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Such findings indicate that perhaps a proportion of neonatal hyperbilirubinemia secondary to G6PD deficiency has a different mechanistic pathway other than an acute hemolytic crisis with exposure to oxidants, as seen in favism
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ISSN 0035-8843
This natural lipid is normally dislodged on receptor engagement, leading to a structural shift involving radial expansion and the appearance of pores in the capsid, forming the C antigenic conformation 7
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