Role-models could demonstrate the benefits of consuming a healthy diet, or the consequences of consuming a poor diet to convince them about the importance of eating a healthful diet.
Transplantation of these cells into a parkinsonian rat model could demonstrate behavioral recovery [ 210].
Further, modelling could demonstrate that the existing evidence is sufficient, such that further empirical studies may not be necessary.
By using the difference of log-likelihood, ln (L1/L0), between the PUM and uniform Poisson models, we could demonstrate that this model is better than a uniform Poisson model with regard to time and space (depth) for M ≥ 7.5 and M ≥ 7.3 earthquakes.
In our VILLIN-HA/CL4-TCR transgenic mouse model we could demonstrate that chronic antigen stimulation in the gut and the gut-associated lymph nodes leads to the peripheral induction of antigen-specific CD8+Foxp3+ T cells with inhibitory capacity for both CD4 and CD8 T cell proliferation.
With our model, we could demonstrate that this effect is at least partially mediated by the kinetics of Arr oligomer dissociation.
In this genetically modified animal model we could demonstrate a marked deficiency in the number of new neurons generated in the hippocampi of p50−/− mice [ 86].
Given the previous history of anti-CD40L antibody evaluation in the clinic, a key requirement for progressing new entities targeting CD40L has been to understand the mechanisms for induction of TE and to design a suitable in vivo model that could demonstrate that the risk of TEs associated with anti-CD40L antibodies has been eliminated.
By analyzing the interactions between DCs and T cells in this in vivo model, they could demonstrate conventional DC (cDC) activation and antigen presentation associated with breach of self-tolerance, an ability of these cells to transfer autoimmunity, together with a central role for cDCs in the TNFα-dependent development of self-reactivity and RA pathogenesis.
In a three-dimensional tumour spheroid model in vitro, we could demonstrate that the secreted fusion protein bound nontransduced cells and caused efficient killing of colon cancer cells in the presence of CPT-11.
