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[49] [50] Liver damage is further characterized into hepatocellular (predominantly initial Alanine transferase elevation) and cholestatic (initial alkaline phosphatase rise) types

Intriguingly, the replication track lengths were quite similar in T315I-Bcr-Abl-32D and 32D cells

Clinical Information a familial form of congenital hyperbilirubinemia transmitted as an autosomal recessive trait

AbolajiAOAdedaraAOMaduJCOwaludeOTOgunyemiOMOmoboyowaDAet al

Mutations in GBA1 represent one of the most common genetic risk factors for PD, leading to significantly reduced GCase protein activity in cholinergic neurons and impairing -syn metabolism, thereby elevating -synuclein levels in these neurons [179]