Titlebook: Iron Chelation Therapy; Chaim Hershko Book 2002 The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Scien

范例

ensemble

渐变

Role of Non-Transferrin-Bound Iron in The Pathogenesis of Iron Overload and Toxicity,. The second one, identified by Hershko and colleagues., is called Non-Transferrin-Bound Iron (NTBI). The latter source is increasingly acknowledged as being of primary importance in iron overload situations, due to its high uptake by parenchymal cells and its potential toxicity.

仔细检查

nurture

他去就结束

Results of Long Term Iron Chelation Treatment with Deferoxamine,eral Institute of Technology and Ciba Ltd on isolation of the iron-containing antibiotic ferrimycin from.it had become apparent that the antibiotic effect of ferrimycin was abolished by culture filtrates from other actinomycetes (.). Further work revealed that one of the main ferrimycin antagonists

漫不经心

Long Term Deferiprone Chelation Therapy,tory anaemias receiving regular blood transfusions. Parenteral preparations which have been evaluated clinically include desferrioxamine (DFO), diethylene triamine penta-acetic acid (DTPA), desferrithiocin and HBED (N,NL bis (2-hydroxy-benzyl ethylenediamine - NNI diacetic acid). Orally active chela

勤勉

Iron Chelator Chemistry,widely used iron chelator in haematology over the past thirty years, has a major disadvantage of being orally inactive’. Consequently, the successful design of an orally active, non-toxic, selective iron chelator has become a much sought after goal.

梯田

Structure-Activity Relationships Among Desazadesferrithiocin Analogues,Fe(VI), occurring in such diverse forms as iron disulfide (FeS., “fool’s gold”), iron oxides, including magnetite (Fe.0.), and hemoglobin. However, the Fe(II) and Fe(III) oxidation states (Equation 1) are of the most relevance in the present discussion.

RECUR

ICL670A: Preclinical Profile,f repeated transfusions, e.g. in ß-thalassemia major, or due to excessive dietary iron uptake in anemias and hereditary hemochromatosis. Excess iron is deposited in the form of hemosiderins (insoluble “iron cores” of ferritin) mainly in the liver, spleen, many endocrine organs and in the myocardium.