As one would expect, diseases such as polio are still rife in Africa and other parts of the Third World.
We expect disease-specific and generic instruments to be moderately correlated because similar, though distinct, constructs are targeted.
Therefore, we would expect disease-associated genes to cluster most strongly in the interactomes specific to the disease-manifesting cell types, providing us with a method of identifying these cell types.
We would therefore expect diseases involving the immune system or immunosuppressive therapies to be more frequent in patients with a history of SCC.
Determining expected disease incidence was critical to calculating power and determining trial sample size.
Fitting of these models often computes expected disease counts via internal standardization.
This disease reaction pattern agreed with the expected disease reaction attributed to the xa5 gene (Nino-Liu et al. 2006).
As expected, disease severity, as measured by both the number of chronic conditions and the Carlson Comorbidity Index, increased across the range.
All PBS-dosed mice displayed expected disease with the peak average clinical score of 4 (Figure 1C).
