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Indeed, ADP could distinguish all three mouse models examined.
We agree with the reviewers' observation and note the distinct GC B cell responses in the two mouse models examined in our study.
This same pattern of amyloid-associated TREM2, DAP12 and Tmem176b expression was also observed in all other APP and APP/PS1 transgenic mouse models examined (data not shown).
All five mouse models examined in this study have previously shown face validity for autism (Silverman et al., 2010), with alterations in social behavior, ultrasonic vocalization, and repetitive behaviors.
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Additionally, transgenic knockout mouse models examining prostaglandin F2α receptor [ 11] and testosterone 5-α-reductase type 1 [ 12], respectively, exhibit an absence of parturition, although screening for mutations in these candidate dystocia-related genes in humans proved unsuccessful [ 13].
Subsequently this mechanism leads to a suppression of α-synuclein aggregation, reduced α-synuclein-induced toxicity and extended survival in the mouse model examined [ 86].
A statistical difference for severe hearing impairment (> 80 dB) in GLY vs no GLY recipients was shown in one study [ 4] but has not later been confirmed [ 2, 10], which fits the negative results of our adult mouse model examining hearing loss 40 h after infection.
While the majority of mouse ARHL models examined most closely resemble sensory ARHL, recent work has identified mice possessing the essential characteristics of neural and strial ARHL.
Hence to determine the concentration of nicotine in our mouse models, we examined cotinine levels in the urine of the experimental mice.
The N171-82Q modelsmodels we examined indicated that the assembly of C-II was defective at relatively early stage of the disease.
No matter how many cell lines or mouse models we examined, the question would still remain – how relevant are these xenotransplant data to human breast cancer?
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