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Both transgenic mouse lines develop fatal BPL.
Both of these transgenic mouse lines develop premalignant lesions that then evolve into invasive mammary tumors that eventually metastasize.
Different human αSyn-A30P and -A53T transgenic mouse lines develop severe motor impairments, partly resembling symptoms of human PD, accompanied by a degeneration of the nigrostriatal neuronal system and LB-like pathology.
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Following TAC, all three JNK knockout mouse lines developed cardiac hypertrophy similar to wild-type mice (WT), but only JNK1 mice displayed a significant reduction in fractional shortening after 3 and 7 days of pressure overload, associated with a significant increase in terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling staining and marked inflammatory infiltrate.
Both mouse lines developed both pulmonary inflammation and fibrosis with minor differences from WT mice (Fig. 8), indicating a redundant role of TNF receptors in the development of PF and/or the existence of compensatory mechanisms.
Accordingly, we employed Lean and Fat mouse lines developed from the same base population by long-term (over 60 generations) divergent selection for low or high body fat % [ 9].
Cc2d1a knockout mouse studies have only provided limited information on the role of this gene because both mouse lines developed so far lead to lethality immediately after birth despite the lack of gross abnormalities (Al-Tawashi et al., 2012; Zhao et al., 2011).
Masumori, N. et al. A probasin-large T antigen transgenic mouse line develops prostate adenocarcinoma and neuroendocrine carcinoma with metastatic potential.
We discovered that an established MHC class II transgenic (tg) mouse line, developed by Ito and coworkers as a model for autoimmunity [12] developed spontaneous tumors starting around eight months of age.
In the APP23 mouse line, developed by Novartis Pharma, the 751 isoform of hAPP with the double Swedish mutation is expressed under the control of a mouse Thy-1.2 promoter [ 292] (the same cDNA under the control of a human Thy-1 promoter had no pathology).
We previously described clinically-relevant cyclin E-transgenic mouse lines that develop pulmonary pre-malignant lesions and lung adenocarcinomas [ 31].
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