First, we modelled treatment of unilateral DME based on RESTORE data, but did not estimate the cost-effectiveness of treating bilateral DME.
This is used to model treatment regimes of cancer with oncolytic viruses.
The quality of the predictions depends on the accuracy of the generalized Born electrostatics model, treatment of protonation equilibria, high-resolution rotamer sampling, a final local energy minimization step, and explicit modeling of the bound, unbound, and unfolded states.
In animal models, treatment of type 2 diabetes mellitus rats with BBR lowered fasting blood glucose and fasting serum insulin, increased insulin sensitivity, and elevated InsR mRNA as well as PKC activity in the liver.
In preclinical models, treatment of cynomolgus monkeys with milatuzumab led to a decrease of peripheral blood mononuclear cells (PBMCs) but not to systemic toxicity or enhanced mortality [ 1].
In preclinical models, treatment of ER-positive breast cancer cells with HDAC inhibitors leads to transcriptional downregulation and protein modification of the ER (Yi et al, 2008).
For example, in an ovarian cancer mouse model, treatment of bevacizumab can inhibit tumor growth but accelerate metastasis with the formation of vasculogenic mimicry [ 36].
In the orthotopic Hep3b2.1-7 Hep3b2.1-7r cancer model, treatment of mice (n=10) began 14 days after inoculation of 2.5 × 10 cells.
In a CML xenograft model, treatment of mice with exosomes caused a greater increase in tumor size compared with controls (PBS-treated mice).
In our in vitro experimental model, treatment of N2a-Rβ cells with TCDD induced functional TH protein expression and elevated dopamine synthesis in a ligand-dependent manner.
