As an initial velocity model, we utilized a simple 1D P-wave velocity model with the Vp/ Vs ratio fixed to 1.73 (Fig. 5).
Considering the fitness and adjustability of the surface-based model, we utilized Rhino 3D Version 5 for the main modeling environment; this is recognized as a typical non-parametric software.
Similar to the study of (Everett et al. 2003), in order to construct the model, we utilized two types of data, namely, (1) geometry of each boundary and (2) lateral distributions of conductivity within each layer.
To determine if the UPR is activated in our tauopathy model we utilized a UAS-Xbp1-EGFP reporter system developed by Ryoo et al. [22].
In order to test the ability of LNP-Bry to activate latent virus in a primary cell model we utilized the SCID-hu (Thy/Liv) mouse model for HIV latency [7], [37], [38], [39], [40], [41], [42].
In order to unify the ITR and Rep elements involved in specificity into a single model, we utilized the chimeric Reps separating region 1 and region 2 along with the chimeric ITRs separating the nicking stem and spacer.
Therefore, to better mimic events that might occur when testing the activity of these antibodies in the mouse infection model, we utilized strain FA1090F62 por5–8, which produces a recombinant hybrid porin that does not bind hC4BP and is thus serum sensitive.
For adequate sample size and ease of comparison to the final fit model, we utilized all available data combining multiple NHANES cohorts as the sample to conduct these three tests, described below.
For a more physiologically relevant model, we utilized the metatarsal organ culture model.
