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Alloxan-induced diabetic rat model has been widely used in several studies [34, 35].
Dopamine conjugated on the surface of chitosan nanoparticle administered in rat model has resulted in less cytotoxic long-term release than dopamine alone.
Therefore the present study was designed to investigate whether the cognitive impairment of AD rat model has relation to the change of NMDAR.
A preliminary in-vivo study using Long Evans rat model has demonstrated a significant reduction in spike-wave discharge after the ESM was burst released from the chip under the same magnetic induction as in-vitro, indicating the potential application of the drug delivery chip.
In previous studies, the loss of DARPP32 phenotype in our HD rat model has been correlated with loss of the neuronal marker NeuN, suggesting that it represents severe dysfunction and/or disappearance of striatal neurons and not only transcriptional alterations [11].
The rat model has some limitations.
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Previous studies in a rat model have shown no correlation between induction of apoptosis in the salivary gland and either the immediate or chronic decrease in salivary function following γ-radiation treatment.
Studies in a rat model have shown that exposure to adverse maternal care giving in the first postnatal week following birth is associated with differential methylation of the 5' region of the Bdnf gene and changes in Bdnf mRNA expression in prefrontal cortex from adult rats and that this is transferred to the next generation [8].
Strong antibody responses to allogeneic MHC-I molecules after MHC mismatched transplantation of fresh bone in this rat model have been observed [ 24].
Similarly, in the curves from the mean rate of ROS fluorescence, the rat model had two large O2– bursts, whereas the mouse model only had one, which is ∼60% smaller.
Because previous studies using the high-dose MIA rat model have reported the involvement of subchondral bone as early as two weeks after injection [ 21], two weeks was chosen as the early time point in this study.
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