1,721,144 research outputs found
Tributyrin plus all-trans-retinoic acid efficiently induces fetal hemoglobin expression in human erythroleukemia cells
No full textFourteen butyrate derivatives and retinoic acid were tested with respect to the hemoglobin F-inducing activity using the K562 erythroleukemia cell line as a model system. Four novel butyrate derivatives with hemoglobin F-inducing activity have been identified. Combined treatment with the butyrate derivative tributyrin and retinoic acid in vitro led to a 7-fold increase of hemoglobin synthesis. Tributyrin and retinoic acid might be promising drugs for clinical trials to treat patients with beta-hemoglobinopathies. Am. J, Hematol, 64:319-321, 2000, (C) 2000 Wiley-Liss, Inc
Diabetes mellitus type I, coeliac disease and Imerslund-Graesbeck-syndrome: simply an unusual combination of rare diseases?
No full textWe describe the clinical course of a girl with onset of type I diabetes mellitus at the age of 3 years. At the age of 10, coeliac disease and shortly thereafter a vitamin B-12 deficiency anemia (Imerslund-Graesbeck-syndrome) was diagnosed. Her younger sister also suffered from Imerslund-Graesbeck-syndrome when she was 11 year old. This unusual, so far not described association of rare diseases suggests a common autoimmune etiology
Butyrate-induced erythroid differentiation of human K562 leukemia cells involves inhibition of ERK and activation of p38 MAP kinase pathways
No full textButyrate induces cytodifferentiation in many tumor cells of different origin, suggesting that an as yet unidentified common mechanism inherent to malignant cells is the target of butyrate action. This study determined the role of different mitogen-activated protein (MAP) kinase signal transduction pathways in butyrate-induced erythroid differentiation of K562 human leukemia cells. Using a panel of anti-ERK, JNK, and p38 phosphospecific antibodies, the study showed that phosphorylation of ERK and JNK is decreased following treatment of cells with butyrate, whereas phosphorylation of p38 is increased. In contrast, a K562 subline defective in butyrate-mediated induction of erythroid differentiation did not reveal these changes in phosphorylation patterns. Inhibition of ERK activity by UO126 induces erythroid differentiation and acts synergistically with butyrate on hemoglobin synthesis and inhibition of cell proliferation, whereas inhibition of p38 activity by SB203580 completely abolished induction of hemoglobin expression by butyrate. Taken together, our data suggest a model in which butyrate induces erythroid differentiation of K562 cells by inhibition of ERK and activation of p38 signal transduction pathways. (Blood, 2000;95:2391-2396) (C) 2000 by The American Society of Hematology
Increase in band 3 density and aggregation in hereditary spherocytosis
No full textPurpose: Red cells in hereditary spherocytosis are characterized by a reduced surface area/volume ratio. The mechanisms leading to the loss of membrane material and subsequent elimination of the cells have still not been clarified. It was the aim of the present study to analyze band 3 distribution in the red cell membrane and its putative role in red cell elimination. Methods/Results: Immunogold histochemistry was performed to detect band 3 in red cell membranes. Band 3 density and distribution were visualized by electron microscopy. Unsplenectomized spherocytosis patients (n = 12) showed reduced band 3 density and aggregation compared to controls (n = 15) (density: 1.2 +/- 0.1 gold particles/mum circumference of red cell membrane vs 1.5 +/- 0.07 gold particles/mum, x +/- SEM; P < 0.05; aggregation: 0.26 +/- 0.02 aggregates/mum vs 0.3 +/- 0.02 aggregates/mum). By contrast, band 3 density and aggregation were increased in spherocytosis patients who had undergone splenectomy (density: 2.8 +/- 0.1 gold particles/mum vs 2.0 +/- 0.1 gold particles/mum; P < 0.05; aggregation: 1.5 +/- 0.1 aggregates/mum vs 0.5 +/- 0.03 aggregates/mum; P < 0.01). Artificial ageing of red cells from healthy controls (n = 6) led to a significant increase in band 3 aggregation (2.06 +/- 0.2 aggregates/mum vs 0.33 +/- 0.1 aggregates/mum; P-Wilcoxon < 0.01) but no change in band 3 density. In hereditary spherocytosis (n = 6), both band 3 density and aggregation increased significantly, after artificial ageing of the red cells. The elevated band 3 aggregation was associated with a stimulated erythrophagocytosis in vitro. Conclusion: Band 3 aggregation characterizes the red cells in hereditary spherocytosis. It may be the cause of selective splenic phagocytosis of both spherocytes and senescent erythrocytes, (C) 2001 Academic Press
Accidental cisplatin overdose in a child: Reversal of acute renal failure with sodium thiosulfate
No full textInduction of fetal hemoglobin synthesis by valproate: Modulation of MAPkinase pathways
No full textValproate has been found to stimulate fetal hemoglobin (HbF) synthesis in patients with sickle cell disease. In accordance with these clinical observations, we found a moderate induction of HbF synthesis in K562 erythroid cells in vitro. Investigation of the role of the mitogen-activated protein kinase (MAPK) pathways by Western blot analysis and use of specific kinase inhibitors suggests that inhibition of ERK pathway and activation of the p38 pathway may contribute to the HbF-inducing activity of valproate. (C) 2002 Wiley-Liss, Inc
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