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This suppressor cell subset is often identified as CD4+CD25high cells [ 27] or as CD4+FoxP3+ lymphocytes [ 41], even if these markers are unable to uniquely define a regulatory T cell phenotype.
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The best set of markers associated with response to golimumab treatment included week-4 changes from baseline; however, even these markers were unable to achieve high enough specificity and sensitivity to be routinely useful predictors.
In our study, the classical serum and urine markers were unable to accurately reflect the changes on renal function after both the short- and long-term treatments, despite the presence of renal lesion, which were more pronounced for the longer CsA exposure; that failure demonstrates the need of better biomarkers of renal dysfunction/damage.
The Pi9-Pro marker was unable to differentiate between the Pi2 and Piz-t alleles.
This marker was unable to discriminate between the studied bowel complications despite it being an organ specific protein.
Thus, the marker was unable to serve as a useful adjunctive tool to assess short-term mortality risk in this patient population.
As a primary screening tool, this marker is unable to distinguish between normal pathological conditions especially in the so-called "grey zone" (PSA value from 2.5 to 10 ng/mL) [ 24].
A single measure of this marker was unable to predict incidence or progression of radiographic knee or hip OA, osteophytes, or joint space narrowing in either men or women [ 71].
However, inconsistencies and contradictions have been pointed out, in particular because of the use of endothelial markers which are unable to distinguish true angiogenic endothelial activity [ 4- 6].
Intrinsic properties of DC subsets or different maturation programs may lead to tolerogenic DCs which do express known maturation markers, but are unable to prime sustained proliferation of T cells and their differentiation into memory cells (Jiang et al, 2007; Platt et al, 2010).
For polyploid species such as cotton, these platforms can be problematic when the SNP assay amplifies both homeologous (At and Dt) copies of a locus, i.e., they act as "dominant" SNP markers and are unable to discriminate between a heterozygous plant and one that is homozygous for one of the two possible alleles at that locus being assayed, such as Genotype 1 in Figure 5A.
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