GF17563293
Copper - O.F.H.C.
foil, 300x1000mm, thickness 2.0mm, half hard, 99.95+%
Sinônimo(s):
Copper, CV000765
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About This Item
Ensaio
99.95%
forma
foil
fabricante/nome comercial
Goodfellow 175-632-93
resistividade
1.673 μΩ-cm, 20°C
tamanho × espessura
300 x 1000 mm × 2.0 mm
pb
2567 °C (lit.)
pf
1083.4 °C (lit.)
densidade
8.94 g/mL at 25 °C (lit.)
cadeia de caracteres SMILES
[Cu]
InChI
1S/Cu
chave InChI
RYGMFSIKBFXOCR-UHFFFAOYSA-N
Categorias relacionadas
Descrição geral
For updated SDS information please visit www.goodfellow.com.
Informações legais
Product of Goodfellow
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Environmental pollution (Barking, Essex : 1987), 194, 78-85 (2014-08-06)
Copper (Cu) is known to accumulate in agricultural soils receiving urban waste products as fertilizers. We here report the use of the leucine incorporation technique to determine pollution-induced community tolerance (Leu-PICT) to Cu in a long-term agricultural field trial. A
Proceedings of the National Academy of Sciences of the United States of America, 111(16), 5866-5871 (2014-04-09)
The human fungal pathogens Candida albicans and Histoplasma capsulatum have been reported to protect against the oxidative burst of host innate immune cells using a family of extracellular proteins with similarity to Cu/Zn superoxide dismutase 1 (SOD1). We report here
Annals of the New York Academy of Sciences, 1314, 6-14 (2014-04-05)
Copper is an important cofactor in numerous biological processes in all living organisms. However, excessive copper can be extremely toxic, so it is vital that the copper level within a cell is tightly regulated. The damaging effect of copper is
Metallomics : integrated biometal science, 5(10), 1346-1356 (2013-08-02)
Copper (Cu) is an essential redox active metal that is potentially toxic in excess. Multicellular organisms acquire Cu from the diet and must regulate uptake, storage, distribution and export of Cu at both the cellular and organismal levels. Systemic Cu
Proceedings of the National Academy of Sciences of the United States of America, 111(14), E1364-E1373 (2014-04-08)
Wilson disease (WD) is a monogenic autosomal-recessive disorder of copper accumulation that leads to liver failure and/or neurological deficits. WD is caused by mutations in ATP7B, a transporter that loads Cu(I) onto newly synthesized cupro-enzymes in the trans-Golgi network (TGN)
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