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Biomedical subjects

L Fryklund

Publications and source records attributed to L Fryklund.

At least 37 records · Page 2Linked to original sources
PubMed1986

Experimental research on IGF-1.

IGF-1 has been produced by recombinant DNA technology; the host cell is a yeast. Studies in hypophysectomized rats show that IGF-1 has little growth promoting effect unless given by infusion at high doses, and priming with bovine growth hormone did not produce any potentiation. In vitro studies reveal that IGF-1 cross-reacts with the insulin receptor on adipose cells. Immunohistochemical studies have revealed high IGF-1 immunoreactivity in proliferating and differentiating cells in the testes, lymphoid organs and pancreatic islets and particularly in regenerating nerves. Local application of IGF-1 may stimulate regeneration in damaged peripheral nerves. Key words:

Adipose Tissue↗
PubMed1986

Evidence indicating trophic importance of IGF-I in regenerating peripheral nerves.

The mechanisms influencing regeneration of peripheral nerves are incompletely known, but growth factors are supposed to play a key role. In the present study, we demonstrate, with the aid of immunohistochemical methods, that somatomedin C (Sm-C/insulin-like growth factor I/IGF-I) rapidly increased from low to high concentrations, reaching peak values in 2 weeks, in regenerating sciatic nerves of adult rats. In addition, IGF-I was demonstrated extracellularly, never observed in the control nerves. Reactive Schwann cells appeared to be the major source for IGF-synthesis. Higher concentrations were seen in tubulated nerves as compared to sutured ones. It is proposed that IGF-I exerts important growth supporting effects on regenerating peripheral nerves.

Animals↗
PubMed1984

Monoclonal antibodies and specific cell surface receptors do not discriminate between human growth hormone prepared by DNA recombinant techniques and the native hormone.

Native and E. coli-derived human growth hormone (hGH) have been compared in their ability to react with four different monoclonal antibodies (MAbs) as well as with the specific cell surface receptors of cultured human IM-9 lymphocytes and liver membranes of pregnant rabbit. For all the tests used, the competition curves obtained using both hormone preparations were superimposable. The results suggest a close similarity in the immunological and biological (binding reaction) properties of native and recombinant hGH.

Antibodies, Monoclonal↗
PubMed1983

Ontogenesis of somatomedin and insulin receptors in the human fetus.

This study examines the ontogenesis of somatomedin and insulin receptors in man. Particulate plasma membranes were prepared by ultracentrifugation from various tissues removed from fetuses after abortion and classified as less than 17, 17-25, and greater than 25 cm in length. The binding of iodinated insulinlike growth factors 1 (IGF-1) and 2 (IGF-2), somatomedin A (SMA), multiplication-stimulating activity (MSA), and insulin was examined at the different ages. In the liver, cross-reaction studies revealed separate insulin and IGF-2 receptors. The Scatchard plots of insulin binding to liver membranes were curvilinear and showed an increase in the concentration of insulin receptors with advancing age. A single IGF-2 receptor was found on liver and no alteration was observed during development. The brain contained a lower concentration of insulin receptors. A change in the brain receptors for somatomedins occurred during development. Early in gestation, a high concentration of a low-affinity IGF-1 receptor was found. After approximately the 17th wk of gestation a higher affinity IGF-1 receptor appeared, which then increased in concentration. Cross-reaction studies also revealed changes in the specificity of these receptors during development. In the youngest fetal group IGF-2 was preferentially bound. Around midgestation a separate IGF-1 receptor, indicated by the preferential displacement of iodinated IGF-1 by IGF-1, appeared. In contrast, iodinated IGF-2 bound to a receptor where IGF-1 and IGF-2 were equipotent.

Brain↗
PubMed1981

Somatomedin B: mitogenic activity derived from contaminant epidermal growth factor.

The mitogenic effect of somatomedin B on human cultured glial cells was neutralized by the addition of antibodies to mouse epidermal growth factor. Somatomedin B contained epidermal growth factor--like activity, competing for binding to the epidermal growth factor receptor. It is concluded that contaminating epidermal growth factor may explain the entire mitogenic activity of somatomedin B.

Cell Division↗
PubMed1981

Serum somatomedin A and non-dialyzable urinary hydroxyproline in girls with idiopathic scoliosis.

Serum somatomedin A was determined by radioreceptor assay in 31 girls with idiopathic scoliosis and 30 controls, with ages ranging from 9.7-16.2 years. In the material as a whole no significant difference could be found between scoliotics and controls. Similarly no differences were found in the girls under 13 years of age. However, in girls older than 13 years the controls had significantly higher somatomedin A levels than the scoliotics. In the second part of the study 26 girls with idiopathic scoliosis and 22 controls were examined with regard to the urinary excretion of non-dialyzable hydroxyproline,. which has been suggested to be correlated with collagen synthesis. The percentage non-dialyzable fraction of the total hydroxyproline was found to be significantly higher in the control girls. The mean age was 12.8 years for both groups. The results suggest a higher growth rate in the controls than in the scoliotics for girls over 12 years. There is, however, no definite evidence as to the function of the somatomedins or of the relationship between non-dialyzable hydroxyproline and growth.

Adolescent↗
PubMed1980

Serum levels of immunoreactive somatomedin A in the rat: some developmental aspects.

Immunoreactive somatomedin A (SMA) was determined in rat serum collected at 20 days of gestation and at 5, 15, 25, and 50 days of postnatal age. Adult levels were shown to be GH dependent. A rapid rise in immunoreactive SMA was observed after 15 days of postnatal age, and this was attributed to the triggering of the SMA-GH regulatory system by nutritional factors at weaning. Circulating levels of immunoreactive SMA were reduced during early development and in pregnancy, raising the possibility that early growth is regulated by an embryonic form of SM which is not detected by the SMA RIA.

Aging↗
PubMed1980

Somatomedin A levels in serum from healthy children and from children with growth hormone deficiency or delayed puberty.

Serum somatomedin A (SMA) has been determined in healthy children (n = 188) in relation to age using both a radioimmunoassay and a radioreceptor assay. The SMA levels, only 50% of adult values at birth, rise gradually with age and reach adult levels at 10 years of age. There is a significant correlation (r = 0.46 P less than 0.001) between SMA determined by the two methods throughout childhood except during puberty. Immunoreactive SMA shows a marked pubertal rise in values with a peak 2 years earlier for girls than boys, which is not observed by the radioreceptor assay technique. In boys with delayed puberty the increase in immunoreactive SMA is seen first when the testes reach a size of 5 ml. Children with growth hormone deficiency (n = 30) had significantly lower levels of SMA than health age-matched controls. Immunoreactive SMA gives a better separation of these groups than the values obtained by radioreceptor assay.

Adolescent↗
PubMed1979

Immunoreactive somatomedin A in human serum.

A RIA has been developed for somatomedin A (SM-A) utilizing Sepharose-bound antibodies. This assay, measuring SM-A, the insulin-like growth factors 1 and 2, and somatomedin C, allows determination in serum samples. In comparison with a serum standard, the mean serum levels in patients with acromegaly or GH deficiency and healthy subjects were 8.7 %/- 0.7 (n = 25), 0.24 +/- 0.02 (n = 25), and 1.15 +/- 0.11 U/ml, respectively. The correlation coefficient between immunoreactive SM-A and SM-A by radioreceptor assay was highly significant (r = 0.93), although the potency ratio of SM-A between the two groups of patients was higher in the RIA than in the radioreceptor assay. Gel chromatography revealed that SM-A in acromegalic serum is bound to a carrier protein which is absent in patients with GH deficiency. After gel chromatography at low pH, 90% of applied immunoreactive SM-A was recovered in the low molecular weight fraction and consisted mainly of neutral polypeptides.

Acromegaly↗
PubMed1977

Increasing growth with raised circulating somatomedin but normal immunoassayable growth hormone.

Two patients are described with elevation of circulating somatomedin A concentration but normal growth hormone levels. One,a young male, appeared clinically acromegalic; the other, a young female, was tall with kyphoscoliosis, and her appearance resembled Marfan's syndrome. In both patients plasma growth hormone concentration was suppressible by hyperglycaemia. It is suggested that their clinical syndromes resulted from excessive somatomedin activity.

Acromegaly↗
PubMed1977

Identification of a receptor for somatomedin-like polypeptides in human fibroblasts.

We have demonstrated a specific receptor for somatomedin-like growth polypeptides in human fibroblasts in culture using the closely related polypeptide, multiplication stimulating activity (MSA), as the radioligand. Polypeptides purified from human plasma, somatomedin A and acid soluble nonsuppressible insulin-like activity (NSILA-s), competed potently for 125I-MSA binding, as did unlabeled MSA. Although insulin and proinsulin also strongly inhibited MSA binding, the properties of the growth peptide receptor differed from those of the human fibroblasts insulin receptor. Somatomedin A, NSILA-s, MSA, insulin and proinsulin all stimulated the incorporation of [3H]thymidine into DNA in human fibroblasts. We propose that these polypeptides induce DNA synthesis through their interaction with the growth peptide receptor.

Cells, Cultured↗