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PubMed2001

Feeding problems in Silver-Russell syndrome.

In order to identify the prevalence and severity of feeding problems in children with Silver-Russell syndrome (SRS) the feeding difficulties of 32 children with SRS and 32 age- and sex-matched control children were assessed using the Feeding Assessment Questionnaire (Harris and Booth 1992). Children's ages ranged from 2 to 11 years, with 19 male and 13 female pairs. In a subset of matched pairs, parent-child interaction at mealtimes was examined using video recording; food intake was also assessed over a 3-day period using weighed food diaries. Children with SRS experienced significantly more feeding problems than children without growth disorders. Common feeding problems for children with SRS were poor appetite, fussiness, slow feeding, and problems associated with oral-motor dysfunction. Feeding problems did not significantly affect intake of kilocalories, protein, fat, or carbohydrates. Mealtime interaction between children with SRS and their parents was significantly more negative than interactions between control-group children and their parents. The focus of intervention packages in SRS should be to reduce negative parent-child interactions and reduce parental anxiety about feeding, growth, and weight.

Abnormalities, Multiple↗

PubMed2001

Mutant laboratory mice with abnormalities in hair follicle morphogenesis, cycling, and/or structure: annotated tables.

Numerous transgenic, targeted mutagenesis (so-called knockouts), conditional (so-called "gene switch") and spontaneous mutant mice develop abnormal hair phenotypes. The number of mice that exhibit such abnormalities is increasing exponentially as genetic engineering methods become routine. Since defined abnormalities in hair follicle morphogenesis, cycling and/or structure in such mutant mice provide important clues to the as yet poorly understood functional roles of many gene products, it is useful to summarize and classify these mutant mice according to their hair phenotype. This review provides a corresponding, annotated table of mutant mice with hair abnormalities, classifying the latter into 6 categories, 1) abnormally low number of hair follicles, 2) disorders of hair morphogenesis, 3) of hair follicle cycling, 4) of hair follicle structure 5) of sebaceous gland structure, and 6) hair growth disorders as a consequence of immunological abnormalities. This annotated table should serve as a useful source of reference for anyone who is interested in the molecular controls of hair growth, for investigators who are looking for mouse models to explore or compare the functional activities of their gene of interest, and for comparing the hair phenotype of newly generated mouse mutants with existing ones.

Animals↗

PubMed2001

Obstetric ultrasound: What the radiologist needs to know.

Obstetric ultrasound forms an integral part of modern obstetric care. This includes the use of ultrasound for screening as well as in diagnostic and therapeutic roles. Radiologists involved in this field must have the appropriate training and expertise to match the type of investigation or screening procedure to be undertaken. There should be an explicit understanding of this training and expertise both for the referring obstetrician and expectant mother. All radiologists involved in the care of women should have a thorough understanding of the normal and abnormal appearances of the first trimester as early pregnancy disorders present to the generalist; however, a smaller number of radiologists are involved in anomaly screening and management of growth disorders and still fewer in tertiary referral work. Obstetric medical practice is increasingly litigious and the aims of screening ultrasound and the limitations (false-negative and false-positive rates) should be explicit not only to the referring clinician but also to the expectant parents prior to screening. The diagnostic accuracy of ultrasound should be known in order that the expectant mother can give informed consent.

Female↗

PubMed2003

PTEN: tumour suppressor, multifunctional growth regulator and more.

The tumour suppressor gene PTEN is mutated in a wide range of human cancers at a frequency roughly comparable with p53. In addition, germline PTEN mutations are associated with several dominant growth disorders. The molecular and cellular basis of these disorders has been elucidated by detailed in vivo genetic analysis in model organisms, in particular the fruit fly and mouse. Studies in the fly have shown that PTEN's growth regulatory functions are primarily mediated via its lipid phosphatase activity, which specifically reduces the cellular levels of phosphatidylinositol 3,4,5-trisphosphate. This activity antagonizes the effects of activated PI3-kinase in the nutritionally controlled insulin receptor pathway, thereby reducing protein synthesis and restraining cell and organismal growth, while also regulating other biological processes, such as fertility and ageing. Remarkably, this range of functions appears to be conserved in all higher organisms. PTEN also plays a role as a specialized cytoskeletal regulator, which, for example, is involved in directional movement of some migratory cells and may be important in metastasis. Furthermore, conditional knockouts in the mouse have recently revealed functions for PTEN in other processes, such as cell type specification and cardiac muscle contractility. Genetic approaches have therefore revealed a surprising diversity of global and cell type-specific PTEN-regulated functions that appear to be primarily controlled by modulation of a single phosphoinositide. Together with evidence from studies in cell culture that suggests links between PTEN and other growth regulatory genes such as p53, these studies provide new insights into PTEN-linked disorders and are beginning to suggest potential clinical strategies to combat these and other diseases.

Cell Division↗

PubMed2005

Transforming growth factor-beta, cell signaling and cardiovascular disorders.

Transforming growth factor-beta (TGF-beta) is a multifunctional growth factor with a wide range of potential effects on growth, differentiation, extracellular matrix accumulation and the immune system. It has been implicated in many cardiovascular disorders. TGF-beta's actions are mediated via a complex between its type I and type II receptors resulting in the phosphorylation of receptor-specific Smads followed by their passage to the nucleus where they influence many transcriptional responses. TGF-beta has important roles in the development of the neointima and constrictive remodeling associated with angioplasty. In atherosclerosis its actions are yet to be fully elucidated but its ability to control the immune system has profound effects on lesion development, particularly by influencing the types of lesions that develop. TGF-beta can also induce arteriogenesis and markedly influences angiogenic processes, possessing both pro- and anti-angiogenic effects. It is also a major contributor to the development of various cardiovascular fibrotic disorders including those in the vasculature, heart and kidney. Targeting TGF-beta prevents neointima formation and the constrictive remodeling associated with angioplasty and also prevents the development of many fibrotic disorders. This review summarizes TGF-beta signaling pathways, the mechanisms by which TGF-beta contributes to many of these cardiovascular diseases and examines the therapeutic potential of targeting TGF-beta actions in preventing these disorders.

Animals↗

PubMed2000

Involvement of hepatocyte growth factor/scatter factor and met receptor signaling in hair follicle morphogenesis and cycling.

HGF/SF and its receptor (Met) are principal mediators of mesenchymal-epithelial interactions in several different systems and have recently been implicated in the control of hair follicle (HF) growth. We have studied their expression patterns during HF morphogenesis and cycling in C57BL/6 mice, whereas functional hair growth effects of HGF/SF were assessed in vivo by analysis of transgenic mice and in skin organ culture. In normal mouse skin, follicular expression of HGF/SF and Met was strikingly localized: HGF/SF was found only in the HF mesenchyme (dermal papilla fibroblasts) and Met in the neighboring hair bulb keratinocytes. Both HGF/SF and Met expression peaked during the initial phases of HF morphogenesis, the stage of active hair growth (early and mid anagen), and during the apoptosis-driven HF regression (catagen). Met+ cells in the regressing epithelial strand appeared to be protected from undergoing apoptosis. Compared to wild-type controls, transgenic mice overexpressing HGF/SF under the control of the MT-1 promoter had twice as many developing HF and displayed accelerated HF development on postnatal day 3. They also showed significant catagen retardation on P17. In organ culture and in vivo, HGF/SF i.c. resulted in a significant catagen retardation. These results demonstrate an important role of HGF/SF and Met in murine hair growth control and suggest that Met-mediated signaling might be exploited for therapeutic manipulation of human hair growth disorders.-Lindner, G., Menrad, A., Gherardi, E., Merlino, G., Welker, P., Handjiski, B., Roloff, B., Paus, R. Involvement of hepatocyte growth factor/scatter factor and Met receptor signaling in hair follicle morphogenesis and cycling.

Animals↗

PubMed1989

The parathyroid glands in chronic renal failure: a study of their growth and other properties made on the basis of findings in patients with hypercalcemia.

We investigated the growth of hyperplastic parathyroid glands removed at operation from 16 patients with chronic renal failure complicated by hypercalcemia, by incubating fresh tissue with tritiated thymidine. In each gland the proportion of cells synthesizing DNA was determined directly by counting labeled nuclei after autoradiography and indirectly from incorporation of label into DNA, and the mean diameter of chief cell nuclei was measured. Both DNA synthesis and mean nuclear diameter were positively correlated with plasma calcium level. Assuming the mean duration of S phase to be 12 hours, the birthrate of new cells (mean +/- SD) was 18.5% +/- 23.6% per year, significantly (p less than 0.05) greater than the 11.5% +/- 7.4% per year found in 63 parathyroid adenomas previously studied. On the basis of estimated disease duration, the minimum birthrate needed to grow glands of the observed weight was 23.4% +/- 16.5% per year. The similarity between observed and needed birthrates indicates that the glands were growing almost as fast as when renal failure began, and that parathyroid growth was no longer regulated in accordance with normal plasma calcium homeostasis. To account for this, we propose that the disordered growth is a consequence of an increase in secretory set point, which in turn is a consequence of calcitriol deficiency. Because the effectiveness of parathyroid hormone is impaired in renal failure, a large increase in total hormone secretion is needed to raise the plasma calcium level to the new set point, and the necessary increase in gland size can be achieved only by a sustained increase in the rate of cell division.

DNA↗

PubMed2004

Neonatal hypoglycaemia: aetiologies.

Diagnosis of glucose status requires knowledge of the homeostatic mechanisms that maintain the blood glucose concentration between the narrow range of 2.5 and 7.5 mmol/l during periods of eating or fasting. Hypoglycaemia occurring within the first few hours after eating is suggestive of hyperinsulinism. Most glucose is subsequently converted into glycogen in the liver, and hypoglycaemia occurring during this phase is suggestive of glycogenosis. During fasting, gluconeogenesis progressively replaces glycogen as the major source of blood glucose, and hypoglycaemia occurring during this period is suggestive of impaired gluconeogenesis or fatty acid disorders. Growth hormone, glucagon, cortisol and insulin-like growth factor 1 deficiencies may also play a role. Other causes of hypoglycaemia have also been identified recently, namely glucose transporter disorders, respiratory chain disorders and congenital disorders of glycosylation.

Humans↗

PubMed1989

Growth factors and the regulation of pre- and postnatal growth.

Peptide growth factors represent a largely paracrine level of intercellular communication that is basic to the process of life. Growth factors are present in the ovum and are amongst the first products expressed by the embryonic genome. They function as both signals and progression factors for embryonic tissue growth, induction, differentiation, maturation and function. While a widespread tissue expression is demonstrable during fetal development, and in certain postnatal tissues such as the epiphyseal growth plate, growth factor presence in the adult is restricted to tissues sharing rapid cellular turnover such as ovary. However, a transient re-expression of peptide growth factors occurs during adult tissue repair. In addition to mitogenic peptides such as IGFs or EGF, the family of growth factors also includes physiological growth inhibitors such as TGF beta and certain neuropeptides. Insulin is mitogenic in the early embryo and evidence is presented to support a continuation of this role, under defined nutritional conditions, in late gestation. The importance of insulin to pre- and postnatal growth has prompted an expanding literature dealing with the interactions of nutrients, hormones and growth factors during the growth and functional maturation of the islets of Langerhans. While the expression of growth factors in the early embryo is apparently autonomous, some, such as IGFs, become increasingly dependent on nutrient, insulin and GH availability during fetal development and in childhood growth. This has resulted in circulating IGF I and II determinations becoming useful diagnostic markers of endocrine-based growth disorder and nitrogen balance.

Embryonic and Fetal Development↗

PubMed1998

Plasma levels of carboxy terminal propeptide of type I procollagen and pyridinoline cross-linked telopeptide of type I collagen in healthy school children.

The aim of this study was to reveal the relationship of the plasma levels of the carboxy terminal propeptide of type I procollagen (PICP) and the pyridinoline cross-linked carboxyterminal telopeptide domains of type I collagen (ICTP) to age and height velocity (HV), and to compare PICP and ICTP levels in those who have not reached their final height with those who have. PICP and ICTP levels were measured by RIA in 271 healthy children (161M, 110F) aged from 10 to 15 y. The HV was calculated from their health check-up cards. The subjects were divided into two groups in this study: the final height (FH) group whose HV was <1.0 cm/y, and the non-final height (NFH) group whose HV in the last year was > or =1.0 cm/y. PICP and ICTP levels almost paralleled the values of age-related changes of HV. Furthermore PICP and ICTP levels significantly correlated with HV. PICP and ICTP levels of the FH group were higher than those of adults previously reported. The values will be useful as reference for healthy children and growth disorder. Before reaching final height, PICP and ICTP can be useful makers of not only bone turnover but also of linear growth. Bone turnover rate is still increasingly active just after linear growth has been completed, and then it become similar to the levels of adults.

Adolescent↗

PubMed1999

Resistance to CD95 (APO-1/Fas)-mediated apoptosis in human renal cell carcinomas: an important factor for evasion from negative growth control.

Disorders in negative growth control by CD95 (APO-1/Fas)-mediated apoptosis have been suggested to facilitate immune evasion of neoplastic cells and resistance to anticancer drugs. The present report describes the expression and function of CD95 receptor and ligand in human renal cell carcinomas (RCC) of all major histological types, presenting in vitro data on RCC cell lines (n = 30) and ex vivo observations in RCC tissue samples (n = 30). Using RT-PCR, flow cytometry and immunostaining, expression of CD95 receptor and ligand was found in human RCC of all major histological types. The expression levels of CD95 ligand, however, were rather low. Despite constitutive CD95 receptor expression, resistance to CD95-mediated apoptosis became evident from the weak response to agonistic anti-CD95 antibodies, which induced a low increase of apoptosis in only 9 of 30 RCC cell lines. After IFN-gamma pretreatment, however, apoptosis triggered by agonistic anti-CD95 antibodies was observed in 22 of 30 RCC cell lines. These data indicated that the machinery required for CD95-induced cell death was present, albeit inactive in most RCC. Inhibition of protein synthesis by cycloheximide resulted in increased sensitivity to agonistic anti-CD95 antibodies, suggesting a role for short-lived apoptosis-protective proteins in the resistance of RCC to CD95-mediated apoptosis. Moreover, we demonstrated the secretion of soluble CD95 receptor which might contribute to this resistance as well. In conclusion, resistance rather than responsiveness to CD95-mediated apoptosis is a key feature of human RCC. This resistance might facilitate evasion from negative growth control and contribute to the failure of cytotoxic drugs in the treatment of human RCC.

Apoptosis↗

PubMed1989

Fibroblast growth factor and glutamate: opposing roles in the generation and degeneration of hippocampal neuroarchitecture.

Neuritic regression and cell death (neurodegeneration) are common features of both normal nervous system development and neurodegenerative disorders. Growth factors and excitatory amino acid neurotransmitters have been suggested independently to play roles in neurodegenerative processes. The present study investigated the combined effects of fibroblast growth factor (FGF) and glutamate on the development and degeneration of cultured hippocampal neurons. Consistent with previous data, we found that FGF, but not NGF, promoted neuronal survival and dendritic outgrowth. In contrast, a low level of glutamate (50 microM) caused a reduction in dendritic outgrowth, and high levels (100 microM-1 mM) reduced neuronal survival in a dose-dependent manner. When cultures were maintained in the presence of FGF, there was a striking reduction in neuronal death normally caused by 100-500 microM glutamate. FGF raised the threshold for glutamate neurotoxicity. FGF also antagonized the outgrowth-inhibiting actions of glutamate. Measurements of intracellular calcium levels with fura-2 demonstrated a direct relationship between glutamate-induced rises in intracellular calcium and neurodegeneration. FGF reduced the glutamate-induced increases in intracellular calcium levels. However, when cultures were pretreated with the RNA synthesis inhibitor actinomycin D or with the protein synthesis inhibitor cycloheximide, FGF did not prevent glutamate-induced increases in intracellular calcium or neurodegeneration. Taken together, these results suggest that (1) interactions between growth factors and neurotransmitters may be important in brain development; (2) imbalances in these systems may lead to neurodegeneration; and (3) cellular calcium-regulating systems may be a common focus of growth factor and neurotransmitter actions.

Animals↗

PubMed1986

Serum bone GLA-protein in growth hormone deficient children.

Serum bone GLA-protein (BGP), a sensitive and specific marker of bone formation, was measured in 54 normal children and in 50 children with growth disorders. In normal children, the pattern of variations of serum BGP with age was similar to the pattern of variations of the growth velocity. Mean serum BGP was very high during the first year of life (25.3 +/- 8.5 ng/ml), decreased to 14.8 +/- 2.2 ng/ml from 2 to 6 years, increased to 18.4 +/- 4.1 ng/ml from 7 to 10 years and to 18.8 +/- 6.5 ng/ml from 11 to 14 years. After puberty, mean sBGP decreased to 12.9 +/- 5.4 ng/ml from 15 to 18 years and to 6.5 +/- 1.4 ng/ml in young adults. In 32 patients with untreated growth hormone (GH) deficiency, mean sBGP was markedly lower than in age matched controls (6.8 +/- 4.4 ng/ml vs. 17.5 +/- 4.9 ng/ml, p less than .001). In 19 patients with GH deficiency who were undergoing treatment with human GH, sBGP was higher than in untreated patients (20.5 +/- 9.3 ng/ml vs. 6.8 +/- 4.4 ng/ml, p less than .001) and was not different from controls. Repeated measurements performed in 14 GH-deficient patients under chronic GH therapy showed that serum BGP: (1) increased in most patients during treatment (p less than .005); (2) was correlated with the duration of treatment (p less than .001); (3) decreased to pretreatment values after discontinuing therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1996

Metabolic effects of recombinant human insulin-like growth factor-I in humans: comparison with recombinant human growth hormone.

Many of the metabolic actions of growth hormone (GH) are mediated through insulin-like growth factors or somatomedins. Recombinant human insulin-like growth factor-I (rhIGF-I) has a dichotomous insulin-like and GH-like action when used in different clinical situations in humans. Its effects on carbohydrate metabolism show a prominent increase in total insulin sensitivity, causing hypoglycemia in higher doses and maintaining normal glucose homeostasis in lower doses. This polypeptide selectively stimulates whole body protein synthesis with no effect on proteolysis when given in doses of 100 micrograms/ kg subcutaneously twice daily for at least 5-7 days, effects which are indistinguishable from those of GH. This contrasts with the marked suppression of proteolysis observed when higher doses are given, similar to the effects observed with insulin. When used in combination with rhGH, rhIGF-I has a synergistic effect, improving total nitrogen retention in calorically deprived subjects, yet it does not cause any greater enhancement of whole body protein anabolism in normally fed volunteers than giving rhGH and rhIGF-I individually. This suggests a common pathway for IGF-I and GH enhancing protein anabolism in the normally fed state. rhIGF-I also stimulates linear growth in children with defects in the GH receptor. Recent data show that this potent growth factor has a potential advantage over GH in the treatment of severe protein catabolic states, particularly the glucocorticosteroid-dependent model, as it ameliorates the marked increase in protein catabolism caused by the steroids, but without a diabetogenic effect. Here, a brief overview is provided of available human data on the actions of this peptide on carbohydrate, lipid, and protein metabolism, linear growth, and its anabolic effects. rhIGF-I offers promise in the treatment of selective growth disorders and in protein catabolic and insulin-resistant states.

Growth Hormone↗

PubMed2006

Catch-up growth follows an abnormal pattern in experimental renal insufficiency and growth hormone treatment normalizes it.

The primary goal of this study was to determine if the ability to undergo catch-up growth following a transient injury is preserved in an experimental model of moderate chronic renal failure (CRF) and the effect of growth hormone (GH) administration on such phenomenon. Young rats were subtotally nephrectomized (days 0 and 4) (Nx). From days 11 to 13, food intake was restricted in subgroups of Nx and control (C) rats (NxR and CR). After refeeding, subgroups of NxR and CR rats received GH from days 14 to 20 (NxRGH and CRGH). Rats were killed on days 14 (C, CR, Nx, NxR), 17 and 21 (C, CR, CRGH, Nx, NxR, NxRGH), and 36 (C, CR, Nx, NxR). Longitudinal growth rate was measured by osseous front advance in the proximal tibiae. With refeeding, growth rate of CR, NxR, and NXrGH rats became significantly greater than that of C, indicating catch-up growth. This occurred later and with lower growth rate in NxR than in CR rats, whereas the characteristics of catch-up growth in CR and NxRGH animals were similar. Changes in growth rate were associated with modifications in the morphology and proliferative activity of growth cartilage. We conclude that catch-up growth occurs in renal insufficiency but follows a different pattern from that observed with normal renal function. GH treatment normalizes the pattern of catch-up growth in CRF. Changes in growth velocity are associated to modifications in the structure and dynamics of growth cartilage.

Animals↗

PubMed2003

Systemic and local regulation of the growth plate.

The growth plate is the final target organ for longitudinal growth and results from chondrocyte proliferation and differentiation. During the first year of life, longitudinal growth rates are high, followed by a decade of modest longitudinal growth. The age at onset of puberty and the growth rate during the pubertal growth spurt (which occurs under the influence of estrogens and GH) contribute to sex difference in final height between boys and girls. At the end of puberty, growth plates fuse, thereby ceasing longitudinal growth. It has been recognized that receptors for many hormones such as estrogen, GH, and glucocorticoids are present in or on growth plate chondrocytes, suggesting that these hormones may influence processes in the growth plate directly. Moreover, many growth factors, i.e., IGF-I, Indian hedgehog, PTHrP, fibroblast growth factors, bone morphogenetic proteins, and vascular endothelial growth factor, are now considered as crucial regulators of chondrocyte proliferation and differentiation. In this review, we present an update on the present perception of growth plate function and the regulation of chondrocyte proliferation and differentiation by systemic and local regulators of which most are now related to human growth disorders.

Animals↗

PubMed2003

[Normal and abnormal alveolar development].

INTRODUCTION: Alveolar growth predominantly occurs post-natally and is characterised by the multiplication of alveoli, the thinning of inter-alveolar walls, and the maturation of capillary vessels. STATE OF THE ART: Alveolar growth is controlled by numerous factors whose interactions remain poorly understood. Many phenomena can interfere with normal alveolar growth resulting in abnormal development and a reduction in alveolar surface. This is especially the case in premature human neonates, whose lungs are structurally and functionally immature. Oxygen therapy, mechanical ventilation, and airway inflammation may induce alveolar growth disorders in these children, resulting in the development of bronchopulmonary dysplasia. PERSPECTIVES AND CONCLUSIONS: Further studies are needed to improve our knowledge about alveolar growth regulatory mechanisms so that better strategies can be developed to prevent these respiratory complications in premature neonates.

Bronchopulmonary Dysplasia↗

PubMed1993

Growth factors in behavioral teratology.

Polypeptide Growth Factors are protein molecules which regulate cell proliferation and/or differentiation. A number of different Growth Factors (GFs) have been identified and characterized in recent years, and they have been shown to control several physiological processes, such as growth, repair, differentiation, and development of specific cell populations. In particular Nerve Growth Factor, the best characterized among the about 30 GF molecules, is endowed with specific activities on cholinergic and peptidergic CNS neurons. Several GFs originally named according to their biological activity (Epidermal Growth Factor, EGF; Fibroblast Growth Factor: FGF; Transforming Growth Factor: TGF; Insulin-like Growth Factor: IGF) have been recently found in the central nervous system. The effects of in vivo GF administration on the ontogenesis of altricial rodents are reported. Indexes of neurobehavioral maturation are accelerated upon neonatal NGF and bFGF exposure, while a similar treatment with EGF exerts both growth-promoting and growth-inhibiting effects on mouse somatic and behavioral development. Administration of IGF appears to affect ultrasonic vocalization in mouse pups. Moreover, NGF given intracerebroventricularly to newborn mice anticipates both the appearance of the scopolamine-induced hyperactivity and the maturation of behaviours under cholinergic control. The present findings are in agreement with a model where different GFs can "switch on" developmental events leading sometimes to dramatic changes in the normal ontogenetic pattern.

Age Factors↗