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Although some mast-cell-deficient mouse strains (W/Wv) are protected from developing K/BxN serum-transferred arthritis [ 11, 16] whereas others (Wsh) are not [ 26, 27], both the W/Wv and Wsh strains lack the early vascular response induced by administration of serum from K/BxN mice, verifying the mast-cell-dependence of this response [ 22] (BAB, RW, CB and DM, unpublished work).
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The survival studies in conjunction with the difference in pathology between aged and young mice verified the presence of age related differences in the host response to Francisella.
As shown in fig. 4d, treatment with anti-IL12/23p40, but not with anti-TNFα, effectively suppressed expansion of Th17 cells in GW501516-treated PPARβ/δ transgenic mice, verifying that the treatment had the expected effect.
Muscles from C57 and mdx mice treated with D-arginine exhibited connective tissue concentrations similar to untreated mice verifying that the inactive isomer had no effect on fibrosis.
Pluripotent differentiation ability was confirmed in the ES T-1 cells by intraperitoneally injecting them into young adult C57BL/6 mice and verifying the formation of teratomas.
SKF83959-induced locomotor and grooming behaviors were eliminated in D1 receptor knockout mice, verifying a key role for D1-like receptor activation.
We chose inbred BALB/c and C57BL/6 mice and outbred ICR mice to verify the infectivity of the novel H7N9 virus in mice.
In this study, we crossed the heterologous CII transgenic mice with anti-heterologous CII-specific TCR transgenic mice to verify the mechanism of T-cell tolerance to self-CII.
Additional studies comparing the effect of the tri-agonist on wild-type, MyD88, and TRIF knockout mice verified activation of MyD88 and TRIF pathways, thus contributing to a synergistic increase in the immune response.
Increased expression of the HIF1 targets Adm, Vegf, Glut1, Pdk1, and Egl-9 family hypoxia-inducible factor 1 (Egln1) in rodΔVhl and rodΔVhl;Hif2a mice verified that HIF1 was transcriptionally active at 11 weeks of age (Fig. 5).
A former study using coronin-1A knockout mice verified that this factor exerts an inhibitory effect on F-actin formation via an Arp2/3-dependent mechanism.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com