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Progress in multiple fields of human and mouse model research has advanced our knowledge of what leads to cognitive decline in AD (for full review [ 5]).
This means expanding the focus of mouse model research to include cognition, behavior, and measures closely correlated with these, such as synaptic and network function.
A possible reason for the lack of direct applicability of mouse model research for drug discovery is the unfortunate focus on gross phenotypes that may be either at best secondary to the mutation or result from mouse-unique factors that do not scale evolutionarily.
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Moreover, in C57Bl/6J mice model, research showed that in resveratrol-treated high fat-fed mice, there was a significant decrease in ambulatory locomotor activity as well as a tendency to decrease the number of rears.
The method reported here represents an important step towards building a generally applicable humanized mouse model for research and offers an improved and robust culture method for expanding human HSCs for clinical follow-up.
Although our study showed an effect of 5-Aza-CdR on the delay of the onset of androgen-independent disease in the mouse model, further research is necessary to evaluate whether 5-Aza-CdR can prolong survival and how long 5-Aza-CdR can delay the onset of androgen-independent disease in the castrated mouse model.
Okada et al. reported that consecutive administration of Poly I C to C57BL/C induced PBC like lesions and serological AMA similar to features of PBC [ 11], and was considered as mouse model for research at the early stage of PBC [ 12- 14].
The interest in the use of humanized mouse models for research topics like Graft versus Host Disease (GvHD), allograft studies and other studies to the human immune system is growing.
Using AMPK signaling-deficient transgenic mouse models, various research groups have demonstrated that the skeletal muscle enriched catalytic α2 AMPK isoform is necessary to increase glucose uptake into skeletal muscle with certain stimuli, including 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), hypoxia and metabolic uncoupling[2] [4].
The advantage of mouse models in research has already been shown by the detection of HCC initiation and progression in transgenic mouse models such as alb-myctg with clinical 1.5-T MR scanners and gadoxetate acid enhancement by revealing hypointense lesions.
Here, we propose a strategy for the design of a new mouse model for HIV research, the HIS-CNS mouse.
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