive correlation between change in serum ICT and tumour mass.

Aged↗
PubMed1981

Disturbances in the glucose metabolism in intestinal ischemia shock.

Intestinal ischemia shock is obtained in fasted rats by 40-minute splanchnic arterial occlusion (SAO) or by 35-minute portal vein occlusion (PVO). Survival is prolonged by plasma treatment; further prolongation is obtained by additional administration of glucose. After SAO early hyperglycemia is marked. Plasma adrenaline rises steeply after opening of the arteries and remains high, while plasma insulin remains unaltered. The hyperglycemia is abolished by adrenalectomy and section of the major splanchnic nerves (MSN) proximal to the adrenals but not by section of the MSN distal from the adrenals or by vagotomy. It is concluded that the sympathetic nervous system is stimulated by a substance, possibly related to VIP, released from the intestines. After PVO hyperglycemia is less marked. Plasma adrenaline as well as insulin are increased. During late and fatal hypoglycemia after PVO plus plasma treatment, the liver still appears to be functionally intact. It is assumed that gluconeogenesis is reversibly inhibited by as yet unknown factors. The hypoglycemia cannot be abolished by injection of common substrates of gluconeogenesis but the combination fructose plus glucagon plus NAD is highly effective.

Adrenal Medulla↗
PubMed1980

Dosage of acetylsalicylic acid for inhibition of platelet function.

In normal males, platelet prostaglandin synthesis as measured by malondialdehyde (MDA) production is blocked by more than 90% after administration of 600 mg of calciumacetylsalicylic acid and by more than 50% after 100 mg. Repeated doses of 100 mg at 12 h intervals progressively decrease MDA production to below 10% of the basic value. Bleeding time increases from 3.38 +/- 0.36 min to 7.73 0.91 min (mean +/- SEM). The data indicate that 12 h 100 mg doses of calciumacetylsalicylic acid (equal to 80 mg of aspirin) adequately inhibit platelet function.

Aspirin↗
PubMed1980

Pitfalls of salicylhydroxamic acid plus glycerol treatment of T. vivax infected goats.

A dosage regime of SHAM (260 to 355 mg/kg) plus glycerol (890 to 1216 mg/kg), cleared T. vivax from peripheral blood of infected goats. Relapses occurred on two occasions in one goat and death during infusion of the drug in two other goats. Pharmacokinetic studies showed that both SHAM and glycerol are rapidly eliminated, the elimination possibly being slower in infected than in uninfected goats. For this reason and also because of the poor solubility of SHAM, very large volumes (500-1000 ml) had to be infused intravenously to obtain therapeutic plasma concentrations. The difficulties of adjusting the pH, the large volumes to be injected combined with the narrow margin between therapeutic and lethal dose preclude practical application of this form of treatment. Toxicity became apparent as a marked increase in heart rate and cessation of the ruminal movements which lasted for about 6 hours. A Herxheimer reaction may play an additional role in infected goats. Relapses may be due either to the fact that the levels of the drugs in the tissue were too low, or to the presence of a sub-population of T. vivax which is not susceptible to the treatment with SHAM plus glycerol.

Animal Diseases↗
PubMed1980

Regional intravascular sympathetic (RIS) block with guanethidine (Ismelin).

Regional intravascular sympathetic (RIS) block was produced in the rabbit ear by intra-arterial injection using guanethidine, during tourniquet occlusion of the ear vessels. Dose-effect relations were studied for the fall in mean arterial blood pressure after tourniquet release 30 seconds and 10 minutes after guanethidine administration. Compared to systemic intravenous injection, the effects after 30 seconds' occlusion were reduced by 64% and after 10 minutes' occlusion by 80%, irrespective of the dose used. This indicates a rapid and a-specific 'binding' of guanethidine in the tissues. After a RIS block (10 minutes' occlusion), vasoconstriction during a cold provocation test was abolished. Skin temperature in the treated ear remained high while the temperature of the untreated contralateral ear fell sharply. The block lasted 3 days at 0.625 mg and 5 days at 2.5 and 10 mg. A second block applied within 5 days was less effective, but applied after three weeks it was as effective as the first block. If the results obtained may be applied to man, it may be concluded that RIS block is a relatively safe method, since the major part of the administered dose will rapidly become unavailable for an immediate systemic effect.

Animals↗
PubMed1979

Regulation of the immune response by macrophages.

Regulation of the immune response by macrophages was studied with cellular resistance to Listeria monocytogenes as parameter. The use of agents which suppress macrophage activity during the induction-phase of immunity enabled the induction of protective immunity with killed listeria. Fractionation of the cell content of listeria yielded an RNA'se sensitive fraction which in a dose of 300 ng and in combination with the cationic surfactant dimethyl dioctadecyl ammonium bromide induced protective immunity against listeria.

Adjuvants, Immunologic↗
PubMed1977

The mechanism of action of two bradykinin-potentiating peptides on isolated smooth muscle.

Bradykinin-induced contractions in the guinea-pig ileum were potentiated by the peptides A-VI-5 (Val-Glu-Ser-Ser-Lys) and BPP5a (Pyr-Lys-Trp-Ala-Pro), while the contractions induced by other agonists were not affected. Neither peptide added alone caused any response. Previous addition of the peptides shortened the latent period following the addition of bradykinin to a value corresponding to the contraction height with an equivalent dose of bradykinin added alone. Bradykinin in contact with a piece of ileum was inactivated at a relatively slow rate. This inactivation was not inhibited by either A-VI-5 or BPP5a in doses causing potentiation. Suppression of the cholinergic activity by cooling, atropine, morphine or tetrodotoxin did not influence the potentiating activity. Addition of the peptides at the moment a submaximal contraction due to bradykinin had been fully established, increased the contraction height within seconds. The two peptides caused a parallel shift to the left of the dose-effect curve of bradykinin, whereas the maximum bradykinin effect remained unchanged. It is concluded that sensitization of bradykinin receptors due to an increased affinity of the receptor for bradykinin is the hypothesis which best fits the experimental findings.

Animals↗