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Regardless of the potential for differences in blood alcohol levels achieved within and between the paradigms, the results obtained using these mouse models serve as an effective means to examine the long-term consequences of FAE to the developing brain at distinct time points (Clancy et al., 2001; Rice and Barone, 2000).
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Here we review and propose how genetically engineered mouse models can serve as valuable tools to predict targeted therapy toxicity, as well as to identify allelic variants that predispose individuals to side effects.
For studying the development of neuropathological features, these mouse models may serve as testing platforms for early interventional studies.
However, quantifiable and heritable traits in the mouse models can serve as markers providing mechanistic insight into the pathophysiology of the disease.
Importantly, Rs1-KO mouse models have served to show the possibility of gene therapy via intravitreal delivery of viral vectors carrying the normal gene, in preparation for application of this treatment in patients with retinoschisis (Byrne et al., 2014; Park et al., 2009; Zeng et al., 2004).
Taken together, this mouse model may serve as an alternative noninvasive, cost-effective and accurate in vivo representative model of a post-arthroplasty S. aureus infection.
This novel mouse model will serve as an important tool to define the cellular and molecular mechanisms by which Cdc42 overexpression affects mammary tumor formation, progression, and metastasis in vivo.
Therefore, this novel transgenic mouse model may serve as a platform to study the basic mechanisms that underlie cardiac remodeling which are Hp genotype dependent and to search for interventions aimed to modulate this process and attenuate the rapid progression of heart failure and decrease the high mortality rate after MI in Hp 2-2 DM individuals which make up 40% of the DM community.
However, the diet-induced obese mouse model best serves research studies relevant to the cause-and-effect relation between periodontal health and obesity [ 3].
This difference might be attributed to the effect that the host genome can have on numerous metabolic factors, such as insulin secretion or peripheral and hepatic sensitivity (Doetschman, 2009; Kahle et al., 2013), particularly in the C57BL/6J mouse model, which serves as a common in-bred strain of diet-induced T2D (Freeman et al., 2006; Toye et al., 2005).
These reporter mouse models can therefore serve as useful tools to study the neuropathological consequences of excitotoxicity and neurotoxicants.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com