The effectiveness of a twice‐daily skin‐moisturising regimen for reducing the incidence of skin tears

A cluster randomised controlled trial was conducted to evaluate the effectiveness of a twice‐daily moisturising regimen as compared to ‘usual’ skin care for reducing skin tear incidence. Aged care residents from 14 Western Australian facilities (980 beds) were invited to participate. The facilities were sorted into pairs and matched in terms of bed numbers and whether they provided high or low care. One facility from each matched pair was randomised to the intervention group. Consenting residents in an intervention facility received a twice‐daily application of a commercially available, standardised pH neutral, perfume‐free moisturiser on their extremities. Residents in the control facilities received ad hoc or no standardised skin‐moisturising regimen. Participant numbers were sufficient to detect a 5% difference in incidence rate between the two groups with 80% power and a significance level of P = 0·05, and the inter‐cluster correlation coefficient was 0·034. Data were collected over 6 months. A total of 1396 skin tears on 424 residents were recorded during the study. In the intervention group, the average monthly incidence rate was 5·76 per 1000 occupied bed days as compared to 10·57 in the control group. The application of moisturiser twice daily reduced the incidence of skin tears by almost 50% in residents living in aged care facilities.     

The effects of aerobic exercise on glucose and counterregulatory hormone concentrations in children with type 1 diabetes

OBJECTIVE: To examine the acute glucose-lowering effects of aerobic exercise in children and adolescents with type 1 diabetes. RESEARCH DESIGN AND METHODS: Fifty children and adolescents with type 1 diabetes (ages 10 to <18 years) were studied during exercise. The 75-min exercise session consisted of four 15-min periods of walking on a treadmill to a target heart rate of 140 bpm and three 5-min rest periods. Blood glucose and plasma glucagon, cortisol, growth hormone, and norepinephrine concentrations were measured before, during, and after exercise. RESULTS: In most subjects (83%), plasma glucose concentration dropped at least 25% from baseline, and 15 (30%) subjects became hypoglycemic (< or = 60 mg/dl) or were treated for low glucose either during or immediately following the exercise session. The incidence of hypoglycemia and/or treatment for low glucose varied significantly by baseline glucose, occurring in 86 vs. 13 vs. 6% of subjects with baseline values <120, 120-180, and >180 mg/dl, respectively (P < 0.001). Exercise-induced increases in growth hormone and norepinephrine concentrations were marginally higher in subjects whose glucose dropped < or = 70 mg/dl. Treatment of hypoglycemia with 15 g of oral glucose resulted in only about a 20-mg/dl rise in glucose concentrations. CONCLUSIONS: In youth with type 1 diabetes, prolonged moderate aerobic exercise results in a consistent reduction in plasma glucose and the frequent occurrence of hypoglycemia when preexercise glucose concentrations are <120 mg/dl. Moreover, treatment with 15 g of oral glucose is often insufficient to reliably treat hypoglycemia during exercise in these youngsters.     

Multiple DICER1‐related tumors in a child with a large interstitial 14q32 deletion

Germ‐line interstitial deletions involving the 14q32 chromosomal region, resulting in 14q32 deletion syndrome, are rare. DICER1 is a recently described cancer‐predisposition gene located at 14q32.13. We report the case of a male child with a ～5.8 Mbp 14q32.13q32.2 germ‐line deletion, which included the full DICER1 locus. We reviewed available clinical and pathological material, and conducted genetic analyses. In addition to having congenital dysmorphic features, the child developed multiple DICER1 syndrome‐related tumors before age 5 y: a pediatric cystic nephroma (pCN), a ciliary body medulloepithelioma (CBME), and a small lung cyst (consistent with occult pleuropulmonary blastoma Type I/Ir cysts seen in DICER1 mutation carriers). He also developed a cerebral spindle‐cell sarcoma with myogenous differentiation. Our investigations revealed that the deletion encompassed 31 protein‐coding genes. In addition to the germ‐line DICER1 deletion, somatic DICER1 RNase IIIb mutations were found in the CBME (c.5437G > A, p.E1813K), pCN (c.5425G > A, p.G1809R), and sarcoma (c.5125G > A, p.D1709N). The sarcoma also harbored a somatic TP53 mutation: c.844C > T, p.R282W. Additional copy number alterations were identified in the CBME and sarcoma using an OncoScan array. Among the 8 cases with molecularly‐defined 14q32 deletions involving DICER1 and for whom phenotypic information is available, our patient and one other developed DICER1‐related tumors. Biallelic DICER1 mutations have not previously been reported to cause cerebral sarcoma, which now may be considered a rare manifestation of the DICER1 syndrome. Our study shows that DICER1‐related tumors can occur in children with 14q32 deletions and suggests surveillance for such tumors may be warranted.