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Rodent models of thyroid system dysfunction were presented.
Therefore, the analysis of the experimental models of thyroid carcinogenesis seems to confirm that the UbcH10 overexpression is essentially restricted to the undifferentiated histotype.
In addition to this we have enumerated flaws in the construction of animal models of thyroid autoimmunity recently (Section 4.8 in [8]).
The molecular mechanisms behind a considerable proportion of thyroid carcinomas remain nevertheless unclear, and extensive effort has been placed in creating in vitro and in vivo models of thyroid carcinogenesis.
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ROSI was also able to reduce thyrocyte growth by 40% in a murine knock-in model of thyroid hormone receptor β [ 107].
During this research, a model of thyroid carcinoma progression based on genome-wide expression datasets has been built by using three different approaches and two validation sets.
However, activation of AMPK has also been associated with increased GLUT1 expression in a rat model of thyroid cells, and increased glucose uptake in thyroid cancer cells has been linked to thyroid cancer progression and aggressiveness [ 24– 26].
Src activity has been observed to be elevated in a murine model of thyroid cancer, and hyper-activation of Src is associated with HIF activity, at least in this model (20).
We recently identified mutations in two mitochondrial DNA-encoded subunits resulting in severe loss of mitochondrial activity in a cell model of thyroid oncocytic tumours (Bonora et al, 2006).
As there was a strong apoptotic response ranging from 83 to 99% in the three sensitive cell lines, we tested the in vivo efficacy of this novel antibody in an orthotopic animal model of thyroid cancer using one of the sensitive cell lines, BCPAP.
This is the basic assumption that we have included in the musculoskeletal model of thyroid-associated orbitopathy [76].
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