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Having shown in vitro power generation by our Quinone-Ubiquinone GBFC, we next ascertained whether it was able to work when implanted in an animal.
Therefore we next ascertained whether IL-1+IL-6+TNF-α winfectedcted xenogeneic (THP-1) macrophages (xIM-1.6.α) could provide similar outcome as observed in the case of syngeneic infected macrophages (sIM-1.6.α) (Figure 1, 2, 3).
We next ascertained MMP-9 expression in both normal breast tissue and in human breast carcinoma tissue microarrays.
We next ascertained whether miR-148a-mediated down-regulation of PAI-1, VAV2, ITGA5, and ITGB8 expression resulted in the inhibition of malignant progression of tumor cells.
DOI: http://dx.doi.org/10.7554/eLife.01906.011 We next ascertained whether Erm associates with other components of the Brm remodeling complex, such as BAP60 and Snr1.
We next ascertained whether MEK5, ERK5, NF- κB and I κB steady-state levels and NF- κB activation in human colon adenocarcinoma samples were correlated with tumour clinicopathological characteristics.
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After confirming the transfer of immune cells and determining the majority phenotype, we next sought to ascertain whether these cells migrated to other organs or regions.
We next sought to ascertain the expression pattern of EMT drivers along the EMT Spectrum.
We next sought to ascertain the pathophysiological role of INPP1 in cancer.
We next wished to ascertain if the Ub conjugates were derived from nascent polypeptides that were linked to tRNA.
We next sought to ascertain whether AMs play an active role in the resolution of HDM-induced AAD.
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