Showing papers on "Red blood cell published in 1995"
Book•
01 Apr 1995TL;DR: The author examines the immune system through the lens of Epstein-Barr Virus-Associated Diseases, as well as the biology of Stem Cells and Disorders of Hematopoiesis, and the approach to the Adult and Child with Anemia.
Abstract: Part I: Mollecular and Cellular Basis of Hematology. Anatomy and Physiology of the Gene. Protein Synthesis and Intracellular Sorting. Protein Architecture: Relationship of Form and Function. Membrane Biology. Cell Adhesion. Cellular Regulatory and Control Mechanism. Part II: Immunologic Basis of Hematology. Overview of the Immune System (including Compartmentalization of the Immune Response). Generation of B-cells. T-cell Immunity. Regulation of Activation of B and T-cells. Tolerance and Autoimmunity. Part III: Biology of Stem Cells and Disorders of Hematopoiesis. Stem Cell Model of Hematopoiesis. Anatomy and Physiology of Hematopoiesis. Growth Factors and the Control of Hematopoiesis. Biology of Erythropoiesis, Erythroid Differentiation and Maturation. Granulopoiesis and Monocytopoiesis. Thrombocytopoiesis. Inherited Forms of Bone Marrow Failure. Aplastic Anemia. Paroxysmal Nocturnal Hemoglobinuria. Pure Red Blood Cell Aplasia. Part IV: Red Blood Cells. Pathobiology of the Red Cell. Approach to the Adult and Child with Anemia. Anemia of Chronic Diseases. Erythrocytosis. Disorders of Iron Metabolism: Iron Deficiency and Overload. Heme Biosynthesis and Its Disorders: Porphyrias and Sideroblastic Anemias. Megaloblastic Anemias. Thalassemia Syndromes. Sickle Cell Disease. Hemoglobin Variants Associated with Hemolytic Anemia, Altered Oxygen Affinity, and Methemoglobinemias. Enzymopathies. Red Cell Membrane Disorders. Autoimmune Hemolytic Anemias. Extrinsic Nonimmune Hemolytic Anemias. Part V: Host Defense and Its Disorders. Immunoglobulins: Structure, Function, and Uses. Complement Biology. Neutrophil Structure and Function. Monocyte and Macrophage Development and Function. Eosinophils and the Hypereosinophilic Syndrome. Disorders of the Phagocyte Function. Disorders of the Lymphocyte Function. Histiocytic Syndromes. Lysosomal Storage Disease. Infectious Mononucleosis and Other Epstein-Barr Virus-Associated Diseases. Spleen and Its Disorders. Systemic Mastocytosis. Part VI: Hemat
1,646 citations
TL;DR: It is concluded that deficiency of fibrinogen develops earlier than any other hemostatic abnormality when plasma-poor RCCs are used for the replacement of major blood loss.
Abstract: The purpose of this study was to assess the change of platelet and fibrinogen concentrations and the change of activities of prothrombin and factors V and VII when major surgical blood loss was replaced with plasma-poor red cell concentrates (RCCs) and colloid plasma substitutes. Sixty patients were studied. The average blood loss was 65% +/- 41% of the calculated blood volume (CBV). Blood loss was monitored carefully and replaced without delay to ensure stable blood volume. Blood samples were obtained at the induction of anesthesia and at the end of the recovery room period, or before the patient was given fresh frozen plasma. In addition, a platelet count was determined after each 20% blood loss. The results were converted to relative values, and simple linear regression with logarithmic transformation was applied. The initial platelet concentration was 257 +/- 89 x 10(3)/mm3 and the extrapolation of the regression line intercepted the critical level of 50 x 10(3)/mm3 at 230% (confidence interval 169%-294%) blood loss. The initial fibrinogen concentration was 3.7 +/- 1.1 g/L and the hemostatically significant level of 1.0 g/L was already reached at 142% (117%-169%) blood loss (r2 = 0.90). Activities of prothrombin and coagulation factors V and VII reached their critical levels at 201% (160%-244%), 229% (167%-300%), and 236% (198%-277%) blood loss, respectively. We conclude that deficiency of fibrinogen develops earlier than any other hemostatic abnormality when plasma-poor RCCs are used for the replacement of major blood loss.
632 citations
TL;DR: An improved protocol was applied to the use of carboxyhemoglobin (HbCO) saturation for the estimation of body hemoglobin mass, red blood cell volume, and blood volume and was appraised in normal volunteers, finding the method is sensitive and precise.
Abstract: An improved protocol was applied to the use of carboxyhemoglobin (HbCO) saturation for the estimation of body hemoglobin (Hb) mass, red blood cell volume, and blood volume and was appraised in norm...
211 citations
TL;DR: It is shown that reduced glutathione (GSH) is able to degrade heme in solution with a pH optimum of 7.5, which explains the origin of non-heme iron found in the membrane of sickle cells and the oxidative stress that is observed in these and other abnormal erythrocytes.
206 citations
TL;DR: The results suggest that young reticulocytes bind to endothelial cell VCAM-1 via VLA-4 integrin, which is similar to the binding of normal and sickle RBCs to E-selectin-transfected COS cells.
191 citations
TL;DR: In two cases of marrow transplantation, reticulocyte volume fell during the aplastic phase after conditioning chemotherapy and then rapidly increased up to values higher than before; this production of macroreticulocytes was the earliest sign of engraftment.
173 citations
TL;DR: In this new method for studying the shape recovery of deformed red blood cells, three optical traps induce a parachute-shaped red cell deformation, which is comparable to the deformation in small capillaries.
149 citations
TL;DR: Results strongly suggest that a member of the chondroitin-glycosaminoglycan family, CSA, represents an additional receptor used by P. falciparum PRBC to cytoadhere to microvascular endothelial cells.
139 citations
TL;DR: Examination of the amino acid sequence and Wrb antigen expression of GPA-related hybrid glycophorins suggests that Arg61 of GPA interacts with Glu658 of band 3 to form the Wr(a+b-) antigen.
122 citations
TL;DR: A transformed bovine peritoneal macrophage cell line was developed and characterized and showed non-specific esterase activity, suggesting that this cell line should be useful to study interactions between the bovines and intracellular pathogens.
118 citations
TL;DR: It is suggested that the R760Q substitution, and probably the other arginine subsitutions, produce band 3 deficiency either by precluding incorporation of the mutant protein into the red blood cell membrane or by leading to loss of mutant protein from differentiating erythroid precursors.
TL;DR: Results indicate that L1 can remove pathologic deposits of chelatable iron from thalassemic and sickle RBC membranes, a therapeutic potential not shared by DFO.
Patent•
02 Feb 1995TL;DR: In this article, a modified secretable erythropoietin (SSEI) protein was used to regulate the growth and differentiation of red blood cell progenitors.
Abstract: DNA encoding modified, secretable erythropoietin proteins whose ability to regulate the growth and differentiation of red blood cell progenitors are different from the wildtype recombinant erythropoietin and to methods of modifying or altering the regulating activity of a secretable erythropoietin and using modified secretable erythropoietin proteins.
TL;DR: The data suggest that cord blood nucleated red blood cells could assist in the timing of fetal neurologic injury, and in general, the closer the birth was to the asphyxial event, the lower was the number of nucleatedred blood cells.
TL;DR: A simple accumulation of mutations in hematopoietic stem cells over time may explain the age-dependent increase in the frequency of glycophorin A mutants, but a balance between mutant cell generation and loss should be taken into account for the mechanism of the increase of T-cell mutations.
Abstract: Using either the colony formation assay or flow cytometry, it is feasible to measure the frequency of rare mutant lymphocytes or erythrocytes in human peripheral blood Accordingly, we have investigated the mutant cell frequencies of the hypoxanthine-guanine phosphoribosyltransferase and T-cell receptor genes in T lymphocytes and of the glycophorin A gene in erythrocytes of several hundred persons aged 0-96 years The mutant frequency of every one of these genes increased significantly with age A simple accumulation of mutations in hematopoietic stem cells over time may explain the age-dependent increase in the frequency of glycophorin A mutants In contrast, a balance between mutant cell generation and loss should be taken into account for the mechanism of the increase of T-cell mutations
TL;DR: The data suggest that a mechanism for adaptation to oxidative conditions may be present in CAPD and its effects on RBC integrity are discussed in comparison with the hemodialysis conditions previously studied.
Journal Article•
TL;DR: The coexistence of new cell formation in the bone marrow and failure of cells to be released into the blood is consistent with ineffective erythropoiesis, and it is concluded that the initial adaptation is a reduction in PV resulting in plethora.
Journal Article•
TL;DR: It seems likely that oxidation processes and accumulation of malondialdehyde can contribute directly to changes in the properties of ¿diabetic¿ red blood cells and may cause the development of long-term complications.
Abstract: The oxidation processes in normal and diabetic erythrocytes after cell exposure to H2O2 and t-butyl hydroperoxide, as well as the effect of malondialdehyde (a stable end product of lipid peroxidation) on erythrocyte membrane structure and stability were studied. The malondialdehyde level began to increase only after oxidation of most of the red blood cell glutathione by peroxides. The activation energy of malondialdehyde was 53 +/- 7 kj/mol. Sodium azide inhibited the oxidation processes induced by t-butyl hydroperoxide. The modification of erythrocytes by malondialdehyde decreased the fluidity of the membrane lipid bilayer measured by fluorescence anisotropy and increased the osmotic stability of the cells. The level of endogenous thiobarbituric acid-reactive species was higher and antioxidative activity was lower in diabetic cells. It seems likely that oxidation processes and accumulation of malondialdehyde can contribute directly to changes in the properties of ?diabetic? red blood cells and may cause the development of long-term complications.
TL;DR: The results reveal that HRPRP act as a new type of peroxidase supported by Trx/TR system in human RBC.
TL;DR: The anemia caused by IL-6 is caused by an increase in plasma volume, and simple regression analysis indicated that the decrease in hematocrit level and increase in Plasma volume were related.
TL;DR: Single human red blood cells, in which the hemoglobin molecules exist in their native, tetrameric states, were analyzed and the amounts of glycated Hb and total Hb in a given cell were found to be uncorrelated.
TL;DR: Fluorescent-labeled erythrocytes provide unique and reliable qualitative and quantitative data about pancreatic microcirculatory changes, thereby improving intravital analysis of blood flow in pancreatic exchange capillaries.
TL;DR: To determine the mechanism of action by which angiotensin-converting enzyme (ACE) inhibitors lower hematocrit in patients with posttransplant erythrocytosis, indices of red blood cell production andred blood cell destruction were obtained serially for 6 months from 10 renal transplant patients receiving treatment with enalapril for this problem.
TL;DR: Human and murine blood cells treated with ZnCl2 and bis(sulfosuccinimidyl)suberate (BS3) (a cross linking agent) undergo band 3 clustering and binding of hemoglobin to red blood cell membrane proteins, thus favouring the phagocytosis of Zn Clay treated cells by macrophages.
Abstract: Human and murine blood cells treated with ZnCl2 and bis(sulfosuccinimidyl)suberate (BS3) (a cross linking agent) undergo band 3 clustering and binding of hemoglobin to red blood cell membrane proteins. These clusters induce autologous IgG binding and complement fixation, thus favouring the phagocytosis of ZnCl2/BS3 treated cells by macrophages. The extension of red blood cell opsonization can be easily modulated by changing the ZnCl2 concentration in the 0.1–1.0 mM range thus providing an effective way to affect blood cell recognition by macrophages. In fact, murine erythrocytes treated with increasing ZnCl2 concentrations have proportionally reduced survivals when reinjected into the animal. Furthermore, the organ sequestration of ZnCl2/BS3 treated cells strongly resembles the typical distribution of the senescent cells. Since the ZnCl2/BS3 treatment can also be performed on red blood cells loaded with drugs or other substances, this procedure is an effective drug-targeting system to be used for the delivery of molecules to peritoneal, liver and spleen macrophages.
TL;DR: These results are the first documentation that human red blood cells contain ACBP and that this protein can affect the utilization of acyl-CoA in plasma membranes of these cells.
Abstract: Acyl-CoA-binding protein (ACBP) has been identified in a number of tissues and shown to affect the intracellular distribution and utilization of acyl-CoA. We have detected ACBP in the cytosol but not the membrane of human red blood cells and, using an e.l.i.s.a. with antibodies prepared against human liver ACBP, found that its concentration was 0.5 microM. To investigate the role of ACBP in human red blood cells, we added purified human liver ACBP and radiolabelled acyl-CoA to isolated membranes from these cells. ACBP prevented high concentrations of acyl-CoA from binding to the membrane but could not keep the acyl-CoA in the aqueous phase at low concentrations. This suggested the presence of a pool in the membrane with a binding affinity for acyl-CoA that was greater than that of ACBP for acyl-CoA. In the presence of lysophospholipid, this membrane-bound pool of acyl-CoA was rapidly used as a substrate by acyl-CoA:lysophospholipid acyltransferase (LAT) to generate phospholipid from lysophospholipid. We also found that ACBP-bound acyl-CoA was preferred over free acyl-CoA as a substrate by LAT. These results are the first documentation that human red blood cells contain ACBP and that this protein can affect the utilization of acyl-CoA in plasma membranes of these cells. The interactions between acyl-CoA, ACBP and the membrane suggest that there are several pools of acyl-CoA in the human red blood cell and that ACBP may have a role in regulating their distribution and fate.
TL;DR: It is suggested that viremia occurs during the acute phase of infection, the virus is present in various organs and there the virus gene is transiently expressed, and the virus enters the blood stream possibly through capillaries of the infected alveolar wall.
TL;DR: It is suggested that, in the rabbit lung, NO is a determinant of PVR in the presence of blood, and that aspect of blood that permits the generation of NO appears to be related to the RBC and not to perfusate viscosity.
Abstract: Nitric oxide (NO) is produced by and relaxes pulmonary arteries and veins; however, a role for NO as a participant in the control of pulmonary vascular resistance (PVR) remains to be defined. Here we investigated the hypothesis that for NO to serve as a determinant of PVR in the rabbit requires the presence of blood. In isolated blood-perfused rabbit lungs, NG-nitro-L-arginine methyl ester (L-NAME, 100 microM) increased PVR and the slope of the pressure-flow relationship. These effects of L-NAME were prevented by pretreatment with L-arginine. In contrast, in lungs perfused with a physiological salt solution, L-NAME had no effect on PVR or the pressure-flow relationship. The addition of washed red blood cells (RBCs) to physiological salt solution, but not the addition of plasma and platelets, restored the response to L-NAME. This effect of RBCs was not reproduced by increasing perfusate viscosity with dextran. These results suggest that, in the rabbit lung, NO is a determinant of PVR in the presence of blood. Moreover, that aspect of blood that permits the generation of NO appears to be related to the RBC and not to perfusate viscosity.
TL;DR: It is shown that chemical cross-linking resulting in alpha-DBBF induces an increased tendency to form ferryl radical in the presence of H2O2 and stabilizes the radical once formed.
TL;DR: Six commercial red blood cell lysing methods were investigated for possible leukocyte permeabilization effect and only one method was applicable for complete permeabilizations of leukocytes and for detection of intracellular antigens alone or simultaneously with the cell surfaceAntigens.
Abstract: When analyzing leukocyte cell surface antigens by flow cytometry, leukocytes are usually first labeled in whole blood and the red blood cells are finally lysed with lysing solutions. The erythrocytes are lysed, but the leukocytes are expected to remain intact. Six commercial red blood cell lysing methods were investigated for possible leukocyte permeabilization effect. The effectiveness of permeabilization was studied by propidium iodide staining, and the detectability of intracellular antigens was studied by using monoclonal antibodies toward two model antigens. Most of the lysing methods caused permeabilization of at least part of the leukocytes, but only one method, already found in our previous studies, was applicable for complete permeabilization of leukocytes and for detection of intracellular antigens alone or simultaneously with the cell surface antigens.
TL;DR: In this paper, the authors measured serum and red blood cell magnesium levels in juvenile migraine patients with and without aura interictally, and found that they had significantly lower levels of magnesium compared with normal subjects.
Abstract: Recently an important role for magnesium in establishing the threshold for migraine attacks has become evident. Accordingly, we measured serum and red blood cell magnesium levels in juvenile migraine patients with and without aura interictally. In comparison with normal subjects, migraineurs had significantly lower serum and red blood cell magnesium levels.