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Genetic or pathological disruption of hepatic UCEs and GLUL leads to hyperammonemia, encephalopathy, and even death due to ammonia toxicity ( 1 4 )

In the overall Japanese population, about 57% of individuals are homozygous for the normal allele (sometimes termed ALDH2*1), 40% are heterozygous for glu487lys, and 3% are homozygous for glu487lys

1 April 2021

Differential features were assessed using parametric ( t test) and non-parametric (Wilcoxon rank sum) statistical tests to account for the degree, direction, and rank of differences between the patient and control groups