Parent-Focused Childhood Obesity Intervention Improves Family Functioning and Children\u27s Well-Being

An Extension-implemented parent-focused childhood obesity intervention designed to improve family functioning around healthful eating and exercise was evaluated. Thirty-six parents and their children, aged 5–13, were randomized to a 12-week intervention condition or control condition. Intervention parents, compared to control group parents, felt more confident in promoting children\u27s healthful eating and exercise, worried less about their children\u27s weight, and engaged in fewer counterproductive parenting behaviors. The children of these parents, as compared to children of control group parents, lost weight and displayed better social-emotional functioning. These results highlight Extension\u27s important role in disseminating evidence-based childhood obesity interventions

Cultural and Contextual Adaptation of a Childhood Obesity Preventive Intervention Program

This article describes the adaptation of a parent-focused evidence-based childhood obesity intervention program for implementation by county-based Extension educators in coordination with school district personnel in rural Pennsylvania. The Lifestyle Positive Parenting Program was designed and evaluated in Australia in clinical settings. Several minor and more serious adaptations, such as featured recipes and content of follow-up telephone calls, were made so that the program would be more appropriate for and appealing to target families. Conceptual issues regarding the adaptation of evidence-based programs are reviewed

Childhood Sexual Abuse and Early Timing of Puberty

AbstractPurposeThe purpose was to examine whether the timing of puberty, indexed by breast development and pubic hair development, was earlier for sexually abused females compared with a matched comparison group of nonabused females, controlling for key alternative confounds.MethodsA cohort of sexually abused females and matched comparisons was followed longitudinally at mean ages 11 through 20 years. Sexually abused participants (N = 84) were referred by protective services. Comparison participants (N = 89) were recruited to be comparable in terms of age, ethnicity, income level, family constellation, zip codes, and nonsexual trauma histories. Stage of puberty was indexed at each assessment by nurse and participant ratings of breast and pubic hair development using Tanner staging—the gold standard for assessing pubertal onset and development. Cumulative logit mixed models were used to estimate the association between sexual abuse status and the likelihood of transitioning from earlier to later Tanner stage categories controlling for covariates and potential confounds.ResultsSexual abuse was associated with earlier pubertal onset: 8 months earlier for breasts (odds ratio: 3.06, 95% CI: 1.11–8.49) and 12 months earlier for pubic hair (odds ratio: 3.49, 95% CI: 1.34–9.12). Alternative explanations including ethnicity, obesity, and biological father absence did not eradicate these findings.ConclusionsThis study confirms an association between exposure to childhood sexual abuse and earlier pubertal onset. Results highlight the possibility that, due to this early onset, sexual abuse survivors may be at increased risk for psychosocial difficulties, menstrual and fertility problems, and even reproductive cancers due to prolonged exposure to sex hormones

Hippocampal plasticity underpins long-term cognitive gains from resistance exercise in MCI

Dementia affects 47 million individuals worldwide, and assuming the status quo is projected to rise to 150 million by 2050. Prevention of age-related cognitive impairment in older persons with lifestyle interventions continues to garner evidence but whether this can combat underlying neurodegeneration is unknown. The Study of Mental Activity and Resistance Training (SMART) trial has previously reported within-training findings; the aim of this study was to investigate the long-term neurostructural and cognitive impact of resistance exercise in Mild Cognitive Impairment (MCI). For the first time we show that hippocampal subareas particularly susceptible to volume loss in Alzheimer's disease (AD) are protected by resistance exercise for up to one year after training. One hundred MCI participants were randomised to one of four training groups: (1) Combined high intensity progressive resistance and computerised cognitive training (PRT+CCT), (2) PRT+Sham CCT, (3) CCT+Sham PRT, (4) Sham physical+sham cognitive training (SHAM+SHAM). Physical, neuropsychological and MRI assessments were carried out at baseline, 6 months (directly after training) and 18 months from baseline (12 months after intervention cessation). Here we report neuro-structural and functional changes over the 18-month trial period and the association with global cognitive and executive function measures. PRT but not CCT or PRT+CCT led to global long-term cognitive improvements above SHAM intervention at 18-month follow-up. Furthermore, hippocampal subfields susceptible to atrophy in AD were protected by PRT revealing an elimination of long-term atrophy in the left subiculum, and attenuation of atrophy in left CA1 and dentate gyrus when compared to SHAM+SHAM (p = 0.023, p = 0.020 and p = 0.027). These neuroprotective effects mediated a significant portion of long-term cognitive benefits. By contrast, within-training posterior cingulate plasticity decayed after training cessation and was unrelated to long term cognitive benefits. Neither general physical activity levels nor fitness change over the 18-month period mediated hippocampal trajectory, demonstrating that enduring hippocampal subfield plasticity is not a simple reflection of post-training changes in fitness or physical activity participation. Notably, resting-state fMRI analysis revealed that both the hippocampus and posterior cingulate participate in a functional network that continued to be upregulated following intervention cessation. Multiple structural mechanisms may contribute to the long-term global cognitive benefit of resistance exercise, developing along different time courses but functionally linked. For the first time we show that 6 months of high intensity resistance exercise is capable of not only promoting better cognition in those with MCI, but also protecting AD-vulnerable hippocampal subfields from degeneration for at least 12 months post-intervention. These findings emphasise the therapeutic potential of resistance exercise; however, future work will need to establish just how long-lived these outcomes are and whether they are sufficient to delay dementia

Return to the sea, get huge, beat cancer: an analysis of cetacean genomes including an assembly for the humpback whale (Megaptera novaeangliae)

Cetaceans are a clade of highly specialized aquatic mammals that include the largest animals that have ever lived. The largest whales can have 1,000 more cells than a human, with long lifespans, leaving them theoretically susceptible to cancer. However, large-bodied and long-lived animals do not suffer higher risks of cancer mortality than humans—an observation known as Peto’s Paradox. To investigate the genomic bases of gigantism and other cetacean adaptations, we generated a de novo genome assembly for the humpback whale (Megaptera novaeangliae) and incorporated the genomes of ten cetacean species in a comparative analysis. We found further evidence that rorquals (family Balaenopteridae) radiated during the Miocene or earlier, and inferred that perturbations in abundance and/or the interocean connectivity of North Atlantic humpback whale populations likely occurred throughout the Pleistocene. Our comparative genomic results suggest that the evolution of cetacean gigantism was accompanied by strong selection on pathways that are directly linked to cancer. Large segmental duplications in whale genomes contained genes controlling the apoptotic pathway, and genes inferred to be under accelerated evolution and positive selection in cetaceans were enriched for biological processes such as cell cycle checkpoint, cell signaling, and proliferation. We also inferred positive selection on genes controlling the mammalian appendicular and cranial skeletal elements in the cetacean lineage, which are relevant to extensive anatomical changes during cetacean evolution. Genomic analyses shed light on the molecular mechanisms underlying cetacean traits, including gigantism, and will contribute to the development of future targets for human cancer therapies

Partial Loss of USP9X Function Leads to a Male Neurodevelopmental and Behavioral Disorder Converging on Transforming Growth Factor β Signaling

The X-chromosome gene USP9X encodes a deubiquitylating enzyme that has been associated with neurodevelopmental disorders primarily in female subjects. USP9X escapes X inactivation, and in female subjects de novo heterozygous copy number loss or truncating mutations cause haploinsufficiency culminating in a recognizable syndrome with intellectual disability and signature brain and congenital abnormalities. In contrast, the involvement of USP9X in male neurodevelopmental disorders remains tentative. We used clinically recommended guidelines to collect and interrogate the pathogenicity of 44 USP9X variants associated with neurodevelopmental disorders in males. Functional studies in patient-derived cell lines and mice were used to determine mechanisms of pathology. Twelve missense variants showed strong evidence of pathogenicity. We define a characteristic phenotype of the central nervous system (white matter disturbances, thin corpus callosum, and widened ventricles); global delay with significant alteration of speech, language, and behavior; hypotonia; joint hypermobility; visual system defects; and other common congenital and dysmorphic features. Comparison of in silico and phenotypical features align additional variants of unknown significance with likely pathogenicity. In support of partial loss-of-function mechanisms, using patient-derived cell lines, we show loss of only specific USP9X substrates that regulate neurodevelopmental signaling pathways and a united defect in transforming growth factor β signaling. In addition, we find correlates of the male phenotype in Usp9x brain-specific knockout mice, and further resolve loss of hippocampal-dependent learning and memory. Our data demonstrate the involvement of USP9X variants in a distinctive neurodevelopmental and behavioral syndrome in male subjects and identify plausible mechanisms of pathogenesis centered on disrupted transforming growth factor β signaling and hippocampal function