Many game-theoretical studies of social cooperation are based on models, in which all individuals are assumed to have the same properties.
Results of several studies based on in-vitro or in-vivo models indeed suggest that more than inhibition of VEGF (which is not the only factor controling REC proliferation) is needed to suppress neovascularization.
Experimental studies based on animal models or in vitro assays have provided inconsistent findings regarding the effects of brominated compounds on MN frequency.
Few local, validated studies based on these models are available in NWP, NI, and SI.
Reporting studies based on one tumor type in one animal model is not unusual.
Over the past years, studies based on in vitro model systems revealed several mechanisms that may contribute to diminished efficacy with PIs and acquisition of resistance.
Studies based on various in vivo models suggest that the immune system not only protects the host from early-stage tumors, but also promotes tumor growth through a process described as immunoediting, immunosculpting or cancer immune system, which can result in the outgrowth of more aggressive tumor cells via exposure to immune effectors and loss of immunogenicity [ 18, 20, 21].
In studies based on statistical modeling to adjust for lead-time, estimates of overdiagnosis are consistently below 5% [ 42, 43].
Still, it is rare to find studies based on explicitly non-autonomous models in the literature, and most authors avoid the challenge of dealing with dynamical systems where the parameters representing external cues are time-dependent.
In our previous studies based on the iBREC model, we showed that ranibizumab, in addition to efficient inhibition of VEGF-stimulated proliferation and migration, can completely restore the VEGF-induced impairment of the endothelial barrier; this provided a rationale for using this antibody fragment in DME therapy.
Some of these factors are also revealed in studies based on anti-TNF therapy in the AA model.
