As such, the statistical significance of the NPA scores can be assessed by estimating confidence intervals around the score, or, equivalently, by evaluating the null hypothesis of the score equaling zero at a given type-I error risk α (often, and herein, α = 0.05).
Hence, in this subsection, we will confirm our hypothesis by evaluating the PDRs of STDMA with various physical transmission rates.
We tested this hypothesis by evaluating the presence of the phosphorylated form of the histone H2A variant, γH2AX, and 53-binding protein 1 (53BP1).
Here we explored this hypothesis by evaluating the direct reinforcing effects of nicotine in experimentally-naive squirrel monkeys using a fixed-ratio (FR) schedule of reinforcement.
We tested this hypothesis by evaluating the differences in effect size of the high risk SPINK1 N34S haplotype on CP from multiple etiologies after combining clinical reports of SPINK1 N34S frequency using meta-analysis.
This study explored this hypothesis by evaluating the functional overlap of the signatures on the basis of annotated gene sets.
We further validated this hypothesis by evaluating the ability of TIMELESS mutants that do not bind PARP1 to be recruited to sites of laser-induced DNA damage.
Further prospective investigations may shed light on this hypothesis by evaluating the complex interplay between insulin and fetuin-A in relation to future cardiometabolic risk.
We tested this hypothesis by evaluating the extent to which controlling for A1C and markers of vascular, neurologic, and inflammatory pathology explained the greater prevalence of hearing impairment among subjects with diabetes (1).
We undertook the current pilot study to test our hypothesis by evaluating the mRNA expressions of three randomly selected cancer-related genes, PIK3C3, PIM3, and PTEN, using quantitative real-time RT-PCR approach.
