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PubMedDate not supplied

[Clinical aspects of cranio-mandibular disorders. II. Symptom profiles of subgroups].

The more frequent clinical variables of cranio-mandibular disorders in a sample of 406 patients of both sexes, aged between 9 and 78 (mean age 30.47), were used to classify the different pathologies of the stomatognatic dysfunction. Radiological imaging completed and improved the diagnostic assessment. The breakdown of the total patient population into diagnostic subgroups was: functional disorders, with a mainly myogenous component (19.7%); disk displacement with reduction (24.1%); disk displacement without reduction (11.7%); osteoarthrosis (10.8%); synovitis of various origin (8.8%); growth disorders (0.9%). A mixed group consisted of many patients displaying signs of internal derangement and contemporary pronounced muscular disorders (20.4%); finally some subjects did not show true disturbances of the masticatory system (3.6%). Considerable differences were found among the subgroups and the findings formed the basis of specific symptom profiles, that mainly considered the chief complaints as masticatory algia, earache, cephalalgia, migraine and neck and shoulders postural disturbances. The prevalence of specific pathogenetic factors confirmed the multifactorial aetiology and the need of a more directed choice of treatment.

Adolescent↗

PubMed1995

GM2 ganglioside and pyramidal neuron dendritogenesis.

GM2 ganglioside, although scarce in normal adult brain, is the predominant ganglioside accumulating in several types of lysosomal disorders, most notably Tay-Sachs disease. Pyramidal neurons of cerebral cortex in Tay-Sachs, as well as many other types of neuronal storage disorders, are known to exhibit a phenomenon believed unique to storage disorders: growth of ectopic dendrites. Recent studies have shown that a common metabolic abnormality shared by storage diseases with ectopic dendrite growth is the abnormal accumulation of GM2 ganglioside. The correlation between increased levels of GM2 and the presence of ectopic dendrites has been found in both ganglioside and nonganglioside storage disorders, the latter including sphingomyelin-cholesterol lipidosis, mucopolysaccharidosis, and alpha-mannosidosis. Quantitative HPTLC analysis has shown that increases in GM2 occur in proportion to the incidence of ectopic dendrite growth, whereas other gangliosides, including GM1, lack similar increases. Immunocytochemical studies of all nonganglioside storage diseases which exhibit ectopic dendritogenesis have revealed heightened GM2 ganglioside-immunoreactivity in the cortical pyramidal cell population, whereas nerurons in normal adult brain exhibit little or no staining for this ganglioside. Further, studies examining disease development have consistently shown that accumulation of GM2 ganglioside precedes growth of ectopic dendrites, indicating that it is not simply occurring secondary to new membrane production. These findings have prompted an examination for a similar relationship between GM2 ganglioside and dendritogenesis in cortical neurons of normal developing brain. Results show that GM2 ganglioside-immunoreactivity is consistently elevated in immature neurons during the period when they are undergoing active dendritic initiation, but this staining diminishes dramatically as the dendritic trees of these cells mature. Collectively, these studies on diseased and normal brain offer compelling evidence that GM2 ganglioside plays a pivotal role in the regulation of dendritogenesis in cortical pyramidal neurons.

Adult↗

PubMed1980

Growth patterns, ultrastructure, and chromosomal constitution of normal kidney and nephroblastoma cells in short-term culture.

Nephrectomies were performed on four children with nephroblastomas (Wilms' tumor). Tumor tissue and normal kidney tissue were taken from each patient and were cultured. The in vitro characteristics of the cultured cells were then compared with their known in vivo characteristics. The normal kidney cells showed uniform cell morphology, had a relatively slow and orderly growth pattern and had the usual diploid chromosomal constitution. The tumor cells on the other hand were irregular in morphology and had a rapid and disorderly growth pattern. Electron microscopic examination confirmed the variation in the tumor cell morphology. In addition, microfilaments were seen to be abnormally abundant in many of the cells and some cells contained membrane-bound granules. Desmosomes were absent. Chromosome analyses showed cells from three of the nephroblastoma samples to maintain a constant hyperdiploid karyotype during the first few passages in vitro, whereas the normal kidney cells continued to have the normal diploid karyotype. Our study suggests that nephroblastoma and normal kidney cells are stable in culture, that is they retain most of their cellular characteristics in vitro and do not undergo rapid dedifferentitation in short-term culture.

Cell Division↗

PubMed2001

Dual function of polysialic acid during zebrafish central nervous system development.

Polysialic acid (PSA), a carbohydrate epitope attached to the neural cell adhesion molecule, serves as a modulator of axonal interactions during vertebrate nervous system development. We have used PSA-specific antibodies and whole-mount immunocytochemistry to describe the spatiotemporal expression pattern of PSA during zebrafish central nervous system development. PSA is transiently expressed on all cell bodies and, except for the posterior commissure, it is not found on axons. Floorplate cells in the spinal cord and hindbrain strongly express PSA throughout development. Enzymatic removal of PSA leads to a defasciculated growth pattern of the posterior commissure and also affects distinct subsets of commissural axons in the hindbrain, which fail to cross the midline. Whereas the disordered growth pattern of hindbrain commissures produced by PSA-removal could be mimicked by injections of soluble PSA, the growth of axons in the posterior commissure was unaffected by such treatment. These results suggest that there are distinct mechanisms for PSA action during axon growth and pathfinding in the developing zebrafish CNS.

Animals↗

PubMed1989

[Intervertebral disk calcification in children].

Thirty one intervertebral space calcifications (I.S.C.) were studied in 21 children (12 boys, 9 girls), with mean age of 7 years; 25 calcifications had been followed for an average of 71.5 months. The main symptom was pain (Crisis) which relieved in a delay of 1 month in 70 per cent of cases. "Crisis" and radiographic fragmentation of the calcification are both criteria of going out of 18 calcifications, in a delay ranged from 28 days to 6 months. The calcification appears as a sign which disclose a general disease of spine, interesting vertebral body, growth plate, and disc; therefore we have observed 15 lesions due to growth disorders in 16 cervical I.S.C., at dorsal level we have described 4 cases of intrasomatic cavitation containing calcified material, opened in the intervertebral space. This growth disturbance has been noted either on first radiograph, or has appeared later, after disappearance of the I.S.C.; we found more over absence of listel and lesion of multiple plates distant from the calcification. This disease is identified to vertebral osteochondrosis where residual deformities are more worrying than the benign calcification; they have concluded management of I.S.C. as early as possible to avoid great deformities of vertebral bodies.

Adolescent↗

PubMed1986

Insulin-like growth factor I (IGF-I) in healthy children, adolescents and adults as determined by a radioimmunoassay specific for the synthetic 53-70 peptide region.

A radioimmunoassay (RIA) specific for the synthetic 53-70 peptide region of human insulin-like growth factor I (IGF-I) was used to determine IGF-I in the serum of 191 healthy newborns, children and adolescents and in 26 adults. The results compare favourably with reported values obtained using RIA systems for the native IGF-I molecule. Intra- and inter-assay CV were 3.3 and 7.2% respectively. In childhood, mean +/- SD IGF-I levels rise from 6.0 +/- 3.5 nmol/l in newborns to 16.5 +/- 4.0 nmol/l at 8-11 years in both sexes. At the onset of puberty, IGF-I levels in females (24.9 +/- 6.6 nmol/l) are significantly (P greater than 0.005) higher than in males (17.2 +/- 4.2 nmol/l). With further pubertal development IGF-I levels continue to rise, reaching peak values at pubertal stage P4 (40.6 +/- 4.5 nmol/l in males, 42.8 +/- 5.1 nmol/l in females) and decline thereafter to lower values during adulthood: 16.5 +/- 5.8 nmol/l (males) and 24.2 +/- 7.0 nmol/l (females) (P greater than 0.001). In pubertal males, IGF-I correlates significantly with height (r = 0.66, P less than 0.001), bone age (r = 0.69, P less than 0.001) and growth velocity (r = 0.64, P = 0.025) as well as with testosterone levels (r = 0.69, P less than 0.001). In pubertal females a significant correlation is found between IGF-I and height (r = 0.55, P less than 0.020). The ready availability of a simple, precise and reproducible IGF-I RIA, should contribute much to evaluating the importance of IGF-I measurements in normal growth and in the diagnosis and therapy of various growth disorders.

Adolescent↗

PubMed1985

Insulin as a growth factor.

Insulin is a potent mitogen for many cell types in vitro. During tissue culture, supraphysiological concentrations of insulin are necessary to promote cell replication in connective or musculoskeletal tissues. Insulin promotes the growth of these cells by binding, with low affinity, to the type I insulin-like growth factor (IGF) receptor, not through the high affinity insulin receptor. In other cell types, such as hepatocytes, embryonal carcinoma cells, or mammary tumor cells, the type I IGF receptor is virtually absent, and insulin stimulates the growth of these cells at physiological concentrations by binding to the high affinity insulin receptor. Both receptor systems activate phosphorylation reactions within the cell which extend to ribosomal proteins. Insulin acts synergistically with other factors, such as platelet-derived growth factor and epidermal growth factor, to stimulate the progression of cells through the cycle of proliferation. Abnormal insulin secretion or action, before or after birth, often is associated with disordered growth suggesting that insulin may function as a growth factor in vivo. Poor growth follows impaired insulin secretion in diabetes mellitus. This is associated with reduced circulating levels of IGF's which may be partly responsible for the growth failure. Insulin has a direct action on release of IGF's from the liver in vitro, but during experimental diabetes there is a reduced number of hepatic somatotropic receptors which could limit the ability of growth hormone to regulate IGF release. Diabetic children, treated conventionally, have normal circulating IGF levels, but both growth rate and serum IGF concentration may increase dramatically when diabetic control is optimized.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1997

Obstruction of the fetal urinary tract.

Understanding the mechanisms of fetal obstructive uropathy will be essential for the specific management of the wide clinical spectrum of congenital obstructive conditions, including selecting observational therapy for mild cases and attempting to maximize renal function in severe cases. Recognition of the unique aspects of fetal renal obstruction is essential to formulate a useful research program, as the lessons of postnatal acquired obstruction are not directly transferable to congenital obstruction. Experimental studies of renal obstruction have demonstrated alterations in the developmental regulation of growth and differentiation in the fetal kidney. Depending on the gestational timing and severity of obstruction, growth may be impaired or accelerated. Similarly, patterns of altered differentiation may indicate immaturity or accelerated maturation, as well as aberrant differentiation. Concomitant with altered development, there is evidence that normal renal regulatory mechanisms, including the renin-angiotensin system and renal hemodynamics, may be affected by obstruction, possibly as compensatory responses. The mechanisms of these various alterations remain to be defined, but are likely to involve combinations of biomechanical signal transduction, growth factor expression, and responses of specific renal autoregulatory mechanisms. Fetal renal obstruction remains incompletely defined. The body of experimental evidence indicates that investigation of mechanisms regulating growth and differentiation is likely to yield important understanding of fetal renal obstruction to permit more accurate prognosis and management. Viewing fetal renal obstruction as a disorder of kidney development, with disordered growth and differentiation, suggests a definition of obstruction as a condition, that--if uncorrected--will lead to impairment in the ultimate functional potential of the kidney. Intervention should aim to maximize functional potential rather than to simply maintain the status quo.

Animals↗

PubMed1997

Quantitative analysis of trabecular morphogenesis in the human costochondral junction during the postnatal period in normal subjects.

BACKGROUND: Quantitative histomorphometric features of the bone growth plate in the human rib have been investigated in infants, ranging in age from 3-36 weeks (mean 18.6 weeks) to provide data currently not available. METHODS: Measurements were taken in each histological zone of the growth plate. Data from 20 cases were pooled and parameters describing the characteristic features of trabecular bone calculated using morphometric formulae. The measurements were made from the resting zone of the cartilage to the secondary spongiosa, 3.78 mm from the starting point. RESULTS: Cartilage volume fraction decreased from 78% in the resting zone to a bone volume fraction of between 20% and 30% in the secondary cancellous bone. Cartilage matrix surface increased rapidly in the cartilage and bone mineral surface declined in correspondence with the development of primary bone. The distance between chondrocyte lacunae was observed to decrease throughout the cartilage to a transverse septa thickness of 18 microns in the hypertrophic zone. A rapid increase in trabecular thickness to 128 microns was observed in the primary spongiosa, the secondary spongiosa ranging between 137 microns and 168 microns. Spacing, chondrocyte profile transverse diameter, increased to 30 microns in the hypertrophic zone, following which an increase in trabecular separation to 347 microns was observed in the primary spongiosa. The number of transverse intervals between individual chondrocyte lacunae was observed to increase in the cartilage to a maximum of 21.3 cartilaginous or mineralised septa per mm of growth plate length in the hypertrophic zone. Trabeculae in the metaphysis then decreased in number to approximately 1.5 trabeculae per mm in the secondary spongiosa. CONCLUSIONS: These data thus provide new insight into the development of trabecular structure during growth and normal values for the comparison of tissue from skeletal dysplasias and growth disorders.

Achondroplasia↗

PubMed1993

Dysspondylochondromatosis.

We report on 3 unrelated patients with an unusual form of neonatal dwarfism with unequal limb length. Radiographs show multiple enchondromatosis of the tubular and the flat bones and severe segmentation abnormalities of the vertebral column. These observations differ from the hitherto described forms of multiple enchondromatosis with growth disorders of the spine, spondyloenchondroplasia, and others. Therefore we propose to delineate this disorder as a new entity.

Abnormalities, Multiple↗

PubMed1997

Neural mechanisms of hair growth control.

Clinical and experimental observations have long suggested that skin nerves have "trophic" functions in hair follicle development, growth and/or cycling, even though the molecular and cellular basis of the underlying neuroepithelial interactions has remained obscure. Here, we critically review currently available evidence arguing in favor of or against the existence of neural mechanisms of hair growth control, and outline why the murine hair cycle provides an excellent experimental system for characterizing and manipulating piloneural interactions. Summarizing relevant, recent data from the C57BL/6 mouse model, it is pointed out that the sensory and autonomic innervation of normal pelage hair follicles, the substance P skin content, and cutaneous mast cell-nerve contacts show striking changes during synchronized hair follicle cycling. Furthermore, the murine hair follicle appears to be both a source and a target of neurotrophins, whereas neuropharmacologic manipulations alter murine hair follicle cycling in vivo. For example, anagen is induced by substance P or adrenocorticotropin (ACTH), and by the experimentally triggered release of neuropeptides from sensory nerves and of neurotransmitters from adrenergic nerves. Taken together, this argues in favor of neuroepithelial interactions as regulatory elements in hair growth control and suggests that the study of piloneural interactions promises important insights into general principles of neuroepithelial communication, namely during epithelial morphogenesis and remodeling. We delineate a hypothetical working model of piloneural interactions and propose that targeted manipulations deserve systematic exploration as a novel strategy for managing hair growth disorders.

Animals↗

PubMed1982

Homologous IM-9 lymphocyte radioreceptor and receptor modulation assays for human serum growth hormone.

Radioreceptor assays for human GH (hGH) have been developed using the IM-9 cultured human lymphoid cell receptor. Varying degrees of nonspecific interference with [125I] hGH binding to these cells occurs in the presence of serum. We have modified the traditional IM-9 competitive binding assay for hGH and abolished the nonspecific serum effects. The modified competitive assay is sensitive to as little as 2 ng/ml hGH, and it has been validated by the quantitative recovery of purified pituitary hGH in hypopituitary serum. Sera from stimulated normals, acromegalics, and patients with severe growth retardation were assayed. The RIA to radioreceptor assay ratios for these groups were 0.98 +/- 0.10, 0.97 +/- 0.18, and 2.43 +/- 0.54, respectively. The assay has potential usefulness in screening and predicting growth-retarded patients most likely to respond to exogenous hGH therapy. In addition, a sensitivity receptor modulation assay, which uses the ability of hGH to regulate its homologous IM-9 receptors, is described. This is 8- to 10-fold more sensitive than the nonregulatory assays and has been applied to the measurement of hGH in sera from unstimulated normals and acromegalics. The ratios of RIA to receptor modulation assay for the two groups were 1.17 +/-0.68 ad 1.07 +/- 0.26, respectively. These sensitive receptor assays offer a powerful technique for the measurement of biologically active and inactive GH peptide in serum, and may be particularly useful in the evaluation of statural growth disorders.

Acromegaly↗

PubMed1990

[Growth parameters of female athletes during periods of high training load].

Studies of children participating in elite sport training programmes revealed growth disorders. Longitudinal analyses of female gymnasts (whose bone age was distinctly below chronological age) over a period of two years do not suggest a general tendency to growth inhibition. However, the marked variation in the longitudinal data may indicate retardation in individual cases. An evaluation of the growth parameters is of practical importance for the medical care of children participating in intensive training programmes.

Adolescent↗

PubMed2000

Oxidant-induced intestinal barrier disruption and its prevention by growth factors in a human colonic cell line: role of the microtubule cytoskeleton.

Reactive oxygen metabolites (ROM) are increased in the inflamed mucosa of inflammatory bowel disease (IBD) and may contribute to loss of intestinal barrier function in this disorder. Growth factors (GF) are protective. But the mechanisms of disruption and protection remain elusive. In the present investigation, we hypothesized that the microtubules (a critical cytoskeletal element) play a key role in the molecular mechanism of intestinal barrier dysfunction induced by ROM and in GF-mediated protection. Utilizing monolayers of a human colonic cell line (Caco-2), we evaluated the effects of ROM (H(2)O(2) or HOCl), in the presence or absence of GF (epidermal growth factor [EGF]; transforming growth factor-alpha [TGF-alpha]), on intestinal barrier function, tubulin (microtubule structural protein), and microtubule stability. Monolayers were also processed for two highly sensitive western immunoblots: fractionated polymerized tubulin (S2; an index of stability); monomeric tubulin (S1; an index of disruption) to detect the oxidation and disassembly/assembly of tubulin. ROM exposure led to a significant increase in the oxidation of tubulin, decrease in the stable S2 polymerized tubulin, and increase in the unstable S1 monomeric tubulin. In concert, each ROM in a dose dependent manner damaged the microtubule cytoskeleton and disrupted barrier function. GF pretreatment not only increased the S2 stable tubulin and decreased tubulin oxidation but also, concomitantly, prevented the disruption of microtubules and loss of barrier function in monolayers exposed to ROM. Antibody against the GF-receptor and inhibitors of GF-receptor tyrosine kinase abolished GF protection, indicating the involvement of epidermal growth factor receptor (EGFR) signaling pathway. As predicted, colchicine, an inhibitor of microtubule assembly, caused barrier dysfunction and prevented GF protection whereas taxol, a microtubule-stabilizing agent, mimicked the protective effects of GF. Thus, organization and stability of the microtubule cytoskeleton appears to be critical to both oxidant-induced mucosal barrier dysfunction and protection of intestinal barrier mediated by GF. Therefore, microtubules may be useful targets for development of drugs for the treatment of IBD.

Caco-2 Cells↗

PubMed1999

Novel aspects of the insulin-like growth factor binding proteins.

The insulin-like growth factors (IGFs), IGF binding proteins (IGFBPs), and IGFBP proteases regulate somatic growth and cellular proliferation both in vivo and in vitro. IGFs are potent mitogens whose actions are determined by the availability of free IGFs to interact with IGF receptors. IGFBPs comprise a family of six proteins that bind IGFs with high affinity and specificity and thereby regulate IGF-dependent actions. IGFBPs have also recently emerged as IGF-independent regulators of cell growth. Several IGFBP association proteins have been discovered recently which can affect IGFBP action. Cleavage of IGFBPs by specific proteases modulates levels of free IGFs and IGFBPs and thereby their actions. IGFBP-related proteins (IGFBP-rPs) are an emerging group of proteins which bind IGFs with low affinity and also play important roles in cell growth and differentiation. The IGFBPs appear to have emerging roles in the mechanisms underlying human cancer. The GH-IGF-IGFBP axis is complex and powerful. Future research on its physiology promises exciting insights into cell biology as well as advancements in the treatment of a wide range of disease states including cancer, diabetes, vascular disease, asthma, and growth disorders.

Humans↗

PubMed1988

Autoradiographic localization of technetium-99 methylene diphosphonate in growth sites of young mice.

Conflicting reports about the localization of 99mTc-MDP in bone and cartilage are found in the literature. Possible binding sites include hydroxyapatite and non-osteoid matrix such as immature collagen. The present study used autoradiographs of demineralized and non-demineralized growth sites in young mice to demonstrate localization of 99Tc-MDP, and consequently 99mTc-MDP, in mineralizing cartilage and bone. Uptake of the isotope was seen in mineralizing bone and cartilage, associated with the mineral in contrast to the organic phase. The results indicate that bone seeking radiopharmaceutical uptake (BSRU) may detect alterations in the rate of mineralized phase in growth sites and thus has the potential to disclose skeletal growth disorders.

Animals↗

PubMed1986

Mid-arm circumference/head circumference ratios for identification of symptomatic LGA, AGA, and SGA newborn infants.

Mid-arm circumference/head circumference ratios (MAC/HC) and birth weights obtained in 73 neonates were studied to compare which of these growth measurements could more accurately predict risk of metabolic complications resulting from either acceleration or retardation of fetal growth. The MAC/HC ratio was more sensitive than birth weight in distinguishing symptomatic large for gestational age (LGA) infants who were born to diabetic mothers from other LGA infants who were asymptomatic, and symptomatic from asymptomatic small for gestational age infants. In addition, the MAC/HC ratio identified symptomatic appropriate for gestational age (AGA) infants born to diabetic mothers and AGA infants with signs and symptoms of growth retardation. The MAC/HC is more useful than birth weight in assessing newborn infants at risk for the metabolic complications associated with fetal growth disorders.

Anthropometry↗

PubMed2001

Dehydroepiandrosterone sulphate and corticotropin levels are high in young male patients with conduct disorder: comparisons for growth factors, thyroid and gonadal hormones.

Childhood conduct disorder (CD) may originate in a stressful upbringing, and be associated with unusual physical or sexual development and thyroid dysfunction. We therefore explored circulating levels of hormones from adrenal, gonadal and growth hormone axes associated with stress, aggression and development in 28 CD patients and 13 age-matched healthy children (10-18 years old). The CD group had higher levels of dehydroepiandrosterone sulphate (DHEA-S), corticotropin (ACTH) and free tri-iodothyronine (fT(3)) if under 14 years. There were no differences for gonadal hormones or maturity ratings which were not associated with aggression. Smaller physical measures in CD children correlated with DHEA-S and growth factors (e.g. insulin-like growth factor I) increased ACTH and fT(3) correlated with restless-impulsive ratings, and DHEA-S with 'disruptive behaviour'. Imbalances in the adrenal and growth axes may have neurotropic repercussions in development.

Adolescent↗