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In addition, original data from a recently published LQT3 mouse model presenting with atrial fibrillation and increased late Na current showed early afterdepolarizations in the presence of long atrial action potentials.
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The adenomatous polyposis coli multiple intestinal neoplasia (ApcMin/+) mouse model presents phenotypes reminiscent of Familial Adenomatous Polyposis (FAP) in humans [18], [19].
Additional genetic studies, such as the chromosomal deletion of the complete stefin gene cluster mapped on mouse chromosome 16 or the cystatin gene cluster mapped on chromosome 2, would be required to potentially uncover and dissect compensation mechanisms that might be occurring in the mutant mouse model presented here.
In both cases, the mouse model presents problems specific to a therapy depending on immune effector cells and their products.
Interestingly, in the mouse model presented here, we observe slowed pacemaking, yet with little variation between the WT and mutant mice across age.
The Cln1 ko mouse model presents with a severe neurodegenerative disease, whereas Cln5 ko mice have a much milder phenotype that progresses more slowly.
Thus, the mouse model presented here has advantages in respect to investigate the multiplicity and tissue sampling for gene expression analysis.
Concluding, the human melanoma xenograft scid mouse model presented in this study (i) closely reflects the clinical situation and (ii) underlines the complexity of metastasis formation.
This metabolism could be altered by the insertion of human CYP2C18&19 genes in the mouse model presented and, thereby, influence cerebral blood flow and possibly also the brain weight.
In conclusion, we have shown that the mouse model presented here can be used to detect activation of ERs by maternally applied BPA and that other estrogens can be detected in living embryos in utero.
The Int6sh transgenic mouse model presented here provides the first and to date only in vivo evidence that the expression of truncated Int6 leads to persistent mammary hyperplasia and increased predisposition to mammary tumors.
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