Role of muscle mass in the association between handgrip strength and blood pressure in children and adolescents.

Studies have reported conflicting results on the association between handgrip strength (HGS) and blood pressure during childhood and adolescence. High multicollinearity involving somatic components that influence both HGS and blood pressure might be an important source of bias. This study sought to investigate the independent effects of HGS and muscle mass on blood pressure levels in children and adolescents. Muscle mass and fat mass (Multifrequency Electrical Bioimpedance) and systolic (SBP) and diastolic (DBP) blood pressure (Automatic oscillometric device) were assessed in 833 volunteers aged 6-18 years, of both sexes. Handgrip strength-for-age quartiles were calculated and participants were assigned to groups by HGS quartiles. Analysis of covariance was conducted to address the linear association between HGS and SBP adjusted for height, muscle mass, and fat mass. To test for linear trend, contrast analysis was conducted. Partial eta-squared was used to confirm or rule out a small significant effect of the independent variables on SBP. The effect size of HGS on SBP was not significant in both sexes. In girls, 1.7% of the between-groups variance in SBP was accounted for by muscle mass (P = 0.016). In boys, 2.3% and 1.8% of the between-groups variance in SBP was accounted for by muscle mass (P = 0.001) and height (P = 0.005), respectively. In conclusion, children with a more advanced physical maturity for their age, that is, who are taller, stronger, and have greater fat-free mass, may be nearly reaching the physiological parameters of adulthood, and consequently have higher systolic blood pressure.

Molecular detection of XO - Turner syndrome.

Turner syndrome is caused by haploinsufficiency of the short arm of X-chromosome, and is usually diagnosed by karyotyping. This procedure is time-consuming, expensive and unfeasible for population screening. We propose molecular detection of 45XO Turner patients based on the ability of HpaII, a methylation sensitive endonuclease, to induce the cleavage of non-methylated DNA in the active X-allele. Genomic DNA was obtained from 22 patients with Turner syndrome confirmed by karyotype (45XO, N = 18; 45XO/46XX, N = 4). After digestion, DNA was amplified with primers directed to exon 1 of the androgen receptor (AR) gene and to the GAPDH control gene. Normal control females or mosaic patients, with a second methylated X-chromosome, escaped from HpaII digestion and produced a band corresponding to AR gene amplification. 45XO patients have just one active non-methylated X-chromosome, completely digested by HpaII, thus preventing the amplification of the AR gene. Three of the 45XO cases gave amplified bands, suggesting low-frequency mosaicisms that are not detected by karyotyping. Compared to classical karyotype studies for the detection of 45XO Turner patients, this new molecular method is simpler, faster and less expensive.