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Journal articles on the topic 'RBC destruction'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Alfrey, C. P., M. M. Udden, C. Leach-Huntoon, T. Driscoll, and M. H. Pickett. "Control of red blood cell mass in spaceflight." Journal of Applied Physiology 81, no. 1 (1996): 98–104. http://dx.doi.org/10.1152/jappl.1996.81.1.98.

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The effect of spaceflight on red blood cell mass (RBCM), plasma volume (PV), erythron iron turnover, serum erythropoietin, and red blood cell (RBC) production and survival and indexes were determined for six astronauts on two shuttle missions, 9 and 14 days in duration, respectively. PV decreased within the first day. RBCM decreased because of destruction of RBCs either newly released or scheduled to be released from the bone marrow. Older RBCs survived normally. On return to Earth, plasma volume increased, hemoglobin concentration and RBC count declined, and serum erythropoietin increased. We

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2

Chadebech, Philippe, Marc Michel, Daniel Janvier та ін. "IgA-mediated human autoimmune hemolytic anemia as a result of hemagglutination in the spleen, but independent of complement activation and FcαRI". Blood 116, № 20 (2010): 4141–47. http://dx.doi.org/10.1182/blood-2010-03-276162.

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Abstract Autoimmune hemolytic anemia (AIHA) due to warm-acting IgA autoantibodies is rare. We explored the pathogenic mechanisms underlying destruction of red blood cells (RBCs) in a patient with severe AIHA mediated exclusively by polymeric immunoglobulin A (pIgA) anti-Band 3 autoantibodies. The follow-up period was 17 months. RBCs were not destroyed by complement activation as no deposition of complement was observed on the patient's RBCs. pIgA eluted from the patient's RBCs did not induce RBC destruction through phagocytosis by monocytes or antibody–dependent cell–mediated cytotoxicity by n

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3

Wouters, Diana, Stephan Femke, Masja de Haas, et al. "C1-Inhibitor Rescues Red Blood Cells From Complement Mediated Destruction in Autoimmune Hemolytic Anemia." Blood 118, no. 21 (2011): 716. http://dx.doi.org/10.1182/blood.v118.21.716.716.

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Abstract Abstract 716 In autoimmune hemolytic anemia (AIHA) autoantibodies (auto-Ab's) to red blood cells (RBCs) may induce complement activation via the classical pathway of complement resulting in complement deposition on RBCs. RBCs coated with auto-Ab and/or complement (C3b) are removed by extravascular destruction in the spleen and liver. In a minority of cases complement activation proceeds until insertion of the membrane attack complex (MAC) resulting in intravascular hemolysis. The inflammatory response and the anoxia induced by hemolysis significantly contribute to the morbidity and fa

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4

Allhorn, Maria, Juana G. Briceño, Lucie Baudino, et al. "The IgG-specific endoglycosidase EndoS inhibits both cellular and complement-mediated autoimmune hemolysis." Blood 115, no. 24 (2010): 5080–88. http://dx.doi.org/10.1182/blood-2009-08-239020.

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Abstract EndoS from Streptococcus pyogenes is an immunomodulating enzyme that specifically hydrolyzes glycans from human immunoglobulin G and thereby affects antibody effector functions. Autoimmune hemolytic anemia is caused by antibody-mediated red blood cell (RBC) destruction and often resists treatment with corticosteroids that also cause frequent adverse effects. We show here that anti-RhD (anti-D) and rabbit anti–human-RBC antibodies (anti-RBC) mediated destruction of RBC, ie, phagocytosis, complement activation, and hemolysis in vitro and in vivo was inhibited by EndoS. Phagocytosis by m

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5

Angus, Brian J., Kesinee Chotivanich, Rachanee Udomsangpetch, and Nicholas J. White. "In Vivo Removal of Malaria Parasites From Red Blood Cells Without Their Destruction in Acute Falciparum Malaria." Blood 90, no. 5 (1997): 2037–40. http://dx.doi.org/10.1182/blood.v90.5.2037.

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Abstract During acute falciparum malaria infection, red blood cells (RBC) containing abundant ring-infected erythrocyte surface antigen (Pf 155 or RESA), but no intracellular parasites, are present in the circulation. These RESA-positive parasite negative RBC are not seen in parasite cultures in vitro. This indicates that in acute falciparum malaria there is active removal of intraerythrocytic parasites by a host mechanism in vivo (probably the spleen) without destruction of the parasitized RBC. This may explain the observed disparity between the drop in hematocrit and decrease in parasite cou

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Zidova, Zuzana, Daniel Garcia-Santos, Katarina Kapralova, et al. "Oxidative Stress and Increased Destruction of Red Blood Cells Contribute to the Pathophysiology of Anemia Caused By DMT1 Deficiency." Blood 124, no. 21 (2014): 4027. http://dx.doi.org/10.1182/blood.v124.21.4027.4027.

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Abstract Inactivating mutations in divalent metal transporter 1 (DMT1) are associated with a severe defect in erythroid iron utilization and cause moderate to severe hypochromic microcytic anemia in human patients and two rodent models. We have previously shown that DMT1 deficiency impairs erythroid differentiation, induces apoptosis of erythroid precursors and causes the suppression of colony-forming capacity of erythroid progenitors. Using in vitro cultures of fetal liver cells we were able to recapitulate this in vivo defect. We confirmed abnormal pattern of erythroid differentiation and in

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7

Ashikaga, Kohei, Marco Alfonso Perrone, Antonio Gianfelici, et al. "Reticulocyte Count and Exercise Performance in Elite Athletes: A Retrospective Study." Sports 13, no. 6 (2025): 169. https://doi.org/10.3390/sports13060169.

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Athletes engaged in dynamic sports experience a shortened red blood cell (RBC) lifespan and accelerated turnover due to RBC destruction. This accelerated RBC turnover might have a positive impact on exercise performance by increasing the number of young red blood cells with a high oxygen-carrying capacity. However, accelerated turnover might also be a result of intravascular haemolysis caused by RBC destruction during exercise, impairing RBC function and oxygen transport. Therefore, we aimed to evaluate the relationship between reticulocyte count as an indicator of short-term RBC profile chang

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8

Arias, Clemente Fernandez, and Cristina Fernandez Arias. "How do red blood cells know when to die?" Royal Society Open Science 4, no. 4 (2017): 160850. http://dx.doi.org/10.1098/rsos.160850.

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Human red blood cells (RBCs) are normally phagocytized by macrophages of splenic and hepatic sinusoids at 120 days of age. The destruction of RBCs is ultimately controlled by antagonist effects of phosphatidylserine (PS) and CD47 on the phagocytic activity of macrophages. In this work, we introduce a conceptual model that explains RBC lifespan as a consequence of the dynamics of these molecules. Specifically, we suggest that PS and CD47 define a molecular algorithm that sets the timing of RBC phagocytosis. We show that significant changes in RBC lifespan described in the literature can be expl

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9

Vercaemst, Leen. "Hemolysis in Cardiac Surgery Patients Undergoing Cardiopulmonary Bypass: A Review in Search of a Treatment Algorithm." Journal of ExtraCorporeal Technology 40, no. 4 (2008): 257–67. http://dx.doi.org/10.1051/ject/200840257.

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Hemolysis is a fact in all extracorporeal circuits, as shown in various studies by the increasing levels of plasma-free hemoglobin (PfHb) and decreasing levels of haptoglobin during and after cardiopulmonary bypass (CPB). Beside complete red blood cell (RBC) destruction or hemolysis, RBCs can also be damaged on a sublethal level, resulting in altered rheological properties. Increased levels of free RBC constituents together with an exhaust of their scavengers result in a variety of serious clinical sequela, such as increased systemic and pulmonary vascular resistance, altered coagulation profi

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10

Yazdanbakhsh, Karina, Stanley Kang, Daniel Tamasauskas, Dorothy Sung, and Andromachi Scaradavou. "Complement receptor 1 inhibitors for prevention of immune-mediated red cell destruction: potential use in transfusion therapy." Blood 101, no. 12 (2003): 5046–52. http://dx.doi.org/10.1182/blood-2002-10-3068.

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AbstractActivation of complement cascade via the antibody-mediated classical pathway can initiate red blood cell (RBC) destruction, causing transfusion reactions and hemolytic anemia. In the present study, we have assessed the ability of a human recombinant soluble form of complement receptor 1 (sCR1) to inhibit complement-mediated RBC destruction in vitro and in vivo. Using an in vitro alloimmune incompatibility model, sCR1 inhibited complement activation and prevented hemolysis. Following transfusion of human group O RBCs into mice lacking detectable pre-existing antibodies against the trans

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11

Ahn, Kyu-Hong, and Jae-Soo Chang. "Performance Evaluation of Compact RBC-Settling Tank System." Water Science and Technology 23, no. 7-9 (1991): 1467–76. http://dx.doi.org/10.2166/wst.1991.0599.

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A laboratory study was conducted to investigate the performance of RBC-Settling tank system on wastewater treatment in comparison with conventional RBC. The same synthetic wastewater was fed parallel into four stage laboratory scale cascade-connected RBC-Settling tank and conventional RBC reactors at a fixed rotational speed and hydraulic loading. At three different organic loading rates of 6.14, 13.44 and 23.31 g SCOD/m2/day, the results of the systems are presented in terms of ammonia nitrogen (NH3-N), total kjeldahl nitrogen (TKN), organic and suspended solids (SS) loading and removal. Disk

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12

Weiss, D. J., and J. S. Klausner. "Neutrophil-induced Erythrocyte Injury: A Potential Cause of Erythrocyte Destruction in the Anemia Associated with Inflammatory Disease." Veterinary Pathology 25, no. 6 (1988): 450–55. http://dx.doi.org/10.1177/030098588802500608.

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Activated neutrophils at effector/target ratios of 1:20 to 1:2,000 induced depletion of red blood cell (RBC)-reduced glutathione, increased membrane-bound hemoglobin and methemoglobin, and promoted immunoglobulin binding to the cell membrane. Superoxide dismutase/catalase ameliorated the decrease in reduced glutathione and the increase in methemoglobin and immunoglobulin binding. This is interpreted as evidence that activated neutrophils can alter the antigenic nature of the RBC membrane through generation of toxic oxygen radicals.

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13

Kiran Kumar Reddy, Y. Ravi, Saiprasad Onkareshwar Kavthekar, Narahari Venkata Susmitha, Nivedita Balasaheb Patil, Priti Kamble, and Chilukuru J. Satyamani Deepika. "Mefenamic acid triggered autoimmune hemolytic anemia in a child: a rare case report." International Journal of Contemporary Pediatrics 10, no. 10 (2023): 1587–89. http://dx.doi.org/10.18203/2349-3291.ijcp20232889.

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Autoimmune hemolytic anemia (AIHA) is characterized by the abnormal production of antibodies that bind to antigens on the surface of red blood cells (RBC), resulting in RBC destruction. Here we describe a rare case of mefenamic acid-induced AIHA in a 3-year-old boy who developed acute hemolysis after ingestion of mefenamic acid for febrile illness. The aim is to draw the attention of pediatricians to one of the side effects of mefenamic acid, the drug which is very commonly used as an antipyretic.

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14

Alnnasouri, M., C. Dagot, and M. N. Pons. "Comparison of four methods to assess biofilm development." Water Science and Technology 63, no. 3 (2011): 432–39. http://dx.doi.org/10.2166/wst.2011.239.

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Two nondestructive methods of biofilm quantification (optical density via a flatbed scanner and biofilm thickness) have been evaluated and compared to two destructive methods (Crystal Violet staining after biofilm disintegration and dry weight). The methods were tested on biofilms that developed on a modified rotating biological contactor (RBC) that was inoculated with urban wastewater and fed with a synthetic medium that mimicked slaughterhouse wastewater. The results of the different methods were highly correlated (coefficient of correlation greater than 0.8). This validation experiment conf

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15

Rock, E., E. Gueux, A. Mazur, C. Motta, and Y. Rayssiguier. "Anemia in copper-deficient rats: role of alterations in erythrocyte membrane fluidity and oxidative damage." American Journal of Physiology-Cell Physiology 269, no. 5 (1995): C1245—C1249. http://dx.doi.org/10.1152/ajpcell.1995.269.5.c1245.

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This study was designed to make precise the nature and the mechanism of the anemia induced by dietary copper (Cu) deficiency. Male Wistar rats were pair fed from weanling for 6 wk either a Cu-deficient or a control diet. The reduced red blood cell (RBC) 51Cr survival indicates an increased destruction of RBC during Cu deficiency. 1,6-Diphenyl-1,3,5-hexatriene fluorescence polarization studies revealed an increase in the fluidity of erythrocyte membranes from deficient rats. The reduced cholesterol-to-phospholipid ratio was consistent with the increased fluidity. Other results indicate an incre

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16

Jordan, Michael B., Nico van Rooijen, Shozo Izui, John Kappler, and Philippa Marrack. "Liposomal clodronate as a novel agent for treating autoimmune hemolytic anemia in a mouse model." Blood 101, no. 2 (2003): 594–601. http://dx.doi.org/10.1182/blood-2001-11-0061.

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Autoimmune hemolytic anemia (AIHA) is a disease in which autoantibodies against red blood cells (RBCs) lead to their premature destruction. Most clinically significant autoantibodies are of the immunoglobulin G (IgG) type, which leads primarily to the uptake and destruction of RBCs by splenic and hepatic macrophages. Therapies such as corticosteroids and splenectomy are directed at interfering with this process. Liposomally encapsulated clodronate (dichloromethylene diphosphonate) has previously been found to be a potent antimacrophage agent. It selectively depletes animals of macrophages with

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17

Smith, John A., David T. Martin, Richard D. Telford, and Samir K. Ballas. "Greater erythrocyte deformability in world-class endurance athletes." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 6 (1999): H2188—H2193. http://dx.doi.org/10.1152/ajpheart.1999.276.6.h2188.

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Because athletes during endurance events require rapid uptake of oxygen, the ability of red blood cells (RBC) to move through capillaries may limit performance. Using ektacytometry, we determined whether RBC deformability (RCD) differed between elite road cyclists ( n = 9) and sedentary controls ( n = 5). Density profiles and standard hematological measurements were also performed. The deformability index (DI) was higher in the cyclists (0.723 ± 0.027) compared with that in controls (0.619 ± 0.040, P < 0.001). Cyclists also had a larger percentage of low-density RBCs ( P < 0.001), and me

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18

Morelli, A., M. Grasso, T. Meloni, G. Forteleoni, E. Zocchi, and A. De Flora. "Favism: impairment of proteolytic systems in red blood cells." Blood 69, no. 6 (1987): 1753–58. http://dx.doi.org/10.1182/blood.v69.6.1753.1753.

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Abstract Red blood cells (RBC) from favic patients are characterized by (a) severe oxidative damage (contributed by autoxidation of divicine and isouramil, two pyrimidine aglycones present in fava beans) and (b) greatly increased calcium levels. In vitro, both autoxidation of divicine and calcium loading produced marked alterations of proteolytic systems in intact RBC. Specifically, autoxidizing divicine inactivated procalpain, the proenzyme species of calcium-activated cytosolic neutral proteinase, or calpain. Inactivation was much greater with glucose-6-phosphate dehydrogenase (G6PD)-deficie

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Morelli, A., M. Grasso, T. Meloni, G. Forteleoni, E. Zocchi, and A. De Flora. "Favism: impairment of proteolytic systems in red blood cells." Blood 69, no. 6 (1987): 1753–58. http://dx.doi.org/10.1182/blood.v69.6.1753.bloodjournal6961753.

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Red blood cells (RBC) from favic patients are characterized by (a) severe oxidative damage (contributed by autoxidation of divicine and isouramil, two pyrimidine aglycones present in fava beans) and (b) greatly increased calcium levels. In vitro, both autoxidation of divicine and calcium loading produced marked alterations of proteolytic systems in intact RBC. Specifically, autoxidizing divicine inactivated procalpain, the proenzyme species of calcium-activated cytosolic neutral proteinase, or calpain. Inactivation was much greater with glucose-6-phosphate dehydrogenase (G6PD)-deficient RBC th

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20

Hathaway, T. K., J. L. Adams, and C. Heckman. "Evaluation of erythrocyte membranes by immunocytochemical techniques following the transfusion of incompatible blood." Proceedings, annual meeting, Electron Microscopy Society of America 46 (1988): 378–79. http://dx.doi.org/10.1017/s0424820100103954.

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The hemolytic transfusion reaction (HTR) is the most formidable complication in blood transfusion therapeutics. Immune clearance and destruction of red blood cells (RBC) following infusion of incompatible blood have generally been thought to involve opsonic proteins, i.e., immunoglobulins (IgG, IgM) and complement. Fibronectin (FN), a multifunctional plasma and tissue protein, participates in many significant biological and pathophysiological activities and has opsonic characteristics. Plasma fibronectin (PFN) has been associated with acute HTR and the use of dogs as effective models for HTR r

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21

Thomas, T. H., C. Mason, and K. M. Illingworth. "Changing effects on erythrocyte sodium and potassium during the development of chronic renal failure with anaemia in rats." Clinical Science 71, no. 6 (1986): 639–46. http://dx.doi.org/10.1042/cs0710639.

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1. Rats were studied 7 days and 17 days after the onset of renal failure which was induced by a surgical technique. 2. Plasma urea, creatinine (PCr) and potassium had increased after 7 days; plasma potassium increased much more after 17 days but PCr was slightly lower. 3. Renal failure caused resetting of erythropoietic control to a lower level of packed cell volume (PCV). After 7 days renal failure some rats had a low PCV, whereas others still had a normal PCV apparently due to slower erythrocyte destruction of pre-renal failure cells. 4. After 7 days renal failure, rats with a normal PCV had

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Barker, JE, and EC McFarland-Starr. "Marrow transplantation in the treatment of a murine heritable hemolytic anemia." Blood 73, no. 7 (1989): 2014–17. http://dx.doi.org/10.1182/blood.v73.7.2014.2014.

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Abstract Mice with hemolytic anemia, sphha/sphha, have extremely fragile RBCs with a lifespan of approximately one day. Neither splenectomy nor simple transplantation of normal marrow after lethal irradiation cures the anemia but instead causes rapid deterioration and death of the mutant unless additional prophylactic procedures are used. In this report, we show that normal marrow transplantation preceded by sublethal irradiation increases but does not normalize RBC count. The mutant RBCs but not all the WBCs are replaced by donor cells. Splenectomy of the improved recipient causes a dramatic

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23

Barker, JE, and EC McFarland-Starr. "Marrow transplantation in the treatment of a murine heritable hemolytic anemia." Blood 73, no. 7 (1989): 2014–17. http://dx.doi.org/10.1182/blood.v73.7.2014.bloodjournal7372014.

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Mice with hemolytic anemia, sphha/sphha, have extremely fragile RBCs with a lifespan of approximately one day. Neither splenectomy nor simple transplantation of normal marrow after lethal irradiation cures the anemia but instead causes rapid deterioration and death of the mutant unless additional prophylactic procedures are used. In this report, we show that normal marrow transplantation preceded by sublethal irradiation increases but does not normalize RBC count. The mutant RBCs but not all the WBCs are replaced by donor cells. Splenectomy of the improved recipient causes a dramatic decrease

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24

Li, Jiu-Hong, Jun-Feng Luo, Ying Jiang, et al. "Red Blood Cell Lifespan Shortening in Patients with Early-Stage Chronic Kidney Disease." Kidney and Blood Pressure Research 44, no. 5 (2019): 1158–65. http://dx.doi.org/10.1159/000502525.

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Background: Although reduced red blood cell (RBC) lifespan has been reported to be a contributory factor to anemia in patients with end-stage chronic kidney disease (CKD), there are limited data regarding RBC lifespan in early-stage CKD. Serum erythropoietin (EPO) is considered a primary causative factor of renal anemia. The aims of this study were to compare the RBC lifespan, serum EPO levels, and other renal anemia indicators across CKD-stage groups of patients and to analyze the impacts of etiological factors on renal anemia. Methods: A cohort of 74 non-smoking patients with CKD were enroll

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25

Olgun, Abdullah, Serif Akman, and M. Kemal Erbil. "The role of RBC destruction in vascular regions with high turbulence on atherosclerosis." Medical Hypotheses 63, no. 2 (2004): 283–84. http://dx.doi.org/10.1016/j.mehy.2004.02.034.

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26

Barroso, Tiago, Leila Costa, Lisa Gonçalves, et al. "CDK4/6 Inhibitors-Induced Macrocytosis Is Not Associated with Hemolysis and Does Not Impact Hemoglobin Homeostasis." Cancers 17, no. 9 (2025): 1567. https://doi.org/10.3390/cancers17091567.

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Background: CDK 4/6 inhibitors (CDK4/6is) are the first-line treatment for metastatic luminal-like breast cancer (BC). These drugs induce macrocytosis without anemia in most patients. The mechanism for the red blood cell (RBC) changes is unknown. In vitro and animal studies show that RBCs from CDK6-knockout mice have increased membrane fragility, but the clinical impact of CDK4/6is on human RBC lifespan is not known. We sought to determine the impact of CDK4/6is on RBC lifespan and detect changes in the regulation of hemoglobin production. Using the mean corpuscular volume (MCV) measurements a

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27

Sloand, Elaine M., Jaroslaw P. Maciejewski, Daniel Dunn, et al. "Correction of the PNH Defect by GPI-Anchored Protein Transfer." Blood 92, no. 11 (1998): 4439–45. http://dx.doi.org/10.1182/blood.v92.11.4439.

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Abstract Hemolytic anemia is a major feature of paroxysmal nocturnal hemoglobinuria (PNH). Intravascular red blood cell (RBC) destruction is caused by increased sensitivity of the abnormal erythrocyte to complement-mediated lysis, due to the GPI absence of a membrane-bound glycosylphosphatidylinositol (GPI)-linked protein, which functions as an inhibitor of reactive lysis (CD59). Both in vivo and in vitro models have suggested the feasibility of cell-to-cell transfer of GPI proteins, and patients with hemolysis could potentially benefit from transfer of CD59 to their deficient erythrocytes. We

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Sloand, Elaine M., Jaroslaw P. Maciejewski, Daniel Dunn, et al. "Correction of the PNH Defect by GPI-Anchored Protein Transfer." Blood 92, no. 11 (1998): 4439–45. http://dx.doi.org/10.1182/blood.v92.11.4439.423k24_4439_4445.

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Hemolytic anemia is a major feature of paroxysmal nocturnal hemoglobinuria (PNH). Intravascular red blood cell (RBC) destruction is caused by increased sensitivity of the abnormal erythrocyte to complement-mediated lysis, due to the GPI absence of a membrane-bound glycosylphosphatidylinositol (GPI)-linked protein, which functions as an inhibitor of reactive lysis (CD59). Both in vivo and in vitro models have suggested the feasibility of cell-to-cell transfer of GPI proteins, and patients with hemolysis could potentially benefit from transfer of CD59 to their deficient erythrocytes. We studied

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29

Hoca, Emre, Fatma Pınar Ziyadanoğlu, Atay Can Kula, and Hayriye Esra Ataoğlu. "Cold agglutinin disease related mismatch between hematocrit and hemoglobin values." International Journal Of Community Medicine And Public Health 7, no. 2 (2020): 770. http://dx.doi.org/10.18203/2394-6040.ijcmph20200465.

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Autoimmune hemolytic anemia is a disease characterized by destruction of red blood cells (RBC) and anemia, caused by production of antibodies released against the body’s own RBCs. While this condition is more commonly idiopathic, it may accompany autoimmune diseases as well. Cold agglutinin disease (CAD) is a rare subtype of acquired autoimmune hemoliytic anemia, however, is an idiosyncratic clinical and pathological terminology, usually seen in older ages. This condition is caused by IgM antibodies called “cold agglutinins” formed against I antigens on RBC membranes which cause agglutination

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d’Agostino, Chiara, Andre Dejam, Mildred Pelletier, Nathawut Sibmooh, Fabiola Rizzatti, and Alan N. Schechter. "Nitrite Ion Fluxes in Human Erythocytes." Blood 106, no. 11 (2005): 3731. http://dx.doi.org/10.1182/blood.v106.11.3731.3731.

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Abstract Our recent studies suggest that nitrite ions serve as a storage pool of nitric oxide (NO•) bioactivity, with reduction of nitrite to NO• within red blood cells (RBC), thus potentially explaining endocrine effects of NO•. We have investigated nitrite uptake and decay in human RBC using recently described methodologies based on assaying after stabilization of nitrite to reaction with hemoglobin by treatment with ferricyanide and quantificating by reductive chemiluminescence. Uptake of nitrite added to whole blood is very rapid (sec) and independent of temperature (from 4°C to 37°C) and

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31

Westerman, Maxwell, Arnold Pizzey, Jocelyn Hirschman, et al. "Plasma Hemoglobin: Potential Sources." Blood 108, no. 11 (2006): 3814. http://dx.doi.org/10.1182/blood.v108.11.3814.3814.

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Abstract Plasma hemoglobin(Hb) is a measure of circulating red blood cell(RBC) destruction and is considered to be the basic indicator of intravascular hemolysis. We have examined the effects of splenectomy on levels of plasma Hb and circulating RBC-derived vesicles in patients with thalassemia intermedia (TI) and compared the results to patients with sickle cell anemia (SCA). Plasma Hb levels in splenectomized patients with TI were 48.5 ± 3.7 mg/ml (5)(Mn ± SEM)(No.of patients) and vesicle levels were 11.29 ± 1.12 x 10 3 /ul blood (9). In contrast, plasma Hb levels in patients with SCA were (

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32

Mohamed, Liban Ali, Osman Yazicioglu, and Oguz Borat. "Design of Blood Supply Chain and Application to Marmara Region in Turkey." European Journal of Engineering Research and Science 4, no. 3 (2019): 27–36. http://dx.doi.org/10.24018/ejers.2019.4.3.1179.

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Blood transfusion is needed due to operations, diseases or accidents. Millions of people's health depends on the success of their blood transfusion. Planning and management is required to supply blood, test against diseases, produce blood products, store t hem and transport them to hospitals. A blood supply chain network design such as Blood Donation Centers (CBM), Regional Blood Centers (RBC), Destruction Centers (DM), and hospitals are addressed. To formulate the problem, the General Algebraic Modeling System (GAMS) software was applied to the Mixed Integer Model. When the number of RBC in M

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Mohamed, Liban Ali, Osman Yazicioglu, and Oguz Borat. "Design of Blood Supply Chain and Application to Marmara Region in Turkey." European Journal of Engineering and Technology Research 4, no. 3 (2019): 27–36. http://dx.doi.org/10.24018/ejeng.2019.4.3.1179.

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Blood transfusion is needed due to operations, diseases or accidents. Millions of people's health depends on the success of their blood transfusion. Planning and management is required to supply blood, test against diseases, produce blood products, store t hem and transport them to hospitals. A blood supply chain network design such as Blood Donation Centers (CBM), Regional Blood Centers (RBC), Destruction Centers (DM), and hospitals are addressed. To formulate the problem, the General Algebraic Modeling System (GAMS) software was applied to the Mixed Integer Model. When the number of RBC in M

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34

Vasievich, Matthew, Bin Zhang, Jesse Rinehart, Morgan Jones, Ivan Maillard, and David Ginsburg. "Sec23b deficiency In Mice Results In Pancreatic Destruction and Defective long Term Hematopoietic Stem Cell Function." Blood 116, no. 21 (2010): 2038. http://dx.doi.org/10.1182/blood.v116.21.2038.2038.

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Abstract Abstract 2038 Congenital Dyserythropoietic Anemia type II (CDAII) is an autosomal recessive disorder caused by mutations in the gene SEC23B. SEC23B is a component of the COPII coat complex that transports proteins from the endoplasmic reticulum (ER) to the Golgi apparatus. CDAII is characterized by mild to moderate anemia and >10% bi- or multi- nucleate erythroblasts in the bone marrow. We generated Sec23b deficient mice (Sec23b gt/gt) from ES cells with a genetrap cassette inserted into the last intron of Sec23b. Sec23b gt/gt mice die at birth with destruction of the exocrine panc

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35

Addiego, Joseph E., Deborah Hurst, and Bertram H. Lubin. "Congenital Hemolytic Anemia." Pediatrics In Review 6, no. 7 (1985): 201–8. http://dx.doi.org/10.1542/pir.6.7.201.

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Anemia due to premature destruction of RBCs is classified as hemolytic, and may be secondary to acquired or inherited (congenital) abnormalities in RBC membrane, hemoglobin, or metabolism. This article reviews the topic of congenital hemolytic anemias and points out a practical approach to diagnosis and therapy. PATHOPHYSIOLOGY The primary function of RBCs is to transport oxygen from the lungs to the tissues. The normal RBC circulates within the vascular system for about 120 days. Survival to its full life span depends upon effective metabolism of glucose to generate high-energy phosphates suc

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Hair, Pamela S., Kenji M. Cunnion, and Neel K. Krishna. "Peptide Inhibitor of Complement C1 Inhibits the Peroxidase Activity of Hemoglobin and Myoglobin." International Journal of Peptides 2017 (September 10, 2017): 1–10. http://dx.doi.org/10.1155/2017/9454583.

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Hemoglobin is the natural carrier of oxygen in red blood cells (RBCs). While intracellular hemoglobin provides life-sustaining oxygen transport, extracellular free hemoglobin displays toxicity due to inherent peroxidase activity generating reactive oxygen species that subsequently react with the hemoglobin molecule to produce toxic heme degradation products resulting in free radicals, oxidative stress damage, and lipid peroxidation. We have recently demonstrated that Peptide Inhibitor of Complement C1 (PIC1) inhibits peroxidase activity of the heme-based enzyme myeloperoxidase. To elucidate wh

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Dean, Melinda M., Ju Ji, YuanTong Gu, Emilie Sauret, and Robert L. Flower. "Visualising interaction of monocytes with red blood cells (RBC) sensitised with “clinically significant” antibodies." Journal of Immunology 202, no. 1_Supplement (2019): 58.16. http://dx.doi.org/10.4049/jimmunol.202.supp.58.16.

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Abstract Background Anti-RBC antibodies in plasma are regarded as clinically significant when they promote clearance of transfused RBC by monocytes/macrophages. To date, processes involved in the attachment or phagocytosis of sensitised RBC by monocytes have been investigated using light or fluorescent microscopy. We used scanning electron microscopy (SEM) to facilitate a closer examination of the interaction between monocytes and RBCs sensitised with antibodies of specificities classified as clinically significant. Methods Peripheral blood mononuclear cells (PBMC) were seeded onto glass cover

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Fibach, Eitan, Johnny Amer, Eliezer Rachmilewitz, Ella Guy, and Stefano Rivella. "Oxidative Stress of RBC in a Murine Model of Beta-Thalassemia Can Be Reversed by Treatment with Antioxidants." Blood 106, no. 11 (2005): 3643. http://dx.doi.org/10.1182/blood.v106.11.3643.3643.

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Abstract Oxidative stress is a prominent contributor to the premature destruction of RBC as well as anemia in thalassemia and sickle cell anemia. The oxidative status within RBC is maintained by the balance between oxidative systems, such as Reactive Oxygen Species (ROS), and antioxidative systems, such as reduced glutathione (GSH). Using flow cytometric methods, we previously showed that RBC obtained from patients with thalassemia (Amer et al. Eur J Haematol70:84,2003; Cytometry60:73,2004) or sickle cell anemia (Amer et al. Blood, 104:972a,2004) exhibit oxidative stress. In the present study,

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Aubin, Eric, Renée Bazin та Réal Lemieux. "Inhibition of IL-1β and TNFα Gene Expression by IVIg or Anti-Red Blood Cell Antibodies in a Mouse Model of ITP." Blood 106, № 11 (2005): 2186. http://dx.doi.org/10.1182/blood.v106.11.2186.2186.

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Abstract Plasma-derived human IgG (IVIg) have been used for more than 2 decades for the treatment of several autoimmune diseases such as ITP, even if their mechanism of action is still not fully understood. Recently, several studies with IVIg-treated patients have shown that IVIg can modulate the serum level of both pro-inflammatory and anti-inflammatory cytokines. In ITP, it is known that the destruction of autoantibody-coated platelets occurs mainly in the spleen. We thus used a mouse model of ITP to evaluate the modulatory effects of IVIg on the expression of several cytokine genes in the s

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Szymanski, Irma O., and Sharyn L. Orton. "Since the Process of Transfusion-Induced Alloimmunization Is Not Harmless, Can We Mitigate It?" Blood 124, no. 21 (2014): 5101. http://dx.doi.org/10.1182/blood.v124.21.5101.5101.

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Abstract Transfusion protocols have remained unchanged for decades. Accordingly, it is necessary to avoid transfusion reactions by giving patients ABO- and irregular antibody-compatible red blood cells (RBC). Prevention of immunization to the Rh antigen D is also required since anti-D may cause a serious hemolytic disease of fetus and newborn. Prevention of transfusion-induced immunization to other blood group antigens is neither required nor feasible for the general transfused population. We consider the process of alloimmunization to be harmful due to the following untoward effects: 1) Destr

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Menakuru, Sasmith R., Adelina Priscu, Vijaypal Dhillon, and Ahmed Salih. "Acute Hyperhemolysis Syndrome in a Patient with Known Sickle Cell Anemia Refractory to Steroids and IVIG Treated with Tocilizumab and Erythropoietin: A Case Report and Review of Literature." Hematology Reports 14, no. 3 (2022): 235–39. http://dx.doi.org/10.3390/hematolrep14030032.

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Patients with sickle cell anemia often receive multiple red blood cell (RBC) transfusions during their lifetime. Hyperhemolysis is a life-threatening phenomenon of accelerated hemolysis and worsening anemia that occurs when both transfused RBCs and autologous RBCs are destroyed. The level of hemoglobin post-transfusion is lower than pre-transfusion levels, and patients are usually hemodynamically unstable. Hyperhemolysis must be differentiated from a delayed hemolytic transfusion reaction during which destruction of transfused RBC is the cause of anemia. Hyperhemolysis syndrome can be differen

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Bauer, Milton C., Douglas J. Weiss, and Victor Perman. "Hematologic alterations in adult cats fed 6 or 12% propylene glycol." American Journal of Veterinary Research 53, no. 1 (1992): 69–72. http://dx.doi.org/10.2460/ajvr.1992.53.01.69.

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Summary Cat foods containing propylene glycol (pg) induce Heinz body formation in feline erythrocytes. To further study the hematologic importance of dietary pg, 21 adult cats were allotted to 3 groups of 7 each and fed diets containing 0,6, or 12% pg on a dry-weight basis. Cats fed pg had a dose-related increase in Heinz bodies within 2 weeks, and the increase persisted throughout the study. Although only slight changes occurred in pcv, hemoglobin concentration, and rbc count, punctate reticulocytes were significantly increased in the group fed 12% pg. Mean rbc survival was decreased in the g

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Osterloh, Kurt, Peter Gaehtgens, and Axel R. Pries. "Determination of microvascular flow pattern formation in vivo." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 4 (2000): H1142—H1152. http://dx.doi.org/10.1152/ajpheart.2000.278.4.h1142.

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Blood flow in microvessels differs significantly from that of red blood cells (RBC) flowing through long, straight glass tubes in vitro. The in vivo situation is characterized by the presence of plasma favoring aggregation, by the irregular geometry of vessel segments, and by frequent branching points. Here, a method is presented to characterize flow patterns in microvascular blood flow during intravital microscopy based on Fourier analysis of recorded light intensity patterns. The interpretation of the resulting power spectra in terms of pattern size distribution was validated by model experi

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Fibach, Eitan, and Eliezer A. Rachmilewitz. "Pathophysiology and treatment of patients with beta-thalassemia – an update." F1000Research 6 (December 20, 2017): 2156. http://dx.doi.org/10.12688/f1000research.12688.1.

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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) or β-globin chains (β-thal) that compose the major adult hemoglobin (α2β2).It is caused by one or more mutations in the corresponding genes. The unpaired globin chains are unstable; they precipitate intracellularly, resulting in hemolysis, premature destruction of red blood cell [RBC] precursors in the bone marrow, and a short life-span of mature RBCs in the circulation. The state of anemia is treated by frequent RBC transfusion

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Mayer, Balázs, Krisztián Németh, Miklós Krepuska, et al. "Vasopressin stimulates the proliferation and differentiation of red blood cell precursors and improves recovery from anemia." Science Translational Medicine 9, no. 418 (2017): eaao1632. http://dx.doi.org/10.1126/scitranslmed.aao1632.

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Arginine vasopressin (AVP) made by hypothalamic neurons is released into the circulation to stimulate water resorption by the kidneys and restore water balance after blood loss. Patients who lack this antidiuretic hormone suffer from central diabetes insipidus. We observed that many of these patients were anemic and asked whether AVP might play a role in red blood cell (RBC) production. We found that all three AVP receptors are expressed in human and mouse hematopoietic stem and progenitor cells. The AVPR1B appears to play the most important role in regulating erythropoiesis in both human and

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Newton, Paul N., Kesinee Chotivanich, Wirongrong Chierakul, et al. "A comparison of the in vivo kinetics of Plasmodium falciparum ring–infected erythrocyte surface antigen–positive and –negative erythrocytes." Blood 98, no. 2 (2001): 450–57. http://dx.doi.org/10.1182/blood.v98.2.450.

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Ring-infected erythrocyte surface antigen (RESA)-positive,Plasmodium falciparum–negative red blood cells (RBCs) are cells from which the malaria parasite has been removed by the host without the destruction of the erythrocyte (“pitting”). The survival of RESA-RBCs in vivo was assessed in 14 severe and 6 uncomplicated falciparum malaria patients. The mean RESA-RBC life of 183 hours (95% confidence interval [CI], 136-246) was longer than the median parasite clearance time of 66 hours (range, 30-108 hours) but shorter than the mean red cell life of 1027 hours (95% CI, 840-1213) (P = .0004), with

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Arthur, Connie M., Amanda Mener, Seema Patel, et al. "Reticuloendothelial Saturation Dictates the Development of RBC Resistance to Antibody-Mediated Clearance Following Incompatible Transfusion." Blood 124, no. 21 (2014): 1559. http://dx.doi.org/10.1182/blood.v124.21.1559.1559.

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Abstract Background: Immune-mediated destruction of red blood cells (RBCs) normally occurs following incompatible transfusion, however some RBCs may remain in circulation after initial cellular clearance despite the presence of RBC specific antibodies. Recent studies suggest that antibody-induced “antigen-modulation” may in part be responsible for this cellular resistance to antibody-mediated removal following the initial phase of RBC clearance. However, the factors that dictate whether cells undergo clearance or antigen modulation immediately following incompatible RBC transfusion remain unkn

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Iida, K., M. B. Whitlow, and V. Nussenzweig. "Membrane vesiculation protects erythrocytes from destruction by complement." Journal of Immunology 147, no. 8 (1991): 2638–42. http://dx.doi.org/10.4049/jimmunol.147.8.2638.

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Abstract Nucleated cells can resist attack by C by exocytosis or endocytosis of the terminal C components C5b-9 (membrane attack complex) (MAC), but it is generally accepted that formation of a single MAC channel on E leads to lysis (one-hit theory). We find that human and guinea pig E, but not SRBC, can eliminate the MAC from the membrane in the form of microvesicles and escape destruction. When guinea pig or human E are incubated with C5b-9, vesiculation proceeds without a lag and is detected at nonlytic doses of C9. Continuous Ca2+ influx is required for vesiculation. The amount of released

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Ataga, Kenneth I., Wally R. Smith, Laura M. De Castro, et al. "Efficacy and safety of the Gardos channel blocker, senicapoc (ICA-17043), in patients with sickle cell anemia." Blood 111, no. 8 (2008): 3991–97. http://dx.doi.org/10.1182/blood-2007-08-110098.

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Abstract Senicapoc, a novel Gardos channel inhibitor, limits solute and water loss, thereby preserving sickle red blood cell (RBC) hydration. Because hemoglobin S polymerization is profoundly influenced by intracellular hemoglobin concentration, senicapoc could improve sickle RBC survival. In a 12-week, multicenter, phase 2, randomized, double-blind, dose-finding study, we evaluated senicapoc's safety and its effect on hemoglobin level and markers of RBC hemolysis in sickle cell anemia patients. The patients were randomized into 3 treatment arms: placebo; low-dose (6 mg/day) senicapoc; and hig

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Cho, Young-Ho, Sechan Youn, and Dong Woo Lee. "Bio-Inspired Cell Concentration and Deformability Monitoring Chips." Journal of Nanoscience and Nanotechnology 7, no. 11 (2007): 4214–19. http://dx.doi.org/10.1166/jnn.2007.001.

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The paper presents a couple of biofluidic devices, whose functions are inspired from biological cell concentration and deformability monitoring functions. The cell concentration monitoring chip is inspired from RBC control mechanism in kidney, performing cell concentration monitoring functions. The cell deformability chip, inspired from selective RBC destruction mechanism in spleen, performs mechanical cell deformability monitoring functions. The structures and principles of the bio-inspired chips are presented and compared with those of the biological organs. The unique features and performan

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