We substituted so-called resonator neural models, which exhibit class 2 excitability and postinhibitory rebound (PIR), for the integrators that are typically used.
In particular we consider two very similar models which exhibit opposite trends for the change of the shear modulus, and explain the origins of this difference as displayed in the various microscopic structures and properties.
Moreover, in diabetic patients and diabetic animal models, which exhibit reduced megalin expression [26], [27], it has been shown that several PPARγ agonists decreased albuminuria [45], [47], [48], [49], [50], [51], [52].
These data are in agreement with our previous findings of a lack of neurodegeneration during the life span of our A53T-SNCA overexpressing mice [13] and suggest that these animals represent a milder form or an earlier stage of pathology compared with other SNCA-overexpressing mouse models which exhibit progressive striatal nerve terminal loss and dopaminergic axon degeneration [14], [15], [16].
The majority of outliers were in regions of the protein models, which exhibit a high degree of disorder.
We used SOD1G93A mice as a model, which exhibit the motor neuron-specific neurodegenerative disease, amyotrophic lateral sclerosis.
We assessed the antinociceptive effects of calcitonin in an ovariectomized (OVX) rat model, which exhibit osteoporosis and hyperalgesia, using the immunohistochemical method.
In transgenic models, which exhibit plaque pathology, both an increase and a decrease in synaptic density was found in the neocortex and in the hippocampus.
Only 21 of the 205 curated models with connected pdorgs show connected pdorgs of type A. For the 75 not curated models, which exhibit connected pdorgs, we found only 7 with type A organizations.
Autoantibody-mediated (lupus-like) cGvHD models, which exhibit a pathology similar to that of lupus, are manifested by nephritis, biliary cirrhosis, salivary gland fibrosis, lymphadenopathy, splenomegaly, autoantibody production and, to a lesser extent, skin pathology.
