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These beneficial effects were corroborated in YAC128 mice which, after one year of DMF treatment, also displayed reduced dyskinesia as well as a preservation of neurons.
To elucidate the role of altered NRG1/Erb B2 signaling in DPN, we used diabetic Swiss Webster mice, which after prolonged diabetes develop severe pathophysiologic symptoms of DPN [ 22].
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Of note, at 48 hours after infection, a low level of Arg1 was noted (data not shown) in the lungs of Klebsiella-infected mice which disappeared after 4 days (as shown).
The vaginal equivalents were implanted subcutaneously in female nude mice, which were sacrificed after 1 and 2 weeks after surgery.
The first evidence demonstrating a scaffolding role of RIPK1 in preventing necroptosis came from studies using transgenic mice showing that loss of RIPK3 protects RIPK1/caspase-8 KO mice, which die shortly after birth16,39,40.
Unlike Ripk1 mice, which die shortly after birth, Ripk1(D138N/D138N) mice are viable.
Similarly, mice which undergo SPL after BMT still show hypercellularity and reticulin fibrosis despite normalized hematocrit (Fig 3, lower panels).
However, data showed a high protein expression of myostatin in ob/ob mice, which was reduced after leptin treatment as compared to the ob/ob (P = 0.026) and pair-fed ob/ob mice (P = 0.015) (Figure 4A), suggesting that leptin enhances muscle growth in ob/ob mice.
Cell-free extracts from mice which developed leukaemia after MSV-M inoculation were tested for oncogenic activity in 1-week old mice.
We detected significantly higher expressions of 53BP1, p53 and 4-HNE in ATII cells isolated from Nrf2−/− mice, which were decreased after treatment with trolox.
There was no effect of arsenic on airway resistance (p = 0.29) in C57BL/6 mice, which was maintained after adjusting for TGV (p = 0.78).
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