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However, fibrosis in the mouse models begins within 30 days of transplantation, which is atypical of human cGvHD, which occurs months to years after transplantation.
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To this end, mouse models are beginning to come into their own as a means to study the role of gene environment interactions in the aetiology of human disorders; by these means, short-term gestational hypoxia has been found to increase the penetrance of vertebral defects in congenital scoliosis (Sparrow et al. 2012).
Work on mouse models is beginning to uncover complex interactions between H. pylori and other bacterial species commonly found in the human gut, such as Clostridium difficile (Rolig et al. 2013), suggesting an intriguing link between dysbiosis and H. pylori -mediated disease.
We used this mouse model to begin to investigate pathogen and host factors that contribute to diarrhea due to S. enterica infections.
A month later there were enough mice models to begin testing.
Then the models begin strutting out.
The models began to show more.
In the NOD mouse model, insulitis typically begins around 3 4 weeks of age, and diabetes occurs in 60 80% of female mice between 12 18 weeks of age depending on the housing conditions.
In the Cln1 ko mouse model, neuron loss begins in the thalamus and only subsequently occurs in the corresponding cortical region (von Schantz et al., 2009).
Mouse models of ALS are beginning to reveal possible principles governing the biology of selective neuronal vulnerability that implicate mitochondria.
Our group is currently examining the potential therapeutic effects of PBA in other AD transgenic mouse models, in which PBA administration begins prior to the pathological onset, and is administered across its anticipated progression.
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