Objective To evaluate whether sugar sweetened beverage consumption, a significant source of dietary fructose, is associated with higher serum uric acid levels and blood pressure in adolescents. Study design We analyzed cross-sectional data from 4867 adolescents aged 12–18 years old in the National Health and Nutrition Examination Survey 1999–2004. Dietary data was assessed from 24-hour dietary recall interviews. Sugar sweetened beverages included fruit drinks, sports drinks, soda, and sweetened coffee or tea. We used multivariate linear regression to evaluate the association of sugar sweetened beverage consumption with serum uric acid and with blood pressure. Results Adolescents who drank more sugar sweetened beverages tended to be older and male. In the adjusted model, serum uric acid increased by 0.18 mg/dL and systolic blood pressure z-score increased by 0.17 from the lowest to the highest category of sugar sweetened beverage consumption (P for trend 0.01 and 0.03, respectively). Conclusions These results from a nationally representative sample of US adolescents indicate that higher sugar sweetened beverage consumption is associated with higher serum uric acid levels and systolic blood pressure, which may lead to downstream adverse health outcomes.

Natural killer (NK) cell alloreactivity is reported to mediate strong GvL (graft versus leukemia) effect in patients after haploidentical stem-cell transplantation (SCT) for acute myeloid leukemia (AML). Because subsequent immune reconstitution remains a major concern, we studied NK-cell recovery in 10 patients with AML who received haplomismatched SC transplants, among whom no GvL effect was observed, despite the mismatched immunoglobulin-like receptor (KIR) ligand in the GvH direction for 8 of 10 patients. NK cells generated after SCT exhibited an immature phenotype: the cytotoxic CD3 ؊ CD56 dim subset was small, expression of KIRs and NKp30 was reduced, while CD94/NKG2A expression was increased. This phenotype was associated to in vitro lower levels of cytotoxicity against a K562 cell line and against primary mismatched AML blasts than donor samples. This impaired lysis was correlated with CD94/NKG2A expression in NK cells. Blockading CD94/NKG2A restored lysis against the AML blasts, which all expressed HLA-E, the ligand for CD94/ NKG2A. Our present study allows a better understanding of the NK-cell differentiation after SCT. These results revealed that the NK cells generated after haplomismatched SCT are blocked at an immature state characterized by specific phenotypic features and impaired functioning, having potential impact for immune responsiveness and transplantation outcome. (Blood. 2005;105:4135-4142)