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This infers that the raised inflammatory gene expression in cardiomyocytes observed in hyperglycemia is secondary to impaired repressive epigenetic histone modifications [200]
E.TurgemanG
If true, such a scenario would pose a formidable challenge to the research community, because distinguishing a physiological form of an otherwise normal endogenous brain protein from a pathologically misfolded/aggregated conformer is not trivial
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