All samples were amplified simultaneously in triplicate in a one-assay run.
However, as multiple assays eventually become available for the marker, a bias in any one assay will complicate the diagnosis and long-term monitoring of patients [ 33].
For example, a number of approaches used different technologies to confirm the findings based on one assay with an additional one [ 92, 93].
As with any set of bioassays, the preparations described in the current study also have potential limitations: differences in drug sensitivities among the preparations might produce conflicting results (a beneficial effect in one assay but a negative response in another).
Our results demonstrate that the phenotypic strength of a strain in one assay is not necessarily predictive of its strength across another.
In one assay, a primer is located over the c.2184+19 common SNP potentially resulting in non-amplification of the mutant allele [ 28].
In all studies, pharmacokinetic assessments were based on the FVII coagulant activity (FVII C) assay, a one-stage assay using thromboplastin tissue factor, which quantifies FVII clotting activity in plasma (Capio Diagnostik A/S, Denmark) [ 21].
Two different rDNA primer sets were tested: one assay amplified a long product including the ITS1, 5.8S and ITS2 regions (LP) and the other a shorter product including the ITS1 only (SP).
In addition, they show little potential for multiplexing capabilities since they can conduct only one assay at a time.
Therefore, since consideration is given to one assay at a time, extracting the similarity scores for the conformer pairs tested in each AID from the all-by-all similarity score matrices computed and stored in the first part of study is described in Figure 16. Figure 16 Analysis method overview.
All laboratory analyses were carried out in batches with all samples from a single subject run in one assay.
