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Both of these genetic marker studies observed a significant amount of genetic diversity among accessions collected from different geographic regions.
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Some studies observed positive associations between inflammatory markers and depressive symptoms, 2 5–9 11 but others did not.
Whereas it is generally known that resistance to rifampicin is a surrogate marker for MDRTB, this study observed a high rate of monoresistance to rifampicin.
In addition to rs1143679, the eight other markers studied were observed to associate significantly in Finnish patients (Tables 3, 4, 5), whereas Swedish patients showed borderline association (Table 5).
Neither study observed improvements in markers of inflammation or oxidative stress.
Another study observed that stem cells and tumor initiating activity could be retrieved from Wnt-induced mammary epithelial cell populations using the cell surface marker CD61 (β3 integrin) [11].
Prognostic marker studies.
Tumor marker studies.
The change in marker sets from the initial exposure to a largely intracellular survival strategy may explain a corresponding shift in the marker sets observed in this study.
Chromosomal rearrangement is known to cause recombination suppression [29], which may be the cause of the marker clustering observed in the present study.
To the best of our knowledge no other studies have associated tPA markers with PTB; however, several studies have observed increased tPA and tissue factors expression in preterm compared to term human decidual tissues [34], [35].
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