01). The effects of these polymorphisms were not modified by personal smoking or secondhand-smoke exposure.\n\nConclusions: Functional promoter variants in CAT and HMOX-1 showed ethnicity-specific associations with new-onset asthma. Oxidant gene protection was restricted to children living in low-ozone communities.”
“Familial aggregation of prostate cancer is likely to be due to multiple susceptibility loci, perhaps acting

in conjunction with shared lifestyle risk factors. Models that assume a single mode of inheritance selleck kinase inhibitor may be unrealistic. We analyzed genetic models of susceptibility to prostate cancer using segregation analysis of occurrence in families ascertained through population-based series totaling 4390 incident cases. We investigated major gene models (dominant, recessive, general, X-linked), polygenic models, and mixed models of susceptibility using the pedigree analysis software MENDEL. The hypergeometric model was used to approximate polygenic inheritance. The best-fitting Sapanisertib molecular weight model for the familial aggregation of prostate cancer was the mixed recessive model.

The frequency of the susceptibility allele in the population was estimated to be 0.15 (95% confidence interval (CI) 0.11-0.20), with a relative risk for homozygote carriers of 94 (95% Cl 46-192), and a polygenic standard deviation of 2.01 (95% Cl 1.72-2.34). These analyses suggest that one or more genes having a strong recessively inherited effect on risk, as well as a number of genes with variants having small multiplicative effects on risk, may account for the genetic susceptibility to prostate cancer. The recessive component would predict the observed higher familial risk for siblings of cases than for fathers, but this could also be due to other factors such as shared lifestyle by siblings, targeted screening effects, and/or non-additive effects of one or more genes.

Genet. Epidemiol. 34:42-50, 2010. (c) 2009 Wiley-Liss, Inc.”
“The AQP9 gene contains a negative insulin response element, suggesting that it Entinostat may be modulated by insulin. Previously, we reported AQP9 overexpression in preeclamptic placentas but a lack of functionality of AQP9 in water and mannitol transport. We also observed high serum levels of insulin and TNF-alpha in preeclamptic women.\n\nObjective: To evaluate whether AQP9 expression is regulated by insulin in the human placenta, and whether the dysregulation of AQP9 observed in preeclamptic placentas may be related to the inability to respond to insulin stimuli.\n\nMethods: Explants from normal and preeclamptic placentas were cultured at different concentrations of insulin. Treatment with TNF-alpha was used to induce phosphorylation of insulin receptor substrate (IRS), which may desensitize insulin action. AQP9 molecular expression and water uptake was determined.\n\nResults: Insulin decreased the molecular expression of AQP9 exclusively in explants from normal placentas in a concentration-dependent manner.