10 research outputs found
Pandemic Flu and the Potential for U.S. Economic Recession: A State-by-State Analysis
Considers how a severe health pandemic outbreak could impact the United States economy and delineates the potential financial loss each state could face
Intellectual disability is associated with increased risk for obesity in a nationally representative sample of U.S. children
BACKGROUND: Data on obesity prevalence in children with intellectual disability (ID) are scarce.
OBJECTIVE: We estimated rates of obesity among children aged 10-17 years with and without ID in a nationally representative dataset that included measures of child weight and ID status, as well as family meal frequency, physical activity, and sedentary behavior.
METHODS: Chi-square tests compared prevalence of obesity, demographic and behavioral characteristics between children with and without ID as reported in the 2011 National Survey of Children\u27s Health. Tests for interaction in logistic regression models determined whether associations between obesity and behavioral characteristics were different between children with/without ID.
RESULTS: Obesity prevalence for children with ID was 28.9% and 15.5% for children without ID. After adjusting for age, sex, race/ethnicity and poverty level, the odds ratio was significantly 1.89 times greater among children with ID than among those without ID (95% CI: 1.14 to 3.12). Among children with ID, 49.8% ate at least one meal with family members every day compared to 35.0% without ID (p \u3c 0.002), and 49.5% with ID participated in frequent physical activity compared to 62.9% (p \u3c 0.005). Prevalence of obesity was higher among all children who ate family meals every day compared to fewer days per week, and the effect was significantly more pronounced among those with ID (p = 0.05).
CONCLUSIONS: Prevalence of obesity among youth with ID was almost double that of the general population. Prospective studies are needed in this population to examine the impact of consistent family mealtimes and infrequent physical activity
Parental concern regarding obesity in children with autism spectrum disorder in the United States: National Survey of Children\u27s Health 2016
BACKGROUND: The prevalence of obesity in children with autism spectrum disorder (ASD) exceeds that of the general population, but the level of parental concern about obesity in these children is unexplored.
OBJECTIVE: We estimate the prevalence of obesity in children 10-17 years in the redesigned National Survey of Children\u27s Health (NSCH) 2016, and compare parental concern about obesity between parents of children with and without ASD.
METHODS: The nationally representative NSCH 2016 oversampled parents of children with parent-report of special health care needs, including ASD. Parents opted to complete the survey via the web or surface mail. Following report of their child\u27s height and weight, parents were asked Are you concerned about their weight? Response options included: Yes, it\u27s too high, Yes, it\u27s too low, or No, I am not concerned. Obesity ( \u3e 95th percentile BMI) was defined using the 2000 CDC growth reference. We used logistic regression to compare odds of obesity, and odds of parental concern, between children with and without ASD.
RESULTS: In 24,251 children, ASD (n=699) increased obesity risk after adjusting for age, sex, and race/ethnicity (OR=1.54, 95%CI: 1.11, 2.14). ASD medication did not significantly affect obesity. ASD increased obesity concern (OR=2.17, 95%CI: 1.53, 4.81) among parents with obese children. Parents of boys with obesity and ASD had less obesity concern if he was taking medication for ASD (OR=0.258, 95%CI: 0.09, 0.78).
CONCLUSION: While the prevalence of obesity is elevated in children with ASD, parental obesity concern is high, suggesting opportunities for the development of parent-focused obesity prevention and treatment interventions for this population
The Effect of Age on the Prevalence of Obesity among US Youth with Autism Spectrum Disorder
BACKGROUND: We sought to assess the association between age and the prevalence of obesity among children with and without autism spectrum disorder (ASD) in the 2011-2012 National Survey of Children\u27s Health.
METHODS: Analyses were restricted to 43,777 children, ages 10-17, with valid measures of parent-reported weight, height, and ASD status. Exploratory analyses describe the impact of sex, race/ethnicity, and household income on the relationship between age and obesity in ASD.
RESULTS: Although the overall prevalence of obesity among children with ASD was significantly (p \u3c 0.001) higher than among children without ASD (23.1% vs. 14.1%, 95% confidence interval for difference 3.6 to 14.4), child age significantly (p = 0.035) modified this difference. In a multivariable logistic regression analysis, adjusted for sex, race/ethnicity, and household income, the odds of obesity among children with ASD compared with children without ASD increased monotonically from ages 10 to 17 years. This pattern arose due to a consistently high prevalence of obesity among children with ASD and a decline in prevalence with advancing age among children without ASD. These findings were replicated using a propensity score analysis. Exploratory analyses suggested that the age-related change in obesity disparity between children with and without ASD may be further modified by sex, race/ethnicity, and household income.
CONCLUSIONS: The patterns of prevalence observed with increasing age among children with and without ASD were unexpected. A better understanding of the etiological and maintenance factors for obesity in youth with ASD is needed to develop interventions tailored to the specific needs of these children
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De Novo Pathogenic Variants in CACNA1E Cause Developmental and Epileptic Encephalopathy with Contractures, Macrocephaly, and Dyskinesias
Developmental and epileptic encephalopathies (DEEs) are severe neurodevelopmental disorders often beginning in infancy or early childhood that are characterized by intractable seizures, abundant epileptiform activity on EEG, and developmental impairment or regression. CACNA1E is highly expressed in the central nervous system and encodes the α1-subunit of the voltage-gated CaV2.3 channel, which conducts high voltage-activated R-type calcium currents that initiate synaptic transmission. Using next-generation sequencing techniques, we identified de novo CACNA1E variants in 30 individuals with DEE, characterized by refractory infantile-onset seizures, severe hypotonia, and profound developmental impairment, often with congenital contractures, macrocephaly, hyperkinetic movement disorders, and early death. Most of the 14, partially recurring, variants cluster within the cytoplasmic ends of all four S6 segments, which form the presumed CaV2.3 channel activation gate. Functional analysis of several S6 variants revealed consistent gain-of-function effects comprising facilitated voltage-dependent activation and slowed inactivation. Another variant located in the domain II S4-S5 linker results in facilitated activation and increased current density. Five participants achieved seizure freedom on the anti-epileptic drug topiramate, which blocks R-type calcium channels. We establish pathogenic variants in CACNA1E as a cause of DEEs and suggest facilitated R-type calcium currents as a disease mechanism for human epilepsy and developmental disorders
De Novo Pathogenic Variants in CACNA1E Cause Developmental and Epileptic Encephalopathy with Contractures, Macrocephaly, and Dyskinesias
International audienceDevelopmental and epileptic encephalopathies (DEEs) are severe neurodevelopmental disorders often beginning in infancy or early childhood that are characterized by intractable seizures, abundant epileptiform activity on EEG, and developmental impairment or regression. CACNA1E is highly expressed in the central nervous system and encodes the α1-subunit of the voltage-gated CaV2.3 channel, which conducts high voltage-activated R-type calcium currents that initiate synaptic transmission. Using next-generation sequencing techniques, we identified de novo CACNA1E variants in 30 individuals with DEE, characterized by refractory infantile-onset seizures, severe hypotonia, and profound developmental impairment, often with congenital contractures, macrocephaly, hyperkinetic movement disorders, and early death. Most of the 14, partially recurring, variants cluster within the cytoplasmic ends of all four S6 segments, which form the presumed CaV2.3 channel activation gate. Functional analysis of several S6 variants revealed consistent gain-of-function effects comprising facilitated voltage-dependent activation and slowed inactivation. Another variant located in the domain II S4-S5 linker results in facilitated activation and increased current density. Five participants achieved seizure freedom on the anti-epileptic drug topiramate, which blocks R-type calcium channels. We establish pathogenic variants in CACNA1E as a cause of DEEs and suggest facilitated R-type calcium currents as a disease mechanism for human epilepsy and developmental disorders
Retrotransposons Are the Major Contributors to the Expansion of the Drosophila ananassae Muller F Element
The discordance between genome size and the complexity of eukaryotes can partly be attributed to differences in repeat density. The Muller F element (∼5.2 Mb) is the smallest chromosome in Drosophila melanogaster, but it is substantially larger (>18.7 Mb) in D. ananassae. To identify the major contributors to the expansion of the F element and to assess their impact, we improved the genome sequence and annotated the genes in a 1.4-Mb region of the D. ananassae F element, and a 1.7-Mb region from the D element for comparison. We find that transposons (particularly LTR and LINE retrotransposons) are major contributors to this expansion (78.6%), while Wolbachia sequences integrated into the D. ananassae genome are minor contributors (0.02%). Both D. melanogaster and D. ananassae F-element genes exhibit distinct characteristics compared to D-element genes (e.g., larger coding spans, larger introns, more coding exons, and lower codon bias), but these differences are exaggerated in D. ananassae. Compared to D. melanogaster, the codon bias observed in D. ananassae F-element genes can primarily be attributed to mutational biases instead of selection. The 5′ ends of F-element genes in both species are enriched in dimethylation of lysine 4 on histone 3 (H3K4me2), while the coding spans are enriched in H3K9me2. Despite differences in repeat density and gene characteristics, D. ananassae F-element genes show a similar range of expression levels compared to genes in euchromatic domains. This study improves our understanding of how transposons can affect genome size and how genes can function within highly repetitive domains