Sentence examples for assays causes from inspiring English sources

The inclusion of ADP at two different concentrations (0.1 and 2.0 mM) in separate ITF [ATP] ligand-binding assays causes a significant increase in the apparent K d of ATP for its Mt-PrsA-binding site (at a concentration of 0.1 and 2.0 mM ADP, respectively), clearly illustrating allosteric inhibition of Mt-PrsA ATP Mt-PrsA ATPmation.

However, not all DSA detected by current assays cause injury in the allograft and not all ABMR phenotypes cause rapid allograft failure.

In some cases, template sequence discrepancies or inaccuracies can lead to failed assays caused by poor or no binding of primers and probes and/or non-specific binding resulting in multiple PCR products.

IgY antibodies can also be used to avoid interference in immunological assays caused by the human complement system, rheumatoid factors, human anti-mouse IgG antibodies (HAMA) or human and bacterial Fc-receptors [ 43].

As with the acquired thermotolerance plate assay, the presence of Gdn-HCl in cultures prior to carrying out the assay causes a major reduction in luciferase refolding activity (due to inhibition of Hsp104, data not shown).

The total quantity of DNA obtained is much smaller and PMAs demand relatively high quantity and quality of DNA, particularly as the bisulphite treatment essential to the assay causes a degree of fragmentation.

In in vitro assays, IC caused a concentration-dependent inhibition of LPS stimulated NO (up to ~ 67.4 % at 50 μM) and TNF-α (~84.5 % at 50 μM) production.

In BH3 profiling assays, MS1 caused depolarization in several human Mcl-1-dependent cell lines with EC50 values of ∼3 μM, contrasted with EC50 values of >100 μM for Bcl-2-, Bcl-xL-, or Bfl-1-dependent celinesnes.

This was in agreement with Mohamed (2011) who found that flow cytometric analysis of cell cycle and comet assay caused DNA damage in Biomphalaria alexandrina hemocytes exposed to Schistosoma mansoni infection when compared to control group.

The 8 genotype-specific amino acids found on group I might contribute to their distinct characterization in in vitro and in vivo marker assay, causing 5 unique mutations located on polymerase related protein.

We do not believe the choice of assay caused the lack of association with mortality in our study, but it cannot be excluded, and direct comparisons of different FGF23 assays will be necessary in the future.