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Developmental Factors (developmental + factor)
Selected AbstractsTetrahydrobiopterin in the prevention of hypertonia in hypoxic fetal brain,ANNALS OF NEUROLOGY, Issue 3 2009Jeannette Vásquez-Vivar PhD Objective Tetrahydrobiopterin (BH4) deficiency is a cause of dystonia at birth. We hypothesized that BH4 is a developmental factor determining vulnerability of the immature fetal brain to hypoxic-ischemic injury and subsequent motor deficits in newborns. Methods Pregnant rabbits were subjected to 40-minute uterine ischemia, and fetal brains were investigated for global and focal changes in BH4. Newborn kits were assessed by neurobehavioral tests following vehicle and sepiapterin (BH4 analog) treatment of dams. Results Naive fetal brains at 70% gestation (E22) were severely deficient for BH4 compared with maternal and other fetal tissues. BH4 concentration rapidly increased normally in the perinatal period, with the highest concentrations found in the thalamus compared with basal ganglia, frontal, occipital, hippocampus, and parietal cortex. Global sustained 40-minute hypoxia-ischemia depleted BH4 in E22 thalamus and to a lesser extent in basal ganglia, but not in the frontal, occipital, and parietal regions. Maternal supplementation prior to hypoxia-ischemia with sepiapterin increased BH4 in all brain regions and especially in the thalamus, but did not increase the intermediary metabolite, 7,8-BH2. Sepiapterin treatment also reduced incidence of severe motor deficits and perinatal death following E22 hypoxia-ischemia. Interpretation We conclude that early developmental BH4 deficiency plays a critical role in hypoxic-ischemic brain injury. Increasing brain BH4 via maternal supplementation may be an effective strategy in preventing motor deficits from antenatal hypoxia-ischemia. Ann Neurol 2009;66:323,331 [source] Bias in the introduction of variation as an orienting factor in evolutionEVOLUTION AND DEVELOPMENT, Issue 2 2001Lev Y. Yampolsky SUMMARY According to New Synthesis doctrine, the direction of evolution is determined by selection and not by "internal causes" that act by way of propensities of variation. This doctrine rests on the theoretical claim that because mutation rates are small in comparison to selection coefficients, mutation is powerless to overcome opposing selection. Using a simple population-genetic model, this claim is shown to depend on assuming the prior availability of variation, so that mutation may act only as a "pressure" on the frequencies of existing alleles, and not as the evolutionary process that introduces novelty. As shown here, mutational bias in the introduction of novelty can strongly influence the course of evolution, even when mutation rates are small in comparison to selection coefficients. Recognizing this mode of causation provides a distinct mechanistic basis for an "internalist" approach to determining the contribution of mutational and developmental factors to evolutionary phenomena such as homoplasy, parallelism, and directionality. [source] Exclusion of coding region mutations in MSX1, PAX9 and AXIN2 in eight patients with severe oligodontia phenotypeORTHODONTICS & CRANIOFACIAL RESEARCH, Issue 3 2006A Gerits Structured Abstract Authors,,, Gerits A, Nieminen P, De Muynck S, Carels C Purpose,,, This paper describes the screening of eight patients with severe oligodontia for PAX9 and AXIN2 mutations. Subjects and Methods,,, Anamnestic data and a panoramic radiograph were collected to study the phenotype of eight patients with oligodontia and their first-degree relatives. A blood sample was taken for a mutational screening for PAX9 and AXIN2 mutations. Results,,, No mutations were discovered, but a unique nucleotide change in a conserved 5, flanking region of PAX9 was revealed. Earlier screening of the same patients for MSX1 mutations also had a negative outcome. Conclusions,,, Considering the discrepancy between the high incidence rate of agenesis and the relatively small number of reported causative mutations in PAX9, MSX1 and AXIN2 genes, the genetic contribution to oligodontia probably is much more heterogeneous than expected so far. Therefore negative results, like the present exclusion data, should be published more often in order to get a better appreciation of the relative contribution of these specific mutations causing oligodontia. In this context the exact number of tested probands also should be mentioned at all cases. Recent evidence of PAX9,MSX1 protein interactions in odontogenesis as well as other genes and developmental factors should receive more attention. [source] Contributions of A. Roberto Frisancho to human population biology: An introduction,AMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 5 2009William R. Leonard Over the span of his career, A. Roberto Frisancho has been one of the prime architects of the development and expansion of human population biology. His research and scholarly publications have helped to move the field beyond simple descriptions of human variation to address the nature and evolutionary origins of human biological diversity. Frisancho's early work in the Peruvian Andes elegantly demonstrated the importance of developmental acclimatization for promoting adaptive responses to the multiple stressors of high-altitude environments. Since mid-1970s, he has played a major role in developing and expanding the use of anthropometric techniques for assessing physical growth and nutritional status. Frisancho's influential publications have helped to make the use of anthropometric methods commonplace in the fields of nutritional science and public health. Throughout his career, Frisancho's work has examined how environmental, genetic, and developmental factors interact to influence human health and nutritional status. His research has addressed topics ranging from the determinants of low-birth weight infants in teenage mothers to the origins of obesity and associated metabolic diseases in populations of the developing world. Both the breadth and impact of Frisancho's work have been truly remarkable. The field of human population biology owes much to the tremendous contributions of A. Roberto Frisancho. Am. J. Hum. Biol., 2009. © 2009 Wiley-Liss, Inc. [source] Transfer of life-history phenology from mothers to progeny in a solitary univoltine parasitoidPHYSIOLOGICAL ENTOMOLOGY, Issue 2 2010ANDREW A. FORBES Among univoltine insects that experience diapause, differences in emergence timing between adult males and females are expected to be dictated by sex-specific developmental factors. In multivoltine insects without a diapause, there is often an additional relationship between the date of oviposition and the date of adult emergence. Differences between male and female emergence timing in the latter case can therefore be influenced by female sex-allocation decisions. In the present study, it is shown that eggs of a univoltine parasitoid wasp Diachasma alloeum Muesebeck (Hymenoptera: Braconidae) that are laid earlier also eclose earlier during the subsequent year, independent of (although complementary to) sex-related differences in development time. The implications of this pattern for sex allocation decisions by female univoltine parasitoids are discussed. [source] Test of a conceptual model of uncertainty in children and adolescents with cancer,RESEARCH IN NURSING & HEALTH, Issue 3 2010Janet L. Stewart Abstract Despite recognition as a significant stressor in childhood cancer, illness-related uncertainty from the perspective of children remains under-studied. We tested a conceptual model of uncertainty, derived from Mishel's uncertainty in illness theory, in 68 school-aged children and adolescents with cancer. As hypothesized, uncertainty was significantly related to psychological distress, but only one hypothesized antecedent (parental uncertainty) significantly predicted children's uncertainty. An alternative model incorporating antecedent developmental factors (age and illness-specific expertise) explained 21% of the variance in child uncertainty; controlling for stage of treatment, uncertainty was higher in children with shorter time since diagnosis, older age, lower cancer knowledge, and higher parental uncertainty. These findings provide the foundation for further studies to understand children's management of uncertainty and its contribution to psychological adjustment to illness. © 2010 Wiley Periodicals, Inc. Res Nurs Health 33:179,191, 2010 [source] Neurobiological Processes in Adolescent Addictive DisordersTHE AMERICAN JOURNAL ON ADDICTIONS, Issue 1 2008Ty S. Schepis PhD The purpose of this review is to summarize the neurobiological factors involved in the etiology of adolescent addiction and present evidence implicating various mechanisms in its development. Adolescents are at heightened risk for experimentation with substances, and early experimentation is associated with higher rates of SUD in adulthood. Both normative (e.g., immature frontal-limbic connections, immature frontal lobe development) and non-normative (e.g., lowered serotonergic function, abnormal hypothalamic-pituitary-adrenal axis function) neurobiological developmental factors can predispose adolescents to a heightened risk for SUD. In addition, a normative imbalance in the adolescent neurobiological motivational system may be caused by the relative underdevelopment of suppressive mechanisms when compared to stimulatory systems. These neurobiological liabilities may correspond to neurobehavioral impairments in decision-making, affiliation with deviant peers and externalizing behavior; these and other cognitive and behavioral traits converge with neurobiological factors to increase SUD risk. The progression to SUD acts as an amplifying feedback loop, where the development of SUD results in reciprocal impairments in neurobehavioral and neurobiological processes. A clearer understanding of adolescent neurobiology is a necessary step in the development of prevention and treatment interventions for adolescent SUD. [source] Comparing cortisol, stress, and sensory sensitivity in children with autismAUTISM RESEARCH, Issue 1 2009Blythe A. Corbett Abstract Previously we reported that children with autism show significant variability in cortisol. The current investigation was designed to extend these findings by exploring plausible relationships between cortisol and psychological measures of stress and sensory functioning. Salivary cortisol values for diurnal rhythms and response to stress in children with and without autism were compared to parent-report measures of child stress, the Stress Survey Schedule (SSS), sensory functioning, Short Sensory Profile (SSP), and Parenting Stress Index. In autism, a negative relationship between morning cortisol and the SSS revealed that higher observed symptoms of stress were related to lower cortisol. Lower cortisol is seen in conditions of chronic stress and in social situations characterized by unstable social relationships. Sensory sensitivity painted a more complicated picture, in that some aspects of SSP were associated with higher while others were associated with lower cortisol. We propose that increased sensory sensitivity may enhance the autistic child's susceptibility to the influence of zeitgeibers reflected in variable cortisol secretion. Evening cortisol was positively associated with SSS such that the higher the level of evening cortisol, the higher the child's parent-reported daily stress, especially to changes, such as in daily routine. Regarding the response to stress, the psychological and parent variables did not differentiate the groups; rather, discrete subgroups of cortisol responders and nonresponders were revealed in both the autism and neurotypical children. The results support a complex interplay between physiological and behavioral stress and sensory sensitivity in autism and plausible developmental factors influencing stress reactivity across the groups. [source] | |||||||||||||