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At least 721 records · Page 40Linked to original sources
PubMed2000

Hypoxic-ischemia-related fetal/neonatal complications and risk of schizophrenia and other nonaffective psychoses: a 19-year longitudinal study.

OBJECTIVE: Epidemiologic evidence linking obstetric complications to schizophrenia has been positive but inconclusive. One reason for the lack of conclusive evidence may be the inconsistency in measuring disturbances of fetal/neonatal brain development based on general obstetric markers of maternal health. The authors used data from the National Collaborative Perinatal Project to examine the relationship between schizophrenia and other nonaffective psychoses and a theoretically derived measure of hypoxic-ischemia-related fetal/neonatal complications. METHOD: Six hundred ninety-three men and women (average age 23) born to a community sample of women between 1959 and 1966 were followed up an average of 19 years after early childhood assessments. Subjects with DSM-IV schizophrenia and other nonaffective psychoses were identified using the Diagnostic Interview Schedule and best-estimate consensus diagnoses. RESULTS: Hypoxic-ischemia-related fetal/neonatal complications were associated with a doubling of the risk of developing a psychotic disorder, compared with no relevant complications (6.9% versus 1.4%). When mood disorders were excluded from the group of psychotic diagnoses, the risk of schizophrenia and other nonaffective psychoses associated with hypoxic-ischemia-related fetal/neonatal complications was strikingly elevated, compared with no relevant complications (5.75% versus 0.39%). Nonpsychotic mood disorders were unrelated to these fetal/neonatal complications. Schizophrenia and other nonaffective psychoses were most strongly associated with hypoxic-ischemia-related fetal/neonatal complications of disordered growth and development. CONCLUSIONS: The data show a strikingly elevated, graded, independent risk of schizophrenia and other nonaffective psychoses associated with this classification of antecedent hypoxic-ischemia-related fetal/neonatal complications.

Adolescent↗
PubMed1990

[The current focus on cardiovascular growth in arterial hypertension].

Recent data have demonstrated that together with an impulsive-conductive function, the cardiovascular system is an organ that synthesizes and secretes several substances involved in the local regulation of its properties. This is the case of endothelial cells and cardiovascular myocytes which produce vasoactive substances and growth factors capable of modulating intra-, auto-, and paracrinally [correction of paraclinically] cardiovascular contractility and growth. It is currently postulated that different genetic or acquired abnormalities in the production of one or more than one of these substances and/or in the response to them, could provoke an excessive increase and/or a disordered growth of the cardiovascular muscles cells. At the same time, both abnormalities could contribute to the initiation and the development of arterial hypertension. The new antihypertensive drugs could be targeted to the cardiovascular endocrine systems.

Cardiovascular System↗
PubMed2004

[Etiology of intrauterine growth retardation. Part I: placental-fetal interrelationship disorder].

Intrauterine growth retardation (IUGR) increases a risk of perinatal complications and may carry a negative influence on a later baby's mental and physical development. Poorer function revealed by many vital organs seems to be the effect of their lower mass and their relative immaturity. In the first part of a paper the authors discuss two groups of factors thought to be responsible for IUGR. The first one has been related to the fetal status-genetic anomalies, other primary developmental defects and different growth patterns.

Embryonic and Fetal Development↗
PubMed2002

Novel treatment of delayed male puberty with aromatase inhibitors.

BACKGROUND: As the evidence for the role of oestrogens in epiphyseal closure appears unequivocal, we hypothesized that boys with constitutional delay of puberty would attain greater adult height if oestrogen action was suppressed. METHODS: We conducted a randomized, double-blind, placebo-controlled study in which we treated boys with constitutional delay of puberty with testosterone plus placebo or testosterone plus a potent fourth-generation aromatase inhibitor, letrozole. FINDINGS: Letrozole effectively inhibited oestrogen synthesis. The 17beta-oestradiol concentrations increased in the untreated group and in the testosterone/placebo-treated group, but in the testosterone/letrozole-treated group no such increase was observed until letrozole treatment was discontinued. Testosterone concentrations were threefold higher in the testosterone/letrozole-treated group than in the other groups. Within 18 months, bone age had advanced by 1.1 +/- 0.3 years in the untreated group and by 1.7 +/- 0.3 years in the testosterone/placebo-treated group, but only by 0.9 +/- 0.2 years in the testosterone/letrozole-treated group (p = 0.02 between treatment groups). Predicted adult height did not change significantly in the untreated group and in the testosterone/placebo-treated group, whereas in the testosterone/letrozole-treated group the increase was 5.1 +/- 1.2 cm (p = 0.004). CONCLUSIONS: Our findings suggest that, if oestrogen action is inhibited in growing adolescents, adult height will increase. This observation provides a rationale for studies aimed at delaying bone maturation in several growth disorders.

Adolescent↗
PubMed1994

The impact of gender and puberty on reference values for urinary growth hormone excretion: a study of 3 morning urine samples in 517 healthy children and adults.

Some recent studies have indicated that measurement of urinary GH (U-GH) excretion may be a useful tool for the evaluation of GH insufficiency in children with growth disorders, although some investigators are skeptical about the diagnostic value of U-GH. Most current assays are only available for specific laboratories or require time-intensive pretreatments of the specimens. This limits the possibility for many centers to compare their patients' data with others or to establish their own reference ranges for U-GH excretion. Therefore, we investigated the performance of a commercially available kit, which allows direct measurement of U-GH in untreated urine specimens. We established a reference range for the geometric mean of 3 morning urine samples in 446 healthy children and 71 adults. U-GH could be determined in all but 9 of 1526 samples (99.4%). U-GH excretion was significantly dependent on pubertal maturation (P < 0.001) and sex (P < 0.001), whereas age had no significant influence in the prepubertal group (P > 0.3). Peak values occurred in Tanner stages 3 and 4 (369 and 391 pg/h in females; 503 and 882 pg/h in males), corresponding to an age interval of 11-18 yr in boys and 9-15 yr in girls. Short collection periods (< 6 h) were related to low values for U-GH excretion (nanograms per night; P < 0.02). This time effect disappeared if U-GH excretion was expressed as picograms per h. If U-GH was related to creatinine output, there was a decrease in U-GH excretion during prepuberty, a blunting of the pubertal peak, and lower values in adults than in prepubertal children (P < 0.0002). The intraindividual variation in U-GH excretion (picograms per h) ranged from 40-61%, constituting approximately two thirds of the interindividual variation. This variation was not lowered by relating U-GH to creatinine. We conclude that the assay was suitable for measurement of U-GH excretion in virtually all healthy volunteers. Sex and pubertal stage as well as urinary volume and clock times for collection periods should be registered when establishing a reference range for U-GH excretion and applying it for clinical purposes. Our reference values may be useful for further studies of patients with GH disorders.

Adolescent↗
PubMed1984

[The thyroid gland, the parathyroid gland and the skin].

Hormones of the thyroid gland (thyroxine, tri-iodothyronine) control the metabolism of cells and tissue of the body, while parathormone and calcitonine are balancing the intra- and extracellular levels of calcium and phosphorus by governing some metabolic functions of bones, kidney and small intestine. Growth, maturation and metabolic homeostasis of the organism depend, among other intrinsic factors, on a normal production and secretory rate of both thyroidal and parathyroidal hormones. Clinical conditions of hyperthyroidism induce 1. increased metabolic turnover of the body with transcutaneous heat loss, 2. disordered growth of hairs and nails, 3. hyperpigmentation of skin, 4. pruritus with or without urticaria. Pretibial (usually symmetrical) myxedema may be associated with conditions of either hyper- or hypothyroidism (e.g., Hashimoto's thyroiditis); if combined with bilateral exophthalmus and acropachyderma of fingers and toes, it is called Diamond syndrome, or E.M.O. syndrome. In hypothyroidism, the skin feels chilly and dry, looks pale, and may present follicular keratoses with or without secondary eczema. The hair appears dull and sparse due to disordered anagen phase. Skin wounds heal with delay. Diffuse myxedema originates in the papillary and periadnexal connective tissue and eventually extends to the dermis as a whole. Clinical conditions of hyperparathyroidism rarely cause secondary calcification of the skin; they may induce severe pruritus, particularly in secondary hyperparathyroidism due to renal failure. Impetigo herpetiformis or generalized pustular psoriasis, resp., may be set off by excessive surgical removal of the goiter. Congenital maldevelopment of both thymus and parathyroid gland leads to cellular immune deficiency with secondary chronic muco-cutaneous candidosis.

Calcium↗
PubMed2000

[Bone growth after finger replantation in childhood].

Following replantation in childhood, growth disorders of the affected epiphysis can influence function and aesthetic appearance of the hand. In a retrospective study long-term results of replantation in the upper limb in childhood were analysed with respect to factors influencing further growth. 22 patients with 29 replanted fingers were reviewed clinically and radiologically after an average interval of ten years. An average bone growth of 93% compared to the contralateral non-injured side was found. With the epiphysis affected, bone growth was reduced to 86% of the contralateral side. Analysis of single phalanges showed a growth rate of 71 to 100% in phalanges distal to the amputation and also in phalanges initially severed. Potential factors influencing bone growth were assessed separately. Best results were achieved in straight injuries without epiphyseal affection. An influence of anoxia time or number of anastomosed vessels could not be found. Even though replantation in childhood affects growing bone, almost normal bone growth can be expected afterwards.

Adolescent↗
PubMed1998

Advances in endocrinology.

Molecular genetics will continue to help us to make precise diagnoses. At present, the expertise to achieve this for a specific disease is often exclusive to one unit with a research interest. It will be important to establish a coordinated approach at a supraregional level to provide molecular diagnosis for rare disorders as a fast reliable clinical service. In addition understanding the molecular mechanisms of disease is likely to direct a search for new treatments. For instance, calcium channel blockers have been used in nesidoblastosis to reduce the hypersecretion of insulin, as a result of the recognition of the role that calcium has in the function of the beta-cell ATP sensitive K+ channel. Although the potential benefits of hGH are now being clearly defined in a range of growth disorders, the treatment is invasive and expensive. It is likely that future endocrine therapeutic developments could include slow release growth hormone preparations, orally active growth hormone mimetics, or even hormone production from an ectopic viral cDNA vector. The next "advances in endocrinology" will also reveal whether leptin will have a therapeutic role in appetite control or even the modulation of pubertal development.

Endocrine System Diseases↗
PubMed1982

Fibroblast growth factor modulates synthesis of collagen in cultured vascular endothelial cells.

Vascular endothelial cells derived from adult bovine aortic arch can be grown in two ways, either in the presence or absence of fibroblast growth factor. The types of collagen produced by cultures under these two conditions have been compared. In the presence of fibroblast growth factor, cells grow in an orderly fashion, express their normal phenotype and synthesize primarily type III collagen plus collagens types IV and V at a ratio of 10:1:3. Cultures grown in the absence of the factor lose their orderly pattern of growth, lose polarity and normal phenotypic expression. They devote twice the proportion of total protein-synthesizing capacity to collagen, and now synthesize type I in addition to the other collagen types. The ratio of collagen types I:III:IV:V is approximately 30:70:1:13. The kinds of type V collagen chains expressed are also altered. Fibroblast growth factor appears to modulate collagen synthesis, the major component of the extracellular matrix, and indirectly modulates the phenotypic expression of cultured vascular endothelial cells. In atherosclerosis, type I collagen is found in association with the intimal layer. The disorderly growth and the abnormal production of type I collagen by these vascular endothelial cells cultured in the absence of fibroblast growth factor is a model for a number of pathological situations including atherosclerotic plaque formation.

Animals↗
PubMed1996

Insulin-like growth factors and their receptors in growth.

The IGFs are essential stimulators of fetal and postnatal growth. Their signals are mediated predominantly by the type I IGF receptor, but another as yet unidentified receptor seems to mediate some actions, especially some of those for IGF-II. During organogenesis, the actions of IGF-I seem to be local (autocrine/paracrine), because it, as well as IGFBPs and IGF receptors, are expressed coordinately in a highly tissue and developmentally specific fashion. IGF-I, however, most likely assumes endocrine functions during postnatal life and provides signals for GH and nutritional status. On the other hand, IGF-II may have only local growth-promoting functions, and its most essential actions may be restricted to in utero life. Both IGFs may be involved in regenerative organ growth, and their uncontrolled expression, especially that of IGF-II, may be involved in the formation of some tumors. The previous conclusions are drawn mainly from in vitro and animal experiments. Although they are generally consistent with data in humans, it is most likely incorrect to extrapolate to man all of the conclusions drawn from the experiments in mice. Differences in placentation are so marked between mice and humans that an exclusive role for IGF-II in human placental growth seems unlikely. On the other hand, it is reasonable to conclude that both IGFs are important stimulants of normal human fetal growth, that IGF-I is a more potent stimulator of human postnatal growth, and that the type I IGF receptor mediates most IGF actions in humans. The fact that no human growth disorders have been linked convincingly to lack of function mutations in IGF or IGF receptor genes suggests that such defects are lethal.

Animals↗
PubMed2006

Imprinting of IGF2 P0 transcript and novel alternatively spliced INS-IGF2 isoforms show differences between mouse and human.

Genomic imprinting is limited to a subset of genes that play critical roles in fetal growth, development and behaviour. One of the most studied imprinted genes encodes insulin-like growth factor 2, and aberrant imprinting and DNA methylation of this gene is associated with the growth disorders Beckwith-Wiedemann and Silver-Russell syndromes and many human cancers. Specific isoforms of this gene have been shown to be essential for normal placental function, as mice carrying paternal null alleles for the Igf2-P0 transcript are growth restricted at birth. We report here the identification of three novel human transcripts from the IGF2 locus. One is equivalent to the mouse Igf2-P0 transcript, whereas the two others (INSIGF long and short) originate from the upstream INS gene that alternatively splices to downstream IGF2 exons. In order to elucidate the molecular mechanisms involved in the complex imprinting of these novel IGF2 transcripts, both the allele-specific expression and methylation for all the IGF2 promoters including P0 and the INSIGF transcripts were analysed in human tissues. Similar to the mouse, the human IGF2-P0 transcript is paternally expressed; however, its expression is not limited to placenta. This expression correlates with tissue-specific promoter methylation on the maternal allele. The two novel INSIGF transcripts reported here use the INS promoter and show highly restricted tissue expression profiles including the pancreas. As previously reported for INS in the yolk sac, we demonstrate complex, tissue-specific imprinting of these transcripts. The finding of additional transcripts within this locus will have important implications for IGF2 regulation in both cancer and metabolism.

Alternative Splicing↗
PubMed2006

Clinical improvement following home parenteral nutrition in pediatric patients with intestinal failure.

BACKGROUND/PURPOSE: Home parenteral nutrition (HPN) is being increasingly used to treat children with intestinal failure. This study evaluated the long-term growth, outcome and complications in Taiwanese pediatric patients with intestinal failure who were treated with HPN. METHODS: This retrospective study included 27 consecutive pediatric patients with intestinal failure who received long-term HPN between 1987 and 2002. These patients were categorized into two groups according to whether they had short bowel syndrome or a bowel motility disorder. Growth, prognosis and complications, including cholestasis, hypoglycemia, hyperglycemia and infections were compared between the two groups. RESULTS: The median age of starting HPN was significantly younger in patients with short bowel syndrome (5 months) than in patients with motility disorders (1.9 years). The median duration of HPN treatment in the overall group was 13.5 months (range, 2.1-113.1 months); weight and height increased 1.7 +/- 2.3 and 1.0 +/- 1.6 in z score, respectively. The most common complications were cholestatic liver disease (52%), hypoglycemia (15%) and hyperglycemia (33%). All patients maintained stable serum glucose levels at follow-up. Cholestatic liver disease developed after 2.3 +/- 2.0 months of total HPN in 13 patients, which subsided after 9.7 +/- 6.9 months in 11 patients, while two patients died. The mean incidence of central venous infection was 3.0 +/- 3.3 per 1000 HPN days. The most common pathogens were Staphylococcus spp. (50%) and Candida spp. (30.6%). CONCLUSION: HPN treatment can successfully provide a bridge to enteral nutrition in pediatric patients with intestinal failure. The metabolic disturbances and cholestasis are usually transient, but infection control is important throughout the period of HPN treatment.

Adolescent↗
PubMed2004

Suppressors of cytokine signalling and regulation of growth hormone action.

The Suppressors of Cytokine Signalling (SOCS) are a family of proteins that are produced in response to signals from a diverse range of cytokines and growth factors and which act to attenuate cytokine signal transduction. Members of the SOCS family form a classical negative feedback loop with key actions involving inhibition of the Janus Kinase-Signal Transducers and Activators of Transcription (JAK-STAT) signalling cascade. Extensive analyses have implicated each of CIS, SOCS1, SOCS2 and SOCS3 in the regulation of Growth Hormone (GH) signal transduction. The expression of each of these SOCS proteins is induced in cells stimulated with GH and their over-expression in cell lines blocks aspects of GH signalling. In vivo studies with genetically modified mice have confirmed important physiological roles for SOCS proteins in regulation of GH action. In particular, mice lacking SOCS2 display gigantism accompanied by evidence of deregulated GH signalling. A precise understanding of the actions of SOCS proteins in GH signalling may offer new opportunities for therapeutic intervention in growth disorders and other conditions involving GH action.

Adaptor Proteins, Signal Transducing↗