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Somatic Development (somatic + development)

Distribution by Scientific Domains

Medical Sciences	83%

Selected Abstracts

Anthropometric and cephalometric measurements in X-linked hypohidrotic ectodermal dysplasia

ORTHODONTICS & CRANIOFACIAL RESEARCH, Issue 4 2007
MO Lexner
Structured Abstract Authors,,, Lexner MO, Bardow A, Bjorn-Jorgensen J, Hertz JM, Almer L, Kreiborg S. Objective,,, To describe the somatic development and craniofacial morphology in males affected with hypohidrotic ectodermal dysplasia (HED) and female carriers and to find clinical markers for early clinical diagnosis of possible female carriers. Design,,, A clinical and radiographic examination of the affected males and the female carriers. Setting and sample population,,, Twenty-four affected males and 43 female carriers with a known mutation in the ED1 gene were examined in a dental clinic in either Copenhagen or Aarhus, Denmark. Experimental variables,,, Height, body mass index (BMI) and head circumference. Cephalometric analysis of the craniofacial morphology. Outcome measure,,, Data on the somatic and craniofacial development in the affected males and female carriers. Results,,, No difference was observed regarding body height in the affected males and female carriers, BMI values were lower than the mean in most affected boys and adolescence and head circumference was somewhat decreased in both groups compared to normative data. The cephalometric analysis showed a reduced maxilla length and prognathism, a normal size and shape of the mandible and a reduced sagittal jaw relationship in both HED groups. Furthermore, affected males had a retroclined nasal bone and a more anteriorly inclined maxilla. A short nose, protruding lips, reduced facial convexity and facial height, characterized the soft tissue profile of the affected males. In female carriers, the lips were significantly retruded when compared with controls. Conclusion,,, No specific somatic or cephalometric markers could be observed, in the female carrier group. [source]

Blocking leukocyte influx and function to prevent chronic lung disease of prematurity

PEDIATRIC PULMONOLOGY, Issue 5 2003
Richard L. Auten MD
Abstract Inflammation is strongly linked to the pathogenesis of chronic lung disease of prematurity (CLD). Premature gas-breathing of ambient or supplemental oxygen in a host with relatively deficient and poorly inducible antioxidant defenses may itself be injurious, and further amplified by mechanical stretch injury in the surfactant-insufficient lung.1 Cellular injury provokes an inflammatory response. Since inflammation is often detected at birth in the lungs of newborns who later develop CLD,2 it has been an attractive strategy to abrogate inflammation, but the arsenal is limited. Glucocorticoids have been widely used but are acknowledged to be potentially harmful to neurologic and somatic development, and are not recommended outside controlled trials.3 The number that benefit is comparable to the number harmed, according to meta-analysis.4 More specific blockade of harmful inflammation could overcome this obstacle. Examination of the inflammatory pathways that initiate and propagate lung injury and subsequent abnormal development points to promising new strategies that may one day be tailored to individual patients. Pediatr Pulmonol. 2003; 35:335,341. © 2003 Wiley-Liss, Inc. [source]

Prenatal diagnosis of tetrasomy 9p with Dandy,Walker malformation

PRENATAL DIAGNOSIS, Issue 8 2004
Markus Hengstschläger
Abstract Objectives To add to the knowledge of chromosomal abnormalities associated with Dandy,Walker malformation. Methods Molecular cytogenetic analyses of a chorionic villus sampling and of an amniocentesis of a fetus with Dandy,Walker malformation and abnormal somatic development. Results All cells examined showed a 47, XY, +idic(9p)(pter,q12::q12,pter) de novo karyotype. This report describes the fourth case of a tetrasomy 9p associated with Dandy,Walker malformation Conclusions This case, together with the three previously reported cases of an association with a tetrasomy 9p, indicate that this chromosomal aberration should be looked for when Dandy,Walker malformation is detected via prenatal ultrasonography. Copyright © 2004 John Wiley & Sons, Ltd. [source]

Minor neurological dysfunction, cognitive development and somatic development at the age of 3 to 11 years in very-low-birthweight infants with transient periventricular echodensities

ACTA PAEDIATRICA, Issue 12 2006
JOERG KUTSCHERA
Abstract Aim: To determine, using strict exclusion criteria, whether transient periventricular echodensities (TPE) in very-low-birthweight infants lead to minor neurological dysfunction and problems in cognitive and somatic development in children without major neurological impairments. Methods: 23 children with TPE were matched to 23 children without TPE. Exclusion criteria were small for gestational age, microcephaly at birth, diplegia, asphyxia, psychomotor retardation, intraventricular haemorrhage grade III/IV, major surgical interventions and malformations. The Kaufman Assessment Battery for Children, Draw-a-Man Test and neuropaediatric examination were used for evaluation. Results: There were no differences in demographic data, growth and socio-economic status. Significant differences with lower results in the TPE group were found in fine motor skills and in the Draw-a-Man Test. In the Kaufman Assessment Battery for Children, all subscales were below average in the TPE group, except the sequential processing scale. In the control group, all subscales were within the average range. Conclusion: By using strict exclusion criteria to eliminate other risk factors for minimal neurological dysfunction and poor cognitive development, we were able to focus on the effect of TPE. TPE seem to affect cognitive development and cause minor neurological dysfunction. [source]

Modulation of growth hormone action by sex steroids

CLINICAL ENDOCRINOLOGY, Issue 4 2006
Udo J. Meinhardt
Summary Growth hormone (GH) is a major regulator of growth, somatic development and body composition. Sex steroids can act centrally by regulating GH secretion and peripherally modulating GH responsiveness. This review addresses data of potential clinical relevance on how sex steroids modulate GH secretion and action, aiming to increase the understanding of sex steroid/GH interactions and leading to improved management of patients. Sex steroids regulate GH secretion directly as well as indirectly through IGF-I modulation. Testosterone stimulates GH secretion centrally, an effect dependent on prior aromatization to oestrogen. Oestrogen stimulates GH secretion indirectly by reducing IGF-I feedback inhibition. Whether oestrogen stimulates GH secretion centrally in females is unresolved. Gonadal steroids modify the metabolic effects of GH. Testosterone amplifies GH stimulation of IGF-I, sodium retention, substrate metabolism and protein anabolism while exhibiting similar but independent actions of its own. Oestrogen attenuates GH action by inhibiting GH-regulated endocrine function of the liver. This is a concentration-dependent phenomenon that arises invariably from oral administration of therapeutic doses of oestrogen, an effect that can be avoided by using a parenteral route. This strong modulatory effect of gonadal steroids on GH responsiveness provides insights into the biological basis of sexual dimorphism in growth, development and body composition and practical information for the clinical endocrinologist. It calls for an appraisal of the diagnostic criteria for GH deficiency of GH stimulation tests, which currently are based on arbitrary cut-offs that do not take into account the shifting baseline from the changing gonadal steroid milieu. In the management of GH deficiency in the hypopituitary female, oestrogen should be administered by a nonoral route. In hypopituitary men, androgens should be replaced concurrently to maximize the benefits of GH. In the general population, the metabolic consequences of long-term treatment of women with oral oestrogen compounds, including selective oestrogen receptor modulators, are largely unknown and warrant study. [source]