PubMed Health⌕ Search

Biomedical subjects

M Kogawa

Publications and source records attributed to M Kogawa.

12 recordsLinked to original sources
PubMed2004

Primary cervical spinal epidural Extra-osseous Ewing's sarcoma.

Cases of primary spinal epidural Extra-osseous Ewing's sarcoma (EES) are rarely seen and a good prognosis for EES cannot be expected since a high incidence of local recurrence and metastasis frequently occur. We present a case of cervical spinal epidural EES in a 7-year-old girl with long survival after tumour resection. She also received adjuvant treatment with peripheral blood stem cell transplantation (PBSCT). This management successfully improved her condition and she was in complete remission without neurological deficit 60 months after surgery. Such a good prognosis of EES in the cervical spine is very rare. It is likely that magnetic resonance imaging (MRI) lead to a diagnosis of this rare type of EES at an early stage of the disease. PBSCT could be useful as an adjuvant to prolong the period of complete remission.

Child↗
PubMed1984

Stimulation of glycosaminoglycan synthesis by somatomedin and insulin in rat chondrocytes via somatomedin receptors.

Using cultured normal rat chondrocytes we have investigated 1) the effects of somatomedin and insulin on glycosaminoglycan (GAG) synthesis and 2) somatomedin and insulin binding sites. We confirmed that somatomedin and insulin stimulate GAG synthesis in normal rat chondrocytes. The maximal responses of somatomedin and insulin in GAG synthesis were the same, but the stimulation of GAG synthesis by maximally effective concentrations of insulin plus somatomedin was not cumulative. Cultured rat chondrocytes had binding sites for somatomedin and insulin, and the binding was displaced by both somatomedin and insulin. Somatomedin is much more effective than even large amounts of unlabelled insulin in displacing both somatomedin and insulin binding. Anti-insulin receptor IgG, which inhibits insulin binding to human placental membrane, did not affect GAG synthesis stimulated by insulin nor did it inhibit insulin binding to chondrocytes. Somatomedin used for GAG synthesis and displacement was the partially purified somatomedin A with a biological activity of 80 U/mg. Therefore the possibility that substances other than somatomedin A, which was contaminated in this preparation, affected this result could not be excluded completely. However, these results suggest that somatomedin and insulin act on normal rat chondrocytes through a somatomedin receptor.

Animals↗
PubMed1983

Effects of somatomedin and other factors on glycosaminoglycan synthesis in cultured rat chondrocytes.

We have investigated the effects of hormones and serum on glycosaminoglycan (GAG) synthesis, using cultured rat chondrocytes isolated from growing cartilage. Somatomedin A stimulated GAG synthesis at a physiological concentration, however in the case of insulin the dose required to stimulate GAG synthesis was 500 times as great as the physiological concentration. Parathyroid hormone also increased GAG synthesis. In contrast, hydrocortisone inhibited GAG synthesis at a pharmacological dosage. None of the following had any effect on GAG synthesis: epidermal growth factor, fibroblast growth factor, triiodothyronine, growth hormone, sex steroid or vitamin D3. Human serum up to a concentration of 1% stimulated GAG synthesis. Serum from patients with acromegaly stimulated GAG synthesis more than that from those with hypopituitarism.

Animals↗
PubMed1983

Short-term study of biosynthesized hGH in man.

Daily injection of 8IU of methionyl human growth hormone (met-hGH), produced by recombinant DNA technology, was performed in healthy young volunteers. Daily injections for four days did not cause any significant change in the results of physical examination, electrocardiogram, blood count or urinalysis. Non-esterified fatty acid levels increased significantly at 4 hours after the first injection of met-hGH in a manner similar to pituitary human growth hormone (pit-hGH). Both hGHs caused a significant increase in serum somatomedin A during the four daily injections. Plasma hGH reached peak levels at 3-4 hours after im injection of met-hGH and 4-6 hours after pit-hGH. The levels were 19.5 +/- 1.6 and 21.3 +/- 2.8 ng/ml, respectively. After iv one bolus administration of 4IU hGH to two volunteers, plasma hGH reached peak levels at 5 minutes at mean levels of 292 ng/ml after met-hGH and 293 ng/ml after pit-hGH. The half life of the two hGHs was 17.2 and 17.1 minutes, respectively, according to the disappearance curve measured after iv administration.

Adult↗
PubMed1983

Insulin stimulation of somatomedin A production in monolayer cultures of rat hepatocytes.

The effect of insulin on the generation of somatomedin by a monolayer culture of rat hepatocytes was investigated. Release of somatomedin into the medium of cultured hepatocytes was observed for at least three days, as determined by a radioreceptor assay for somatomedin A. The addition of 1-100 micrograms/ml insulin to the medium caused dose-related increases in somatomedin A in the conditioned medium for up to three days. The conditioned medium also stimulated DNA synthesis in human fibroblasts. To investigate hormone degradation by hepatocytes, labelled somatomedin A or insulin was added to the medium and the degradation was examined by trichloroacetic acid (TCA) precipitation, and gel chromatography. Although [125I]somatomedin A was slightly degraded even after 24 h of incubation, [125I]insulin was degraded within 6 h and the TCA precipitation at 24 h was 15% only. This degradation of hormones was inhibited by 1 mM bacitracin. Insulin stimulation of somatomedin production was significantly increased to 131.2% as compared with cultures without bacitracin. The molecular size of the somatomedin released into the medium was greater than that of purified somatomedin, suggesting that this somatomedin is bound to carrier proteins.

Animals↗
PubMed1982

Effect of GH and insulin on the generation of somatomedin by perfused rat liver.

The release of somatomedin from perfused livers of normal and hypophysectomized (hypox) rats has been studied. Somatomedin was determined by the radioreceptor assay for somatomedin A. The release of somatomedin in the perfusates of normal livers was observed during the initial 30 minutes and maintained during the second and third 30 minutes of recirculation. The addition of insulin at a concentration of 10 mU/ml to the perfusates caused a significant increase in the release of somatomedin in the 1st, 2nd and 3rd 30-minutes recirculatory perfusates. The addition of human growth hormone (25 micrograms/ml) and/or insulin (1 mU/ml) to the perfusates caused a significant increase in somatomedin after 120 minutes of recirculation. Hypox rats released amounts of somatomedin in perfusates similar to those of normal rats. The effect of insulin on the release of somatomedin was greater in hypox rats than that observed in normal rats. The molecular size of the somatomedin released in the perfusate was greater than that of purified somatomedin, suggesting that this somatomedin is bound to carrier proteins.

Animals↗
PubMed1982

Effects of glucocorticoid on body growth and serum levels of somatomedin A in the rat.

Serum levels of somatomedin A, as measured by radioreceptor assay, and body weight gain were 86.5 +/- 9.2% and 166.9 +/- 7.8% (N = 5) of the initial values, respectively, after 18 days administration of 2.5 mg cortisone acetate (CA). These values were significantly lower than those for saline treated rats (P less than 0.005). Reduced serum somatomedin A and body growth rate were partially restored after halting the injection of CA. Combined administration of daily doses of 100 micrograms hGH with CA did not prevent the decrease in somatomedin activity in treated rats. This observation suggests that GH plays a minor (or no) role in the fall of serum somatomedin A in CA-treated rats. From these data we conclude that glucocorticoids reduce serum somatomedin by inhibiting the effect of GH on the generation of somatomedin.

Animals↗
PubMed1981

A TSH secreting pituitary tumor accompanied by high stature: presentation of a case and review of the literature.

A 23-year-old man of high stature, with hypogonadism and bitemporal-upper-quadrant visual defects was found to have a pituitary tumor. He had a slightly enlarged struma, while he did not show any signs of hyperthyroidism. His serum TSH level (10.4 microunits/ml) was slightly elevated in spite of increased levels of serum thyroid hormone (T3 249 ng/dl, T4 12.0 microgram/dl). Neither the elevated serum TSH levels nor thyroidal uptake of 123I were suppressed after 7 days of 75 microgram triiodothyronine administration. Serum TSH levels did not increase further after TRH administration. Hypofunction of the anterior pituitary gland was observed. Following transsphenoidal hypophysectomy, his serum thyroid hormone and TSH levels returned to the normal range. Immunohistochemical examination revealed the existence of numerous TSH positive cells. From these data we concluded that the patient had a pituitary tumor which secreted inappropriate amounts of TSH.

Adenoma, Chromophobe↗
PubMed1981

Effect of food and GH on the binding of 125I-somatomedin A to the membranes of rat lung and kidney.

Studies were undertaken to examine the relationship between serum levels of somatomedin A and its binding sites in the lung and kidney of rats. After three days of fasting, serum levels of somatomedin A decreased, accompanied by increases of 17.5% and 21.4% in binding to the plasma membranes from lung and kidney, respectively. After two days of refeeding, this binding decreased with the increase in the serum level of somatomedin A. There was observed a negative correlation between the serum level of somatomedin A and the percentage of labelled somatomedin A bound to the membranes. These observations suggest that somatomedin down-regulates its own receptor under these conditions. A similar regulatory mechanism was not observed with either hypophysectomized- or GH-treated rats.

Animals↗
PubMed1980

Effect of insulin and nutrition on serum levels of somatomedin A in the rat.

The serum levels of somatomedin A, as measured by radioreceptor assay, were significantly reduced in rats 2 days after the administration of streptozotocin. The mean decrease was 45.4 +/- 2.9% of the initial values. In rats treated with insulin, blood glucose levels and glycosuria decreased, and serum somatomedin A returned to 108.3% +/- 11.7% of the initial values by the sixth day of treatment. In untreated diabetic rats, serum somatomedin A decreased progressively to 23.4 +/- 4.4% 8 days after streptozotocin administration. The total caloric intakes in the treated and nontreated diabetic rats were similar, suggesting that the low levels of somatomedin A in diabetic rats may be due to lack of insulin. A significant correlation was observed between serum somatomedin A values and body weight (r = 0.90) or the urinary glucose (r = -0.84) or blood glucose levels (r = -0.67). When the diabetic insulin-treated rats were fed a low protein diet, there was no increase in serum somatomedin A. Inhibitory factors in serum which interfere in the bioassay for somatomedin had no effect in our radioreceptor assay.

Animals↗
PubMed1980

Effect of thyroid hormone on the serum level of somatomedin A.

The effect of thyroid hormone on the serum level of somatomedin A was studied using a radioreceptor assay for somatomedin A. In 13 patients with hyperthyroidism, the mean level of somatomedin A was 0.06 +/- 0.05 U/ml, which was within the normal range. Low levels were found in 19 patients with primary hypothyroidism with a mean of 0.39 +/- 0.04 U/ml. After treating these patients with thyroxine, the serum somatomedin A levels returned to the normal range. There was a significant correlation between the somatomedin A level on one hand and T3 (r = 0.49) and T4 (r = 0.55) level on the other. The serum level of somatomedin A did not decrease for 7 days after thyroidectomy nor increase after treating hypophysectomized rats with 2 microgram of thyroxine for 14 days. However, the effect of growth hormone on serum somatomedin A was augmented 42.2% by the combined administration of the same amount of T4 for 7 days. There was a positive correlation between the serum level of somatomedin A and the percentage increase in body weight (4 = 0.73). These data suggest that thyroxine potentiates the effect of GH on synthesis and/or the secretion of somatomedin A.

Adult↗