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Emerging evidence from mouse models has identified the importance of BACE1 in myelination and cognitive performance.
The conducted multivariate analysis, which incorporates all five predictors that are relevant in simple models, has identified four independent predictors.
Work in transgenic mouse models has identified Six2 in the CM as self-renewing nephron stem/progenitor cells (Kobayashi et al, 2008).
In addition, seminal research using animal models has identified tumour and host genes associated with metastatic capacity (quite distinct from tumorigenic potential), and also organotropism [ 149- 151].
Investigation of acute coinfection in mouse models has identified a range of possible mechanisms for IAV– S. pneumoniae coinfection 9, suggesting that multiple factors contribute to bacterial susceptibility.
Work in animal models has identified increased infiltrates of innate immune cells (NK cells and macrophages) and CD4+ lymphocytes drawn in by the proinflammatory secretome (Xue et al, 2007).
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Kinetic models have identified correlations between different characteristics leading to interesting insights on the mechanisms underlying the phenomenon [19, 20].
The pubchem and CDK extended models have identified the epoxide fragment as the only cause of the active prediction.
Clinical models have identified risk factors and laboratory testing to evaluate severity, guide clinical therapy and tell prognosis.
Analytical models have identified a set of social learning strategies that are predicted to be adaptive relative to individual (asocial) learning.
Indeed, genetic screens performed on worm models have identified a wide variety of conserved genes that can suppress or increase disease progression and are thus potential therapeutic drug targets.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com