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Using a CSD rat model, we investigated if valproate and topiramate lower the susceptibility to develop CSD by inducing changes in brain DNA methylation.
Using a rat model, we previously showed that chronic administration of lipopolysaccharide and proteases to gingival sulcus induced both periodontal inflammation and liver injury.
Using a rat model, we tested a new bioengineering strategy for the in vivo and de novo generation of autologous grafts without the addition of extracellular matrix or cells, and analyzed their biomechanical and structural properties.
Using cultured alveolar interstitial fibroblasts and an in vivo perinatal nicotine exposure rat model, we found that PPARγ promoter methylation is strongly correlated with inhibition of PPARγ expression in the presence of nicotine.
Hypermetabolic patterns in PD patients are often interpreted as compensatory changes [31] and so, assuming this to be true for our rat model, we would expect strong correlations with compensatory gait changes (increased IH print area and duration of CH, IF and IH stance).
In the 6-hydroxydopamine (6-OHDA) PD rat model we investigated the effect of STN DBS on deficient prepulse inhibition (PPI) induced by the dopamine (DA) receptor agonist apomorphine, which is an operative measure for disturbed sensorimotor gating seen in certain neuropsychiatric disturbances.
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Based on our own cross-species observations in obese human and rat models, we investigated the role of OPN in the development of insulin resistance.
To facilitate future studies in the rat models we report here the isolation and characterization of rat cDNAs homologous to hiap-1, hiap-2 and xiap as well as the generation of specific anti-IAP antibodies.
Although functional recovery was observed in both rat models, we wanted to better understand the reasons for the reduced survival of grafted neurons in the AAV-α-synuclein model.
Although platelet calcium levels have been measured frequently in other arterial hypertensive rat models, we believe this is the first demonstration of a similar alteration in the L-NAME-treated hypertensive model.
By the successfully established diet-induced hyperhomocysteinemia rat models, we found that, after α-zearalanol treatment, the activity of cystathionine β-synthase, the key enzyme in homocysteine metabolism, was significantly elevated and level of nitrative stress in liver was significantly reduced.
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