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The mechanism leading to a substantially improved survival rate of CLP mice when treated with an anti-N-terminal antibody is not completely clear.
Infected mice when treated with the encapsulated peptide showed 83% survivability and approximately 2 log unit reductions in the bacterial load in the tissues versus 100% mortality observed with the free peptide.
Escape mutants were observed in 80% of mice when treated with 2.5 mg/kg of ch-mAbs.
Recently, it was shown that dystrophic muscle disease symptoms decreased in mdx mice when treated with myostatin antibodies [ 9].
However, there was little difference detected in the IgG1 levels between the transgenic Nek2 mice and the control mice when treated with the T cell dependent antigen).
This finding is in line with an earlier onset of arthritis in mice when treated with the ERα/β antagonist ICI 182780 [ 10].
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Arthritic mice benefited when treated with the FAAH inhibitor JNJ1661010.
This inducer of definitive endoderm (IDE -1 and IDE -1rivandve (its-2) further enablederivativection of pancreatic progenitors furtherusenabledwhen theated along winductionlactam V[63].
Using ChIP assays, we confirmed that ATF4 contributes to VEGFA transcription and furthermore demonstrated that endogenous ATF4 binds to a region ∼+0.9 kb downstream of the transcription start site in mouse cells when treated with a UPR inducer.
For example, BMSCs formed only bone tissue in the mouse model when treated in the same manner as the dental tissue-derived stem cells [ 19, 27].
No mouse died when treated with anti-BjussuCV, anti-alk-BjussuCV, anti-BthTX-I, or anti-BthTX-II, and the mortality was reduced by around 83% in response to anti-alk-BthTX-I and anti-alk-BthTX-II.
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