Blue gold can be made by alloying with iron, and purple gold can be made by alloying with aluminium. Less commonly, addition of manganese, indium, and other elements can produce more unusual colors of gold for various applications.Colloidal gold, used by electron-microscopists, is red if the particles are small; larger particles of colloidal gold are blue. Isotopes
Gold has only one stable isotope, 197Au, which is also its only naturally occurring isotope, so gold is both a mononuclidic and monoisotopic element. Thirty-six radioisotopes have been synthesized, ranging in atomic mass from 169 to 205. The most stable of these is 195Au with a half-life of 186.1 days. The least stable is 171Au, which decays by proton emission with a half-life of 30 µs. Most of golds radioisotopes with atomic masses below 197 decay by some combination of proton emission, α decay, and β+ decay. The exceptions are 195Au, which decays by electron capture, and 196Au, which decays most often by electron capture (93%) with a minor β− decay path (7%). All of golds radioisotopes with atomic masses above 197 decay by β− decay.At least 32 nuclear isomers have also been characterized, ranging in atomic mass from 170 to 200. Within that range, only 178Au, 180Au, 181Au, 182Au, and 188Au do not have isomers. Golds most stable isomer is 198m2Au with a half-life of 2.27 days. Golds least stable isomer is 177m2Au with a half-life of only 7 ns. 184m1Au has three decay paths: β+ decay, isomeric transition, and alpha decay.
Myelokathexis is a congenital disorder of the white blood cells that causes severe, chronic leukopenia (a reduction of circulating white blood cells) and neutropenia (a reduction of neutrophil granulocytes). The disorder is believed to be inherited in an autosomal dominant manner. Myelokathexis refers to retention (kathexis) of neutrophils in the bone marrow (myelo). The disorder shows prominent neutrophil morphologic abnormalities.Myelokathexis is amongst the diseases treated with bone marrow transplantation and cord blood stem cells. WHIM syndrome is a very rare variant of severe congenital neutropenia that presents with warts, hypogammaglobunemia, infections, and myelokathexis. A gain-of-function mutation resulting in a truncated form of CXCR4 is believed to be its cause. The truncated form of the receptor has a 2-fold increase in G-protein coupled intracellular signalling, and this mutation of the receptor can be identified by DNA sequencing. See also
WHIM syndrome

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