P-37 Flow cytometric analysis of cytosolic and mitochondrial ferritins in immature red blood cells from patients with myelodysplastic syndrome

2005 ◽  
Vol 29 ◽  
pp. S38
Author(s):  
M.G. Della Porta ◽  
L. Malcovati ◽  
M. Maffioli ◽  
E. Travaglino ◽  
S. Levi ◽  
...  

1994 ◽  
Vol 56 (3) ◽  
pp. 593-595 ◽  
Author(s):  
Reiko USUI ◽  
Junko HIROTA ◽  
Toshinori OMI ◽  
Sadahiko IWAMOTO ◽  
Shigenori IKEMOTO


1994 ◽  
Vol 17 (2) ◽  
pp. 106-115
Author(s):  
Kimihiko Yanagita ◽  
Minoru Nakamura ◽  
Seiji Kondo ◽  
Hiroshi Nagafuji ◽  
Hiroshi Chifu ◽  
...  


2006 ◽  
Vol 12 (2) ◽  
pp. 82-85 ◽  
Author(s):  
Shoko Sato ◽  
Yuichi Hasegawa ◽  
Toshiro Nagasawa ◽  
Haruhiko Ninomiya


Cytometry ◽  
2004 ◽  
Vol 60A (1) ◽  
pp. 73-80 ◽  
Author(s):  
Johnny Amer ◽  
Ada Goldfarb ◽  
Eitan Fibach


Blood ◽  
2001 ◽  
Vol 98 (12) ◽  
pp. 3492-3494 ◽  
Author(s):  
Udomsak Bunworasate ◽  
Hilal Arnouk ◽  
Hans Minderman ◽  
Kieran L. O'Loughlin ◽  
Sheila N. J. Sait ◽  
...  

Abstract Acute monoblastic leukemia (acute myeloid leukemia [AML], French-American-British type M5a) with leukemia cutis developed in a patient 6 weeks after the initiation of erythropoietin (EPO) therapy for refractory anemia with ringed sideroblasts. AML disappeared from both marrow and skin after the discontinuation of EPO. Multiparameter flow cytometric analysis of bone marrow cells demonstrated coexpression of the EPO receptor with CD45 and CD13 on the surface of blasts. The incubation of marrow cells with EPO, compared to without, resulted in 1.3- and 1.6-fold increases, respectively, in tritiated thymidine incorporation and bromodeoxyuridine incorporation into CD13+ cells. Clinical and laboratory findings were consistent with the EPO-dependent transformation of myelodysplastic syndrome (MDS) to AML. It is concluded that leukemic transformation in patients with MDS treated with EPO may be EPO-dependent and that management should consist of the discontinuation of EPO followed by observation, if clinically feasible.



2006 ◽  
Vol 74 (6) ◽  
pp. 3204-3212 ◽  
Author(s):  
Ingo Borggraefe ◽  
Jie Yuan ◽  
Sam R. Telford ◽  
Sanjay Menon ◽  
Rouette Hunter ◽  
...  

ABSTRACT Babesia microti is a tick-borne red blood cell parasite that causes babesiosis in people. Its most common vertebrate reservoir is the white-footed mouse. To determine whether B. microti invades reticulocytes, as does the canine pathogen B. gibsoni, we infected the susceptible inbred mouse strains C.B-17.scid and DBA/2 with a clinical isolate of B. microti. Staining of fixed permeabilized red blood cells with 4′,6′-diamidino-2-phenylindole or YOYO-1, a sensitive nucleic acid stain, revealed parasite nuclei as large bright dots. Flow cytometric analysis indicated that parasite DNA is primarily found in mature erythrocytes that expressed Babesia antigens but not the transferrin receptor CD71. In contrast, CD71-positive reticulocytes rarely contained Babesia nuclei and failed to express Babesia antigens. Accordingly, the frequency of YOYO-1-positive, CD71-negative cells strongly correlated with parasitemia, defined as the frequency of infected red blood cells assessed on Giemsa-stained blood smears. Importantly, the absolute numbers generated by the two techniques were similar. Parasitemia was modest and transient in DBA/2 mice but intense and sustained in C.B-17.scid mice. In both strains, parasitemia preceded reticulocytosis, but reticulocytes remained refractory to B. microti. In immunocompetent C.B-17 mice, reticulocytosis developed early, despite a marginal and short-lived parasitemia. Likewise, an early reticulocytosis developed in resistant BALB/cBy and B10.D2 mice. These studies establish that B. microti has a tropism for mature erythrocytes. Although reticulocytes are rarely infected, the delayed reticulocytosis in susceptible strains may result from parasite or host activities to limit renewal of the mature erythrocyte pool, thereby preventing an overwhelming parasitemia.



2020 ◽  
Vol 11 (2) ◽  
pp. 51
Author(s):  
Raghda Fouda ◽  
AzzaA Aboul Enein ◽  
NermeenA El-Desoukey ◽  
RandaM Abo Elfetouh ◽  
AhmedM. A Abdel Hafez






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