meinen job.... 
beispiel...?!?
seit heute morgen tipp ich....
....chronic disease is characterized by changes in iron homeostasis, with increased uptake and retention of iron within cells of the reticuloendothelial system resulting in normocytic or microcytic iron-refractory anemia. In patients with anemia of chronic disease, the proliferation and differentiation of erythroid precursors are impaired and are linked to the inhibitory effects of proinflammatory cytokines.....patients with anemia of chronic disease, the proliferation and differentiation of erythroid precursors are impaired and are linked to the inhibitory effects of proinflammatory cytokines. Erythropoietin responses in anemia of chronic disease are mostly inadequate for the degree of anemia (41). Hepcidin contributes to anemia of chronic disease not only through effects on iron metabolism, but also through inhibition of erythroid progenitor proliferation and survival (42). Hepcidin production is also stimulated by lipopolysaccharide (LPS), Freund adjuvant, and turpentine (21,23,43-45). Iron overload or LPS injection stimulates transcription of HAMP, the gene that encodes hepcidin. However, the mechanisms inducing transcription of HAMP are different between inflammation and iron overload. Reduced transcription of HAMP and inappropriate low production of hepcidin may explain iron overload in hemochromatosis patients with mutations in their HFE-, TFR2- and HJV-gene. The various heritable forms of the iron storage disease are due, at least in part, to the inability of iron to stimulate the hepatic production of hepcidin under these conditions (46-48 ). In contrast, up-regulation of HAMP during inflammation occurs even in HFE knockout mice and in animals with mutation in TFR2. These data indicate that hepcidin production may occur during inflammation in the absence of HFE, HJV and/or TFR2 activation. Nemeth et al (27,43) suggested that the only cytokine that stimulates hepatic hepcidin production is interleukin-6 (IL-6). Up-regulation of HAMP is impaired in IL-6 knockout mice after LPS stimulation (49) but not abolished suggesting that other proinflammatory cytokines are also able to induce hepcidin production. Recent data from Lee et al (50) show that hepcidin transcription was stimulated in murine hepatocytes not only by IL-6 but also by IL-1? and IL-1ß. The maximal response of hepcidin expression occurs 6h after LPS injection (51). Thus, hepcidin transcription by proinflammatory cytokines does not require HFE, TFR2 and/or HJV stimulation, suggesting direct up-regulation of HAMP by IL-6, IL-? and IL-1ß (49,50). IL-1 induces hypoferremia (52) and up-regulation of ferritin (53). It may play a primary role in the anemia of chronic inflammation (54), probably by its stimulation of hepcidin....
und das in einem fort...ich kann nicht mehr...bzw versteh ich davon soviel wie die putze die hier grad war und staubgesaugt hat...
beispiel...?!?
seit heute morgen tipp ich....
....chronic disease is characterized by changes in iron homeostasis, with increased uptake and retention of iron within cells of the reticuloendothelial system resulting in normocytic or microcytic iron-refractory anemia. In patients with anemia of chronic disease, the proliferation and differentiation of erythroid precursors are impaired and are linked to the inhibitory effects of proinflammatory cytokines.....patients with anemia of chronic disease, the proliferation and differentiation of erythroid precursors are impaired and are linked to the inhibitory effects of proinflammatory cytokines. Erythropoietin responses in anemia of chronic disease are mostly inadequate for the degree of anemia (41). Hepcidin contributes to anemia of chronic disease not only through effects on iron metabolism, but also through inhibition of erythroid progenitor proliferation and survival (42). Hepcidin production is also stimulated by lipopolysaccharide (LPS), Freund adjuvant, and turpentine (21,23,43-45). Iron overload or LPS injection stimulates transcription of HAMP, the gene that encodes hepcidin. However, the mechanisms inducing transcription of HAMP are different between inflammation and iron overload. Reduced transcription of HAMP and inappropriate low production of hepcidin may explain iron overload in hemochromatosis patients with mutations in their HFE-, TFR2- and HJV-gene. The various heritable forms of the iron storage disease are due, at least in part, to the inability of iron to stimulate the hepatic production of hepcidin under these conditions (46-48 ). In contrast, up-regulation of HAMP during inflammation occurs even in HFE knockout mice and in animals with mutation in TFR2. These data indicate that hepcidin production may occur during inflammation in the absence of HFE, HJV and/or TFR2 activation. Nemeth et al (27,43) suggested that the only cytokine that stimulates hepatic hepcidin production is interleukin-6 (IL-6). Up-regulation of HAMP is impaired in IL-6 knockout mice after LPS stimulation (49) but not abolished suggesting that other proinflammatory cytokines are also able to induce hepcidin production. Recent data from Lee et al (50) show that hepcidin transcription was stimulated in murine hepatocytes not only by IL-6 but also by IL-1? and IL-1ß. The maximal response of hepcidin expression occurs 6h after LPS injection (51). Thus, hepcidin transcription by proinflammatory cytokines does not require HFE, TFR2 and/or HJV stimulation, suggesting direct up-regulation of HAMP by IL-6, IL-? and IL-1ß (49,50). IL-1 induces hypoferremia (52) and up-regulation of ferritin (53). It may play a primary role in the anemia of chronic inflammation (54), probably by its stimulation of hepcidin....
und das in einem fort...ich kann nicht mehr...bzw versteh ich davon soviel wie die putze die hier grad war und staubgesaugt hat...
ich war zuerst da sprach das Ei zum Huhn
