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These findings demonstrate that germ-free IL-10−/− mice develop rapid and severe intestinal inflammation following C. jejuni infection, which correlates with activation of NF-κB signalling.
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C. jejuni mono-associated IL-10−/− mice developed rapid and severe colitis, even in the presence of low bacterial inoculum (102 cfu/mouse).
After arthritis induction, wildtype and knockout mice developed rapid inflammation, indicated by acute joint swelling.
C57BL/6 mice developed rapid and severe arthritis following serum transfer, whereas u-PA-/ mice were essentially resistant: 60% (three out of five) of u-PA-/ mice developed arthritis with an average maximum clinical score of 1.2 ± 0.5, compared with 100% (seven out of seven) of C57BL/6 mice with an average maximum clinical score of 11.1 ± 1.3 (P < 0.005).
The quaking (qk) viable mice (qkv) develop rapid tremors and clonic seizures resulting from their severe dysmyelination [1].
The MRL/ lpr mice develop a rapid and fluminant autoimmune nephritis with 50% mortality at 6 months of age.
66 Ob/ob mice develop a rapid breathing pattern when compared to age-matched wild-type mice and exhibit a depressed hypercapnic ventilatory response (HCVR).
Subsequent studies demonstrated that Bmp6 null mice develop a rapid and massive accumulation of iron in the liver that is related to a marked reduction in liver Hamp expression [ 21, 22].
The SOD1 Tg mice develop a rapid and progressive neurodegenerative disease, ALS, with a massive death of motor neurons and therefore they are a suitable animal model for testing the idea that telomerase increasing compounds, such as AGS-499, may have beneficial therapeutic effects on neurodegenerative diseases (Fossel and Flanary, 2009; Fu et al, 2000; Harley, 2005).
These mice develop an early-onset phenotype with rapid disease progression and as a consequence can realistically be used as a therapeutic screening tool (14).
TGF- β-null mice develop a multiorgan autoimmune inflammatory disease leading to organ failure and rapid death after birth.
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