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In addition to the steady state erythropoiesis, acute anemia probably stimulates another response which results in rapid development of new red blood cells. This has been studied in rats and happens in the liver through the activation of the BMP4-dependent stress erythropoiesis pathway. [12]
In mammals, NRBCs occur in normal development as precursors to mature red blood cells in erythropoiesis, the process by which the body produces red blood cells. NRBCs are normally found in the bone marrow of humans of all ages and in the blood of fetuses and newborn infants .
Rat-children or chuas are children or adults with microcephaly, exploited as beggars situated in Gujrat City, particularly the Shrine of Saint Shah Dola, [1] and elsewhere in Pakistan. They have sloping foreheads, narrow faces that resemble rodents, and are often intellectually disabled and dependent on others.
Latent iron deficiency (LID), also called iron-deficient erythropoiesis, [1] is a medical condition in which there is evidence of iron deficiency without anemia (normal hemoglobin level). [2] It is important to assess this condition because individuals with latent iron deficiency may develop iron-deficiency anemia.
n/a n/a Ensembl n/a n/a UniProt n a n/a RefSeq (mRNA) n/a n/a RefSeq (protein) n/a n/a Location (UCSC) n/a n/a PubMed search n/a n/a Wikidata View/Edit Human Erythropoietin (/ ɪ ˌ r ɪ θ r oʊ ˈ p ɔɪ. ɪ t ɪ n, - r ə -, - p ɔɪ ˈ ɛ t ɪ n, - ˈ iː t ɪ n / ; EPO), also known as erythropoetin, haematopoietin, or haemopoietin, is a glycoprotein cytokine secreted mainly by the kidneys ...
The contribution of Epo and EpoR to neuroprotection and development are not as clearly understood as its role in erythropoiesis in hematopoietic tissue. In a line of mice that expressed EpoR exclusively in hematopoietic cells, the mice developed normally had normal brains and brain function and were fertile, despite the lack of EpoR in ...
Ineffective erythropoiesis is defined by the expansion of early-stage erythroid precursors driven by erythropoietin, accompanied by the apoptosis of late-stage precursors. . This mechanism is principally responsible for the anemia seen in acquired conditions such as certain subtypes of myelodysplastic syndrome (MDS) and inherited disorders such as β-thalassemia, inherited sideroblastic ...
The homozygous Gunn rat, which lacks the enzyme uridine diphosphate glucuronyltransferase (UDPGT), is an animal model for the study of Crigler–Najjar syndrome. Since only one enzyme is working improperly, gene therapy for Crigler-Najjar is a theoretical option which is being investigated.