نتایج جستجو برای: stress polycythemia

تعداد نتایج: 444064  

Journal: :Cancer research 2013
Sangeeta Nischal Sanchari Bhattacharyya Maximilian Christopeit Yiting Yu Li Zhou Tushar D Bhagat Davendra Sohal Britta Will Yongkai Mo Masako Suzuki Animesh Pardanani Michael McDevitt Jaroslaw P Maciejewski Ari M Melnick John M Greally Ulrich Steidl Alison Moliterno Amit Verma

Even though mutations in epigenetic regulators frequently occur in myeloproliferative neoplasms, their effects on the epigenome have not been well studied. Furthermore, even though primary myelofibrosis (PMF) has a markedly worse prognosis than essential thrombocytosis or polycythemia vera, the molecular distinctions between these subgroups are not well elucidated. We conducted the HELP (HpaII ...

Journal: :The Journal of clinical investigation 1978
J F Prchal J W Adamson S Murphy L Steinmann P J Fialkow

Bone marrow cells from two glucose-6-phosphate dehydrogenase (G-6-PD) heterozygotes with polycythemia vera were cultured to determine whether progenitors which wre not of the polycythemia vera clone were present, and, if present, which cell lines contributed to the increase in erythroid colonies observed in response to added erythropoietin (ESF). To accomplish this, the G-6-PD isoenzyme activit...

2006
Catherine Lacout Didier F Pisani Micheline Tulliez Françoise Moreau Gachelin William Vainchenker Jean-Luc Villeval

A JAK2 mutation is frequently found in several BCR/ABL-negative myeloproliferative disorders. To address the contribution of this mutant to the pathogenesis of these different myeloproliferative disorders, we used an adoptive transfer of marrow cells transduced with a retrovirus expressing JAK2 in recipient irradiated mice. Hosts were analyzed during 6 months after transplantation. For a period...

Journal: :Blood 2006
Catherine Lacout Didier F Pisani Micheline Tulliez Françoise Moreau Gachelin William Vainchenker Jean-Luc Villeval

A JAK2(V617F) mutation is frequently found in several BCR/ABL-negative myeloproliferative disorders. To address the contribution of this mutant to the pathogenesis of these different myeloproliferative disorders, we used an adoptive transfer of marrow cells transduced with a retrovirus expressing JAK2(V617F) in recipient irradiated mice. Hosts were analyzed during the 6 months after transplanta...

Journal: :American journal of physiology. Heart and circulatory physiology 2005
JoAnn Lindenfeld John V Weil Victoria L Travis Lawrence D Horwitz

Previous studies have concluded that polycythemia decreases oxygen delivery primarily because of a large fall in cardiac output associated with a rise in systemic vascular resistance that has been attributed to increased blood viscosity. However, because other studies have shown that polycythemia may not reduce oxygen delivery, an alternative hypothesis is that cardiac output falls in response ...

Journal: :Blood 2014
Elisa Rumi Daniela Pietra Virginia Ferretti Thorsten Klampfl Ashot S Harutyunyan Jelena D Milosevic Nicole C C Them Tiina Berg Chiara Elena Ilaria C Casetti Chiara Milanesi Emanuela Sant'antonio Marta Bellini Elena Fugazza Maria C Renna Emanuela Boveri Cesare Astori Cristiana Pascutto Robert Kralovics Mario Cazzola

Patients with essential thrombocythemia may carry JAK2 (V617F), an MPL substitution, or a calreticulin gene (CALR) mutation. We studied biologic and clinical features of essential thrombocythemia according to JAK2 or CALR mutation status and in relation to those of polycythemia vera. The mutant allele burden was lower in JAK2-mutated than in CALR-mutated essential thrombocythemia. Patients with...

2010
Silverio Perrotta Valeria Cucciolla Marcella Ferraro Luisa Ronzoni Annunziata Tramontano Francesca Rossi Anna Chiara Scudieri Adriana Borriello Domenico Roberti Bruno Nobili Maria Domenica Cappellini Adriana Oliva Giovanni Amendola Anna Rita Migliaccio Patrizia Mancuso Ines Martin-Padura Francesco Bertolini Donghoon Yoon Josef T. Prchal Fulvio Della Ragione

BACKGROUND Gain-of-function of erythropoietin receptor (EPOR) mutations represent the major cause of primary hereditary polycythemia. EPOR is also found in non-erythroid tissues, although its physiological role is still undefined. METHODOLOGY/PRINCIPAL FINDINGS We describe a family with polycythemia due to a heterozygous mutation of the EPOR gene that causes a G-->T change at nucleotide 1251 ...

Journal: :The Tohoku Journal of Experimental Medicine 1951

Journal: :Proceedings of the Royal Society of Medicine 1968

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