(C) 2009 American Institute of Physics. [DOI: 10.1063/1.3149696]“
“Some mechanisms have been proposed to explain the role of bradykinin on glucose homeostasis and some studies reported that the BDKRB2 +9/-9 polymorphism was associated to the transcriptional activity of the receptor. In this scenario, the main aim of this study was to evaluate the association of the BDKRB2 +9/-9 polymorphism with diabetes mellitus risk in the Brazilian general population. This study included 1,032 subjects of the general urban population. Anthropometrical, blood pressure, biochemical, and genotype analyses for the BDKRB2 +9/-9 bp insertion/deletion polymorphism were performed. Individuals
carrying +9/+9 or +9/-9 genotypes had higher glucose values (84.5 mg/dL versus 80.6 mg/dL, resp.) and higher frequency of diabetes mellitus (7.6% versus 3.6%, resp.)
compared to individuals check details carrying -9/-9, adjusting Baf-A1 cell line for age and gender. In addition, higher diabetes mellitus risk was associated to presence of the +9/+9 or +9/-9 genotypes (OR = 1.91; 95% CI = 1.09-4.19; P = 0.03). Our data suggest that the BDKRB2 +9/-9 polymorphism may act as a genetic modulator of glucose homeostasis. It was previously associated to insulin sensitivity, glucose uptake, and insulin secretion, and, in this study, data suggest that the polymorphism may increase susceptibility to chronic metabolic conditions such as diabetes in the Brazilian population.”
“BACKGROUND: The tuberculin skin test (TST) is used to help diagnose tuberculosis (TB) in acutely ill hospitalised children.
OBJECTIVE: To investigate the potential augmentative effect of
topical calcipotriol (a vitamin D analogue) or zinc on TST induration.
METHODS: Three TSTs were performed among 64 hospitalised children; each site was covered with topical aqueous cream (control), calcipotriol or zinc and assessed 24 and 48 h later by investigators blinded to all topical applications.
RESULTS: Rabusertib supplier TSTs were reactive in 15 (23.4%) children, of whom 13 (20.3%) were TST-positive. Topical calcipotriol and zinc induced TST positivity in two children with reactive but negative control TSTs. These treatments, however, did not significantly increase TST positivity rates. In children with reactive TSTs, the median 48 h induration diameter was not significantly different between the control, calcipotriol- or zinc-treated groups, which were respectively 12.0 (25%-75% IQR 5.0-18.0), 14.0 (25%-75% IQR 10.0 – 15.0) and 12.0 (25%-75% IQR 8.0 – 15.0) mm. Topical treatments did not induce TST reactivity or TST positivity in children with culture-confirmed TB disease (n=4), human immunodeficiency virus infection (n=18) or kwashiorkor (n=9).
CONCLUSIONS: Topical calcipotriol or zinc does not induce TST reactivity or significantly increase TST positivity rates in acutely ill hospitalised children.