Academic literature on the topic 'Diseased red cell'
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Journal articles on the topic "Diseased red cell"
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Yang, Lan, Shiqi Huang, Zhirong Zhang, Zhenmi Liu, and Ling Zhang. "Roles and Applications of Red Blood Cell-Derived Extracellular Vesicles in Health and Diseases." International Journal of Molecular Sciences 23, no. 11 (May 25, 2022): 5927. http://dx.doi.org/10.3390/ijms23115927.
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Red blood cell-derived extracellular vesicles (RBCEVs) are vesicles naturally produced by red blood cells and play multiple roles such as acting as cell-to-cell communication messengers in both normal physiological and diseased states. RBCEVs are highly promising delivery vehicles for therapeutic agents such as biomolecules and nucleic acids as they are easy to source, safe, and versatile. RBCEVs autonomously target the liver and pass the blood–brain barrier into the brain, which is highly valuable for the treatment of liver and brain diseases. RBCEVs can be modified by various functional units, including various functional molecules and nanoparticles, to improve their active targeting capabilities for tumors or other sites. Moreover, the RBCEV level is significantly shifted in many diseased states; hence, they can also serve as important biomarkers for disease diagnoses. It is clear that RBCEVs have considerable potential in multiple medical applications. In this review, we briefly introduce the biological roles of RBCEVs, presented interesting advances in RBCEV applications, and discuss several challenges that need to be addressed for their clinical translation.
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CHEN, YONG, JIYE CAI, and JINGXIAN ZHAO. "DISEASED RED BLOOD CELLS STUDIED BY ATOMIC FORCE MICROSCOPY." International Journal of Nanoscience 01, no. 05n06 (October 2002): 683–88. http://dx.doi.org/10.1142/s0219581x02000899.
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In recent years, many mammalian cells, especially erythrocytes because of simpleness of their membrane surfaces, were widely studied by atomic force microscopy. In our study, diseased erythrocytes were taken from patients of lung cancer, myelodisplastic syndrome (MDS), and so on. We obtained many clear topographical images of numerous erythrocytes, single erythrocyte, and ultramicrostructure of erythrocyte membrane surfaces from normal persons and patients. By studying the red cells of lung cancer patients, we found that many erythrocytes of lung cancer patient have changed into echinocytes. One erythrocyte has 10–20 short projections, most of which, with a mean width of 589.0 nm and a length of 646.7 nm, are on the edge of cell. The projections in the center of echinocytes are lodged and embedded, but in conventional model of echinocytes, the projections in the center stretch outside cell membrane, so a novel model of erythrocytes was designed in our paper. After observation of microstructure of MDS patient's erythrocyte membrane surface, we found that many apertures with different diameters of tens to hundreds nanometers appeared on the surface of cell membrane. It can be concluded that AFM may be widely applied in clinic pathological inspection.
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Mattè, Alessandro, Enrica Federti, Elena Tibaldi, Maria Luisa Di Paolo, Giovanni Bisello, Mariarita Bertoldi, Andrea Carpentieri, et al. "Tyrosine Phosphorylation Modulates Peroxiredoxin-2 Activity in Normal and Diseased Red Cells." Antioxidants 10, no. 2 (February 1, 2021): 206. http://dx.doi.org/10.3390/antiox10020206.
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Peroxiredoxin-2 (Prx2) is the third most abundant cytoplasmic protein in red blood cells. Prx2 belongs to a well-known family of antioxidants, the peroxiredoxins (Prxs), that are widely expressed in mammalian cells. Prx2 is a typical, homodimeric, 2-Cys Prx that uses two cysteine residues to accomplish the task of detoxifying a vast range of organic peroxides, H2O2, and peroxynitrite. Although progress has been made on functional characterization of Prx2, much still remains to be investigated on Prx2 post-translational changes. Here, we first show that Prx2 is Tyrosine (Tyr) phosphorylated by Syk in red cells exposed to oxidation induced by diamide. We identified Tyr-193 in both recombinant Prx2 and native Prx2 from red cells as a specific target of Syk. Bioinformatic analysis suggests that phosphorylation of Tyr-193 allows Prx2 conformational change that is more favorable for its peroxidase activity. Indeed, Syk-induced Tyr phosphorylation of Prx2 enhances in vitro Prx2 activity, but also contributes to Prx2 translocation to the membrane of red cells exposed to diamide. The biologic importance of Tyr-193 phospho-Prx2 is further supported by data on red cells from a mouse model of humanized sickle cell disease (SCD). SCD is globally distributed, hereditary red cell disorder, characterized by severe red cell oxidation due to the pathologic sickle hemoglobin. SCD red cells show Tyr-phosphorylated Prx2 bound to the membrane and increased Prx2 activity when compared to healthy erythrocytes. Collectively, our data highlight the novel link between redox related signaling and Prx2 function in normal and diseased red cells.
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Aoki, T., and T. Inoue. "Glycophorin in red blood cell membranes of healthy and diseased carp, Cyprinus carpio L." Journal of Fish Diseases 34, no. 7 (May 18, 2011): 573–76. http://dx.doi.org/10.1111/j.1365-2761.2011.01262.x.
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Li, He, Lu Lu, Xuejin Li, Pierre A. Buffet, Ming Dao, George E. Karniadakis, and Subra Suresh. "Mechanics of diseased red blood cells in human spleen and consequences for hereditary blood disorders." Proceedings of the National Academy of Sciences 115, no. 38 (September 6, 2018): 9574–79. http://dx.doi.org/10.1073/pnas.1806501115.
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In red blood cell (RBC) diseases, the spleen contributes to anemia by clearing the damaged RBCs, but its unique ability to mechanically challenge RBCs also poses the risk of inducing other pathogenic effects. We have analyzed RBCs in hereditary spherocytosis (HS) and hereditary elliptocytosis (HE), two typical examples of blood disorders that result in membrane protein defects in RBCs. We use a two-component protein-scale RBC model to simulate the traversal of the interendothelial slit (IES) in the human spleen, a stringent biomechanical challenge on healthy and diseased RBCs that cannot be directly observed in vivo. In HS, our results confirm that the RBC loses surface due to weakened cohesion between the lipid bilayer and the cytoskeleton and reveal that surface loss may result from vesiculation of the RBC as it crosses IES. In HE, traversing IES induces sustained elongation of the RBC with impaired elasticity and fragmentation in severe disease. Our simulations thus suggest that in inherited RBC disorders, the spleen not only filters out pathological RBCs but also directly contributes to RBC alterations. These results provide a mechanistic rationale for different clinical outcomes documented following splenectomy in HS patients with spectrin-deficient and ankyrin-deficient RBCs and offer insights into the pathogenic role of human spleen in RBC diseases.
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Wilkes, Mark C., Aya Shibuya, and Kathleen M. Sakamoto. "Signaling Pathways That Regulate Normal and Aberrant Red Blood Cell Development." Genes 12, no. 10 (October 19, 2021): 1646. http://dx.doi.org/10.3390/genes12101646.
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Blood cell development is regulated through intrinsic gene regulation and local factors including the microenvironment and cytokines. The differentiation of hematopoietic stem and progenitor cells (HSPCs) into mature erythrocytes is dependent on these cytokines binding to and stimulating their cognate receptors and the signaling cascades they initiate. Many of these pathways include kinases that can diversify signals by phosphorylating multiple substrates and amplify signals by phosphorylating multiple copies of each substrate. Indeed, synthesis of many of these cytokines is regulated by a number of signaling pathways including phosphoinositide 3-kinase (PI3K)-, extracellular signal related kinases (ERK)-, and p38 kinase-dependent pathways. Therefore, kinases act both upstream and downstream of the erythropoiesis-regulating cytokines. While many of the cytokines are well characterized, the nuanced members of the network of kinases responsible for appropriate induction of, and response to, these cytokines remains poorly defined. Here, we will examine the kinase signaling cascades required for erythropoiesis and emphasize the importance, complexity, enormous amount remaining to be characterized, and therapeutic potential that will accompany our comprehensive understanding of the erythroid kinome in both healthy and diseased states.
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Nayani, Karthik, Arthur A. Evans, Saverio E. Spagnolie, and Nicholas L. Abbott. "Dynamic and reversible shape response of red blood cells in synthetic liquid crystals." Proceedings of the National Academy of Sciences 117, no. 42 (October 2, 2020): 26083–90. http://dx.doi.org/10.1073/pnas.2007753117.
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Mammalian cells are soft, and correct functioning requires that cells undergo dynamic shape changes in vivo. Although a range of diseases are associated with stiffening of red blood cells (RBCs; e.g., sickle cell anemia or malaria), the mechanical properties and thus shape responses of cells to complex viscoelastic environments are poorly understood. We use vapor pressure measurements to identify aqueous liquid crystals (LCs) that are in osmotic equilibrium with RBCs and explore mechanical coupling between RBCs and LCs. When transferred from an isotropic aqueous phase into a LC, RBCs exhibit complex yet reversible shape transformations, from initially biconcave disks to elongated and folded geometries with noncircular cross-sections. Importantly, whereas the shapes of RBCs are similar in isotropic fluids, when strained by LC, a large variance in shape response is measured, thus unmasking cell-to-cell variation in mechanical properties. Numerical modeling of LC and cell mechanics reveals that RBC shape responses occur at constant cell membrane area but with membrane shear moduli that vary between cells from 2 to 16 × 10−6N/m. Temperature-dependent LC elasticity permits continuous tuning of RBC strains, and chemical cross-linking of RBCs, a model for diseased cells, leads to striking changes in shape responses of the RBCs. Overall, these results provide insight into the coupling of strain between soft mammalian cells and synthetic LCs, and hint at new methods for rapidly characterizing mechanical properties of single mammalian cells in a population and thus cell-to-cell variance.
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Li, He, Dimitrios Papageorgiou, Hung-Yu Chang, Lu Lu, Jun Yang, and Yixiang Deng. "Synergistic Integration of Laboratory and Numerical Approaches in Studies of the Biomechanics of Diseased Red Blood Cells." Biosensors 8, no. 3 (August 10, 2018): 76. http://dx.doi.org/10.3390/bios8030076.
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In red blood cell (RBC) disorders, such as sickle cell disease, hereditary spherocytosis, and diabetes, alterations to the size and shape of RBCs due to either mutations of RBC proteins or changes to the extracellular environment, lead to compromised cell deformability, impaired cell stability, and increased propensity to aggregate. Numerous laboratory approaches have been implemented to elucidate the pathogenesis of RBC disorders. Concurrently, computational RBC models have been developed to simulate the dynamics of RBCs under physiological and pathological conditions. In this work, we review recent laboratory and computational studies of disordered RBCs. Distinguished from previous reviews, we emphasize how experimental techniques and computational modeling can be synergically integrated to improve the understanding of the pathophysiology of hematological disorders.
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Polák, J., M. Jokes, and Marie Ulrychová. "Cell wall disintegration consistently found in tissues of reversion diseased red currant cv. Heinemann’s rote spätlesse." Biologia Plantarum 27, no. 6 (November 1985): 462–64. http://dx.doi.org/10.1007/bf02894718.
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Prodanovic, Radisa, Ivan Vujanac, Danijela Kirovski, Vojin Ivetic, Bozidar Savic, Milenko Zutic, Branislav Kureljusic, and Oliver Radanovic. "Paratuberculosis in breeding stock of red Holstein cows." Veterinarski glasnik 65, no. 3-4 (2011): 179–90. http://dx.doi.org/10.2298/vetgl1104179p.
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This paper describes paratuberculosis in an isolated breeding herd of 25 high-yield dairy cows of the Red Holstein breed. The animals were examined clinically and then given the test for ldelayed type hypersensitivity and their blood serum was examined for the presence of specific antibodies against Mycobacterium avium subsp. paratuberculosis (Map). The clinical examination revealed that two cows exhibited symptoms of the disease that indicated an advanced stage of paratuberculosis. The following parameters were examined in the blood of the cows that showed clinical signs of the disease: leukocytes and erythrocytes count, concentrations of total proteins, albumin, iron, sodium, potassium, and activity of creatine kinase. The analysis of the red blood cell count revealed certain digressions that indicated the existence of hypochromic microcytic anaemia. The number of leukocytes was within the physiological values, but the neutrophil-lymphocyte ratio was disrupted and stood at almost 1:1. The results of the biochemical analyses of the blood serum of diseased cows indicated hypoproteinaemia, hypoalbuminaemia, hypoferremia, hyposodiumaemia, hypokalemia, and increased activities of creatine kinase enzymes. A suspect reaction on the site of application of avian tuberculin was determined in two animals. Animals with clinical signs of the disease reacted negative to the test of delayed type hypersensitivity. The presence of specific antibodies against the cause of paratuberculosis was proven in four animals (16%), including two animals with clinical signs of the disease and one that had a suspect reaction on the site of application of avian tuberculin. Furthermore, one animal that died exhibited macroscopic and microscopic changes regarding the intensity and distribution of lesions, the type of cellular infiltrate, and the number of present acidresistent bacteria, and the changes were characterized as diffuse changes of multibacillary type. The cause of bovine paratuberculosis was isolated from the altered organs.
Dissertations / Theses on the topic "Diseased red cell"
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Cytlak, Urszula Malgorzata. "Phosphatidylserine exposure in red blood cells from patients with sickle cell disease." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708601.
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Barber, Latorya Arnold. "The Activity of Lipid Transport Proteins in Normal and Sickle Red Blood Cells." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1243353188.
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Al, Balushi Halima. "Novel approach towards pathogenesis and treatment of sickle cell disease." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/288739.
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Sickle cell disease (SCD) is one of the most common genetic diseases worldwide. HbS polymerisation causes altered red blood cell (RBC) rheology and fragility, increase in blood viscosity with blockage of small blood vessels, and RBC membrane permeability changes. Excessive levels of cell-free Hb, high autoxidation of Hb, contribute to the production of reactive oxygen species (ROS) in SCD patients. In this work, oxidants showed direct and indirect effects on the main cation permeability pathways involved in dehydration of HbS/S RBCs - Psickle, the Gardos channel and the KCl cotransporter (KCC) - and thus on RBC volume causing polymersation. Psickle and Gardos channel activities showed significant correlation, consistent with the hypothesis that Ca2+ entry via Psickle causes activation of the Ca2+-dependent K+ channel. Treatment of SCD remains inadequate relying on the blood transfusion and supportive therapy depending on the organ affected. In the present study antioxidants and aromatic aldehydes showed some promising results towards future alternative treatments for SCD. Antioxidants showed inhibitory effects on the cation permeability pathways leading to inhibition of polymerisation and haemolysis and thus maintained RBC volume. Aromatic aldehydes interact with HbS and are usually given to increase oxygen affinity, thereby reducing its tendency to polymerise. GBT1118 had a marked inhibitory effect on all three cation permeability pathways. It reduced sickling, Psickle and Gardos activity. It inhibited KCC by affecting the regulatory protein phosphorylation cascade. It maintained RBC hydration, and stabilised RBCs. Historically Oman was the principal trading port of the Persian Gulf region, resulting in the complex mix of social and ethnic backgrounds. In 1989 a second mutation in the β chain of Hb, at position β121 was found in an Omani patient in addition to the usual HbS mutation at the β6 position, and termed HbS-Oman. At low percentage of HbS-Oman patients show severe SCD symptoms. Despite RBCs containing at most 25% HbS-Oman, there was high sickling percentage and K+ permeability showed many features similar to those seen in homozygous HbS/S patients. The presence of α thalassaemia was protective and represents an obvious potential prognostic marker for this rare SCD genotype. Overall, the present work contributes to elucidation of the pathogenesis of SCD, suggests approaches to the development of novel therapies and increases our understanding of a rare SCD genotype, HbS-Oman.
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Lizarralde, Iragorri Maria. "Impact of mechanical and oxidative stress on red blood cell properties in sickle cell disease." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCC324.
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Le globule rouge est une cellule simple avec l’une des fonctions les plus importantes de l’organisme : participer aux échanges gazeux et fournir l’oxygène aux tissus. C'est un disque biconcave hautement élastique grâce à un réseau de protéines du cytosquelette et de protéines membranaires spécifiques. La fonction, ainsi que la structure des globules rouges sont altérées dans plusieurs pathologies humaines telles que les hémoglobinopathies et les anomalies de membrane. La drépanocytose est une maladie héréditaire génétique caractérisée par une hémoglobine anormale qui polymérise en conditions hypoxiques provoquant la déformation des globules rouges circulants. La drépanocytose se caractérise également par une anémie hémolytique chronique et des crises vaso-occlusives douloureuses dues à l'obstruction des capillaires.Dans le but de mieux comprendre les mécanismes responsables des manifestations cliniques, nous avons étudié les propriétés mécaniques et adhésives des globules rouges de patients atteints de drépanocytose en évaluant 1) l'impact de contraintes mécaniques répétées sur la survie des globules rouges à l'aide d'un appareil microfluidique qui mime la microcirculation et 2) le rôle du stress oxydant dans l'activation des protéines d'adhérence érythroïde.Nous avons conçu une puce microfluidique et montré que le stress mécanique est un paramètre critique sous-jacent à l'hémolyse intravasculaire dans la drépanocytose et que des taux intracellulaires élevés d'hémoglobine fœtale préviennent cette lyse. Outre ces résultats, nous avons constaté que le traitement à l'hydroxyurée protège les globules rouges de la lyse lors d'un stress mécanique, même en l'absence d'expression de l'hémoglobine fœtale. D'autre part, nous avons étudié la structure et la fonction de la protéine d'adhérence érythroïde Lu/BCAM dans des conditions oxydantes en utilisant des approches biochimiques et d'imagerie. Nous avons observé que le stress oxydant active la fonction adhésive de Lu/BCAM par des modifications post-traductionnelles qui modifient sa distribution membranaire. Nous décrivons un nouveau mécanisme qui affecte les interactions en cis de Lu/BCAM à la surface cellulaire et qui pourraient expliquer l'adhérence anormale des globules rouges à la laminine en l'absence d'événements de phosphorylation.En conclusion, nous avons développé un modèle microfluidique reproduisant les dimensions physiologiques des microvaisseaux humains, permettant d’évaluer les caractéristiques cellulaires jusque-là inexplorées dans la drépanocytose. Nous montrons que le stress mécanique répété est en partie responsable de l'hémolyse chez les patients atteints d'anémie falciforme, ce qui pourrait contribuer aux niveaux élevés de stress oxydant en raison de l'hème libre dans la circulation. Nos travaux démontrent l'importance de la dimension mécanique dans l’obstruction des capillaires et la contribution critique du stress oxydant dans l'adhérence anormale des globules rouges dans cette maladie. Améliorer la déformabilité des globules rouges et cibler le stress oxydant pour inhiber l'adhérence des globules rouges serait une stratégie prometteuse pour cibler les principales caractéristiques de cette pathologie et alléger le fardeau de la maladieThe red blood cell is a simple cell with one of the most important functions in the organism, that is fulfilling the gas exchange function and delivering oxygen to the tissues. It is a highly elastic biconcave disk thanks to a network of specific skeletal and membrane proteins. The function and structure of the red cell are altered in several human pathologies like hemoglobinopathies and membrane disorders. Sickle cell disease is a genetic hereditary disorder characterized by abnormal hemoglobin that polymerizes under hypoxic conditions leading to the sickling and alteration of circulating red cells. The hallmarks of sickle cell disease are hemolytic anemia and painful vaso-occlusive crises due to the obstruction of fine capillaries.With the aim of better understanding the mechanisms behind these clinical manifestations we investigated the mechanical and adhesive properties of red blood cells from patients with sickle cell disease by assessing 1) the impact of repeated mechanical stress on red cell survival using a microfluidic device that mimic human microcirculation, and 2) the role of oxidative stress in the activation of erythroid adhesion proteins.We designed a microfluidic device that allowed us to show that mechanical stress is a critical parameter underlying intravascular hemolysis in sickle cell disease and that high intracellular levels of fetal hemoglobin protect against lysis. Furthermore, we found that treatment with hydroxyurea protects red blood cells from lysis upon mechanical stress even in the absence of fetal hemoglobin expression. On the other hand, we investigated the structure and function of the erythroid adhesion protein Lu/BCAM under oxidative conditions using biochemical and imaging approaches. We observed that oxidative stress activates the adhesive function of Lu/BCAM through post-translational modifications that alter its membrane distribution. We describe a novel mechanism that affects Lu/BCAM cis-interactions at the cell surface that might account for the abnormal adhesion of sickle red cells to laminin in the absence of phosphorylation events.In conclusion, we developed a microfluidic device replicating the physiological dimensions of human microvessels that allows assessing previously unexplored cellular characteristics in sickle cell disease. We show that repeated mechanical stress is partly responsible for hemolysis in patients with sickle cell disease, which might contribute to the high levels of oxidative stress because of free heme in the circulation. Our work demonstrates the importance of the mechanical dimension in the blockade of small capillaries and the critical contribution of oxidative stress in the abnormal adhesion of red cells in this disease. Improving red cell deformability and targeting oxidative stress to inhibit red cell adhesion would be promising strategies to target the main hallmarks of this pathology and alleviate the disease burden
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Simionato, Greta [Verfasser]. "The influence of hypoxia in erythropoiesis and morphology of red blood cells in sickle cell disease and hereditary spherocytosis. / Greta Simionato." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2020. http://d-nb.info/1221599666/34.
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Boa-Amponsem, Kwame Jr. "Genetics, humoral immunoresponsiveness, and disease resistance in chickens." Diss., Virginia Tech, 1998. http://hdl.handle.net/10919/30580.
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Lines of White Leghorn chickens selected > 20 generations for (HA) and against (LA) antibody response to SRBC injected i.v. from 41 to 51 days of age, are now known to have diverged in primary antibody response to SRBC. Experiments described in this dissertation were designed to further evaluate the immune competence of these lines as influenced by age, diet, and a disease agent. A crossing experiment was also conducted to further describe the mode of inheritance of such competence.
Humoral immunocompetence was evaluated by primary, memory, and maternal antibody responses to SRBC. Primary antibody response, measured 5, 10, and 20 days after inoculation with SRBC was greater in HA than LA chicks inoculated at 14, 21, and 28 days of age. In chicks injected at 7 days of age, a higher frequency of responders was observed for HA than LA chicks suggesting an earlier onset of immunocompetence in the high than low antibody line.
Immunological memory antibody responses (secondary and tertiary) was studied in parallel experiments on two groups of chicks hatched at a 14-day interval. Chicks in both hatches were from the same matings of parental Lines HA and LA. Memory responses were evident in chicks at 14 days of age. Antibody responses to a second and third inoculation with SRBC were similar for both lines suggesting that genetic factors that influence primary and memory responses are not the same. The responses of LA chicks to repeat inoculations with SRBC were anamnestic whereas those of HA chicks initially inoculated at 28 days of age were not anamnestic. This study did not establish any major influence of nutrient density on either primary or memory immune responses even though the higher nutrient density diet improved growth performance.
Assays in chicks indicated that maternal antibodies were transferred earlier into eggs laid by HA hens than in those of LA hens ( 7 to 9 days vs 10 to 12 days after inoculation) regardless of dosage administered. Response patterns whether assessed in terms of frequency of detection or magnitude of response showed divergence between the lines.
Chicks of parental, reciprocal F , F , and backcrosses of 1 2 mating combinations of Lines HA and LA were injected with SRBC at 36 days of age. Contrasts between parental lines for antibody titers measured 5 and 12 days later showed higher antibody titers in HA than LA chicks. Sex-linked effects were evident because reciprocal contrasts for F crosses, individual heterosis, and 1 maternal heterosis were sex dependent.
Response to marble spleen disease virus ( MSDV) measured 6 days after inoculation of chicks from parental, reciprocal F1, F2, and backcross matings of the lines, indicated that the mode of inheritance of spleen weight differed after infection. In the infected chicks, parental contrasts for absolute and relative spleen weights showed greater resistance to MSDV in LA than HA chicks. No other genetic effect was consistently important after infection.Ph. D.
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Panknin, Christina Monika [Verfasser]. "Characterization of red blood cell functions in health and coronary artery disease / Christina Monika Panknin." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2017. http://d-nb.info/1136421815/34.
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Kucukal, Erdem. "BIOMIMETIC MICROFLUIDIC PLATFORMS FOR MONITORING CELLULAR INTERACTIONS IN MICROSCALE FLOW." Case Western Reserve University School of Graduate Studies / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=case1576231265150031.
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Claveria, Pizarro Viviana Andrea. "Flow of healthy and sickle red blood cells in microcirculatory conditions : clustering process and self-margination phenomenon." Thesis, Montpellier, 2017. http://www.theses.fr/2017MONTS081/document.
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J'ai caractérisé expérimentalement la formation de clusters au cours du passage de globules rouges (GRs) sains et drépanocytaires dans microcapillaires droites. L'effet de l'agrégation a été également étudié. J'ai montré que la formation des clusters dans des conditions physiologiques est due à la combinaison des interactions hydrodynamiques et des celles causées par les macromolécules du plasma. En effet, les interactions macromoléculaires ne sont pas complètement atténuées sous contraintes de cisaillement physiologiques et au contraire ils contribuent à la stabilité des clusters. En outre, j'ai découvert la présence d’une distribution bimodale en ce qui concerne les distances entre les cellules constituant les clusters hydrodynamiques.En plus, j'ai étudié expérimentalement le comportement collectif des globules rouges drépanocytaires oxygénés et leur distribution radiale le long de microcapillaires cylindriques avec un diamètre comparable à ces des veinules et des artérioles humaines. J'ai trouvé que les GRs montrent une distribution hétérogène en fonction de leur densité: les cellules plus légères ont tendance à rester prés du centre du canal, alors que la plupart des cellules denses (et aussi plus rigides) auto-marginent sous des conditions définies. L'agrégation semble d'inhiber l'auto-margination en fonction des patients et en particuliers des facteurs d’agrégation: le dextrane, par exemple, favorise l'auto-margination dans certains patients et il la diminue dans des autres. Le plasma montre de contraster l'auto-margination des GRs dans tous les sujets, en soulignant l'importance des protéines et des molécules adhésives du plasma dans les phénomènes d'agrégation. Finalement, j'ai observé que l'auto-margination se manifeste naturellement au cours de l’écoulement de globules rouges drépanocytairesI experimentally characterized the clustering formation of healthy and sickle red blood cells (RBCs) flowing through straight micro-capillaries. The effect of aggregation was also investigated. I found that cluster formation under physiological conditions is most likely caused by a combination of hydrodynamic and macromolecule-induced interactions. Macromolecule-induced interactions are not fully overcome by shear stresses within the physiological range, and they contribute to cluster stability. Moreover, I found that a pronounced bimodal distribution of the cell-to-cell distances in the hydrodynamic clusters is produced.Additionally, I investigated experimentally the collective behavior of oxygenated sickle RBCs and their distribution along cylindrical micro-capillaries with diameters comparable to a human venule or arteriole. I have shown that there is a heterogeneous distribution of RBCs according to their density: low-density cells tend to stay closer to the center of the channel, while most dense cells (also more rigid) self-marginated under defined conditions. Aggregation seems to inhibit self-margination depending on the aggregative factor and patient: dextran allows self-margination in some patients and inhibits it in others. Plasma inhibits self-margination of cells in all cases, highlighting the importance of the plasma proteins and adhesive molecules in the aggregation phenomena
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El, Hoss Sara. "Novel insights into the role of fetal hemoglobin in spleen function, red cell survival and ineffective erythropoiesis in sickle cell disease." Thesis, Université de Paris (2019-....), 2019. https://theses.md.univ-paris-diderot.fr/ELHOSS_Sara_va2_20190924.pdf.
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La drépanocytose est une maladie génétique héréditaire récessive causée par la substitution d'un acide aminé dans la chaîne β-globine aboutissant à la production d'hémoglobine anormale (HbS). Dans des conditions hypoxiques, l’HbS polymérise entraînant une falciformation et une perte de déformabilité des globules rouges (GR). Au cours de la drépanocytose, le dysfonctionnement splénique entraîne des complications potentiellement mortelles, en particulier chez les jeunes enfants. Généralement, une asplénie fonctionnelle précède la survenue d’une asplénie anatomique avec cependant une grande variabilité inter-individuelle du fait de facteurs modulateurs génétiques et environnementaux. L’hémoglobine fœtale (HbF) est le principal modulateur de la gravité de la maladie, car la présence d’HbF inhibe la polymérisation d’HbS, retardant et prévenant ainsi les complications graves, améliorant la qualité de vie des patients et augmentant leur survie. Il existe une hétérogénéité assez bien caractérisée de la concentration et de la distribution cellulaire d'HbF dans les GR circulants, mais le rôle de l'HbF au cours de l'érythropoïèse est mal documenté.Dans le but de mieux comprendre le rôle de l’HbF dans la perte de fonctionnalité splénique, la survie des GR et l'érythropoïèse inefficace, nous avons étudié 1) l'histoire naturelle du dysfonctionnement splénique chez les enfants drépanocytaires, 2) l'expression cellulaire et la distribution de l'HbF comparativement chez les enfants, chez les patients naïfs et ceux traités par hydroxycarbamide (HC) et 3) le rôle de l'HbF au cours de l'érythropoïèse terminale.Nous avons d’abord développé une méthode de cytométrie en flux à haut débit pour mesurer la fonction de filtration splénique et avons montré que la perte de fonction splénique est présente très tôt dans la vie, dès 3 à 6 mois chez les enfants drépanocytaires, puis diminue avec l'âge. Nous avons également mis en évidence que les cellules irréversiblement falciformées (ISC) jouaient un rôle dans la survenue de la séquestration splénique aiguë, laquelle entraîne à son tour une perte supplémentaire de fonction. Dans la deuxième partie de ce travail, nous avons mis en place une approche originale pour déterminer la distribution d'HbF à l’échelle cellulaire. En utilisant une cohorte longitudinale de patients traités par HC (inducteur d'HbF), nous avons montré que celui-ci avait un impact positif global sur les GR, en augmentant non seulement le contenu en HbF, mais également le volume de tous les GR, indépendamment de leur contenu en HbF. Nous avons par ailleurs montré que les cellules riches en HbF (High-F) étaient un marqueur précis d’efficacité de l'HC. Dans la dernière partie de la thèse, nous avons démontré pour la première fois une érythropoïèse inefficace chez les patients drépanocytaires et avons révélé un nouveau rôle de l'HbF au cours de l'érythropoïèse terminale, celui de protéger les érythroblastes de l'apoptose.En conclusion, ce travail montre que l'HbF a un effet bénéfique supplémentaire sur la drépanocytose en conférant non seulement une survie préférentielle des cellules F dans la circulation, mais en diminuant également l'érythropoïèse inefficace. Ce résultat suggère que la persistance d’HbF dans la drépanocytose serait davantage la conséquence d’un enrichissement en F-érythroblastes au cours de la différenciation érythroïde terminale survenant peu après la naissance plutôt qu’un retard du switch des hémoglobinesSickle cell disease (SCD) is caused by a single point mutation in the β-globin gene generating sickle hemoglobin (HbS). Hypoxia drives HbS polymerization that is responsible for red blood cell (RBC) sickling and reduced deformability. In SCD, splenic dysfunction results in life-threatening complications, particularly in early childhood. During the course of the disease, the spleen functionally declines and anatomically disappears, although with great individual variability depending on modulating genetic and environmental factors. The key modulator of disease severity is fetal hemoglobin (HbF), as the presence of HbF inhibits HbS polymerization, thus delaying and preventing severe complications, ameliorating patients’ quality of life and increasing survival. There is a rather well characterized hetero cellular concentration of HbF and distribution in circulating RBCs but the role of HbF during erythropoiesis, is poorly documented. With the aim of better understanding the role of HbF in spleen function, red cell survival and ineffective erythropoiesis we investigated 1) the natural history of spleen dysfunction in SCD children, 2) the cellular expression and distribution of HbF in SCD children, in untreated patients and patients treated with Hydroxycarbamide and 3) ineffective erythropoiesis and the role of HbF during terminal erythropoiesis.We developed a flow cytometry high-throughput method to measure splenic filtration function and showed that splenic loss of function is present very early in life at 3-6 months in SCD children and further declines with age. We also highlighted that irreversibly sickled cells (ISCs) are a potential contributor to acute splenic sequestration (ASS) which in turn results in further loss of splenic function. In the second part of this work, we set up an original approach to determine HbF distribution per cell. Using a longitudinal cohort of patients treated with hydroxycarbamide (HC - an inducer of HbF), we showed that HC has a global positive impact on RBCs, by not only increasing HbF content but also by increasing the volume of all RBCs independent of HbF. We moreover showed that High F-cells are a more precise marker of HC efficacy. In the last part of the thesis, we showed for the first time clear evidence of ineffective erythropoiesis in SCD and revealed a new role of HbF during terminal erythropoiesis protecting erythroblasts from apoptosis. In conclusion, this work shows that HbF has an additional beneficial effect in SCD by not only conferring a preferential survival of F-cells in the circulation but also by decreasing ineffective erythropoiesis. Importantly, it suggests that the delay in hemoglobin switch in SCD might be also due to an enrichment in F-erythroblasts during terminal erythroid differentiation occurring very early in infancy, shortly after birth
Books on the topic "Diseased red cell"
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Bernhardt, Ingolf, and J. Clive Ellory, eds. Red Cell Membrane Transport in Health and Disease. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-662-05181-8.
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Bernhardt, Ingolf. Red Cell Membrane Transport in Health and Disease. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003.
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R, Bridges Kenneth, and Pearson Howard A, eds. Anemias and other red cell disorders. New York: McGraw-Hill, 2007.
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Tsuyoshi, Ohnishi S., and Ohnishi Tomoko, eds. Membrane abnormalities in sickle cell disease and in other red blood cell disorders. Boca Raton, Fla: CRC Press, 1994.
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Malaria resistance or susceptibility in red cells disorders. Hauppauge, NY: Nova Science, 2009.
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1949-, Agre Peter, and Cartron Jean Pierre, eds. Protein blood group antigens of the human red cell: Structure, function, and clinical significance. Baltimore: Johns Hopkins University Press, 1992.
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The match: "savior siblings" and one family's battle to heal their daughter. Boston: Beacon Press, 2010.
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Lichtman, Marshall A., and Josef T. Prchal. Red Cell and Its Diseases. McGraw-Hill Education, 2021.
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Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Red cell disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0002.
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The peripheral blood film in anaemias - Anaemia in renal disease - Anaemia in endocrine disease - Anaemia in joint disease - Anaemia in gastrointestinal disease - Anaemia in liver disease - Iron (Fe) deficiency anaemia - Vitamin B12 deficiency - Folate deficiency - Other causes of megaloblastic anaemia - Anaemia in other deficiency states - Haemolytic syndromes - Genetic control of haemoglobin production - Sickling disorders - HbS—sickle-modifying therapies - Sickle cell trait (HbAS) - Other sickling disorders - Other haemoglobinopathies - Unstable haemoglobins - Thalassaemias - α thalassaemia - β thalassaemia - Other thalassaemias - Hereditary persistence of fetal haemoglobin - Hb patterns in haemoglobin disorders - Non-immune haemolysis - Hereditary spherocytosis - Hereditary elliptocytosis - Glucose-6-phosphate dehydrogenase (G6PD) deficiency - Pyruvate kinase deficiency - Other red cell enzymopathies - Drug-induced haemolytic anaemia - Methaemoglobinaemia - Microangiopathic haemolytic anaemia - Acanthocytosis - Autoimmune haemolytic anaemia - Cold haemagglutinin disease - Leucoerythroblastic anaemia - Aplastic anaemia - Paroxysmal nocturnal haemoglobinuria - Pure red cell aplasia - Iron (Fe) overload - Transfusion haemosiderosis
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Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, Banu Kaya, and Angela Theodoulou. Red cell disorders. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0002_update_001.
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The peripheral blood film in anaemias - Anaemia in renal disease - Anaemia in endocrine disease - Anaemia in joint disease - Anaemia in gastrointestinal disease - Anaemia in liver disease - Iron (Fe) deficiency anaemia - Vitamin B12 deficiency - Folate deficiency - Other causes of megaloblastic anaemia - Anaemia in other deficiency states - Haemolytic syndromes - Genetic control of haemoglobin production - Sickling disorders - HbS—sickle-modifying therapies - Sickle cell trait (HbAS) - Other sickling disorders - Other haemoglobinopathies - Unstable haemoglobins - Thalassaemias - α thalassaemia - β thalassaemia - Other thalassaemias - Hereditary persistence of fetal haemoglobin - Hb patterns in haemoglobin disorders - Non-immune haemolysis - Hereditary spherocytosis - Hereditary elliptocytosis - Glucose-6-phosphate dehydrogenase (G6PD) deficiency - Pyruvate kinase deficiency - Other red cell enzymopathies - Drug-induced haemolytic anaemia - Methaemoglobinaemia - Microangiopathic haemolytic anaemia - Acanthocytosis - Autoimmune haemolytic anaemia - Cold haemagglutinin disease - Leucoerythroblastic anaemia - Aplastic anaemia - Paroxysmal nocturnal haemoglobinuria - Pure red cell aplasia - Iron (Fe) overload - Transfusion haemosiderosis
Book chapters on the topic "Diseased red cell"
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Brovelli, Augusta, and Giampaolo Minetti. "Red Cell Ageing." In Red Cell Membrane Transport in Health and Disease, 673–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-662-05181-8_29.
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Brugnara, Carlo. "Sickle Cell Disease." In Red Cell Membrane Transport in Health and Disease, 549–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-662-05181-8_23.
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Bien, Christian G., Christian E. Elger, Ali R. Afzal, Sirajedin Natah, Ritva Häyrinen-Immonen, Yrjö Konttinen, George S. Zubenko, et al. "Red Cell Pyruvate Kinase Deficiency." In Encyclopedia of Molecular Mechanisms of Disease, 1809–10. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_1526.
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Orbach, Hedi, Gisele Zandman Goddard, Asher Winder, and Yehuda Shoenfeld. "Acquired Adult Pure Red Cell Aplasia." In Diagnostic Criteria in Autoimmune Diseases, 525–28. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-285-8_96.
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Tauler Riera, Pedro, Maurizio Volterrani, Ferdinando Iellamo, Francesco Fallo, Andrea Ermolao, William J. Kraemer, Nicholas A. Ratamess, Avery Faigenbaum, Andrew Philp, and Keith Baar. "Red Blood Cell Rheological Properties." In Encyclopedia of Exercise Medicine in Health and Disease, 750. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_4491.
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Patrinos, George P., and Frank G. Grosveld. "Transgenic Models of Red Cell Disorders." In Red Cell Membrane Transport in Health and Disease, 643–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-662-05181-8_28.
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Tauler Riera, Pedro, Maurizio Volterrani, Ferdinando Iellamo, Francesco Fallo, Andrea Ermolao, William J. Kraemer, Nicholas A. Ratamess, Avery Faigenbaum, Andrew Philp, and Keith Baar. "Red Blood Cell Capillary Transit Time." In Encyclopedia of Exercise Medicine in Health and Disease, 750. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2950.
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King, Karen E., and Paul M. Ness. "Red Cell Transfusions in Patients with Hematologic Malignancies." In Neoplastic Diseases of the Blood, 1139–52. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-64263-5_53.
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King, Karen E., and Paul M. Ness. "Red Cell Transfusions in Patients with Hematologic Malignancies." In Neoplastic Diseases of the Blood, 1251–63. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3764-2_55.
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Jones, D. B. "The Origin of the Reed-Sternberg Cell." In Lymphoproliferative Diseases, 91–106. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-0739-3_7.
Full textConference papers on the topic "Diseased red cell"
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Liu, Jia, Yuhao Qiang, and E. Du. "Measurement of Electrical Properties of Sickle Cells From Electrical Impedance of Cell Suspension." In ASME 2017 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/imece2017-71734.
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Analysis of the electrical properties of a biological cell can provide useful information about its characteristic features, such as the intracellular composition, charge distribution and composition changes in cell membrane, as well as the extracellular environment. Electrical impedance spectroscopy of a cell suspension can be used to extract an average measure of the electrical properties of single cells. In sickle cell disease, the disease state of a sickle red blood cell is closely related to the intracellular hemoglobin composition and concentration. This study presents an electrical impedance measurement of sickle cell suspension with normal red blood cells as control. Electrical impedance spectra of cell suspensions are obtained in the range of 1000 Hz to 1MHz. Based on Maxwell’s mixture theory, average values of membrane capacitance and cytoplasm resistance of single cells are extracted for both normal and sickle blood samples. Comparing to traditional parallel-plate setup for cell suspension subjected to frequency sweep, this method requires low quantity of blood specimens and can be potentially valuable for patients that are already anemic.
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Ferrant, A., N. Leners, E. K. Gini, J. P. Osselaerey, and J. Sonnet. "EFFECT OF PIRACETAM ON THE MEAN INTRASPLENIC RED CELL TRANSIT TIME (MST) IN SICKLE CELL DISEASE AND SICKLE CELL THALASSAEMIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644215.
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The effect of Piracetam on the MST has been evaluated in 3 children with homozygous sickle cell disease, and in 1 child and 2 adults with sickle cell β thalassaemia. The MST was measured using 99 Tern labelled autologous red cells before and during treatment with Piracetam (160 mg/kg/d). Tests for in vitro fi1terabi1ity of red cells were performed and an improvement of the in vitro deformabi1ity was observed in all the patients.A shortening of the MST was also observed :
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Kuroda, H., M. Iribe, M. Matsubara, M. Watanabe, and T. Sanada. "Image Analysis of Human Nailfold Capillary With High Speed Digital Video Capillaroscopy." In ASME/JSME 2007 5th Joint Fluids Engineering Conference. ASMEDC, 2007. http://dx.doi.org/10.1115/fedsm2007-37464.
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Diagnoses of skin diseases are considerably difficult tasks due to the multiply-folded factors. Nailfold capillaroscopy has been developed to diagnosis microvascular disturbances mainly in connective tissue diseases, including systemic sclerosis, dermatomyositis, systemic lupus erythematosus, and Raynaud’s phenomenon. Capillaroscopy is non-invasive, easy to use, low cost and suitable for observation of these typical phenomena. We improved conventional capillaroscopy by constructing “high speed digital video capillaroscopy”, by integrating high speed digital video camera, deep-focus zoom lens, appropriate light source and light collecting adaptor. High speed digital video camera enabled us to observe the individual red blood cell in human nailfold capillary in vivo. The light collecting adaptor is effective for preventing skin from excessive light exposure, which causes serious damage. The first objective of this study is to extract the shape of nailfold capillary quantitatively by using binarization and the level-set method. By using the level-set method, the function, which distinguishes outside from inside of the capillary and also evaluates radius distribution along the capillary center line, is calculated. Based on this mathematical description of capillary shape, more rigorous definition of the capillary red blood cell velocity than the conventional method is obtained. The second objective of this study is to propose the innovative measurement method of red blood cell velocity in nailfold capillary. As plasma gaps show high brightness we trace them and estimate the velocities of blood cells on the center line of capillary. The last objective of this study is to observe the behavior of red blood cell. We evaluate the movement of individual red blood cell, not only in the axial direction but also the lateral direction. We analyze the series of images of red blood cells in capillary and discuss their behavior.
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Habib, GS, W. Saliba, and P. Froom. "FRI0129 Lupus and pure red cell aplasia." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.164.
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Galpayage Dona, Kalpani Nisansala Udeni, Jia Liu, Yuhao Qiang, E. Du, and A. W. C. Lau. "Electrical Equivalent Circuit Model of Sickle Cell." In ASME 2017 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/imece2017-70677.
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Mature red blood cell (RBC) consists of cytoplasm, mainly normal hemoglobin (HbA) within a plasma membrane. In sickle cell disease, abnormal sickle hemoglobin (HbS) molecule polymerizes and forms into rigid fibers at low oxygen tension, which contributes to variation in the biophysical properties of sickle cells from healthy RBCs. This paper presents an electrical equivalent circuit (EEC) model of sickle cell that considers the phase transition of oxy-HbS solution to deoxy-HbS polymers. Briefly, we model the oxy-HbS solution following healthy RBCs using a resistor and deoxy-HbS fibers as a capacitor. To validate the model, electrical impedance measurements of cell suspensions for normal RBCs and sickle cells are performed, using a multi-channel lock in amplifier in the frequency range of 1 kHz to 10 MHz in a customized microfluidic chamber. Quantitative measurements of the classical components of EEC model are extracted using the developed EEC sickle cell model, allowing us to better understand the biophysics of cell sickling event in sickle cell disease.
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Shaked, Natan T., Lisa L. Satterwhite, Marilyn J. Telen, George A. Truskey, and Adam Wax. "Dynamic quantitative microscopy and nanoscopy of red blood cells in sickle cell disease." In SPIE BiOS, edited by Jose-Angel Conchello, Carol J. Cogswell, Tony Wilson, and Thomas G. Brown. SPIE, 2012. http://dx.doi.org/10.1117/12.907659.
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Erjavec, Vladimira, and Alenka Nemec Svete. "Brachycephalic Dogs with Brachycephalic Obstructive Airway Syndrome Have Increased Variability in Red Blood Cell Size." In Socratic Lectures 7. University of Lubljana Press, 2022. http://dx.doi.org/10.55295/psl.2022.d8.
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Brachycephalic obstructive airway syndrome (BOAS) is a conformation-related respiratory disorder of dog breeds with congenitally flattened facial and skull anatomy. BOAS is characterized by chronic shortness of breath and subsequent difficulty in exercising, a tendency to overheat, increased and abnormal respiratory noise, and low oxygen levels. The aim of our retrospective study was to inves-tigate the level of red blood cell distribution width (RDW), a biomarker of chronic hypoxemia, in groups of BOAS patients with different degrees of BOAS and a group of healthy non-brachycephalic dogs. Red blood cell distribution width provides information on the variability in the red blood cell volume. It is a simple and inexpensive variable included in the complete blood count report. Seventy-two BOAS patients and 24 non-brachycephalic dogs were included in this retrospective study. Pa-tients with BOAS were classified into grade 1 (13 dogs), grade 2 (27 dogs), and grade 3 (32 dogs) according to the severity of the disease. In our study, a significantly (p < 0.05) higher RDW was found in all groups of BOAS patients compared to the non-brachycephalic dog group. However, we found no significant difference in RDW between the groups of BOAS patients. Thus, we may conclude that BOAS patients have increased variability in the size of red blood cells compared with healthy non-brachycephalic dogs. Our results warrant further studies to determine the potential utility of RDW in BOAS and to clarify the role of RDW in BOAS patients in relation to the severity of BOAS and cardiovascular risk. Keywords: Brachycephaly; Brachycephalic obstructive airway syndrome; Dogs; Haematology; Erythrocytes; Red blood cell distribution width
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CHEN, YONG, JIYE CAI, and JINGXIAN ZHAO. "DISEASED RED BLOOD CELLS STUDIED BY ATOMIC FORCE MICROSCOPY." In Proceedings of the Asian Symposium on Nanotechnology and Nanoscience 2002. WORLD SCIENTIFIC, 2003. http://dx.doi.org/10.1142/9789812796714_0054.
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Farhat, Hassan, and Joon Sang Lee. "The Study of RBC Deformation in Capillaries With a Lattice Boltzmann Method for Surfactant Covered Droplets." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-12629.
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This study aims at analyzing the shape change of red blood cells in the process of streaming through a capillary smaller than the red blood cell diameter. The characteristics of its shape change and velocity can potentially lead to an indicator of a variety of diseases. We approach this problem with considering red blood cells as surfactant covered droplets. This assumption is justified by the fact that the cell membrane liquefies under high pressure in small capillaries, and this allows the marginalization of the mechanical properties of the membrane. The red blood cell membrane is in fact a macro-colloid containing lipid surfactant. When liquefied, it can be treated as a droplet of immiscible hemoglobin covered with lipid surfactant in plasma surrounding. The merit is to analyze the effect of the flow condition and domain geometry on the surfactant concentration change over the droplet interface, and the effect of this change on the surface tension of the droplet. The distribution of the surfactant is calculated by enforcing conservation of the surfactant mass concentration on the interface, leading to a convection diffusion equation. The equation takes account of the effects of the normal and Marangoni stresses as a boundary condition on the interface between the immiscible fluids. The gradient in the surface tension adversely determines the droplet shape by effecting a local change in the capillary number, and influences its velocity by retarding the local surface velocity. The choice of the Gunstensen model is motivated by its capability of handling incompressible fluids, and the locality of the application of the surface tension. We used the same concept to investigate the dynamic shape change of the RBC while flowing through the microvasculature, and explore the physics of the Fahraeus, and the Fahraeus-Lindqvist effects.
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Dintenfass, L. "VERY LARGE AND COMPACT AGGREGATES OF RED CELLS IN HEART DISEASE AND CANCER: POSSIBLY AN ANALOGOUS ROLE IN THE MICROCIRCULATION AS PLATELET AGGREGATES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644213.
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Very large aggregates of red blood cells, showing compact morphology, are easily observed in vitro, and might be of importance in the in vivo microcirculation. Blood from patients with myocardial infarction, WaldenstrBm1s macroglobulinaemia, or varoous carcinomas. etc., was anticoagulated with EDTA, and adjusted to haematocrit of 0.30, using native plasma. All tests were carried out in the slit-capillary photoviscometer, at temp, of 22°C. Micro and macrophotographs were taken during flow and stasis, using slits of 12.5 and 50 micron gaps. Studies showed that very large (two-dimensional) red cell aggregates are formed, such aggregates (clumps) containing up to 50,000 red cells in a single clump. The architecture of such aggregates differed according to the origin of blood: both rouleaux type and random / compact type of aggregates were observed; in principle, a spectrum of morphologies can be seen. These observations form a link between the earlier work of FAHRAEUS, on the one hand, and that of KNISELY, on the other; whic works appeared at the time to be contradictory and irreconcilable.
Reports on the topic "Diseased red cell"
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Banks, H. T., Karen M. Bliss, and Hien Tran. Modeling Red Blood Cell and Iron Dynamics in Patients with Chronic Kidney Disease. Fort Belvoir, VA: Defense Technical Information Center, February 2012. http://dx.doi.org/10.21236/ada556965.
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Davidson, Irit, Hsing-Jien Kung, and Richard L. Witter. Molecular Interactions between Herpes and Retroviruses in Dually Infected Chickens and Turkeys. United States Department of Agriculture, January 2002. http://dx.doi.org/10.32747/2002.7575275.bard.
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Tumors in commercial poultry are caused mainly by infection with avian herpes and retroviruses, the herpesvirus Marek's disease virus (MDV) and the retroviruses, reticuloendotheliosis (REV), lymphoid leukosis, subgroups A-I and J (ALV and ALV-J) in chickens, or Iymphoprolipherative disease (LPDV) in turkeys. Infection with one virus aggravates the clinical outcome of birds that are already infected by another oncogenic virus. As these viruses do not interfere for infection, MDV and one or more retroviruses can infect the same flock, the same bird and the same cell. While infecting the same cell, herpes and retroviruses might interact in at least three ways: a) Integration of retrovirus genomes, or genomic fragments (mainly the LTR) into MDV;b) alteration of LTR-driven expression of retroviral genes by MDV immediate- early genes, and c) by herpesvirus induced cellular transcriptional factors. The first type of molecular interaction have been demonstrated to happen efficiently in vitro by Dr. Kung, in cases multiple infection of cell cultures with MDV and REV or MDV and ALV. Moreover, Dr. Witter showed that an in vitro-created recombinant, RM1, had altered in vitro replication and in vivo biological properties. A more comprehensive characterization of RM1 was carried out in the present project. We sought to highlight whether events of such integrations occur also in the bird, in vivo. For that, we had first to determine the prevalence of dually-infected individual birds in commercial flocks, as no systematic survey has been yet reported. Surprisingly, about 25% of the commercial flocks infected with avian oncogenic viruses had a multiple virus infection and 5% of the total samples ana lysed had multiple virus sequences. Then, we aimed to evaluate and characterize biologically and molecularly the resulting recombinants, if formed, and to analyse the factors that affect these events (virus strains, type and age of birds and time interval between the infection with both viruses). The perception of retrovirus insertions into herpesviruses in vivo is not banal, as the in vivo and in vitro systems differ in the viral-target cells, lymphocytes or fibroblasts, in the MDV-replicative type, transforming or productive, and the immune system presence. We realized that previous methods employed to study in vitro created recombinant viruses were not adequate for the study of samples taken directly from the bird. Therefore, the Hot Spot-combined PCR was developed based on the molecularly known RM1 virus. Also, the PFGE that was used for tissue cultured-MDV separation was inefficient for separating MDV from organs, but useful with feather tips as a source of bird original MDV. Much attention was dedicated now to feathers, because if a recombinant virus would be formed in vivo, its biological significance would be evident by horizontal dissemination through the feathers. Major findings were: a) not only in vitro, but also in vivo MDV and retrovirus co-infections lead to LTR integrations into MDV. That was shown by the detection of chimeric molecules. These appeared in low quantities and as quasispecies, thus interfering with sequence analysis of cloned gel-purified chimeric molecules. Mainly inserts were located in the repeat long MDV fragments. In field birds chimeric molecules were detected at a lower frequency (2.5%) than in experimentally infected birds (30-50%). These could be transmitted experimentally to another birds by inoculation with chimeric molecules containing blood. Several types of chimeric molecules were formed, and same types were detected in birds infected by a second round. To reproduce viral integrations, in vivo infection trials were done with field inoculate that contained both viruses, but the chimeric molecule yield was undetectable.
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Ficht, Thomas, Gary Splitter, Menachem Banai, and Menachem Davidson. Characterization of B. Melinensis REV 1 Attenuated Mutants. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7580667.bard.
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Brucella Mutagenesis (TAMU) The working hypothesis for this study was that survival of Brucella vaccines was directly related to their persistence in the host. This premise is based on previously published work detailing the survival of the currently employed vaccine strains S19 and Rev 1. The approach employed signature-tagged mutagenesis to construct mutants interrupted in individual genes, and the mouse model to identify mutants with attenuated virulence/survival. Intracellular survival in macrophages is the key to both reproductive disease in ruminants and reticuloendothelial disease observed in most other species. Therefore, the mouse model permitted selection of mutants of reduced intracellular survival that would limit their ability to cause reproductive disease in ruminants. Several classes of mutants were expected. Colonization/invasion requires gene products that enhance host-agent interaction or increase resistance to antibacterial activity in macrophages. The establishment of chronic infection requires gene products necessary for intracellular bacterial growth. Maintenance of chronic infection requires gene products that sustain a low-level metabolism during periods characterized little or no growth (1, 2). Of these mutants, the latter group was of greatest interest with regard to our originally stated premise. However, the results obtained do not necessarily support a simplistic model of vaccine efficacy, i.e., long-survival of vaccine strains provides better immunity. Our conclusion can only be that optimal vaccines will only be developed with a thorough understanding of host agent interaction, and will be preferable to the use of fortuitous isolates of unknown genetic background. Each mutant could be distinguished from among a group of mutants by PCR amplification of the signature tag (5). This approach permitted infection of mice with pools of different mutants (including the parental wild-type as a control) and identified 40 mutants with apparently defective survival characteristics that were tentatively assigned to three distinct classes or groups. Group I (n=13) contained organisms that exhibited reduced survival at two weeks post-infection. Organisms in this group were recovered at normal levels by eight weeks and were not studied further, since they may persist in the host. Group II (n=11) contained organisms that were reduced by 2 weeks post infection and remained at reduced levels at eight weeks post-infection. Group III (n=16) contained mutants that were normal at two weeks, but recovered at reduced levels at eight weeks. A subset of these mutants (n= 15) was confirmed to be attenuated in mixed infections (1:1) with the parental wild-type. One of these mutants was eliminated from consideration due to a reduced growth rate in vitro that may account for its apparent growth defect in the mouse model. Although the original plan involved construction of the mutant bank in B. melitensis Rev 1 the low transformability of this strain, prevented accumulation of the necessary number of mutants. In addition, the probability that Rev 1 already carries one genetic defect increases the likelihood that a second defect will severely compromise the survival of this organism. Once key genes have been identified, it is relatively easy to prepare the appropriate genetic constructs (knockouts) lacking these genes in B. melitensis Rev 1 or any other genetic background. The construction of "designer" vaccines is expected to improve immune protection resulting from minor sequence variation corresponding to geographically distinct isolates or to design vaccines for use in specific hosts. A.2 Mouse Model of Brucella Infection (UWISC) Interferon regulatory factor-1-deficient (IRF-1-/- mice have diverse immunodeficient phenotypes that are necessary for conferring proper immune protection to intracellular bacterial infection, such as a 90% reduction of CD8+ T cells, functionally impaired NK cells, as well as a deficiency in iNOS and IL-12p40 induction. Interestingly, IRF-1-/- mice infected with diverse Brucella abortus strains reacted differently in a death and survival manner depending on the dose of injection and the level of virulence. Notably, 50% of IRF-1-/- mice intraperitoneally infected with a sublethal dose in C57BL/6 mice, i.e., 5 x 105 CFU of virulent S2308 or the attenuated vaccine S19, died at 10 and 20 days post-infection, respectively. Interestingly, the same dose of RB51, an attenuated new vaccine strain, did not induce the death of IRF-1-/- mice for the 4 weeks of infection. IRF-1-/- mice infected with four more other genetically manipulated S2308 mutants at 5 x 105 CFU also reacted in a death or survival manner depending on the level of virulence. Splenic CFU from C57BL/6 mice infected with 5 x 105 CFU of S2308, S19, or RB51, as well as four different S2308 mutants supports the finding that reduced virulence correlates with survival Of IRF-1-/- mice. Therefore, these results suggest that IRF-1 regulation of multi-gene transcription plays a crucial role in controlling B. abortus infection, and IRF-1 mice could be used as an animal model to determine the degree of B. abortus virulence by examining death or survival. A3 Diagnostic Tests for Detection of B. melitensis Rev 1 (Kimron) In this project we developed an effective PCR tool that can distinguish between Rev1 field isolates and B. melitensis virulent field strains. This has allowed, for the first time, to monitor epidemiological outbreaks of Rev1 infection in vaccinated flocks and to clearly demonstrate horizontal transfer of the strain from vaccinated ewes to unvaccinated ones. Moreover, two human isolates were characterized as Rev1 isolates implying the risk of use of improperly controlled lots of the vaccine in the national campaign. Since atypical B. melitensis biotype 1 strains have been characterized in Israel, the PCR technique has unequivocally demonstrated that strain Rev1 has not diverted into a virulent mutant. In addition, we could demonstrate that very likely a new prototype biotype 1 strain has evolved in the Middle East compared to the classical strain 16M. All the Israeli field strains have been shown to differ from strain 16M in the PstI digestion profile of the omp2a gene sequence suggesting that the local strains were possibly developed as a separate branch of B. melitensis. Should this be confirmed these data suggest that the Rev1 vaccine may not be an optimal vaccine strain for the Israeli flocks as it shares the same omp2 PstI digestion profile as strain 16M.
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Horwitz, Benjamin, and Nicole M. Donofrio. Identifying unique and overlapping roles of reactive oxygen species in rice blast and Southern corn leaf blight. United States Department of Agriculture, January 2017. http://dx.doi.org/10.32747/2017.7604290.bard.
Full textAbstract:
Plants and their fungal pathogens both produce reactive oxygen species (ROS). CytotoxicROS act both as stressors and signals in the plant-fungal interaction. In biotrophs, a compatible interaction generates little ROS, but is followed by disease. An incompatible interaction results in a strong oxidative burst by the host, limiting infection. Necrotrophs, in contrast, thrive on dead and dying cells in an oxidant-rich local environment. Rice blast, Magnaportheoryzae, a hemibiotroph, occurs worldwide on rice and related hosts and can decimate enough rice each year to feed sixty million people. Cochliobolusheterostrophus, a necrotroph, causes Southern corn leaf blight (SLB), responsible for a major epidemic in the 1970s. The objectives of our study of ROS signaling and response in these two cereal pathogens were: Confocal imaging of ROS production using genetically encoded redox sensor in two pathosystems over time. Forward genetic screening of HyPer sensor lines in two pathosystems for fungal genes involved in altered ROSphenotypes. RNA-seq for discovery of genes involved in ROS-related stress and signaling in two pathosystems. Revisions to the research plan: Library construction in SLB was limited by low transformation efficiency, compounded by a protoplasting enzyme being unavailable during most of year 3. Thus Objective 2 for SLB re-focused to construction of sensor lines carrying deletion mutations in known or candidate genes involved in ROS response. Imaging on rice proved extremely challenging, so mutant screening and imaging were done with a barley-infecting line, already from the first year. In this project, ROS imaging at unprecedented time and spatial resolution was achieved, using genetically-encoded ratio sensors in both pathogens. This technology is currently in use for a large library of rice blast mutants in the ROS sensor background, and Southern corn leaf blight mutants in final stages of construction. The imaging methods developed here to follow the redox state of plant pathogens in the host tissue should be applicable to fungal pathogens in general. Upon completion of mutant construction for SCLB we hope to achieve our goal of comparison between intracellular ROS status and response in hemibiotroph and necrotroph cereal pathogens.
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Hovav, Ran, Peggy Ozias-Akins, and Scott A. Jackson. The genetics of pod-filling in peanut under water-limiting conditions. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7597923.bard.
Full textAbstract:
Pod-filling, an important yield-determining stage is strongly influenced by water stress. This is particularly true for peanut (Arachishypogaea), wherein pods are developed underground and are directly affected by the water condition. Pod-filling in peanut has a significant genetic component as well, since genotypes are considerably varied in their pod-fill (PF) and seed-fill (SF) potential. The goals of this research were to: Examine the effects of genotype, irrigation, and genotype X irrigation on PF and SF. Detect global changes in mRNA and metabolites levels that accompany PF and SF. Explore the response of the duplicate peanut pod transcriptome to drought stress. Study how entire duplicated PF regulatory processes are networked within a polyploid organism. Discover locus-specific SNP markers and map pod quality traits under different environments. The research included genotypes and segregating populations from Israel and US that are varied in PF, SF and their tolerance to water deficit. Initially, an extensive field trial was conducted to investigate the effects of genotype, irrigation, and genotype X irrigation on PF and SF. Significant irrigation and genotypic effect was observed for the two main PF related traits, "seed ratio" and "dead-end ratio", demonstrating that reduction in irrigation directly influences the developing pods as a result of low water potential. Although the Irrigation × Genotype interaction was not statistically significant, one genotype (line 53) was found to be more sensitive to low irrigation treatments. Two RNAseq studies were simultaneously conducted in IL and the USA to characterize expression changes that accompany shell ("source") and seed ("sink") biogenesis in peanut. Both studies showed that SF and PF processes are very dynamic and undergo very rapid change in the accumulation of RNA, nutrients, and oil. Some genotypes differ in transcript accumulation rates, which can explain their difference in SF and PF potential; like cvHanoch that was found to be more enriched than line 53 in processes involving the generation of metabolites and energy at the beginning of seed development. Interestingly, an opposite situation was found in pericarp development, wherein rapid cell wall maturation processes were up-regulated in line 53. Although no significant effect was found for the irrigation level on seed transcriptome in general, and particularly on subgenomic assignment (that was found almost comparable to a 1:1 for A- and B- subgenomes), more specific homoeologous expression changes associated with particular biosynthesis pathways were found. For example, some significant A- and B- biases were observed in particular parts of the oil related gene expression network and several candidate genes with potential influence on oil content and SF were further examined. Substation achievement of the current program was the development and application of new SNP detection and mapping methods for peanut. Two major efforts on this direction were performed. In IL, a GBS approach was developed to map pod quality traits on Hanoch X 53 F2/F3 generations. Although the GBS approach was found to be less effective for our genetic system, it still succeeded to find significant mapping locations for several traits like testa color (linkage A10), number of seeds/pods (A5) and pod wart resistance (B7). In the USA, a SNP array was developed and applied for peanut, which is based on whole genome re-sequencing of 20 genotypes. This chip was used to map pod quality related traits in a Tifrunner x NC3033 RIL population. It was phenotyped for three years, including a new x-ray method to phenotype seed-fill and seed density. The total map size was 1229.7 cM with 1320 markers assigned. Based on this linkage map, 21 QTLs were identified for the traits 16/64 weight, kernel percentage, seed and pod weight, double pod and pod area. Collectively, this research serves as the first fundamental effort in peanut for understanding the PF and SF components, as a whole, and as influenced by the irrigation level. Results of the proposed study will also generate information and materials that will benefit peanut breeding by facilitating selection for reduced linkage drag during introgression of disease resistance traits into elite cultivars. BARD Report - Project4540 Page 2 of 10