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As previously reported [21], [22], Vav1 /– mice also manifested T lymphopenia as inferred by the increased in the percentage of B220+ B cells in the spleen (Figure 3B).
These mice also manifested forelimb dystonia.
Progressive muscle pathology in SOD1 G93Adl B6 mice also manifested as a change in the fatigue characteristics of EDL and soleus muscles.
Glibenclamide-treated mice also manifested significant fall of the SOD, GSH-Px, and CAT activities in liver and kidney compared to STZ-treated mice.
Importantly, this apoptogenic effect of calcarea carbonica was not cell line-specific since S-180-bearing mice also manifested significant tumor cell apoptosis (30%) when treated with calcarea carbonica.
ApoC3Tg mice also manifested severe hepatic insulin resistance assessed by a hyperinsulinemic-euglycemic clamp, which could mostly be attributed to increased hepatic diacylglycerol content, protein kinase C-ε activation, and decreased insulin-stimulated Akt2 activity.
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Aging humans and mice also manifest a mild anemia with a shift from lymphoid to myeloid lineages (Janzen et al., 2006).
A greater severity of pancreatitis in these mice was also manifested by an extensive acinar cell loss, pronounced leukocyte infiltration and robust activation of p38 kinase (Fig 1B,C and Supplementary Figs 3 5).
Our data demonstrates a p75NTR/TrkB imbalance in the striatum of two different HD mouse models, HdhQ111/111 homozygous knockin mice and R6/1 mice that was also manifested in the putamen of HD patients.
In this study, we found an imbalance between p75NTR and TrkB expression in two distinct HD mouse models: HdhQ111/111 mutant knockin mice and R6/1 transgenic mice that was also manifested in the putamen of HD patients supporting the idea that p75NTR/TrkB imbalance is relevant to HD pathology.
This is consistent with our earlier studies in aldh5a1 −/− mice, who also manifest significantly increased GABA levels.
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