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Interestingly, aggregates of an HTT exon1-Q94 protexpressedssed in the brains of a mouse model required 3 weeks to dissociate after HTT exon1 expression was turned off.
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Consistent with our data highlighting the importance of full-length huntingtin, disrupted calcium signaling in an HD mouse model requires the polyglutamine expansion in the context of the full huntingtin protein (66).
Our findings suggest that investigation of these genetically altered mouse models requires careful optimization of restricted feeding protocols.
From a physiological perspective, a proper understanding of the metabolic phenotypes of various mouse models requires quantitative integration of these variables and how they change over time.
Precision mouse models require minimal off-target effects.
The preclinical studies with DHA in AD mouse models require encapsulation of DHA in the chow to minimize oxidation [ 10, 11].
However, all mouse models require direct administration of human complement into the central nervous system, as the mouse complement system is ineffective because, in part, of circulating complement-inactivating protein(s) [ 32].
Further, working with mouse models requires significant time and expense to create and study the appropriate phenotypes, thus preventing the use of these animal models in high-throughput screens for genetic pathways that may either enhance or suppress the phenotype.
Our cellular analyses suggest that maximizing efficacy in (NZB × NZW F1 mouse models requires not only targeting the components of MZ B cells but also depleting other B cell subsets such as naive/activated B cells.
To compare for the pharmacokinetic properties of α-mangostin, a major bioactive compound, in mangosteen extract and pure α-mangostin, the pharmacokinetics as well as tissue distribution, in vitro metabolism, plasma protein binding and safety evaluation were conducted in mice because a mouse model is required a small amount of compounds and useful to develop disease models.
A satisfactory mouse model is required to fight the devastating effects of muscular dystrophy (MD).
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