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At least 19 recordsLinked to original sources
PubMed1977

Embryonic and postnatal growth of rat and mouse. V. Prenatal growth of organs and tissues, general principles: allometric growth, absence of growth, and the genetic regulation of the growth process.

(1) The investigation yielded several general growth principles, i.e., types of growth occurring rather frequently: (a) allometric growth, (b) a non-changing growth rate, persisting when the growth rate changes in the majority of tissues, (c) a growth rate equal to that of the whole embryo, (d) absence of growth and (e) jumps, i.e., changes in the volume or surface of organs completed within about half a day or less and probably due to changes in the cell volume or surface area; these histological changes tend to start simultaneously with the changes in growth rate. (2) Growth constants tend to have a value of about 2.0 in the prenatal period, as in the post-natal period. During development, however, their value increases slightly but significantly. (3) Further arguments are given for the mitosis-regulating model described in Part III. (4) The mitosis-regulating model combined with the general growth principles derived here and in earlier parts of this report constitute a comprehensive model for the genetiv regulation of the growth process.

Age Factors↗
PubMed1975

The embryonic and postnatal growth of rat and mouse. III. growth of the whole animal in the puberty, adult, and senescence phases in two inbred mouse strains (cpb-s and kba/2). Exponential growth, sudden changes in the growth rate, and a model for the regulation of the mitotic rate.

1. The growth model forumlated for prenatal and postnatal growth up to the middle of the puberty phase seems to be valid for the later postnatal phases as well, including adulthood and senescence. 2. In this model, growth consists of phases with exponential growth (constant specific growth rate) separated by sudden changes in the rate. 3. In the period described here, 7 phases can be distinguished, beginning with puberty (phase IV) and ending with senescence (phase X). 4. In 4 of these phases the growth rate does not differ significantly between the four groups of mice used. In the other 3 phases there are no differences between three of the groups but the fourth, one of the sexes of the CPB-S strain, differs very definitely from the rest. 5. Absence of growth occurred in some phases in one of the groups. 6. Some of the phases do not occur in all individual animals; this holds especially for phase VIII, which occurred in only about 25% of the animals. 7. The 'growth constants' postulated in Part I and now studied in the individual mice, tend to have a value of about 2. A theoretical model is described for the regulation of the mitotic rate giving 'growth constants' of about the same numerical value.

Animals↗
PubMed1979

The effect of hypothyroidism on growth, serum growth hormone, the growth hormone-dependent somatomedin, insulin-like growth factor, and its carrier protein in rats.

To study the possible mechanisms involved in growth retardation associated with hypothyroidism, serum T4, GH, the GH-dependent somatomedin, insulin-like growth factor (IGF), and its carrier protein (CP) were measured in hypothyroid rats and their age-matched controls. Three groups of rats were studied: infant, immature, and adult. Marked hypothyroidism (serum T4, less than 1 microgram/dl) was produced in experimental animals by providing them with drinking water containing 0.05% propylthiouracil. Infant and immature hypothyroid rats weighed markedly less than normal controls and had significantly reduced serum levels of GH, IGF, and CP. Normal adult rats, treated with propylthiouracil for 60 days, also weighed considerably less than control animals and exhibited a significant drop in serum GH, IGF, and CP during this period. The administration of bovine GH to hypothyroid adult rats for 7 days did not restore either IGF or CP levels to normal, indicating that their decrease in serum was, in part, a direct result of hypothyroidism per se. These results indicate that serum levels of GH, IGF, and CP are at least partly under thyroid hormone control. Furthermore, these studies suggest that the growth retardation associated with hypothyroidism may be mediated through somatomedin activity.

Aging↗
PubMed1977

Collaborative study of the effects of human growth hormone in growth hormone deficiency: IV. Treatment with low doses of human growth hormone based on body weight.

In order to define the minimum effective dose of human growth hormone (GH) in growth hormone deficient children, GH was administered to three groups of patients based on their body weight. Five children who received 0.01 International Unit (IU) GH/kg three times a week (tiw) failed to respond with a significant increase in their rate of growth. A dose of 0.03 IU GH/kg tiw increased the growth rate of 12 patients from 3.5 +/- 0.4 (SE) cm/year to 6.4 +/- 0.4 (SE) cm/year (P less than 0.001) during the first 12 months of therapy. Eight children (67%) larger than or equal to 6.0 cm/year. A similar increase growth rate from 3.6 +/- 0.4 (SE) cm/year to 7.3 +/- 0.4 (SE) cm/year (P less than 0.001) was observed over the first 12 months of therapy in 16 growth hormone deficient children who were given 0.06 IU GH/kg tiw. Thirteen children (81%) grew larger than or equal to 6.0 cm/year. During a second year of treatment, children receiving either 0.03 or 0.06 UI GH/kg tiw again showed a significant increase in their rate of growth. However, the response was significantly less than that observed during the first year of treatment. Comparison of these results with those available in the literature suggests that the most efficient, although not necessarily the optimal, initial dose of GH in children with growth hormone deficiency is 0.06 IU GH/kg administered three times a week.

Adolescent↗
PubMed1975

Energetics of Bacillus stearothermophilus growth: molar growth yield and temperature effects on growth efficiency.

The major growth yield of a prototrophic strain of Bacillus stearothermophilus under aerobic conditions on salts medium containing ammonium nitrate as the nitrogen source and glucose or succinate as the carbon source was maximal at the lowest growth temperature employed and decreased steadily as the temperature was raised. The temperature optima for growth yield and for growth rate were thus different. The molar growth yield values of the thermophile, especially at the lower growth temperatures, were similar to those reported for aerobically grown mesophilic bacteria, both on glucose and on succinate. At the higher growth temperatures, a lower proportion of glucose carbon was incorporated into cells and a correspondingly greater proportion was left incompletely utilized in the medium, mostly as acetate. This suggests a greater inefficiency in the coordination of the nonoxidative and oxidative phases of glucose metabolism at the gigher temperatures. Another factor causing a decreased cell yield at higher temperatures was possibly an uncoupling of energy production from respiration. The rates of respiration by intact cells of the thermophile on glucose and on succinate followed the Arrhenius relationship from 55 C to 20 C, which is some 20 C below the minimal growth temperature of the organism. The Arrhenius constant was 17.1 kcal/mol for glucose oxidation and 13.5 kcal/mol for succinate oxidation. These results are comparable to those reported for some mesophiles, and they suggest that the inability of the thermophile to grow at temperatures below about 41 C is not due to an abnormally high temperature coefficient for the uptake and oxidation of the carbon source.

Acetates↗
PubMed1976

Relative importance of growth hormone and sex steroids for the growth at puberty of trunk length, limb length, and muscle width in growth hormone-deficient children.

We have followed the growth of stature, sitting height, skinfolds, muscle widths measured radiologically, and skeletal maturity in growth hormone-deficient patients in whom hGH was given and withheld in alternating three-month periods throughout puberty (referred to as "off-hGH" and "on-hGH" periods). Six boys and four girls had true isolated GH deficiency and developed puberty spontaneously. Two boys had gonadotrophin deficiency plus GH deficiency, and five boys had multiple deficiencies; in these boys the signs of puberty were induced by hormone treatment. Boys with true isolated deficiency grew about two-thirds as much in height in the off-hGH periods as in the on-hGH periods; their total gain in height during the adolescent spurt would have been about 20 cm, instead of 30 cm, if hGH had been discontinued at the beginning of puberty. The effect of hGH was entirely on growth in leg-length, however, which virtually ceased during the off-hGH periods. Growth in sitting height altered little when hGH was withdrawn. Growth in limb muscles, however, was GH dependent throughout puberty; during the majority of periods when hGH was withheld, muscle was actually lost; this occurred in the boys who were receiving large doses of testosterone as well as in those producing their own normal amounts. Subcutaneous fat diminished when hGH was given and increased when it was withdrawn; this occurred independently of administration of testosterone. There was little evidence that growth of pubic and axillary hair progressed faster during on-hGH periods, except perhaps in patients with multiple deficiencies. There was some evidence, however, that bone age progressed less rapidly during on-hGH periods than during off-hGH periods in the patients with isolated deficiency. The results in the girls agreed with those in boys so far as stature was concerned, but the relationship with sitting height and leg length appeared to be different; the reasons for this are discussed. We conclude that all children with GH deficiency should continue on treatment with hGH throughout puberty, ideally until growth ceases.

Adolescent↗
PubMed1979

Combined test of hypothalamic-pituitary function in growth retarded children treated with growth hormone. I. Secretion of growth hormone and somatomedin before and after treatment.

In 23 growth retarded children two consecutive insulin tolerance tests (ITT) were performed to establish a diagnosis of growth hormone (GH) deficiency. Nine children did not respond (GH peak value less than 8 mU/1), whereas 14 were classified as having partial GH deficiency (GH peak value less than 20 mU/1). All were treated for an average period of 40 months with human growth hormone (HGH). In a combined stimulation test at the end of the treatment period 9 children demonstrated a persistent GH deficiency, whereas a normal response was found in 14 of the previous partial GH deficient children. During treatment the monthly growth rate rose from 0.21 cm 0.58 cm in the GH deficient children and from 0.31 cm to 0.70 cm in the partial deficient children, in most of whom spontaneous pubertal development occurred during treatment. Somatomedin (SM) values were decreased in the GH deficient children before and after treatment but increased to normal levels during treatment. Growth velocity in these children during treatment was correlated to SM values before treatment. In the partial GH deficient children SM values were subnormal before but normal after treatment. This supports the assumption that in some children with constitutional delay in puberty a reversible functional hypopituitarism exists, which is normalized after the onset of puberty, due to androgens sensitizing growth hormone releasing mechanisms. Treatment with HGH may induce increased growth velocity in some of these patients.

Body Height↗
PubMed1976

Embryonic and postnatal growth of rat and mouse. IV. Prenatal growth of organs and tissues: age determination, and general growth pattern.

(1) Data on the embryonic growth of several organs and of many different types of tissue in the mouse and rat are presented. (2) The concept developmental age is introduced, because it leads to an age estimate that is better correlated with the developmental stage. (3) The general growth pattern of the organs and tissues studied agrees with that found for the whole animal, consisting of phases with exponential growth separated by breaks. In the majority of the organs the breaks occur at the same time as in the whole animal. (4) The decrease in the growth rate at the end of phase E II is definitely smaller in the majority of the organs than in the whole animal. (5) Breaks occurring at other times than those found in the whole animal seem to take place in a few organs, and in the mouse at the embryonic age of about 17 days in a large number of organs.

Animals↗
PubMed1976

Action of growth hormone on erythropoiesis: changes in red blood cell enzyme activities in growth-retarded patients with and without growth hormone deficiency.

Fifteen red cell enzyme activities of growth-retarded patients with and without growth hormone (GH) deficiency were investigated before and after GH administration. The 15 enzymes were Hexokinase, phosphoglucomutase, glucose phosphate, isomerase, phosphofructokinase, fructose diphosphate aldolase, glyceraldehyde-3-phosphae dehydrogenase, triosephosphate isomerase, 2,3-diphosphoglycerate mutase, 3-phosphoglycerate kinase, 3-phosphoglycerate mutase, enolase, pyruvate kinase, glycose-6-phosphate dehydrogenase, 6-phosphogluconic dehydrogenase, glutathione reducase. Sixty-six subjects were studied: 30 normal control subjects (group N) and 36 patients (aged 5-23 years) with short stature. Complete endocrine evaluation showed 21 (group I) to have GH deficiency (10 patients with isolated GH deficiency) and 15 (group II) to have normal hypothalamic and pituitary function except for two patients with a moderate hypothyroidism. Both had been receiving thyroid hormone treatment for a long time before our studies. All 36 patients were treated with 2 mg human growth hormone intramuscularly for 7 days. Before GH treatment no significant difference was observed between hematologic data in group I (GH deficiency) and group II (no GH deficiency). After GH therapy there was a significant increase in reticulocyte count in both groups of patients with short stature. The mean pretreatment value in group I was 1.294% +/- 0.084 (SEM); the mean post-treatment value was 2.081% +/- 0.287 (SEM)< P less than 0.005. The mean pretreatment value in group II was 1.0% 0.184 (SEM); the mean post-treatment value was 1.407% +/- 0.193 (SEM), P less than 0.01. In group II (no GH deficiency) mean pretreatment erythrocyte enzyme activities were not significantly different from those activities observed in normal control subjects (group N). However, in patients who lacked GH, the pretreatment activities of five red cell enzymes (glucose phosphate isomerase, triosephosphate isomerase, glyceraldehyde-3-phosphate dehydrogenase, 2,3-diphosphoglycerate mutase, 3-phosphoglycerate kinase) were significantly decreased before GH administration compared with the values in normal control subjects...

Adolescent↗
PubMed1977

Effects of growth hormone on protein metabolism. Acute changes in plasma amino acids in growth retarded patients with and without growth hormone deficiency.

39 patients with growth retardation were investigated: 21 (group H) were suffering from GH deficiency and 18 (group N) had no endocrine disease except for two adequately treated patients with mild hypothyroidism. Analysis of 15 plasma amino acid concentrations was carried out before and 1 and 2 hours after intravenous HGH injection at a dosage of 2 mg per m2. Except for one amino acid no significant difference between mean pre-treatment amino acid values was observed in the two groups of patients. In group H there was a highly significant decrease in plasma concentration of 14 amino acids already 1 hour after HGH injection and of all 15 amino acids after 2 hours. This response of plasma amino acids to HGH was less pronounced in group N. For 5 amino acids a moderate correlation was found in group H between acute metabolic response to HGH and growth response to long-term HGH treatment. Our results following HGH injection may reflect increased plasma amino acid transfer into cells due to HGH.

Adolescent↗
PubMed1977

Effects of fibroblast growth factor and epidermal growth factor on the rate of growth of amniotic fluid-derived cells.

Primary cultures of cells derived from human and bovine amniotic fluid were cultivated in Dulbecco's modified Eagles medium with 20% fetal calf serum. Whereas increased concentrations of fetal calf or other types of serum bring about no further mitogenic response, the rate of growth of these cells was nevertheless sharply increased when 100 ng/ml of FGF was added to the culture media. The FGF induced mitogenic effect was statistically significant. EGF at 100 ng/ml had a less pronounced effect which, when analyzed statistically, was not significant. Amniotic fluid-derived cells are used for the prenatal detection of genetic disorders. The use of FGF to increase the rate of growth of these cells should reduce the time required between amniocentesis and diagnosis.

Amniotic Fluid↗
PubMed1978

Collaborative study of the effects of human growth hormone in growth hormone deficiency. V. Treatment with growth hormone administered once a week.

Twenty-two GH-deficient patients received 6 IU GH weekly for 6 months. They increased their growth rate from 1.0 +/- 0.2 to 2.9 +/- 0.3 (SE) cm/6 months (P less than 0.01). However, their rate of growth was significantly less (P less than 0.05) than the rate [4.1 +/- 0.5 (SE) cm/6 months] observed earlier when they had received 2 IU GH three times a week. Seven patients received weekly GH for 18 months and they also grew significantly less (P less than 0.01) than when they had received GH divided over the week. These results suggest that once a week GH does not provide the most effective therapy for GH deficiency.

Drug Administration Schedule↗
PubMed1977

Transitory growth hormone deficiency successfully treated with human growth hormone.

This study was carried out in order to determine whether children with a transitory type of growth hormone deficiency showed an accelerated growth in height velocity on treatment with human growth hormone (HGH). Following careful diagnostic routine procedures 13 extremely short children were diagnosed as having isolated growth hormone deficiency, and were successfully treated with HGH. A true isolated growth hormone deficiency was present in 5 of the children, whereas 8 showed a normal increase in serum growth hormone on repeated growth hormone stimulation tests after their development of puberty and termination of HGH treatment. Three boys with bone ages of 5.5, 8.0 and 9.5 years showed an undisputable effect following HGH administration. They showed an initial growth at the start of treatment, and a second growth spurt during development of puberty. Two of the boys reached final statures of 14 cm taller than the predicted heights. The other patients, including the children with true isolated growth hormone deficiency showed an initial spurt of growth at the start of the HGH treatment immediately followed by a pubertal growth spurt. The mean accleration of height velocity for the children with true isolated growth hormone deficiency was from 3.4 cm during the year before treatment to 7.0 cm during the first year on treatment, as compared to 2.8 and 7.4 cm, respectively, for the children with transitory growth hormone deficiency. A girl with severe anorexia nervosa who had a transitory growth hormone deficiency, showed an accelerated high velocity from 1.1 cm to 7.6 cm during the first year following treatment with HGH.

Adolescent↗
PubMed1977

Effect of administration frequency of growth hormone on longitudinal bone growth in the hypophysectomized rat.

The effect of the administration frequency of growth hormone on longitudinal bone growth was investigated with tetracycline as intravital marker of the bone growth of the proximal tibia in hypophysectomized rats. The total dose of growth hormone (NIH-GH-B16) and the administration period were the same in all compared experiments. It was possible to achieve an optimum growth response for a certain total dose of growth hormone by increasing the injection frequency. The period of hormone administration was 10 or 5 days followed by a 10 days withdrawal period. When the growth hormone was administered alone or in association with L-thyroxine for 10 days, the optimum injection frequency for growth hormone was found to be 1 inj./day in hypophysectomized rats and 2 inj./day in thyroxine-treated hypophysectomized rats. When the administration period was 5 days for growth hormone given in association with L-thyroxine, the growth stimulation induced by one daily growth hormone injection was the same as that induced by two or four daily injections of the same total dose. An increase in the administration frequency for a total daily dose of thyroxine from 1 to 2 inj./day did not increase the longitudinal bone growth either when thyroxine was given alone or in association with growth hormone.

Animals↗
PubMed1976

Growth hormone stimulating the growth of arterial medial cells in vitro. Absence of effect of insulin.

Earlier studies have shown a stimulatory effect of diabetic serum on the growth of rabbit aortic medial cell cultures. Growth media supplemented with normal serum with added insulin (50-2,000 muU./ml. serum) did not enhance the growth of the medial cell cultures. Control media containing serum from recent diabetics with low insulin concentration stimulated the growth (2p less than 0.01). Supplementation of normal serum with human growth hormone (final concentration 1-5 ng./ml. medium) resulted in a significant enhancement of growth (2p less than 0.005). The growth-promoting effect of growth hormone was not detectable with lower concentrations (0.5 ng. and 0.1 ng./ml. medium). The growth effect of the low concentration of growth hormone could not be augmented by increasing the concentration of glucose in the incubation medium. Growth hormone in an amount of 1 ng./ml. medium increased both the number of 3H-thymidine-labeled cells as identified by autoradiography and the number of mitotic bodies (2p less than 0.005 and 2 p less than 0.025). The present results demonstrate that the growth-stimulating factor(s) in diabetic human serum described earlier is not insulin but may well be growth hormone.

Adult↗
PubMed1975

A potent new mesodermal growth factor from mouse submaxillary gland. A quantitative, comparative study with previously described submaxillary gland growth factors.

A new growth factor with potent growth stimulating effects on connective tissue cells of the cornea has been isolated and partially purified from mouse submaxillary glands. A computerized image analysis system has been used to quantitate the growth responses of connective tissue fibroblasts to this new growth factor and to compare its activity with that of four previously described growth factors [nerve growth factor (NGF), epidermal growth factor (EGF), mesodermal growth factor (MGF), and thymocyte-transforming factor (TTF)] also obtained from mouse submaxillary glands. The new factor is as potent a growth stimulator as the previously described MGF. All five of the growth factors possessed esteropeptidase activity (trypsin-like) and general proteolytic activity. There was no correlation between the degree of growth stimulation of the connective tissue cells and either the esteropeptidase or general proteolytic activities of any of the growth factors.

Animals↗