8 10–13 Given the importance of risk stratification, additional biomarkers that probe different neurohormonal pathways may further help to define disease progression and prognosis, which is likely to be dynamic and change over time.
Critically, reliance on a single measurement or non-systematic ascertainment of serum creatinine to define disease prevalence may result in misclassification.
Observations that miRNAs displayed high stability in paraffin-embedded tissues from clinical samples or in human plasma raised the possibility that miRNA expression analysis may be a useful tool to define disease states.
However, as PET images include a greater body area, it may define sites of disease outside the scope of that seen on routine CT scanning.
The statistically significant positive correlations observed between the grade of DCIS and the expression of structures reactive with GS-1 and VVA suggest that these reactive antigens may define a phenotype for disease progression or DCIS transformation to invasive disease.
The presence of disease susceptibility alleles may define subsets of patients with different disease courses, including patients with mild, nonerosive disease and those with a true RA phenotype and progressive disease, with extensive joint damage and ExRA manifestations.
We found that contribution of different non-HLA single nucleotide polymorphisms (SNPs) associated with RA in the development of distinct ACPAs does not overlap, and may define distinct subgroups of disease with an SE-positive or an SE-negative background.
Most of the conditions in which the role of oxidative stress and related mediators has been characterized belong to what one may define as chronic inflammatory/fibrogenic diseases, often involving chronic activation of wound healing.
Therefore we expect that expanding this multigenic approach using in-depth sequencing of other sets of genes, particularly other hubs within the synaptic proteome, will identify other nsSNP clusters, and genetic load that may define a range of neuropsychiatric diseases [19].
Additional research on the isoform-specific roles of the NOXs and on the specific downstream targets that they affect may define suitable therapeutic targets for cardiovascular diseases.
