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Since impaired adult neurogenesis is shown to augment memory deficits in AD mouse models, here we examined the status of adult neurogenesis in AICD transgenic mice.
We therefore examined whether the HCC gene signature identified in the mouse models here is capable of segregating human HCCs of various etiologies.
The dual role in protection and pathology for mast cells revealed in both mouse models here and in our previous studies [3] has implications for human infection as well, as discussed in response to the next question.
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The need of a cardiac stressor in our mouse model (here: pressure overload by TAC) supports the "second hit" hypothesis in titin-based DCM.
Analogously, several miR-200c binding sites are predicted on Mus musculus ZEB1, ZEB2 and NCAM1 3′UTR, indicating its putative role in the mouse model here presented.
Along with a previous transgenic mouse model with FPPS overexpression we reported previously [ 11], the transgenic mouse model here provides a new means of studying FPPS gene function in vivo.
As a necessary first step toward the eventual goal of developing such a mouse model, here we asked whether mammographic density could be altered within the mouse mammary gland.
In the Brotherton et al. study, which compared sALS cases to an A4V fALS case and controls, C4F6 recognized skein like inclusions (similar to what we observed in the L126Z mouse model here) in the spinal motor neurons of A4V fALS cases.
The novel mouse models described here will be useful tools for future studies addressing this question in more details.
In the mouse models studied here, we found that the majority of bacilli were indeed intracellular within macrophages through most of the infection.
The mouse models presented here together with similar recent studies [31] [35] reveal a role for familial LRRK2 mutations in mediating the dysfunction of the nigrostriatal dopaminergic pathway.
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