In our spatially continuous model, we showed that such a seizure can spread as a traveling front where inhibition is leading; see Fig. 11.
By using a random graph model, we showed that the throughput of S-IDNC decreases with increasing an number of receivers.
Using the 5-HT3 receptor as system model, we showed that the pharmacology of the HALO-5HT3 receptor was identical to that of the native receptor.
Upon further investigating the working mechanisms for EGCG's protective effect in the EAE model, we showed that dietary EGCG dose-dependently attenuated the disease's severity.
Additionally, using an orthotopic tumor model, we showed the usefulness of a non-invasive whole-body optical imaging for real-time evaluation of therapeutic efficacy.
With the obtained fuzzy model, we showed the robust stability condition which provides a basis for different robust fuzzy control design.
Finally, using a SCID mice xenograft model, we showed that p75NTR overexpression favors tumor growth and strongly increases tumor resistance to anti-tumoral treatment.
Furthermore, from an in vivo study using a rat common carotid artery anastomosis model, we showed that plasma-heparin grafts had higher patency rate at 2 weeks and 4 weeks compared to plasma-control (untreated) grafts.
Using the rabbit as the animal model, we showed that the system did form a space-filling and transparent gel in the vitreous cavity, and the inflammation response could be controlled to an acceptable level.
In one, our ovarian cancer model, we showed that we observed 100percentt survival.
Using hypertonic induction of the aldose reductase (AR) gene activation as a model, we showed that OREs contained dynamic nucleosomes.
