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At least 19 recordsLinked to original sources
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↗
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↗
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↗
PubMed1979

Rheumatoid arthritis and growth retardation in children: treatment with human growth hormone.

Twenty patients with rheumatoid arthritis or Still's disease associated with growth failure were treated with human growth hormone, 7.5 to 17 U/m2 body surface per week. Five patients did not respond with better growth. In the remainder the mean growth rate increased from 1.9 cm/year (range: 0 to 3.3) to 6.2 cm/year (range: 3.6 to 12) over 5 to 7 months. Twelve patients treated for longer periods increased their mean growth rate from 2.6 cm/year (range: 0.7 to 5.7) to 6.3 cm/year (range: 2.4 to 9.7) and continued to grow during a second year of treatment. Growth velocity decreased in 6 patients when the hGH therapy was discontinued. The causes for this improvement in growth are possibly multifactorial: the growth rate is depressed by the severity of the disease and high-dose glucocorticoid therapy. Increases of growth rate occurred during improvements in the disease, reduction of steroid medication, as a result of therapy with human growth hormone, and because of puberty in some patients. Human growth hormone seemed to improve the underlying condition of four of the patients but had no influence on the disease in the remaining children.

Adolescent↗
PubMed1977

Reactivity of non-primate growth hormones and prolactins with human growth hormone receptors on cultured human lymphocytes.

Ovine placental lactogen is as reactive as human growth hormone with the human growth hormone receptor of cultured human (IM-9) lymphocytes, which confirms the findings of Carr and Friesen with receptors of human liver. We now also show that bovine and ovine growth hormones and ovine prolactin have reactivity for the human growth hormone receptor on IM-9 lymphocytes that is of the same order of magnitude (0.03%) as that previously reported for human placental lactogen. The binding studies predict that these non-primate hormones will have biological effects on skeletal growth in primates, either as agonists or antagonists. Previous studies have shown that when IM-9 lymphocytes are exposed to human growth hormone for 18 h at 37 C, there is a time and concentration dependent loss of human growth hormone receptors, and the magnitude of the loss of receptors after preincubation for 18 h at 37 C is greater than the average occupancy of receptors under steady state conditions for 90 min at 30 C. In the present study we show that human and ovine placental lactogens, ovine prolactin, and bovine and ovine growth hormones also produce this effect on the human growth hormone receptor. Since the cellular process by which a hormone induces loss of its own receptors appears to require binding of the hormone to its receptor as well as one or more subsequent steps in hormone action, it is likely that all of the preparations that induce receptor loss will be shown to have some agonist activity of human growth hormone in promoting skeletal growth in primates. Further, these studies extend the interrelationships between primate and non-primate pituitary and placental hormones from what has been suggested previously from biological and structural studies.

Animals↗
PubMed1979

Practical application of generic growth theory and the significance of the growth curve parameters.

The generic growth curve is developed by plausibility arguments based on simple growth models. Parameters of the generic curve include the maximum size, maximum specific growth rate, and a dimensionless velocity constant which can be related to metabolic efficiency in the case of nutrient-limited growth. Parameter estimates are obtained from estimates of the size and time at the point of inflection, the size and time at any other arbitrarily selected point, and the maximum size. Parameter estimates thus obtained and used as initial estimates in nonlinear least squares analysis often give rapid convergence to a minimum error mean square. [For the growth of Escherichia coli K-12 in liquid medium, the generic curve could be simplified to a form containing only three parameters: the maximum specific growth rate, the maximum size, and the time required to reach maximum size. When the bacteria were inhibited by the addition of increasing amounts of the lactoperoxidase antimicrobial factor, there was no significant change in viable counts or maximum specific growth rate, but the time required to reach maximum growth increased linearly with increasing amounts of added antimicrobial factor.] Analysis of growth in terms of the generic growth curve can be a powerful technique for finding relationships which may not be apparent from qualitative consideration of the data.

Biometry↗
PubMed1978

Growth hormone modulation of murine erythroleukemia cell growth in vitro.

There are few studies showing a biological effect of growth hormone (somatotropin) on cell proliferation in vitro at physiological concentrations. We report here that Friend virus-infected erythroleukemia cells are responsive to growth hormone in vitro. Using a serum-free clonogenic assay we found as little as 0.1 ng of human growth hormone per ml caused a prominent stimulation of cell proliferation. Peak activity of human growth hormone occurred at 200 ng/ml, resulting in a 2-fold increase in cloning. Human chorionic somatomammotropin and the Cys(Cam)53-hGH(1-134) fragment of human growth hormone were also active, but a biologically inert oxidized human growth hormone had no growth-promoting effect in vitro. Cell proliferation was stimulated by insulin with peak potentiation occurring at 1 ng/ml, and prolactin had a demonstrable stimulatory effect between 50 and 100 ng/ml. These observations indicate that growth hormone and related polypeptides have a direct effect on the in vitro proliferation of erythroleukemia cells in the absence of serum. The results confirm a direct action of growth hormone on mammalian cells and suggest that pituitary hormones may affect leukemic cell growth.

Animals↗
PubMed1979

The relationship of growth failure (chronic undernutrition) to the prevalence of clinically severe protein-energy malnutrition and to growth retardation in protein-energy malnutrition.

A total of 72 of 276 children from a rural Mexican village were chronically undernourished as judged by their growth failure between 6 and 36 months of age. Fourteen of the 72 and five of the remaining 204 children developed clinically severe protein-energy malnutrition (PEM) as judged by clinical signs other than weight or length. This amounted to an 8-fold higher prevalence of PEM in the group of children with growth failure. When children were grouped into quartiles of length at 6 months by sex, quartile was not related to the subsequent occurrence of PEM or to the age when PEM developed. However, analysis indicated that the growth of children with PEM and growth failure had slowed relative to their quartiles before PEM developed; they were also retarded according to the Harvard standards. The children with PEM were then compared to others with a similar growth history (growth failure, no growth failure) who never developed PEM. PEM children did not differ significantly in over weight or length and displayed a significant difference in upper arm muscle circumference at only one age. The 14 with growth failure and PEM had poorer overall growth, including arm muscle circumference, than the five with PEM and no growth failure.

Anthropometry↗
PubMed1979

Inhibition by glucocorticoids and choleragen of the conditional growth of poorly adherent mononuclear phagocytes of newborn hamster liver and lung (hormonal control of macrophage growth).

Conditions for in vitro growth of mononuclear phagocytes from newborn hamster liver and lung were studied. In the primary cultures of liver and lung, round cells outgrew and frequently floated off into the culture medium. They were separated from fibroblast-like cells adherent to plastic by collecting the medium. The round cells were identified as mononuclear phagocytes on the criteria of phagocytic capacity of heat-killed bacteria and IgG-coated erythrocytes, fine cell structure and cytochemistry. The phagocytes that had not been activated previously proliferated for about ten generations in F12 medium supplemented with 10% fetal calf serum depending on a growth factor produced by hamster brain, liver or lung cells. Without the factor, the cells quickly cytolysed. Mononuclear phagocytes from blood had the same characteristics of growth and cytochemistry, but had fewer IgG receptors at the cell surface than similar cells from the liver and lung. The effects of a variety of chemical compounds on the growth of the liver and lung cells were studied. Insulin stimulated their growth by 20-30%, but was not replaceable for the growth factor. Glucocorticoids, dexamethasone and hydrocortisone, inhibited the growth of the phagocytes at the physiological concentrations: 3 x 10(-9) M and 2 x 10(-8) M for 50% inhibition, respectively. Indomethacin, non-steroid anti-inflammatory reagent, at 10(-8) M to 10(-6) M gave no effect. Choleragen that increases the intracellular cyclic AMP level, inhibited the growth at a concentration as low as 5 pg/ml. These data suggest that the growth of mononuclear phagocytes is controlled not only by a growth factor produced by other cells but also by glucocorticoids.

Animals↗
PubMed1978

Osmotic effects on radial growth rate and specific growth rate of three soil fungi.

The radial growth rate on osmotically adjusted agar medium and the relative specific growth rate in osmotically adjusted liquid medium were determined for Rhizoctonia solani, Pythium ultimum, and Verticillium dahliae. On basal medium, an isolate of P. ultimum and R. solani had similar radial growth rates of 0.52 and 0.47 mm/h, respectively, whereas V. dahliae grew at a rate of 0.08 mm/h. Radial growth rate was reduced 50% at osmotic potentials of -16, -27, and -32 bars for P. ultimum, R. solani, and V. dahliae, respectively. No growth occurred at -32 bars for P. ultimum, -56.2 bars for R. solani, and -100 bars for V. dahlia. Specific growth rates in liquid culture were 0.011 h-1 for P. ultimum, 0.008 h-1 for V. dahliae, and 0.026 h-1 for R. solani. Ratios of radial growth rate (Kr) to specific growth rate (alphas) were computed for each fungus growing at different osmotic potentials. There was not a constant relationship between Kr on agar and alphas in liquid medium, e.g., Kr/alphas ratios varied from 8-41% from a mean ratio for a particular species. The results indicated that radial growth rate on osmotic agar was not useful as a measure of relative specific growth rate of a fungus in osmotically adjusted liquid medium.

Agar↗
PubMed1977

[Phenomenologic-mathematical modeling of the human-body-length growth through the analysis of growth periods and their quantitative-analytical registration].

The body height growth (of masculine beings) was modelled in a phenomenologic-mathematical manner by partitioning the time course of measured growth curve in parts every of which corresponds to a separated growth period. This partitioning was reached in a natural way so that a superposition of the single spurts yields the whole measured course. Every growth batch will be described in its time course by one term of inverse tangent function. The biological meaning and an explanation of the succession of the growth spurt as an effect of control circuits need further exploratory work. For detailed statements on acceleration phenomena concerning the body height growth this analysis gives possibilities for comparing the single growth spurts of the mean growth process of two populations in question. For measured values given by BROCK (1954) and SALZLER (1967) there are five growth periods in the time intervall reaching from time of conception until the end of the first year. Comparing the mathematical functions of the corresponding growth spurts for these two groups one can conclude that the second spurt (fetal spurt) is responsible for an increase of birth body height and the fourth for an increase of body height in the suckling age of the latter group against the former one.

Adolescent↗
PubMed1979

Application of the principles of enzyme kinetics to clonal growth rate assays: an approach for delineating interactions among growth promoting agents.

The interaction of mitogenic factors on a single cell type and the comparative activity of a given factor in diverse cell types have been studied by applying the principles of Michaelis-Menten kinetics to clonal growth data. Such comparisons are facilitated by derivation of two parameters; Km mitogen, the mitogen concentration that gives half-maximal clonal growth and a theoretical maximal growth rate, RMAX T. Both parameters are analogous to the Km and VMAX as applied to enzymatic reactions. Use of these parameters permits meaningful comparisons between cells with different growth rates. Using kinetic analysis of dose-response data, we found that normal human epithelial cells require 200 times more fetal bovine serum protein (FBSP) than a malignant line to multiply at their respective half-maximal rates. Further, the Km FBSP of normal cells was reduced to that of the malignant line by the inclusion of growth factors (EGF or FGF, and hydrocortisone) in the medium. On the other hand, even though greater levels of serum were required when growth factors and hydrocortisone were not present, their inclusion did not alter RMAX T. Interactions between mitogenic factors were shown to be unidirectional. Although EGF reduced the Km FBSP, FBSP did not change the Km EGF. The same type of analysis revealed that hydrocortisone, which potentiated the mitogenic activity of EGF did not change the Km EGF. Kinetic analysis of cell growth should prove useful in studies on the relation between growth and tumor promotion as well as in the evaluation of growth-inhibiting chemotherapeutic agents.

Blood Proteins↗