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We found that PI4KIIα transgenic (TG) mice have abnormal glucose tolerance and higher serum glucose levels than wild-type mice.
The present study was designed to determine if hypodopaminergic (i.e., reduced brain levels of dopamine) mice have abnormal sleep and waking activity patterns that recapitulate sleep-wake activity in human PD patients.
Mecp2−/y mice have abnormal gait and movements, hypoactivity, hypotonicity, tremor, hindlimb clasping, and irregular breathing.
CAV2 is also associated with caveolae structure, and Cav2 KO mice have abnormal pulmonary function, but no apparent defect in adipocyte structure or function [37].
11β-HSD1KO mice have abnormal HPA axis control and enhanced circadian HPA drive (23).
Cfh –/– mice have abnormal accumulation of glomerular C3 along the glomerular basement membrane (GBM) [ 6].
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46 Although mutations in CASZ1 have not been reported in humans, this gene is located in one of the congenital heart defect critical regions defined by Zaveri et al 10 and in the proximal cardiomyopathy critical region defined by Kang et al. 9 Liu et al 47 demonstrated that CASZ1-deficient mice had abnormal heart morphology with abnormally shaped ventricular apices and ventricular septal defects.
In contrast, the Magel2-null mice had abnormal and extended estrous cycles, with few nucleated smears, and lengthened periods with only cornified smears (Figure 4 C D).
Likewise, the reduction of adiponectin, PPAR-α and PPAR-δ gene expression contributes to our contention that the adipose tissue from N2KO mice has abnormal functionality.
Because TB-RBP-null male mice had abnormal seminiferous tubules and reduced sperm counts but were fertile, it is possible that male germ cells contain redundant pathways to regulate the transport and temporal expression of post-transcriptionally regulated mRNAs [22].
Ocular photodetection testing showed that, compared with WT mice, Bst+/− mice had abnormal PLRs but similar circadian rhythms.
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