On the basis of preclinical models, we hypothesized pharmacodynamic separation, achieved by intermittent delivery of epidermal growth factor receptor tyrosine kinase inhibitors intercalated with chemotherapy, as a reasonable strategy to deliver combination therapy.
Based on literature on human social models we hypothesized that the visual presence of the interface agent would result in more positive attitudes toward engineering and greater self-efficacy than the presence of a human voice alone.
Since we and other groups have reported that the inhibition of FAK activity exhibited a potent anticancer effect in several cancer models, we hypothesized that TAE226, a novel ATP-competitive tyrosine kinase inhibitor designed to target FAK, can prevent the occurrence and progression of peritoneal dissemination.
Moreover, consistent with GxE models we hypothesized that any genotype-related differences in brain function would be most pronounced in patients with PTSD.
Since misfolded tau has been shown to transmit across synapses in AD animal models, we hypothesized that synapses in AD patients may contain misfolded tau.
Given the influence of estrogen on SLE in experimental models, we hypothesized that OCPs with estrogenic effects would similarly accelerate lupus development.
Supported by simple molecular models, we hypothesized that the twist provided by biaryls will place the hydrophilic and the hydrophobic functional groups at a plane orthogonal to that containing the phenolic and the hydroxymethyl functional groups.
According to previous studies of ectopic calcification in osteoporosis patients and their animal models, we hypothesized that long-term warfarin therapy affects both bone mineral metabolism and vascular calcification [5], [6].
On the basis of these two models, we hypothesized that binding of mecamylamine to the NL sites may impede the rotation of the M2 segments, disrupting the hydrophobic to polar residue switching, finally maintaining the receptor in a nonconducting conformation.
