ABSTRACT
BACKGROUND: Differences in genetic influences on disordered eating are present across puberty in girls. Heritability is 0% before puberty, but over 50% during and after puberty. Emerging data suggest that these developmental differences may be due to pubertal increases in ovarian hormones. However, a critical piece of evidence is lacking, namely, knowledge of genetic influences on disordered eating across puberty in boys. Boys do not experience increases in ovarian hormones during puberty. Thus, if pubertal increases in genetic effects are present in boys, then factors in addition to ovarian hormones may drive increases in heritability in girls. The current study was the first to examine this possibility in a sample of 1006 male and female twins from the Michigan State University Twin Registry. METHOD: Disordered eating was assessed with the Minnesota Eating Behavior Survey. Pubertal development was assessed with the Pubertal Development Scale. RESULTS: No significant differences in genetic influences on disordered eating were observed in males across any developmental stage. Heritability was 51% in boys during pre-puberty, puberty and young adulthood. By contrast, in girls, genetic factors accounted for 0% of the variance in pre-puberty, but 51% of the variance during puberty and beyond. Sex differences in genetic effects were only significant during pre-puberty, as the best-fitting models constrained heritability to be equal across all males, pubertal females and young adult females. CONCLUSIONS: The results highlight sex-specific effects of puberty on genetic risk for disordered eating and provide indirect evidence of a role for ovarian hormones and/or other female-specific factors.
Subject(s)
Diseases in Twins , Feeding and Eating Disorders/genetics , Genetic Predisposition to Disease/epidemiology , Puberty/physiology , Registries , Sex Characteristics , Adolescent , Adolescent Development , Adult , Child , Estradiol/metabolism , Feeding and Eating Disorders/diagnosis , Feeding and Eating Disorders/epidemiology , Feeding and Eating Disorders/metabolism , Female , Humans , Male , Models, Theoretical , Puberty/metabolism , Risk Factors , Young AdultABSTRACT
BACKGROUND/AIM: The aim of this study was to examine the extent to which additive genetic, shared environmental and non-shared environmental factors contribute to adolescent and preadolescent sleep problems. METHODS: The sample consisted of a cohort of 270 monozygotic and 246 dizygotic twins from a university-based twin registry. RESULTS: Results demonstrated that genetic and environmental influences each appear to be important to adolescent sleep problems. CONCLUSIONS: While the magnitude of genetic influence on sleep problems was consistent with findings from the adult literature, it was smaller than in studies with younger children, suggesting genetic effects may be less influential in adolescence and adulthood.
Subject(s)
Sleep Wake Disorders/genetics , Social Environment , Twins, Dizygotic/genetics , Twins, Monozygotic/genetics , Adolescent , Age Factors , Child , Female , Humans , Male , Sleep Wake Disorders/etiologyABSTRACT
The aim of this study was to determine the association between temperament and sleep in adolescents. Participants included 516 adolescents and their mothers drawn from the community. Findings indicated that as with younger children, sleep and dimensions of temperament (sociability, impulsivity and negative affect) are related in adolescents.
Subject(s)
Sleep Wake Disorders/psychology , Temperament , Adolescent , Child , Female , Humans , Male , Mothers , Personality , Reproducibility of Results , Surveys and QuestionnairesABSTRACT
Programmed cell death or apoptosis is a highly regulated physiological process that is critical in development, particularly in the central nervous system. The DNA fragmentation factor 45 (DFF45 or ICAD) is a subunit of a heterodimeric DNase complex that is crucial for DNA fragmentation and normal apoptosis. To examine the neurobiological consequences of lacking DNA fragmentation and timely apoptosis during mouse development in vivo, we compared spatial learning behaviors in DFF45 mutant and wild-type control mice. We found that DFF45 mutant mice exhibit enhanced spatial learning and memory compared to wild-type mice. Moreover, both the granule cell density and total granule cell number in the hippocampal dentate gyrus region are higher in the DFF45 mutant brains than in the wild-type brains. We propose that the increase in granule cell number in the dentate region due to the DFF45 mutation changes the neuronal network underlying spatial learning and memory in DFF45 mutant mice.
Subject(s)
Maze Learning/physiology , Memory/physiology , Proteins/genetics , Space Perception/physiology , Animals , Apoptosis/physiology , Apoptosis Regulatory Proteins , Cell Count , DNA Fragmentation/physiology , Dentate Gyrus/cytology , Dentate Gyrus/growth & development , Dentate Gyrus/physiology , Female , Male , Mice , Mice, Inbred C57BL , Mice, Mutant Strains , SwimmingABSTRACT
The effect of removal of Ca2+ bound to thrombospondin (TSP) on the protein structure in solution has been investigated using ESR spin-label techniques. A maleimide spin label was selectively attached to the free thiol group presumably near the carboxyl-terminal domain in which Ca2+-binding sites are situated. The ESR spectra of spin-labeled TSP showed that the bound label undergoes a relatively fast rotational motion with an effective rotational correlation time in the nano-second time regimes. Removal of bound Ca2+ in TSP by dialyzing spin-labeled TSP from a Ca2+-containing buffer into an EDTA-containing buffer resulted in an increase in the mobility of the bound label by a factor of 2.3. The data suggest that EDTA chelation of bound Ca2+ in TSP induces a conformational change of TSP at least near the site of spin labeling.
Subject(s)
Blood Platelets/metabolism , Calcium/metabolism , Glycoproteins/metabolism , Electron Spin Resonance Spectroscopy , Humans , Kinetics , Protein Binding , Protein Conformation , Spin Labels , ThrombospondinsABSTRACT
Proton relaxation enhancement (PRE) values for fatty acid spin labels bound to human serum albumin have been investigated using the inversion-recovery method at 24 MHz. At 0.1 mM protein concentration and a label-to-protein ratio of one-to-one, the PRE value for 12-Doxylsterate-albumin complex is 7.8 +/- 2.3, whereas the PRE values for 5-Doxylstearate and 16-Doxylstearate-albumin complexes are 1.5 +/- 0.6 and 1.7 +/- 0.7, respectively. Addition of 10-fold excess of stearic acid reduced the PRE values nearly to 1, indicating that the strong enhancements arise from direct binding of fatty acid spin labels to human serum albumin. PRE values for all three labels exhibit maxima as a function of the label-to-protein ratio, suggesting multiple binding sites for fatty acid spin labels with labels in the tightest binding sites not resulting in the most effective relaxation. Based on the rates of reduction of ESR signal amplitudes by sodium ascorbate, the difference in PRE values for the three fatty acid spin labels bound to albumin is attributed to the difference in water accessibility of the nitroxide moieties at various positions along the acyl chain, being greater at the C-12 position than at C-5 or C-16 position. The PRE value of 8 for 12-Doxylstearate bound to human serum albumin indicates that this complex may be a suitable paramagnetic contrast agent for in vivo NMR imaging.
