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In contrast, white matter degeneration was observed in Dpl-expressing Ngsk mice yet was not seen in mice expressing either of the two transgenes, PrP_Dpl and CD_Dpl.
Mice carrying floxed alleles in Brca1 and in p53 were crossed with mice expressing either Fshr-Cre or Mis2r-Cre transgenes, or both of these transgenes.
In histopathological analysis, young mice expressing either LRRK2 variant presented with transient vacuolization of striatal white fiber tracts accompanied by accumulation of microglial cells and astrogliosis, but inflammation resolved without permanent damage.
Tumors from mice expressing either allele are dependent upon mutant EGFR for survival.
We had previously reported that CD46 cytoplasmic isoforms had differential roles in inflammation using transgenic mice expressing either isoform.
RGCs from these mice expressing either AKAR2.2 or AKAR3 were depolarized using brief application of high concentration KCl (Figures 2A & B).
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These transgenic mice express either IL-1R1 or TNFR1 cDNA under transcriptional control of neuron-specific enolase or human glial fibrillary acidic protein promoters.
Briefly 1×107 mouse MPCs expressing either EWS-FLI-1, EWS-FLI-1 R340N mutant or an empty pMSCV vector, were cross-linked with 1% folmaldehyde for 10 min. After addition of 0.125 M glycine and washing in cold PBS, cells were lysed and the chromatin fraction was sheared to roughly 700bp fragments by sonication.
Analysis of gastrocnemius muscle weight in control mice showed that muscle weight of the 12-month-old mice was reduced compared with that of 3-month-old mice expressed either as muscle weight/body weight ratio (Fig. 2B) or in terms of absolute muscle weight (not shown).
Transgenic mice constitutively expressing either MMTV-cyclin D1 or MMTV-c-Myc develop mammary hyperplasia and mammary carcinomas [55], [56], [57].
Transgenic mice over expressing either IDE or NEP under the control of the same promoter were developed and subsequently crossed to the J20 line of APP transgenic mice [ 44].
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