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10.1016/j.hoc.2013.11.004 http://scihub22266oqcxt.onion/10.1016/j.hoc.2013.11.004 C3942790!3942790!24589273     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Hematol+Oncol+Clin+North+Am 2014 ; 28 (2): 387-401 Nephropedia Template TP {{tp|p=24589273|t=2014. Modulation of hepcidin as therapy for primary and secondary iron overload disorders: pre-clinical models and approaches |pdf=|usr=}}{{24589273}} gab.com Text Modulation of hepcidin as therapy for primary and secondary iron overload disorders: pre-clinical models and approaches JO: Hematol Oncol Clin North Am http://www.kidney.de/pget.php?&tw=1&pmid=24589273 #FOAvip Correcting ineffective erythropoiesis and iron dysregulation by regulating hepcidin expression: Unbalanced hemoglobin ?- and ?-chain expression in the thalassemias, results in anemia, extramedullary hematopoiesis and ineffective erythropoiesis leading to secondary iron overload even in the absence of transfusion therapy. Severe, chronic ineffective erythropoiesis also leads to iron overload in other anemias, including the dyserythropoietic and sideroblastic anemias. Hereditary hemochromatosis (HH) is a group of human genetic disorders that share the common pathophysiology of an incrementally inappropriate increase in dietary iron uptake, leading to progressive iron overload over a period of years. In all cases, the iron overload may eventuate in toxic levels of iron in the liver, heart and endocrine tissues, leading to a multiplicity of complications, including organ failure. Despite the diversity of the underlying diseases, in each case, the iron overload is a direct effect of the dysregulation of hepcidin, the hormonal negative regulator of iron absorption by the intestine that is produced in the liver. In this article, we will discuss new approaches to treating iron overload diseases such as these, using hepcidin mimetics or by modulating endogenous hepcidin expression. In particular, we will discuss lipid nanoparticle (LNP) encapsulated siRNA and antisense oligonucleotide (ASO)-mediated inhibition of TMPRSS6, an upstream regulator of hepcidin, and treatment with transferrin or hepcidin mimetics, including the recently described ?minihepcidins.? In each case, in animal models of ?-thalassemia, not only do the interventions affect iron absorption, but they also act as disease-modifying agents that ameliorate the ineffective erythropoiesis inciting iron metabolism dysreguation in the first place. Twit Text FOAVip Modulation of hepcidin as therapy for primary and secondary iron overload disorders: pre-clinical models and approaches ????Hematol Oncol Clin North Am http://www.kidney.de/pget.php?&tw=1&pmid=24589273 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24589273 #FOAvip English Wikipedia <ref>{{Cite pmid|24589273}}</ref> Modulation of hepcidin as therapy for primary and secondary iron overload disorders: pre-clinical models and approaches #MMPMID24589273 Schmidt PJ; Fleming MD Hematol Oncol Clin North Am 2014[Apr]; 28 (2): 387-401 PMID24589273show ga Correcting ineffective erythropoiesis and iron dysregulation by regulating hepcidin expression: Unbalanced hemoglobin ?- and ?-chain expression in the thalassemias, results in anemia, extramedullary hematopoiesis and ineffective erythropoiesis leading to secondary iron overload even in the absence of transfusion therapy. Severe, chronic ineffective erythropoiesis also leads to iron overload in other anemias, including the dyserythropoietic and sideroblastic anemias. Hereditary hemochromatosis (HH) is a group of human genetic disorders that share the common pathophysiology of an incrementally inappropriate increase in dietary iron uptake, leading to progressive iron overload over a period of years. In all cases, the iron overload may eventuate in toxic levels of iron in the liver, heart and endocrine tissues, leading to a multiplicity of complications, including organ failure. Despite the diversity of the underlying diseases, in each case, the iron overload is a direct effect of the dysregulation of hepcidin, the hormonal negative regulator of iron absorption by the intestine that is produced in the liver. In this article, we will discuss new approaches to treating iron overload diseases such as these, using hepcidin mimetics or by modulating endogenous hepcidin expression. In particular, we will discuss lipid nanoparticle (LNP) encapsulated siRNA and antisense oligonucleotide (ASO)-mediated inhibition of TMPRSS6, an upstream regulator of hepcidin, and treatment with transferrin or hepcidin mimetics, including the recently described ?minihepcidins.? In each case, in animal models of ?-thalassemia, not only do the interventions affect iron absorption, but they also act as disease-modifying agents that ameliorate the ineffective erythropoiesis inciting iron metabolism dysreguation in the first place. äModulation of hepcidin as therapy for primary and secondary iron overl(epmc).pdf DeepDyve Pubget Overpricing