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Consideration of these equilibria makes it clear that the potential means for increasing the exposure of neurons to bilirubin acid would include increasing the quantity of [bilirubin anion]-albumin (i.e., unconjugated bilirubin ) and especially thereby unbound or free bilirubin, disturbing the binding of bilirubin anion to albumin, decreasing the quantity of albumin that is free to bind bilirubin, and increasing the quantity of hydrogen ions (i.e., lowering pH) ( Table 26.3 )

( vs their C-peptide negative counterparts, patients with a residual -cell function had higher IGF-I levels despite similar glycemic control (50)

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