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During analyses of various ganglioside-lacking mutant mice, we demonstrated that nervous tissues exhibited inflammatory reactions and subsequent neurodegeneration.
Nevertheless, in glioma-bearing nude mice, we demonstrated that the peptide moiety was degraded to various rates according to time after intravenous administration.
Using osteoprotegerin (OPG -knockout mice, we demOPG -knockoutt in vivo the effects of both genistein and 17β-estradiol (E2) on bone micebolism were completely abolishedemonstrated
By using both human breast cancer cells and genetically engineered mice, we demonstrated that RBP2 is critical for breast cancer metastasis to the lung in multiple in vivo models.
For antigen-specific CD8+ Tregs detected in the VILLIN-HA/CL4-TCR transgenic mice we demonstrated the specific expression of CCL4.
In a previous experimental study on mice, we demonstrated that miR-155 and miR-125b play a role in innate immune response [13].
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Using both pharmacologic and genetic approaches in mice, we demonstrate that L1 expression in the adult hippocampus enables long-term memory formation.
Using genetic intercrosses between Nf1 +/− and class I A-PI-3K-deficient mice, we demonstrate that hyperactivation of the p21ras-class IA PI-3K pathway is the mechanism for this phenotype.
Using genetically engineered tracing mice, we demonstrate that, in dystrophic muscle, specialized cells of muscular, endothelial, and hematopoietic origins gain plasticity toward a fibrogenic fate via a TGFβ-mediated pathway.
In mice, we demonstrate that microneedle-mediated delivery of ChAd63.ME-TRAP induced similar numbers of transgene-specific CD8+ T cells compared to intradermal (ID) administration with needle-and-syringe, following a single immunisation and after a ChAd63/MVA heterologous prime-boost schedule.
Using TCF8+/− mice, we demonstrate herein that ZEB1 haploinsufficiency elicited excessive adipose tissue accumulation in female mice early in fat acquisition (Figures 2 and 3).
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