Neck circumference as a complementary measure to identify excess body weight in children aged 13-24 months

Objectives:to analyze the accuracy of neck circumference (NC) as a measure for assessing excess body weight in children aged 13-24 months of life, according to gender.Methods:this is a cross-sectional study comparing the neck circumferences in relation to body mass index (BMI) and other anthropometric measures. The best cut-off point for identifying excess body weight was determined using the Receiver Operating Characteristics curve (ROC curve), according to gender and age groups 13-15 months, 16-19 months and 20-24 months.Results:NC waspositively correlated (p<0.001) with body weight and BMI in both genders, and length in girls (p<0.001). Positive correlations were found between NC and BMI in the three age groups (13-15, 16-19 and 20-24 months) in both boys and girls. The NC cut-off points for boys were 23.6, 23.9 and 24.0 cm, and 23.4, 23.5 and 23.6 cm for girls, for the 1315, 16-19 and 20-24 age groups respectively.Conclusions:NC can be used to screen for excess body weight in children aged 13-24 months. However, further studies with a larger sample will be required in order to complement these results

Kallikrein genes are associated with lupus and glomerular basement membrane-specific antibody-induced nephritis in mice and humans

Immune-mediated nephritis contributes to disease in systemic lupus erythematosus, Goodpasture syndrome (caused by antibodies specific for glomerular basement membrane [anti-GBM antibodies]), and spontaneous lupus nephritis. Inbred mouse strains differ in susceptibility to anti-GBM antibody-induced and spontaneous lupus nephritis. This study sought to clarify the genetic and molecular factors that may be responsible for enhanced immune-mediated renal disease in these models. When the kidneys of 3 mouse strains sensitive to anti-GBM antibody-induced nephritis were compared with those of 2 control strains using microarray analysis, one-fifth of the underexpressed genes belonged to the kallikrein gene family, which encodes serine esterases. Mouse strains that upregulated renal and urinary kallikreins exhibited less evidence of disease. Antagonizing the kallikrein pathway augmented disease, while agonists dampened the severity of anti-GBM antibody-induced nephritis. In addition, nephritis-sensitive mouse strains had kallikrein haplotypes that were distinct from those of control strains, including several regulatory polymorphisms, some of which were associated with functional consequences. Indeed, increased susceptibility to anti-GBM antibody-induced nephritis and spontaneous lupus nephritis was achieved by breeding mice with a genetic interval harboring the kallikrein genes onto a disease-resistant background. Finally, both human SLE and spontaneous lupus nephritis were found to be associated with kallikrein genes, particularly KLK1 and the KLK3 promoter, when DNA SNPs from independent cohorts of SLE patients and controls were compared. Collectively, these studies suggest that kallikreins are protective disease-associated genes in anti-GBM antibody-induced nephritis and lupus