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Biomedical subjects

G Heynen

Publications and source records attributed to G Heynen.

At least 55 records · Page 3Linked to original sources
PubMed1980

[Purification of human cartilaginous proteoglycans and technical aspects of the radioimmunoassay].

Proteoglycans (PG) have been purified by classical methods from human articular cartilage in order to set up a radioimmunoassay. Conditions of labelling, purification of labelled PG, and optimal conditions of buffer, temperature, duration of incubations and dilution of antiserum are described. Separation of free and bound PG is performed by immunoprecipitation. It is demonstrated that human articular PG can be assayed quantitatively by RIA procedure, with the sensitivity of +/- 2 femto-moles (+/- 5 ng) per tube.

Animals↗
PubMed1980

[Demonstration of multiple forms of immunoreactive calcitonin (CTi) in human serum by isotachophoresis. Preliminary results].

Heterogeneity of immunoreactive calcitonin (iCT) in the serum has been studied by preparative isotachophoresis. Under the described technical conditions, it is possible to distinguish several molecular species of iCT characterized by a faster mobility than synthetic CT. Preliminary results suggest that immunoreactive CT profile is not similar in various hypercalcitonemic diseases.

Calcitonin↗
PubMed1979

Treatment of Paget's disease with (3-amino-1-hydroxypropylidene)-1, 1-bisphosphonate (A.P.D.).

18 patients with Paget's disease were treated orally with (3-amino-1-hydroxypropylidene)-1, 1-bisphosphonate (A.P.D.). In most cases bone resorption became normal within a week of treatment, whereas the return to normal bone formation took 3-6 months; this difference produced a transient imbalance between resorption and formation. In biopsy specimens taken during treatment the numbers of osteoclasts and osteoblasts decreased towards normal and excess osteoid disappeared.

Aged↗
PubMed1979

Ethanol induced secretion of calcitonin in chronic renal disease.

Whisky (25-50 ml) increased plasma levels of immunoreactive calcitonin (iCT) in seventeen of nineteen patients with chronic renal failure. The effect was greater in patients with high levels of iCT than in those with normal levels. Changes in plasma iCT were not related to changes in calcium, phosphate or immunoreactive gastrin, but were inhibited by the prior administration of propranolol.

Calcitonin↗
PubMed1979

Double-blind placebo-controlled evaluation of levamisole in chronic rheumatoid arthritis.

Thirty-three out-patients with rheumatoid arthritis completed the study intended to compare under double-blind conditions, 50 mg levamisole tablets with placebo. Patients were given the double-blind medication at a dosage of one tablet t.i.d. for 3 months, and at a dosage of one tablet t.i.d., on 2 consecutive days every week for the next 3 months. Pain score, duration of morning stiffness, articular index and E. S. R. were recorded at the start of treatment, after 3 months of treatment and at the end of treatment. The levamisole patients made significantly better progress than did the placebo patients: for E.S.R. after 3 months of treatment, and for E.S.R., pain and morning stiffness by the end of treatment. Ten levamisole patients and 5 placebo patients reported adverse reactions. These were mainly gastrointestinal symptoms in the levamisole-treated patients.

Adolescent↗
PubMed1979

The relationship between disturbed metabolism of vitamin D and bone disease in chronic renal failure.

Following the discovery that the kidney is involved in the metabolism of vitamin D, a causal relationship has been sought between defective production of 1,25-dihydroxy vitamin D3 and bone disease in chronic renal failure. This paper reviews some of the clinical evidence for and against such a relationship, and considers the possible role of other vitamin D metabolites in the pathophysiology of renal bone disease.

Bone Diseases↗
PubMed1979

[Renal osteodystrophy in two children : a comparison of the effects of 1 alpha-hydroxycholecalciferol (author's transl)].

Two children suffering from renal osteodystrophy were treated by 1 alpha hydroxycholecalciferol (1 alpha OHD3) 1 microgr. each day, for 18 months. In both the level alkaline phosphatase decreased at the same time as endogenous immunoreactive CT increased, iPTH did not change steadily, whereas plasma creatinine rise. As plasma calcium concentration did not increase, it is suggested that the increase in endogenous CT concentration is a part of the favourable response to the treatment by 1 alpha OHD3.

Alkaline Phosphatase↗
PubMed1979

[The effects of 1 alphahydroxycholecalciferol in patients with renal osteodystrophy, Paget's disease of bone and in normal subjects (author's transl)].

The administration of 1 alpha hydroxycholecalciferol (1 alpha OHD3) (2 microgr. per day) increase the plasma immunoreactive calcitonin (i CT) concentration in normal subjects after six days. This effect is also observed in patients suffering from Paget's disease of bone, suggesting that the mechanism responsable for the secretion of CT following the administration of 1 alpha is not disturbed in that disease. By contrast, the absence of increase in plasma iCT in the patients suffering from chronic renal failure suggests an impaired secretion of CT in that disorder.

Calcitonin↗
PubMed1979

Treatment of renal bone disease with 1 alpha-hydroxylated derivatives of vitamin D3. Clinical, biochemical, radiographic and histological responses.

Forty patients with severe bone disease and chronic renal failure were treated with 1 alpha-hydroxycholecalciferol (1 alpha-OHD3) or 1,25-dihydroxycholecalciferol (1,25(OH)2D3) for 7--49 months (total = 738 patient months). There were symptomatic, biochemical and radiographic improvements in the majority of patients (greater than 70 per cent). Paired bone biopsies, taken before and during treatment in 26 patients, showed no change in bone matrix area, whereas matrix area decreased in a control group of 26 patients over the same period. There were small but consistent decreases in bone marrow fibrosis and in bone cell (osteoblast and osteoclast) counts in treated patients but not in controls. However, the proportion of patients who showed histological 'cure', in the sense of complete reversal of marrow fibrosis or excess osteoid was no greater in the treated than in the control group...

Adolescent↗
PubMed1978

Is 24,25-dihydroxycholecalciferol a calcium-regulating hormone in man?

Small doses (1-10 microgram daily) of 24,25-dihydroxycholecalciferol (24,25-(OH)2D3), a renal metabolite of vitamin D of uncertain function, increased intestinal absorption of calcium in normal people and in patients with various disorders or mineral metabolism, including anephric subjects. In five of six patients studied, calcium balance increased, but, unlike 1,25-dihydroxycholecalciferol, 24,25-(OH)2D3 did not increase plasma or urinary calcium concentrations. These results suggest that 24,25-(OH)2D3 may be an important regulator of skeletal metabolism in man with potential value as a therapeutic agent.

Adult↗
PubMed1978

[Calcitonin, gastrin, parathyroid hormone and the autonomic nervous system].

Stimulation of the beta-adrenergic terminations was employed to determine whether calcitonin-secreting thyroid C cells are derived from the neural crest. Calcitonin secretion was increased, whereas parathormone, insulin and gastrin values were not significantly changed. In addition, administration of a beta-blocking drug before ethanol led to a marked fall in calcitonin with respect to the baseline. Once again, other hormone levels were not affected.

Calcitonin↗
PubMed1978

Physiological and pharmacological aspects of 24,25-dihydroxycholecalciferol in man.

The present study describes the response to small oral doses (1--10 microgram/day) of 24,25-DHCC in man. Contrary to expectation, 24,25-DHCC was as potent as 1,25-DHCC in increasing intestinal absorption of calcium both in normal persons and in patients with a variety of disorders of calcium metabolism. Despite this increase in intestinal absorption, plasma and urine calcium did not increase after 24,25-DHCC as they did after 1,25-DHCC. Metabolic balance studies showed calcium balances to increase by 1.6 to 11.5 mmoles/day in 5 of the 6 patients studied. 24,25-DHCC increased intestinal absorption of calcium equally well in anephric patients, suggesting that conversion of 24,25-DHCC to 1,24,25-trihydroxycholecalciferol by the kidney cannot be the sole mechanism by which 24,25-DHCC expresses biological activity, even though in vitamin D deficient rats nephrectomy does abolish the ability of large doses of 24,25-DHCC to increase calcium absorption. It is concluded that 24,25-DHCC may be a calcium-regulating hormone in man. In view of the effects demonstrated here and its relatively high concentration in plasma and slow turnover rate, 24,25-DHCC has the properties that might be ideal for a long-acting stimulator of bone mineralisation. Further work is needed to explain why 24,25-DHCC has effects in man which are not readily seen in other species.

Bone Development↗