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Using ex vivo choroid plexus live imaging and isotope flux in combination with in vivo CSF production determination in mice, we identify a key component in the CSF production machinery.
In mice, we identify the transcription factor Satb2 (Special AT-rich sequence-binding protein 2) as a selective marker for three RGC types: On-Off DSGCs encoding motion in either the anterior or posterior direction, a newly identified type of Off-DSGC and an Off-sustained RGC type.
By combining data from a GWAS screening in >100,000 individuals of European ancestry, mediator lipidomics, and functional validation studies in mice, we identify the AA metabolome as an important regulator of cholesterol homeostasis.
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Among the top upregulated genes in rodΔVhl mice we identified and verified Adm and Edn2 by real-time PCR (Fig. 5).
Using chromatin interaction sequencing, massively parallel reporter assays (MPRA), and transgenic mice, we identified disease-linked, biallelic HAR mutations in active enhancers for CUX1, PTBP2, GPC4, CDKL5, and other genes implicated in neural function, ASD, or both.
Using N-ethyl-N-nitrosourea mutagenesis in mice, we identified a mutant with increased resistance to viral infections because of the presence of hyperresponsive NK cells.
In mice, we identified an essential role for histone 3 lysine 9 (H3K9) dimethylation and the lysine dimethyltransferase G9a in cocaine-induced structural and behavioral plasticity.
In addition to natural anti-Gal alpha 1-3Gal inM in GalT mice, we identified natural IgM which bound alpha-N-acetylgalactosamine (alpha GalNAc) but not Gal alpha 1-3Gal or blood group A. Although unexpected, these antibodies were expressed at 10-fold greater concentrations in GalT mice than in WT mice.
Of 50 recordings (from 29 mice) we identified 9 ChAT+ neurons and 30 ChAT− neurons, leaving 11 neurons unclassified.
In a screening of 128 generation-3 (G3) mice, we identified a mouse mutant (p23-ST1) with enlarged brain ventricles that proved heritable (Supplementary Fig. S1).
In an application of the new model for genetic mapping of iQTL in mice, we identified five significant QTLs on chromosomes 1, 4, 9, and 15 for the overall survival time to hyperoxic acute lung injury (HALI).
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