https://www.selleckchem.com/products/sb239063.html Nonetheless, ongoing success in research and clinical outcomes will increase knowledge of the value of occupational therapy and increase the size of the profession. WHO's focus on function is to be lauded. Yet, occupational therapists must not be content with an emphasis on function. They also need to advocate for contextual changes that eliminate barriers to participation and engagement experienced by people with disability. Copyright © 2020 by the American Occupational Therapy Association, Inc.Hyperbilirubinemia is a prevalent disease in neonates and is also a main reason for hospitalization within the first week after birth, and this disease is mainly caused by the imbalance between production and elimination of bilirubin. Uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1), organic anion transporter polypeptide 2 (OATP2), heme oxygenase 1 (HO-1), and biliverdin reductase A (BLVRA) play crucial roles in the metabolism of bilirubin. More and more studies have revealed the association between the variation of the encoding genes for these enzymes and hyperbilirubinemia. This article reviews the research advances in the association between the gene polymorphisms of bilirubin metabolic enzymes and hyperbilirubinemia.A boy, aged 4 months, had the major clinical manifestations of prolonged jaundice and hepatomegaly. Multiple biochemical tests revealed abnormal liver function along with elevated alpha-fetoprotein and lactate. Genetic analysis confirmed that the boy had the mutations of c.589C>T(p.Gln197Ter) and c.687G>C(p.Trp229Cys) in the DGUOK gene, both of which were novel mutations and were determined to be pathogenic and likely pathogenic respectively, by a variety of bioinformatics tools and the ACMG standard. Therefore, the boy was confirmed to have DGUOK-related mitochondrial DNA depletion syndrome. Literature review showed that onset of liver disease in infancy was the main clinical feature of this disease,