Gold cyanide leaching is inefficient with conventional cyanidation. Bismuth ions can improve the efficiency of gold cyanidation by intensifying gold dissolution. The electrochemical behavior, structure information, and surface product of gold anodic dissolution were studied during the intensification of bismuth ions on gold cyanide leaching. The electrochemical analysis showed that the bismuth ions can not only improve anode current density, but also make gold dissolve at a lower potential, increase the corrosion current and intensify gold anodic dissolution. The microstructure analysis showed that bismuth ions intensified the cyanide corrosion of the gold surface, causing a large number of loose honeycombs, gullies, pits, and large holes on the gold surface. The XPS, FT-IR, and Raman analysis showed that there is weak information of C≡N in the spectrum of Bi intensification contrasting to that of conventional cyanidation. Cyanide compounds may be the insoluble AuCNads, which does not deposit on the surface of gold plate after Bi intensification cyanidation. The insoluble intermediate AuCNads is likely to react promptly with CN- to form soluble Au(CN ) 2 − , making less insoluble AuCNads deposits on the gold surface. Therefore, bismuth ions can promote the dissolution of insoluble AuCNads, prevents its passivation film to cover around the gold plate, keeps cyanide good contact with gold, and finally accelerates the cyanide dissolution of gold.

Introduction Patients with a homozygous β0‐thalassemia mutation usually have a transfusion‐dependent β‐thalassemia major phenotype. However, some β‐thalassemia patients present with a relatively mild and even normal phenotype and always have a high level of Hb F induced by genetic modifiers. Methods In this study, we identified a homozygous β0‐thalassemia mutation (HBB: c.126_129delCTTT) in a 36‐year‐old pregnant woman. She had not presented any clinical symptoms of β‐thalassemia since birth. To investigate her unexpected mild phenotype, known genetic modifiers that ameliorate the severity of β‐thalassemia were analysed. Besides, we described the haematological changes during pregnancy. Results Two genetic modifiers (a heterozygous KLF1: c.519_525dup mutation; and two homozygous HBS1L‐MYB locus SNP variants: rs7776054 and rs9399137) were identified. However, she showed a gradually decreased level of Hb during pregnancy, and serious transfusion complication of hyperhaemolysis was induced and complicated the pregnancy. Conclusion This report is in accordance with previous findings that genetic modifiers can ameliorate the clinical severity of β‐thalassemia, even without obvious clinical symptoms in a prolonged steady state. However, the steady state can be disrupted during pregnancy. In addition, raising awareness of hyperhaemolysis among clinicians treating patients with thalassemia is necessary.

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