Because of the stable, yet modifiable nature of DNA methylation, we hypothesized that bone lead, a marker of cumulative exposure with a half-life measured in years, would be associated with changes in global DNA methylation and that this association would be more evident than an association with a biomarker of concurrent/short-term exposure such as blood lead.
On the basis of previous research, we hypothesized that (1) hyporeactive HPA axis at 18 years would be associated with more severe MS pain at 22 years and (2) the association would be stronger in the presence of relative cold and pressure pain hypersensitivity.
Given data that increasing age is associated with an exaggerated CNS inflammatory response, we examined whether older age (>55 years) would be associated with a greater IFN-alpha-induced increase in CNS glutamate.
To test the hypothesis that a change in glycated hemoglobin (A1c) over a follow-up interval of approximately 2 years would be associated with concomitant changes in fasting lipids in individuals with type 1 diabetes (T1D).
We predicted that more severe post-traumatic stress (PTS) symptoms at age 37 years would be associated with insecure attachment at age 55 and with worse PTS symptoms 24 years later at age 61, and that age 55 attachment would mediate the influence of earlier PTS symptoms on later symptoms.
A 10% reduction in systolic blood pressure is considered clinically worthwhile, (18) and, if sustained for another 4 years, would be associated with an ∼25% reduction in cardiovascular events (22).
This is broadly consistent with the result of the prior analysis which found that once-lifetime testing at age 35 years would be associated with a reduction of between 25-36% in lifetime risk to age 65 years in screened women [ 27].
Designed to address many of the potential limitations of RCTs and observational studies, the GI-REASONS theted thypothesissis that celecoxib use in patients with osteoarthritis of at least moderate GI risk (aged ≥55 years) would be associated with a lower incidence of clinically significant upper and/or lower GI events than nsNSAIDs in standard clinical practice.
We hypothesized that: 1) REE, adjusted for FFM, would be lower in children with DS than in sibling controls, 2) changes in FM over the three year period would be associated with baseline REE, adjusted for baseline FFM, baseline FM, sex, and age.
We hypothesized that both clinical and biological markers of inflammation during the first year of life would be associated with later developmental outcomes.
