Complexes [Cu(SPh)(2)](-), [Cu(SPh)I](-) and K[Cu(SPh)(2)(Ph)](+) were observed by in situ electrospray ionization mass spectrometry (ESI-MS) analysis of the copper(i)-catalyzed C-S coupling reaction under catalytic reaction conditions indicating that they are intermediates in the reaction. A catalytic cycle was proposed based on these observations.

BackgroundHyperbilirubinemia is a common disorder during neonatal period in Taiwan. Gene variants may play an important role in the development of neonatal hyperbilirubinemia. The current study investigated the association between neonatal hyperbilirubinemia and common gene variants involving the production and metabolism of bilirubin.MethodsThis prospective study enrolled 444 healthy infants born in the Chang Gung Memorial Hospital at Taipei from 2013–2015. Hyperbilirubinemia was defined as a total bilirubin ≥ 15 mg/dL. A log-binomial model was used to assess the risk of gene variants.ResultsThe most common genetic variant was short heme oxygenase (HO)-1 promoter GT-allele (<24 repeats) (39.4 %), followed by GA at nt388 in hepatic solute carrier organic anion transporter 1B1 (SLCO1B1) (31.1 %), GA at nt211 in UDP-glucuronosyltransferase 1A1 (UGT1A1) (29.3 %), ABO incompatibility (16.2 %), alpha thalassemia (5.0 %), and G6PD deficiency (3.2 %). The log-binomial analysis demonstrated greater risks of hyperbilirubinemia in infants with GA at nt211 in UGT1A1 (RR = 1.548; 95 % CI = 1.096–2.187), short HO-1 promoter GT-repeat (RR = 2.185; 95 % CI = 1.527–3.125), and G6PD deficiency (RR = 1.985; 95 % CI = 1.010–3.901). The other gene variants – including blood type, alpha thalassemia, and SLCO1B1 – carried no significant risk.ConclusionsG6PD deficiency, short HO-1 promoter GT-repeat and GA at nt211 in UGT1A1 are risk factors of neonatal hyperbilirubinemia. The data provide clinical evidence to explain the high incidence of neonatal hyperbilirubinemia in Taiwan.

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