Sentence examples for mouse model presents from inspiring English sources

The adenomatous polyposis coli multiple intestinal neoplasia (ApcMin/+) mouse model presents phenotypes reminiscent of Familial Adenomatous Polyposis (FAP) in humans [18], [19].

In both cases, the mouse model presents problems specific to a therapy depending on immune effector cells and their products.

The Cln1 ko mouse model presents with a severe neurodegenerative disease, whereas Cln5 ko mice have a much milder phenotype that progresses more slowly.

Compared to other models in which subretinal inflammation occurs secondarily to light-injury or genetic defects (Cruz-Guilloty et al, 2013; Guo et al, 2012; Kohno et al, 2013; Rutar et al, 2012; Suzuki et al, 2012), the Cx3cr1 knockout mouse model presents a primary MP accumulation in the absence of an inherited retinal degeneration (C57BL/6J background) (Combadiere et al, 2007).

In this regard, the NOD mouse model presents an advantage over drug-induced diabetes models because the disease in this mouse strain develops spontaneously; additionally, there is no controversy over whether differences in gene expression in the liver are caused by diabetes-induced agents.

This mouse model presents progressive tau pathology with the first tau deposits in homozygous mice appearing at 2 months of age and developing until the age of 5 6 months when the mice have to be culled due to their motor phenotype (Allen et al., 2002; Delobel et al., 2008).

Heterozygotes for the mutant Fbn1 allele mgΔloxPneo, carrying the same internal deletion of exons 19 24 as the mgΔ mouse model, present defective microfibrillar deposition, emphysema, deterioration of aortic wall and kyphosis.

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.

Interestingly, in the mouse model presented here, we observe slowed pacemaking, yet with little variation between the WT and mutant mice across age.

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.