The maternal-age-associated risk of congenital heart disease is modifiable.

Maternal age is a risk factor for congenital heart disease even in the absence of any chromosomal abnormality in the newborn. Whether the basis of this risk resides with the mother or oocyte is unknown. The impact of maternal age on congenital heart disease can be modelled in mouse pups that harbour a mutation of the cardiac transcription factor gene Nkx2-5 (ref. 8). Here, reciprocal ovarian transplants between young and old mothers establish a maternal basis for the age-associated risk in mice. A high-fat diet does not accelerate the effect of maternal ageing, so hyperglycaemia and obesity do not simply explain the mechanism. The age-associated risk varies with the mother's strain background, making it a quantitative genetic trait. Most remarkably, voluntary exercise, whether begun by mothers at a young age or later in life, can mitigate the risk when they are older. Thus, even when the offspring carry a causal mutation, an intervention aimed at the mother can meaningfully reduce their risk of congenital heart disease.

Continuing Delay in the Diagnosis of Slipped Capital Femoral Epiphysis.

OBJECTIVE: To evaluate whether the time from symptom onset to diagnosis of slipped capital femoral epiphysis (SCFE) has improved over a recent decade compared with reports of previous decades. STUDY DESIGN: Retrospective review of 481 patients admitted with a diagnosis of SCFE at three large pediatric hospitals between January 2003 and December 2012. RESULTS: The average time from symptom onset to diagnosis of SCFE was 17 weeks (range, 0-to 169). There were no significant differences in time from symptom onset to diagnosis across 2-year intervals of the 10-year study period (P = .94). The time from evaluation by first provider to diagnosis was significantly shorter for patients evaluated at an orthopedic clinic (mean, 0 weeks; range, 0-0 weeks) compared with patients evaluated by a primary care provider (mean, 4 weeks; range, 0-52 weeks; r = 0.24; P = .003) or at an emergency department (mean, 6 weeks, range, 0-104 weeks; r = 0.36; P = .008). Fifty-two patients (10.8%) developed a second SCFE after treatment of the first affected side. The time from the onset of symptoms to diagnosis for the second episode of SCFE was significantly shorter (r = 0.19; P < .001), with mean interval of 11 weeks (range, 0-104 weeks) from symptom onset to diagnosis. There were significantly more cases of mildly severe SCFE, as defined by the Wilson classification scheme, in second episodes of SCFE compared with first episodes of SCFE (OR, 4.44; P = .001). CONCLUSION: Despite reports documenting a lag in time to the diagnosis of SCFE more than a decade ago, there has been no improvement in the speed of diagnosis. Decreases in both the time to diagnosis and the severity of findings for the second episode of SCFE suggest that the education of at-risk children and their families (or providers) may be of benefit in decreasing this delay.