scholarly journals Lenalidomide – A Brief Review of its Use in Myelodysplastic Syndromes

2015 ◽  
Vol 11 (2) ◽  
pp. 141
Author(s):  
Jaykumar J Sejpal ◽  
Yogesh R Belagali ◽  
Hanmant V Barkate ◽  
◽  
◽  
...  

Myelodysplastic syndromes (MDS) are a heterogeneous group of blood diseases mainly affecting older people. Deletion of the long arm of chromosome 5 (del[5q]) is reported in approximately 10–15 % of all MDS cases. Lenalidomide is an immunomodulatory, anti-cytokine and anti-angiogenic agent, which leads to red blood cells transfusion independence in patients of lower risk MDS with del(5q). This review briefly describes role of lenalidomide in treatment of lower-risk MDS with del(5q) as well as non-del-5q MDS. Recent evidence also suggest a potential role of lenalidomide in combination with other agents for treatment of higher-risk MDS

2019 ◽  
Vol 91 ◽  
pp. 425
Author(s):  
S. Puente-Marin ◽  
I. Nombela ◽  
V. Chico ◽  
S. Ciordia ◽  
M.C. Mena ◽  
...  

Hematology ◽  
2007 ◽  
Vol 2007 (1) ◽  
pp. 84-90 ◽  
Author(s):  
Marilyn J. Telen

AbstractA number of lines of evidence now support the hypothesis that vaso-occlusion and several of the sequelae of sickle cell disease (SCD) arise, at least in part, from adhesive interactions of sickle red blood cells, leukocytes, and the endothelium. Both experimental and genetic evidence provide support for the importance of these interactions. It is likely that future therapies for SCD might target one or more of these interactions.


Anemia ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Erwin Weiss ◽  
David Charles Rees ◽  
John Stanley Gibson

Phosphatidylserine exposure occurs in red blood cells (RBCs) from sickle cell disease (SCD) patients and is increased by deoxygenation. The mechanisms responsible remain unclear. RBCs from SCD patients also have elevated cation permeability, and, in particular, a deoxygenation-induced cation conductance which mediates entry, providing an obvious link with phosphatidylserine exposure. The role of was investigated using FITC-labelled annexin. Results confirmed high phosphatidylserine exposure in RBCs from SCD patients increasing upon deoxygenation. When deoxygenated, phosphatidylserine exposure was further elevated as extracellular [] was increased. This effect was inhibited by dipyridamole, intracellular chelation, and Gardos channel inhibition. Phosphatidylserine exposure was reduced in high saline. levels required to elicit phosphatidylserine exposure were in the low micromolar range. Findings are consistent with entry through the deoxygenation-induced pathway (), activating the Gardos channel. [] required for phosphatidylserine scrambling are in the range achievablein vivo.


2010 ◽  
Vol 142 (1) ◽  
pp. 2-7 ◽  
Author(s):  
Dimitrios N. Tziakas ◽  
Georgios K. Chalikias ◽  
Dimitrios Stakos ◽  
Harisios Boudoulas

1978 ◽  
Vol 45 (1) ◽  
pp. 7-10 ◽  
Author(s):  
H. Bard ◽  
J. C. Fouron ◽  
J. E. Robillard ◽  
A. Cornet ◽  
M. A. Soukini

Studies were carried out during fetal life in sheep to determine the relationship of 2,3-diphosphoglycerate (DPG), the intracellular red cell and extracellular pH, and the switchover to adult hemoglobin synthesis in regulating the position of the fetal red cell oxygen-affinity curve in utero. Adult hemoglobin first appeared near 120 days of gestation. The mean oxygen tension at which hemoglobin is half saturated (P50) prior to 120 days of gestation remained constant at 13.9 +/- 0.3 (SD) Torr and then increased gradually as gestation continued, reaching 19 Torr at term. During the interval of fetal life studied, the level of DPG was 4.43 +/- 1.63 (SD) micromol/g Hb and the deltapH between plasma and red blood cells was 0.227 +/- 0.038 (SD); neither was affected by gestational age. The decrease in the red cell oxygen affinity after 120 days of gestation ocrrelated with the amount of adult hemoglobin present in the fetus (r = 0.78; P less than 0.001). This decrease can be attributed only to the amount of the adult-type hemoglobin present, and not to DPG, or to changes in the deltapH between plasma and red blood cells, because both remained stable during the last trimester.


1974 ◽  
Vol 29 (9-10) ◽  
pp. 510-515 ◽  
Author(s):  
W Helfrich

Abstract The role of lipid exchange in the curvature elasticity of bilayers is studied theoretically. Blocking of exchange between the monolayers may give rise to a nonequilibrium lipid distribution going hand in hand with a spontaneous curvature. Some possible consequences for vesicular deformations are discussed. Lipid nonequilibrium is tentatively suggest as one possible cause for certain shape transformations of red blood cells


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