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A dominant-negative Gjb2 R75W transgenic mouse model shows incomplete development of the cochlear supporting cells, resulting in profound deafness from birth [Inoshita A et al. (2008) Neuroscience 156:1569–1567].
It is still debated whether endotoxemia in influenza virus infection associates with the pathogenesis of IAE, but the IAE-like mouse model shows hypercytokinemia without direct influenza virus infection in the brain, and that is closely intimate histological and immunopathological features such as BBB breakdown seen in IAE patients.
But here's the problem -- each mouse "model" is different and no single mouse "model" shows all the pathologic features of AD.
Further, a Clusterin knockout mouse model shows an increase in incubation time following inoculation with BSE prions [25].
This mouse model shows close similarity to the pathogenesis of RSV-induced lower airway disease in humans.
This mouse model shows an increase in Ter119+ cellsigh cells and a decrease in enucleated cells [5], [9], [31], similar to our Chk1 mutant mice.
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Further characterization of the RIPK1 KO mouse model showed that the deletion of RIPK1 led to bone marrow aplasia and loss of hematopoietic stem and progenitor cells (HSPCs 16.
In addition, MRI and photothermal effect for mouse model showed enhanced T1 signal and temperature elevation in tumor site with photoirradiation.
In vivo implantation of the LZ scaffolds in a mouse model showed absence of foreign body reaction to the scaffold.
Immunoprecipitation of Akt in pre-symptomatic mSOD1G93A muscle and end-stage atrophic muscle from this mouse model showed binding of CTMP to Akt (Fig. 1E), corresponding to the increased expression of these proteins over time.
Initial characterization of this mouse model showed that under baseline, no-stress conditions, increasing adult neurogenesis enhances pattern separation, but has no effect on anxiety or depression-related behavior (Sahay et al, 2011).
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