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We finally showed that SF CD27+ and CD27- switch memory B cells were activated, as assessed by the expression of CD69, and expressed high levels of the CD86, but not CD80, costimulatory molecule.
The level of retroviral transduction (as assessed by the expression of EGFP) was 20% in the MFE23.CD3ζTDGA CIR-expressing population generated from patient 1.
VIC phenotype was assessed by the expression of alpha-smooth muscle actin (αSMA), vimentin, and collagen production after 28 days.
Furthermore, the chondrogenic differentiation of hASCs was assessed by the expression of chondrogenic-related markers (collagen type II, Sox-9 and Aggrecan) and deposition of cartilage-specific extracellular matrix for up to 28 days.
Interestingly, when functional activity of neutrophils was assessed by the expression of Fcγ receptor I, which is a marker of neutrophil activation recognized by the monoclonal antibodies CD64, we found that neutrophil CD64 expression varied significantly with infection and severity of infection, but not with alcohol consumption.
Differentiation was assessed by the expression of c-Kit, Sca1, Gr-1 and Mac-1 (BD/Pharmingen) by FACS.
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The IFN scores, representative of total IFN type I activity, were assessed by the expression levels of certain IFN type I signature genes such as IFI44, IFI44L, IFIT3, LY6E, and MX1 in CD14+ monocytes by real-time quantitative PCR.
Therefore, the potential of hAMSCs to undergo malignant transformation into TAFs when exposed to GBM CM was assessed by determining the expression of vimentin and alpha sm-actin, both proteins that are highly expressed in TAFs.
In fact, in the absence of PTP1B tissue macrophages display an activated phenotype assessed by the increased expression of CD80 that has a role in the maintenance of inflammation.
The phenotype of DCs after stimulation was assessed by studying the expression of cell surface markers.
These results correlated with the Stat1-driven gene expression as assessed by monitoring the expression of Stat1-mediated IFN-inducible 6-16 mRNA.
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