We have developed an OIR model in mice, and have characterized the expression of the netrin-1 receptors UNC5A-D, DCC, neogenin, and A2b in the retinas of normal and OIR mice.
Through the mouse models we have characterized, we hope to explore several possible mechanisms that may explain the positive health benefits of PKA inactivation or down-regulation.
Of special note to experimental gerontologists, we have characterized novel mice [littermate control mice harboring this transgene (GHR-N RIP::IGHR-N RIP)] that could be used for testing the necessity of insulin sensitivity for the healthspan or longevity of any long-lived, insulin-sensitive micee.
We have characterized a mouse model of acute, acquired lymphedema [5] that closely simulates the volume response, histopathology, and lymphoscintigraphic characteristics of acquired lymphedema [2], [5], [13] [14].
In a mouse burn wound model, researchers have characterized SDF-1 expression in the healing margin of burn wounds [ 52].
Although several studies have characterized the mouse brain synaptosomal proteome [ 9- 11] and age-related proteomic changes in the brain [ 12, 13], the mitochondrial proteomic alterations that occur with age within the synaptosome remain uncharacterized.
To our knowledge, this is the first report that describes electrocardiographic evidence of myocardial ischemia in conscious mice, although ST segment changes have characterized isoproterenol-induced ischemia in rat [ 28] and man [ 29].
We have characterized the mice in detail at the immunological level and show that they allow the growth of a variety of tumor types (both subcutaneously and orthotopically), including tumors stably expressing fluorescent marker proteins.
Using a genetically engineered mouse model of lung adenocarcinoma, we have characterized the effects of circadian rhythm disruption on lung tumorigenesis.
In summary, we have characterized a humanized mouse model with functional DENV-specific adaptive immune responses.
