Eitan Fibach

ORCID: 0000-0002-6658-6126
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About
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Research Areas
  • Hemoglobinopathies and Related Disorders
  • Erythrocyte Function and Pathophysiology
  • Iron Metabolism and Disorders
  • Acute Myeloid Leukemia Research
  • Blood groups and transfusion
  • Neonatal Health and Biochemistry
  • Epigenetics and DNA Methylation
  • Retinoids in leukemia and cellular processes
  • Erythropoietin and Anemia Treatment
  • Prenatal Screening and Diagnostics
  • Trace Elements in Health
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Chronic Myeloid Leukemia Treatments
  • Hematopoietic Stem Cell Transplantation
  • Papaya Research and Applications
  • RNA Interference and Gene Delivery
  • RNA modifications and cancer
  • Fatty Acid Research and Health
  • Virus-based gene therapy research
  • Immune Cell Function and Interaction
  • Toxin Mechanisms and Immunotoxins
  • Heme Oxygenase-1 and Carbon Monoxide
  • Calcium signaling and nucleotide metabolism
  • Cytokine Signaling Pathways and Interactions
  • Glycosylation and Glycoproteins Research

Hadassah Medical Center
2014-2023

Hebrew University of Jerusalem
2006-2023

Hadassah Academic College
2000-2021

University Medical Center
2007-2017

Augusta Victoria Hospital
2017

Hadassah
1999-2007

University of Ferrara
2003-2006

Gamida Cell (Israel)
2004

Sheba Medical Center
2004

National Institute of Diabetes and Digestive and Kidney Diseases
1993-2002

Addition of the potent tumor promoter, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), to murine erythroleukemia cell lines in suspension cultures inhibited both spontaneous differentiation and induced by hexamethylene bisacetamide (HMBA), dimethyl sulfoxide, or butyric acid. Inhibition was unrelated cytotoxicity reversible. When several plant diterpenes were tested, there a positive correlation between tumor-promoting activity inhibition differentiation. TPA HMBA-induced only if added prior...

10.1073/pnas.74.8.3451 article EN Proceedings of the National Academy of Sciences 1977-08-01

Summary Sickle cell disease (SCD) is basically a red blood (RBC) disorder characterised by sickling and haemolysis, but platelets polymorphonuclear neutrophils (PMN) are also involved. Oxidative damage may play role in the pathogenesis of SCD. Using flow cytometry, we measured oxidative‐state markers simultaneously RBC, PMN obtained from 25 normal donors, nine homozygous (SS) patients six SS/beta‐thalassaemia patients. Reactive oxygen species (ROS) reduced glutathione (GSH) were following...

10.1111/j.1365-2141.2005.05834.x article EN British Journal of Haematology 2005-11-25

Cells from a myeloid leukemic line in culture can be induced by the differentiation-inducing protein MGI to form colonies with normal differentiation mature macrophages and granulocytes. This consisted of clones that undergo cell (D(+) clones) (D(-) were not inducible. D(+) able both Normal was even no longer diploid. segregate some D(-) progeny, progeny. This, therefore, provides system for studies on genetic chemical control cells.

10.1073/pnas.70.2.343 article EN Proceedings of the National Academy of Sciences 1973-02-01

Reactive oxygen species (ROS) contribute to the pathogenesis of several hereditary disorders red blood cells (RBCs), including thalassaemia. We report here on a modified flow cytometric method for measuring ROS in normal and thalassaemic RBCs. RBCs were incubated with 0.4 mM 2',7'-dichlorofluorescin diacetate (DCFH-DA), then washed further either or without 2 H2O2. Flow analysis showed that RBC fluorescence increased time; it faster reached higher intensity (by 10-30-fold) H2O2-stimulated as...

10.1034/j.1600-0609.2003.00011.x article EN European Journal Of Haematology 2003-02-01

When added to mouse neuroblastoma cultures, the potent tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA) inhibits spontaneous neurite formation as well that induced in response serum deprivation, prostaglandin E1, 5-bromo-2′-deoxyuridine, and papaverine. Other tumor-promoting macrocyclic plant diterpenes also inhibit formation, whereas nonpromoting do not. Inhibition by TPA was reversible unrelated toxicity.

10.1126/science.644318 article EN Science 1978-05-05

Iron is essential for the survival as well proliferation and maturation of developing erythroid precursors (EP) into hemoglobin-containing red blood cells. The transferrin-transferrin receptor pathway main route iron uptake. Using a two-phase culture system, we have previously shown that placental ferritin macrophages derived from peripheral monocytes could partially replace transferrin support EP growth in transferrin-free medium. We now demonstrate absence transferrin, synthesized secreted...

10.1002/jcb.21499 article EN Journal of Cellular Biochemistry 2007-09-27

Abstract Iron is important for many biological processes, and its deficiency or excess involved in pathological conditions. Although most iron firmly bound (e.g., hemoglobin), some, the labile pool (LIP), to low‐affinity ligands. The level of LIP regulated meet cell's requirements but prevent excess. We describe herein a multiparameter flow cytometry procedure measuring various human hematopoietic cells. Peripheral blood bone marrow (BM) cells were loaded with calcein‐AM, washed, then...

10.1002/cyto.a.20491 article EN Cytometry Part A 2007-11-28

Erythropoiesis in long-term hemodialyzed (LTH) patients is supported by erythropoietin (rHuEpo) and intravenous (IV) iron. This treatment may end up iron overload (IO) major organs. We studied such for the parameters of IO serum organs.Patients were treated with rHuEpo (6-8 x 10(3) units × 1-3/wk) IV 100 mg ferric saccharate.Of 115 patients, 21 had ferritin (SF) > 1000 ng/mL. group was further analyzed. Their SF transferrin saturation (TSAT) 2688 ± 1489 ng/mL 54.2 32.7%, respectively (vs....

10.1111/j.1600-0609.2012.01783.x article EN European Journal Of Haematology 2012-03-22

Low-risk myelodysplastic syndrome (MDS) is characterized by cytopenia, mainly anemia, because of ineffective hematopoiesis. Some the patients with erythropoiesis, or without ring sideroblasts in their bone marrow, develop severe anemia requiring frequent blood transfusions and consequently iron overload. Excess free cells catalyses generation reactive oxygen species (ROS) that cause cell tissue damage. Using flow cytometry techniques, we compared oxidative status red (RBC), platelets...

10.1111/j.1600-0609.2007.00972.x article EN European Journal Of Haematology 2007-10-04

Background The lifespan of red blood cells is terminated when macrophages remove senescent by erythrophagocytosis. This puts at the center systemic iron recycling in addition to their functions tissue remodeling and innate immunity. Thus far, erythrophagocytosis has been studied evaluating phagocytosis erythrocytes that were damaged mimic senescence. These studies have demonstrated acquisition some specific individual senescence markers can trigger macrophages, but we hypothesized mechanism...

10.3324/haematol.2011.057620 article EN cc-by-nc Haematologica 2012-02-13

There are three types of myeloid leukemic cells, IR+D, IR+D- and IR-D-. IR+D+ cells were induced to differentiate granulocytes in mass culture liquid medium by conditioned (CM) from cultures lungs mice injected with endotoxin. About 90% the differentiate, 50% mature 40% intermediate stages. An efficient induction granulocyte differentiation was also obtained CM primary rat embryo or human spleen there a lower activity various other sources. about 20% stages but not granulocytes; IR-D- could...

10.1002/jcp.1040860205 article EN Journal of Cellular Physiology 1975-10-01

Preclinical and clinical studies demonstrate the feasibility of treating β-thalassemia Sickle Cell Disease (SCD) by lentiviral-mediated transfer human β-globin gene. However, previous have not addressed whether ability lentiviral vectors to increase hemoglobin synthesis might vary in different patients.We generated carrying gene with without an ankyrin insulator compared their induce vitro thalassemic mice. We found that insertion leads higher, potentially therapeutic levels through a novel...

10.1371/journal.pone.0032345 article EN cc-by PLoS ONE 2012-03-27

Thalassemia (thal) is an autosomal recessive, hereditary, chronic hemolytic anemia due to a partial or complete deficiency in the synthesis of α-globin chains (α-thal) β-globin (β-thal) that compose major adult hemoglobin (α 2β 2). It caused by one more mutations corresponding genes. The unpaired globin are unstable; they precipitate intracellularly, resulting hemolysis, premature destruction red blood cell [RBC] precursors bone marrow, and short life-span mature RBCs circulation. state...

10.12688/f1000research.12688.1 preprint EN cc-by F1000Research 2017-12-20
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