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The London group has investigated the effect of angiogenesis blockade in murine arthritis, using CIA in genetically susceptible DBA/1 mice.
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Impressive proof of principle has been demonstrated in murine collagen-induced arthritis using dendritic cells that express TRAIL [ 71].
Finally, a murine arthritis model of infection was used to ascertain whether two of the genes highlighted in this study have a role in pathogenesis.
A murine arthritis model of infection was used to determine a role for the LC-uFFA survival genes sasF and vraE in pathogenesis.
The goal of our work was to examine, in well-described glucose-6-phosphate isomerase (G6PI -induced murine arthritis [ 11- 17], whether F-FDG6PI -inducedT can be used for the quantitative in vivo assessmurinef inflarthritisin acute and chronic stages of experimental arthritis.
The potency of bivalent formats was 500-fold increased as compared to monovalent VHHs and even exceeded the potency of clinically used conventional antibodies both in vitro and in a murine arthritis model.
We also conclude that gait analysis represents a valuable addition to the methods currently used for evaluation of the severity of joint changes in murine arthritis models.
In the current studies, we evaluated, for the first time, the use of combined F-FDG PET/CT for in vivo quantification of inflammatory conditions in experimental murine arthritis.
In murine arthritis, synoviolin heterozygous knockout mice are protected against arthritis development associated with reduced synovial hypercellularity.
IL-17 has been described to be implicated in synovial hypercellularity in murine arthritis models [16].
Synoviolin is an E3 ubiquitin ligase implicated in murine arthritis pathogenesis.
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