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Emanuel Necas

Researcher at First Faculty of Medicine, Charles University in Prague

Publications -  121
Citations -  2425

Emanuel Necas is an academic researcher from First Faculty of Medicine, Charles University in Prague. The author has contributed to research in topics: Bone marrow & Haematopoiesis. The author has an hindex of 22, co-authored 121 publications receiving 2326 citations. Previous affiliations of Emanuel Necas include University of Alabama at Birmingham & Charles University in Prague.

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Journal Article

Hepcidin mRNA levels in mouse liver respond to inhibition of erythropoiesis.

TL;DR: It is proposed that hepcidin is exclusively sensitive to iron utilization for erythropoiesis and hepatocyte iron balance, and these changes are not sensed by other genes involved in the control of iron metabolism in the liver.
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A study of intracellular iron metabolism using pyridoxal isonicotinoyl hydrazone and other synthetic chelating agents

TL;DR: Reticulocytes with a high level of non-heme radioiron are envisaged as a useful system for testing biological effectiveness of various iron chelators and Pyridoxal isonicotinoyl hydrazone was shown to be an effective in vivo chelator.
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MYB transcriptionally regulates the miR-155 host gene in chronic lymphocytic leukemia

TL;DR: Evidence that MYB (v-myb myeloblastosis viral oncogene homolog) is overexpressed in a subset of B-CLL patients is presented and evidence of oncogenic activities of MYB in B- CLL that include its stimulatory role in MIR155HG transcription is provided.
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A Sudden Increase in Partial Pressure End-Tidal Carbon Dioxide (PETCO2) at the Moment of Return of Spontaneous Circulation

TL;DR: The rule of 10mm Hg may be extended to include a sudden increase in continuously recorded P(ET)CO(2) by more than 10 mm Hg as an indicator of the possibility of ROSC in constantly ventilated patients.
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TRAIL (Apo2L) suppresses growth of primary human leukemia and myelodysplasia progenitors

TL;DR: Tumor necrosis factor-related apoptosis-inducing ligand TRAIL does not affect normal human hematopoiesis but suppresses the growth of early primary leukemia and myelodysplasia progenitors.