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To verify the successful deletion of NLRP3 in the CMV-NLRP3 KO mice, we differentiated bone marrow-derived macrophages from the wild-type and CMV-NLRP3 KO mice and exposed these cells to NLRP3 stimuli.
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To generate mouse macrophages, we differentiated bone-marrow cells isolated from wild-type C57BL/6 mice and from B6.B10ScN- Tlr4 lps-del mice (Jackson Laboratory) according to standard procedures [ 26].
We differentiated mouse bone marrow cells in the presence of recombinant macrophage colony stimulating (rM-CSF) factor for 14 days during the flight of space shuttle Space Transportation System (STS -126.
In this study, we differentiated mouse ESCs to germ cells.
Several possibilities may contribute to the discrepancy between our study and Iwabuchi-Doi's: First, we differentiated mouse ESCs and EpiSCs in cell aggregates (EBs) in serum-free medium, whereas Iwabuchi-Doi et al. performed EpiSC neural differentiation using monolayers in N2B27 medium.
To determine if our results in P19 cells were applicable to mouse embryonic stem (mES) cells, we differentiated mES cells in hanging drops for 2 days and in suspension culture for an additional 5 days, the latter with 0-50 nM RA.
To assess osteoclastogenesis in vitro, we differentiated osteoclasts from mouse bone marrow cells and from mouse monocytic RAW 264.7 cell line.
To further explore potential differences in the in vivo half-life of sAPP, we differentiated in the Tg2576 mice sAPPα from sAPPβ, both human and murine (Figure 1C).
When these cells were transplanted into cartilage defective mice, they differentiated into hyaline cartilage and also had a high survival rate.
We examined the capacity of splenocytes of IFN-γR KO and wild-type mice to differentiate into osteoclasts in vitro, and we investigated whether the extramedullar splenic CD11b+ cell population, expanded after immunisation with collagen type II in complete Freund's adjuvant (CII/CFA) in the IFN-γR KO mice, can be regarded as possible osteoclast precursors.
To evaluate possible phenotypic differences at early times after gene deletion, we established primary myoblast cultures from Vps15f/f mice, differentiated the myoblasts to myotubes in vitro and transduced them with adenoviral Cre to induce gene deletion.
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