By using the DSS-induced colitis mouse model, we demonstrated that miR-223 deficiency resulted in more severe symptoms.
By applying the model, we demonstrated 83.9% Cu, 96.0% Cr, and 99.3% As removal from treated wood particles.
By using the model, we demonstrated the neuronal growth process from disconnected neurons to fully connected three-dimensional networks.
Using the 6-OHDA model, we demonstrated that SVs derived from LPS-stimulated primary astrocytes significantly accelerated DA neuron loss following 6-OHDA treatment.
In a mouse burn model, we demonstrated differential GR levels, size, and transcriptional activity in CD14 knockout (KO) mice when compared to wild-type (C57BL/6J) after injury.
Using a plasmid-based transient expression model, we demonstrated that N796, N580 and N799 were capable of significantly inhibiting viral replication in vitro and in vivo.
Using a rabbit model, we demonstrated that mechanical loading applied to cancellous bone in situ increased bone formation and altered trabecular morphology.
This is similar with our findings in nervous system except that in our model we demonstrated that SVs contain the increase of miR-34a and display robust effect rather than exosomes in regulating cell apoptosis.
By using synthetic seismograms in a full 3D model, we demonstrated the effects of offshore heterogeneities, such as the subducting oceanic plate and low-velocity layers (accretionary prism and seawater), on the MT inversion of offshore earthquakes in subduction zones.
Here, in a CLP model, we demonstrated that during sepsis development, the levels of SOD2 and SOD3 increased in the lung, but these did not prevent nitrosative damage and inflammation.
In our model, we demonstrated that the blink reflex EMG can be a reliable endpoint to record in the GTN infusion model over several hours with no special measures required to maintain mechanical stability.
