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While it has previously been reported that HIF-1 may induce the formation of MCETs [64], hypoxia caused MCET formation via a HIF-1 independent mechanism while suppressing the release of proinflammatory mediators including TNF-, possibly in an attempt to attenuate the development of an inflammatory state and thus, to prevent tissue injury during hypoxia [64]

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Define your model's neurotrophic state before choosing your peptide, and you'll design studies that generate reproducible, mechanistically interpretable results

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