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Dissertations / Theses on the topic 'Erythrocytes'

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Published: 4 June 2021

Last updated: 31 July 2024

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1

Gonzalez, Laurie J. "The influence of membrane lipid order on cell shape and microvesiculation in human erythrocytes /." Diss., CLICK HERE for online access, 2006. http://contentdm.lib.byu.edu/ETD/image/etd1615.pdf.

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2

Persson, Sylvi. "Erythrocyte deformability studies by viscometry and filtrometry." Lund : Dept. of Medicine, University Hospital of Lund, Lund University, 1994. http://catalog.hathitrust.org/api/volumes/oclc/39207611.html.

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3

Flatt, Joanna Frances. "A study of human erythrocyte membrane structure and function using variant erythrocytes." Thesis, University of Bristol, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.560498.

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Human erythrocytes are highly specialised cells boasting numerous features to maximise gas carriage, exchange and delivery around the body. The role of the highly proteinaceous red cell membrane in these processes is vital. Some membrane proteins such as the Rh-associated glycoprotein (RhAG) and aquaporin-1 (AQP1) are postulated to form gas channels, and disorders affecting membrane proteins can have extensive effects on normal red cell function. In this work, the role and interactions of Rh proteins are probed using rare variant Rh-deficient erythrocytes. The RhCE polypeptide is required for normal expression of other members of the Rh complex. Lack of RhCE is associated with depressed expression of CD44, an adhesion molecule, and may alter expression of proteins involved in complement such as decay acceleration factor and Iymphocyte function-associated antigen 3. Absence of RhAG prevents Rh complex expression and is found to affect band 3 macrocomplex proteins GPA and protein 4.2, highlighting the important role for RhAG in the macrocomplex. AQP1 is increased in the absence of RhAG, which supports the hypothesis that they share similar functions. The hereditary stomatocytoses are disorders that affect the ion permeability of red cell membranes. This work comprises a study of the pleiotropic disorder stomatin-deficient cryohydrocytosis (sdCHC), which is caused by mutations in the red cell glucose transporter, glut1. The mutant proteins show minimal glucose transport and increased permeability to cations when expressed heterologously in Xenopus laevis oocytes - consistent with the disease phenotype. sdCHC erythrocytes have very reduced amounts of stomatin, a monotopic membrane protein, a feature shared by other very leaky red cells. This is accompanied by a concomitant increase in stomatin-like protein 2, whose function in red cells is currently unknown. The fates of stomatin proteins in normal and leaky cells are investigated throughout erythropoiesis and found to differ between cation-leaky phenotypes.

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4

Salles, Christine. "Erythrocytes et hémodialyse." Bordeaux 2, 1992. http://www.theses.fr/1992BOR2B004.

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5

HOLTZCLAW, JOHN DAVID. "CHARACTERIZATION OF LIGHT SICKLE ERYTHROCYTES DERIVED FROM DENSE ERYTHROCYTES IN VITRO." University of Cincinnati / OhioLINK, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=ucin990632508.

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6

Janzen, Johan. "Fibrinogen adsorption to human erythrocytes." Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/25820.

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Fibrinogen adsorption to human erythrocytes has been implicated as the mechanism responsible for the reversible aggregation of red cells. The object of this thesis was to measure the binding of fibrinogen to human erythrocytes and to compare the binding with aggregation behaviour. The binding of isolated ¹²⁵I-fibrinogen to red cells was estimated from the amount of radiolabel removed from solution upon addition of cells, from the amount of radiolabel retained in cell pellets produced by ultracentrifugation and corrected for intracellular radiolabel, and from radiolabel retained by cells after exhaustive washing in protein-free buffer. Binding of human albumin to red cells was determined by the same methods. The free energy of formation of red cell/red cell contacts due to isolated fibrinogen was determined by the method of Evans and Buxbaum (Biophys. J. 3̲4̲, 1-12, 1981). The solution depletion method required corrections for dilution effects and was not sensitive enough for detailed determination of binding of these proteins to red cells. Binding estimated from cell pellets and corrected for intracellular radiolabel increased linearily with protein concentration to 12 mg/mL for fibrinogen and 50 mg/mL for albumin. The binding at 1 mg/mL was between 50 and 250 molecules per cell for fibrinogen and between 1000 and 1400 molecules per cell for albumin. Binding determined from wash analyses was similar to pellet binding corrected for free radiolabel. The surface affinity of red cells for red cell beads was determined to be 1.8 ± 0.5 x 10⁻³ erg/cm² (mean ± SEM, n = 4) and 2.8 ± 0.8 x 10⁻³ erg/cm² (mean ± SEM, n = 28) at 4.4 and 8.8 mg/ml fibrinogen respectively. Adhesion between red cells and red cell beads occurred at 2.2 mg/mL fibrinogen, but was too weak to allow estimation of the surface affinity. The surface affinities and binding estimates allow calculation of the mean binding energy for fibrinogen to the red cell surface. The surface affinity per molecule, assuming 250 molecules per cell at 1 mg/mL, was 30 ± 10 and 24 ± 7 kilocalories/mole at 4.4 and 8.8 mg/mL respectively. The difference was not significant. This result poses a problem as binding energies of this order suggest that the adhesion would be irreversible. If fibrinogen binding were 1500 molecules per cell at 1 mg/mL a binding energy of 4 ± 1 kilocalories/mole would be implied. These results are interpreted as indicating that fibrinogen bound to red cells may be displaced during ultracentrifugation.
Medicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate

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7

Goding, Linda M. "Macrophage Recognition of Xenogeneic Erythrocytes." University of Toledo Health Science Campus / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=mco1197469419.

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8

Dodson, Walter R. "Dynamics of erythrocytes and microcapsules." College Park, Md. : University of Maryland, 2008. http://hdl.handle.net/1903/8153.

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Thesis (Ph. D.) -- University of Maryland, College Park, 2008.
Thesis research directed by: Fischell Dept. of Bioengineering. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.

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9

BOUSCH, WAHL MARIE-ROSE. "Les erythrocytes vecteurs de medicaments." Strasbourg 1, 1993. http://www.theses.fr/1993STR15083.

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10

Rowe, Jane Alexandra. "Rosetting of Plasmodium falciparium infected erythrocytes." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260775.

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11

Yusof, Ashril bin. "Exercise-induced oxidative stress in erythrocytes." Thesis, University of Essex, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.434390.

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12

El-Dweik, Majed. "Optical glucose nanobiosensor encapsulated in erythrocytes." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/4672.

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Thesis (Ph.D.)--University of Missouri-Columbia, 2007.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on March 23, 2009) Vita. Includes bibliographical references.

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13

Goodyer, Ian D. "Glucose transport in malaria infected erythrocytes." Thesis, University of Bath, 1993. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356980.

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14

Snoek, Robert. "Spin labeling and analysis of erythrocyte surfaces." Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/25973.

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Spin labeling the oligosaccharides of the red cell membrane was achieved via selective oxidation of gal/ga1NAc (with galactose oxidase) or sialic acid residues (with mild periodic acid) followed by reductive amination of the oxidized sugars with NaBH₃CN and TEMPAMINE. Spin labeling the galactose residues resulted in low yields and specificity, hindering analysis of the spin labeled cells (SL-RBC). Higher specificity and yields were obtained by labeling sialic acids. A protocol was devised which gave maximum yields with no Heisenberg exchange or membrane alterations (as detected by gel electrophoresis). Detailed analysis of the product showed the majority of the spins to be on the PAS positive membrane proteins (glycophorin A, B and C), only 8% being associated with the lipids. Isolation of glycophorin A, the major sialoglycoprotein of the red cell membrane, revealed two modified sialic acids per molecule. Successful ESR interpretations could only be done by lysing the SL-RBC (producing SL-ghosts), eliminating spins which had become internalized (rather than covalently attached to the surface) during the reductive amination step. Assuming a random distribution of biradicals (since there were two spins per glycophorin), an average separation of 16±2 angstroms was calculated between the nitroxides. The spin labeled sialic acids exhibited relatively mobile spectra with Ʈc = 9 x l0⁻¹⁰s. Upon addition of wheat germ agglutinin (WGA), a lectin known to bind to glycophorin, the mobility of the spin label decreased. Even though WGA binding to SL-ghosts showed complex behaviour as detected by Scatchard plots (which required compensation for WGA impurities and non-specific binding), the ESR was only sensitive to the specific binding, the spin mobility decreasing with increasing WGA. The fact that the spin probe was monitoring sialic acids interactions was confirmed by addition of other lectins. Only lectins which interact with glycophorin altered the ESR signal.
Science, Faculty of
Chemistry, Department of
Graduate

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15

Chen, Chang Wen Preston Robert Leslie. "L-aspartic acid transport in cat erythrocytes." Normal, Ill. Illinois State University, 1987. http://wwwlib.umi.com/cr/ilstu/fullcit?p8806853.

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Thesis (Ph. D.)--Illinois State University, 1987.
Title from title page screen, viewed August 22, 2005. Dissertation Committee: Robert L. Preston (chair), George W. Kidder, Jim N. Tone, John L. Frehn, Wayne A. Riddle. Includes bibliographical references (leaves 209-216) and abstract. Also available in print.

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16

Gilks, C. F. "The surface of Plasmodium chabaudi infected erythrocytes." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233501.

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17

Kriek, Neline. "Protein transport in Plasmodium falciparum infected erythrocytes." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270202.

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18

RollaÌn, Haro Ana MariÌa. "Active erythrocytes, drug delivery and related studies." Thesis, University of Ulster, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274408.

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19

SEKAR, DURAIRAJ. "Effect of TiO2 nanoparticles on Trout Erythrocytes." Doctoral thesis, Università degli Studi di Camerino, 2011. http://hdl.handle.net/11581/401865.

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20

Thawani, Neeta. "The contribution of host-and parasite-derived factors to erythropoietic suppression underlying the development of malarial anemia /." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111901.

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Severe anemia is the most prevalent life-threatening complication of malaria infection. In addition to destruction of red blood cells (RBC), decreased RBC production or erythropoietic suppression has been shown to contribute to malarial anemia. The mechanism of this suppression is unknown, but it is considered to be multifactorial since erythropoietic suppression can be observed in the presence of both inflammatory mediators and parasite-derived factors. Experiments presented in this thesis aimed at determining the role of host cytokines released in response to blood-stage malaria infection and parasite-derived factors in erythropoietic suppression underlying the development of malarial anemia. Pro-inflammatory cytokines released during malaria infection have been proposed to play a central role in erythroid suppression. To dissect the discrete roles of these cytokines in the processes leading to anemia, mice were treated with CpG-oligodeoxynucleotides (CpG-ODN) which, like malaria infection in humans and experimental mouse models, induces an acute type 1 pro-inflammatory response. CpG-ODN treatment induced anemia, which was associated with suppressed erythropoiesis and reduced RBC survival. Importantly, CpG-ODN-induced IFN-gamma was found to be the major factor mediating erythropoietic suppression but not decreased RBC survival. We also studied the roles of Th1, Th2 and anti-inflammatory cytokines produced in response to Plasmodium chabaudi AS infection in the development of erythropoietic suppression during blood-stage malaria. Signal transducer and activator of transcription (STAT)6, required for signaling of the Th2 cytokines IL-4 and IL-13, was shown to play a critical role in malarial anemia by inhibiting the proliferation and differentiation of erythroid cells. We also observed that suppressed erythropoiesis is a general feature in mice infected with various rodent Plasmodium species that differ in their clinical manifestations and immune responses. Since parasite-derived factors have been shown to contribute to malarial pathogenesis including anemia, the contribution of P. falciparum - and P. yoelii-derived products to erythropoietic suppression was investigated. Both Plasmodium-derived and synthetic hemozoin (Hz) suppressed the proliferation but not the maturation of erythroid progenitor cells in vitro. However, P. yoelii-derived Hz but not synthetic Hz induced transient anemia in mice. These findings provide novel insights into the complex interactions between the parasite and host immune system and the regulation of erythropoiesis during severe malarial anemia.

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21

Darmani, Homa. "Erythrocyte adhesion by macromolecules." Thesis, Cardiff University, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.278681.

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22

Brown, Lola A. "The Effects of Sickle Erythrocytes on Endothelial Permeability." Thesis, Georgia Institute of Technology, 2005. http://hdl.handle.net/1853/6960.

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Sickle cell anemia is a hematological disorder that is caused by a single point mutation in the beta-globin chain of hemoglobin. It results in several complications related to the small and large vessels in patients with the disease. Large vessel complications include cerebral infarcts, which are observed in children under ten years old. The mechanism behind this complication is not completely understood. It is the goal of this project to begin to understand the role sickle erythrocytes may play in causing endothelial dysfunction as a precursor to sickle related complications. The hypothesis of this work is that exposure of large vessel endothelium to sickle erythrocytes causes an increase in endothelial permeability through loosening of adherens junctions. In the first goal of this work, bovine aortic endothelial cells (BAECs) are grown on coverslips and exposed to sickle erythrocytes for 5 minutes and either immediately fixed or incubated in 30 minutes and then fixed. Immunofluorescent studies labeling VE cadherin show changes in VE cadherin dynamics, suggesting sickle erythrocytes may be involved in this observation. Next, BAECs were grown on transwell inserts and exposed to sickle erythrocytes for 5 minutes. The erythrocytes are washed off and the BAEC are incubated with 10,000 MW dextran conjugated to lucifer yellow or FITC-BSA or to determine BAEC permeability. When dextran is used as the test molecule, endothelial permeability did not show a significant change from baseline. However, when BSA is used as the test molecule, increases in endothelial permeability are observed. Explanations into the differences between the transport mechanisms of the two molecules are discussed. These experiments show changes in VE cadherin localization due to sickle erythrocyte exposure. This may cause increases in endothelial permeability and an experimental model and preliminary studies are performed. This study provides potential mechanisms to explain the changes in VE cadherin localization and provide suggestions for further studies to test the effect of sickle erythrocytes on endothelial permeability. This work provides a strong foundation for continuing studies on the effects of sickle erythrocytes on endothelial dysfunction within the confines of sickle related complications.

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23

Smeets, Edgar Felix. "Scrambling of membrane phospholipids in platelets and erythrocytes." [Maastricht : Maastricht : Universiteit Maastrich] ; University Library, Maastricht University [Host], 1996. http://arno.unimaas.nl/show.cgi?fid=6693.

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24

Treutiger, Carl Johan. "Host cell adhesion of Plasmodium falciparum-infected erythrocytes /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-2952-1.

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25

Herricks, Thurston E. "Malaria pathogenesis : deformability limits of malaria infected erythrocytes /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8622.

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26

Lancaster, Jo-Ann M. "Volume-sensitive membrane transport in Xenopus laevis erythrocytes." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298236.

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27

Staines, Henry Michael. "Cation transport in Plasmodium falciparum-infected human erythrocytes." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298726.

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28

Maingot, Catherine. "The use of photosensitive erythrocytes in drug delivery." Thesis, University of Ulster, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.554334.

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The development of systems capable of delivering therapeutic agents in a site-specific manner continues to attract considerable attention, particularly for the treatment of focal disease such as many forms of cancer. Although many forms of delivery systems have emerged over the past 2 decades, the focus of my work has been directed towards the study of the erythrocyte as a potential drug delivery vehicle for possible clinical application in the treatment of solid tumours. The erythrocyte, as a drug delivery vehicle, has attracted a considerable degree of attention in the past, although many of the suggested applications depend on either passive delivery of therapeutic agents or in facilitating fortuitous targeting modalities based on sequestration by the reticuloendothelial system (RES). To date no erythrocyte-based system exists where application of an external stimulus can facilitate site-specific release and deposition at a pre-determined target site. The work in this thesis, therefore, describes my attempts to develop and assess such a system in order to facilitate delivery of therapeutic effects to solid tumours. In pursuing such an objective, the work in this thesis describes the development and assessment of an erythrocyte-based carrier system in vitro, exploiting fluorogenic tracers to demonstrate light- and ultrasound-stimulated release from the carrier and retention of the released payload at a target site. The work in this thesis goes beyond the existing state-of-the-art in describing the behaviour of the system in a phantom-based circulation system in order to demonstrate functionality in terms of stimulus-dependant release of payload from the system. Building on those studies, the work in this thesis extends into in vivo studies in mice using the stimulus- responsive erythrocyte-based system to demonstrate deposition of a therapeutic at a target site. In these studies, Iight- and ultrasound-stimulated site-specific deposition of indocyanine green was demonstrated and this was further exploited in order to demonstrate a therapeutic effect (reduction in tumour growth) at the deposition site. The data in this thesis suggest a significant potential role for a stimulus-responsive erythrocyte-based carrier system, particularly in the treatment of solid tumours.

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29

Shapiro, Vladimir Michael. "GOLD UPTAKE BY DICYANOGOLD(I) TREATED HUMAN ERYTHROCYTES." University of Cincinnati / OhioLINK, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=ucin998307802.

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30

Raththagala, Madushi Upendrika. "Defining a novel role of hydroxyurea on erythrocytes." Diss., Connect to online resource - MSU authorized users, 2008.

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31

Bütikofer, Peter. "Membrane vesiculation of normal and pathologic human erythrocytes /." [S.l : s.n.], 1987. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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32

McNamee, Antony. "Physical alterations to erythrocytes following sublethal mechanical stresses." Thesis, Griffith University, 2020. http://hdl.handle.net/10072/394320.

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Mechanical circulatory support (MCS) devices, extracorporeal membrane oxygenators, and dialysis machines are mechanical systems designed to replace and/or support the functionality of specific biological organs. These devices have been extensively developed over recent decades and are increasingly utilised in acute and chronic care, greatly improving patient outcomes and extending survival. Given these devices integrate into the human vasculature, the efficacy of mechanical circulation depends on: successful surgical implantation and infection prevention, long-term functional performance without mechanical failure, and biological compatibility minimising damaging interactions with blood (i.e., haemocompatibility). With improved device design, many current generation MCS devices have the capacity to adequately meet the required functional demands of associated biological organs, operating within parameters that avoid overt haemolysis and other extremes of inadequate haemocompatibility. Nevertheless, unfortunately the use of MCS remains plagued with severe secondary systemic complications which implicate impaired blood health and a functional decline of blood flow. While many precipitating determinants of these secondary complications remain unresolved, the accumulating clinical evidence indicates that the current haemocompatibility criteria is insufficient in predicting declines in blood function without the development of haemolysis (i.e., sublethal damage). Blood trauma may be induced by non-physiological flow environments, largely due to elevated shear forces, turbulence, and collision with other cellular and artificial surfaces within MCS. Consequently, fragmentation of red blood cells (RBCs), shortened cell life-spans, and decreased cell function may be observed at microvascular levels, leading to the development of acute tissue ischaemia, propagating chronic systemic complications (e.g., multi-system organ failure – where mortality is unavoidable). While there is need for improved, more sensitive, markers of haemocompatibility that can detect declining RBC function in non-haemolysed blood, only limited studies have investigated this sublethal trauma. The aim of the present dissertation was to mechanistically elucidate how non-physiological shear environments, typical of MCS, can adversely affect blood function and flow independent of haemolysis, leading to the development of multi-system organ failure and death. The dissertation provides a comprehensive discussion into the haemorheological alterations that occur following exposure of blood to shear stresses that are supraphysiological (i.e., >10 Pa) and subhaemolytic (i.e., less than that required to induce haemolysis), providing novel characterisation and avenues for future inspection. The findings of the current dissertation greatly enhance the understanding of the processes involved in the accumulation of functional blood damage observed in MCS, while progressing current understanding of red cell physiology. Further, the collective findings may in part explain current clinical complications associated with the use of MCS, possibly identifying rheological aetiologies for ischaemic complications, angiodysplasia, and the vascular related incidence of neurological complications. The collective studies conceivably provide the basis for the development of a more sensitive and holistic indicator of haemocompatibility, while facilitating the development of numerical models that will allow in silico optimisation that will rapidly accelerate the advancement of future MCS devices. Understanding the haemorheological interactions associated with blood trauma will also assist the clinical management of current patients exposed to various forms of mechanical circulation, providing potential avenues for targeted rheological pharmacotherapy and improved patient care.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School Allied Health Sciences
Griffith Health
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33

Allen, Bruce Gordon. "Studies on the reaction cycle of the calcium transport atpase from human erythrocytes." Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/24458.

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The plasma membrane calcium-transport ATPase plays a major role in maintaining the low cytosolic calcium concentrations required for normal cellular function. Calcium, magnesium, calmodulin and lanthanum have been shown to alter the activity of the calcium-stimulated, magnesium-dependent ATPase activity in human erythrocytes. In an attempt to examine the reaction sequence of the (Ca²⁺ + Mg²⁺)-ATPase, the effects of these agents on the kinetics of calcium dependent phosphoprotein formation, the first step in the partial reaction sequence, were examined. Calmo-dulin-depleted erythrocyte membranes were prepared by hypotonic lysis in the presence of EDTA, according to the method of Carafoli et al (1980). Calcium-dependent formation of the phosphorylated intermediate was biphasic; the high calcium-affinity component was associated with low levels of E.Ca.P and a shallow response to changing calcium concentrations, whereas in the region of the low calcium-affinity component, E.Ca.P rose sharply in response to increasing calcium concentrations. The low affinity component of E.Ca.P lies in the range of calcium concentrations which inhibit (Ca²⁺ + Mg²⁺)-ATPase activity. When analyzed on LiDS acid PAGE, both components of calcium-dependent phosphoprotein formation were due to hydroxylamine-sensitive phosphorylation of a 135,000-145,000 dalton protein. Hence, the low calcium-affinity component of phosphoprotein formation and calcium-dependent inhibition of (Ca²⁺ + Mg²⁺)-ATPase activity were likely due to calcium-inhibition of dephosphorylation. Kinetic studies of calcium-dependent phosphoprotein formation, at two different calcium concentrations (1.0 μM, 0.4 mM), indicated that a steady-state was reached much sooner at higher calcium concentrations. Lanthanum, which is known to block dephosphorylation of the intermediate complex, increased both the apparent rate of formation and the steady-state level of the phosphorylated intermediate. Calmodulin, which has previously been shown to increase both the maximum velocity and the calcium affinity of the (Ca²⁺ + Mg²⁺)-ATPase, did not affect either calcium-dependent inhibition of (Ca²⁺ + Mg²⁺ )-ATPase activity or the biphasic nature of calcium-dependent phosphoprotein formation. At low calcium concentrations, calmodulin increased the apparent rate of phosphoprotein formation, whereas at higher calcium concentrations (0.4 mM) calmodulin reduced the steady-state level of the phosphoprotein; the apparent rate of formation was unaffected. In the presence of lanthanum, calmodulin increased both the apparent rate of formation and steady-state level of the phosphoprotein, suggesting that the true rate of formation was increased by calmodulin at higher calcium concentrations, but this was normally hidden by a simultaneous increase in the rate of dephosphorylation. Removal of endogenous magnesium, using trans-1,2-diamino-cyclohexane tetraacetic acid (CDTA) did not alter the calcium sensitivity or rate of formation of the phosphorylated intermediate, however turnover of the intermediate was markedly reduced. In the absence of free magnesium, both the velocity and calcium sensitivity of the (Ca²⁺ + Mg²⁺)-ATPase were also found to be lower. The low calcium-affinity component of calcium-dependent phosphoprotein formation, which Schatzmann (1982) has attributed to an action of calcium at a "magnesium-specific" site, was not affected by magnesium concentrations as high as 1 mM. Furthermore, this phosphoprotein could be dephosphorylated along either the forward or reverse pathways. These results indicate that the transformation from E₁.Ca.P to E₂.Ca.P may not be the site of the calcium-dependent inhibition of dephosphorylation. Calmodulin-depleted membrane fragments were prepared from the erythrocytes of cystic fibrosis patients as well as age- and sex-matched controls. Under conditions in which dephosphoryla-tion is inhibited, phosphoprotein formation and (Ca²⁺ + Mg²⁺)-ATPase activities were determined. Both (Ca²⁺ + Mg²⁺)-ATPase activity and phoshoprotein formation were found to be significantly reduced in the preparations derived from patients with cystic fibrosis. Turnover of the phosphorylated intermediate did not differ significantly between the two groups. A reduction in (Ca²⁺ + Mg²⁺)-ATPase activity and phosphoprotein formation suggests that there may be fewer active calcium-pumping sites in the erythrocyte membranes of cystic fibrosis patients compared to normal subjects.
Pharmaceutical Sciences, Faculty of
Graduate

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34

Hughes, Mark Simon. "Lithium interactions with erythrocytes studied by NMR and AAS." Thesis, University of Wolverhampton, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.236152.

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35

Raynard, R. S. "Thermal compensation of transport systems of rainbow trout erythrocytes." Thesis, University of Liverpool, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233880.

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36

Burlak, Christopher II. "Analysis of Porcine Kupffer Cell Recognition of Human Erythrocytes." University of Toledo Health Science Campus / OhioLINK, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=mco1083268448.

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37

Geiss, Loren V. "Freeze tolerance and cryoprotection of erythrocytes from Dryophytes chrysoscelis." University of Dayton / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=dayton1533074960877566.

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38

Desai, Jeremy. "The encapsulation of pharmacologically active peptides into intact erythrocytes." Thesis, Aston University, 1985. http://publications.aston.ac.uk/12462/.

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39

Winski, Shannon Lee 1967. "Metabolism and toxicity of sodium arsenate in human erythrocytes." Diss., The University of Arizona, 1997. http://hdl.handle.net/10150/282320.

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Toxicity of arsenic species is dependent on chemical oxidation state. Inorganic arsenic in the trivalent state, arsenite or As(III), is more biologically active than pentavalent arsenic, arsenate or As(V), and is more toxic by most measures. As(V), however, is more stable and prevalent in the environment. One consequence of environmental exposure is peripheral vascular disease, which is primarily due to vascular changes, but toxicity to the erythrocyte has not been evaluated. To understand toxicity and the implications of arsenic oxidation state, human erythrocytes were utilized to model the uptake, biotransformation (metabolism) and toxicity of sodium arsenate, As(V). It was first established that biotransformation, both in vivo and in vitro, would not be limited by uptake of As(V) into the cell. Evidence suggested that reduction was accomplished by at least two separate pathways. All reductive metabolism was dependent on the presence of reduced thiols including both non-protein thiols (glutathione; GSH) and protein thiols (ProSH). These pathways are: (1) chemically mediated reduction by GSH and (2) protein mediated reduction. It was established that the protein-dependent pathway required a reduced protein thiol and also required the presence of GSH. This points to reduction through a redox coupling to form a protein mixed disulfide (ProSSG). Toxicity to the erythrocyte was evaluated by determining total cell death, morphologic changes and effects on the energy cofactor adenosine triphosphate (ATP). Based on these three parameters, the erythrocyte was more susceptible to As(V) and not As(III) as other tissues are. The morphologic effects on the cell were also consistent with ATP depletion. These changes were characterized by formation of morphologically altered cells that are unable to deform in circulation effectively and occlude the microcirculation. This could contribute to vascular tissue damage associated with arsenic-induced circulatory disorders. In summary, the erythrocyte is able to take in As(V) which is detrimental to the ability of the cell to perform its intended function. Biotransformation to As(III) would therefore be a detoxifying event, and understanding the factors involved in biotransformation will help to understand human susceptibility to arsenic-induced vascular disease.

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40

陳思潁 and Sze-wing Scarlet Chan. "Erythroleukemic cell differentiation factor (EDF): biochemical, cloning, molecular structure, and functionalstudies." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B30269076.

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Dhaliwal, Kanwaljit. "A study of membrane choline transport and renal failure." Thesis, King's College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300380.

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Crick, Alex James. "Live imaging studies of the interactions of the malaria parasite with the human erythrocyte." Thesis, University of Cambridge, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708165.

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43

Greyling, H. J. "The reconstitution of the histone octamer." Doctoral thesis, University of Cape Town, 1987. http://hdl.handle.net/11427/22553.

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Bibliography: pages 110-126.
This thesis describes methodology for the reconstitution of the chicken erythrocyte octamer from acid-denatured histones or the natural H3-H4 tetramer and H2A-H2B dimers. Oligomeric properties of reconstituted octamers were elucidated during column chromatographic and chemical cross-linking studies. The conformational identity of the natural and reconstituted octamers was demonstrated by the ability of all preparations to crystallise as helical octamer tubes. The application of the reconstitution methodology in addressing fundamental problems of chromatin research, was demonstrated during subsequent studies, namely (i) The reconstitution of hybrid histone octamers containing a structural variant of a specific histone. These studies were undertaken to study the effect on histone-histone interactions in hybrid octamers of which erythrocyte H2B was substituted for by sea urchin sperm H2B(l) or erythrocyte H3 and H4 were substituted for by dethiolated H3 and sea urchin sperm H4 respectively. (ii) The reconstitution of an octamer suitable for the sitespecific derivatisation of a specific histone, or covalently labelled with aurothiomalate in a specific histone complex. These studies were concluded to represent general labelling strategies which may be of use in crystallographic or physico-chemical studies of nucleosome structure.

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Chan, Sze-wing Scarlet. "Erythroleukemic cell differentiation factor (EDF) : biochemical, cloning, molecular structure, and functional studies /." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B23472662.

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45

Yau, Tsz Wai. "Erythrocyte membrane dynamics and engineering : studies of the cell's morphology, metabolism, membrane flickering and transport." Thesis, The University of Sydney, 2011. https://hdl.handle.net/2123/28842.

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A cell is the fundamental unit of living things. All cells are encapsulated by a phospholipid bilayer called the cell membrane, which is important for enclosing cellular contents. The cell membrane contains cholesterol, proteins (both peripheral and integral), and carbohydrate chains that attach to either membrane proteins or phospholipids (glycoproteins, or glycolipid, respectively). The cell membrane is generally semipermeable to small solutes (e.g. water, 02, and CO2), and the transmembrane exchange is regulated extensively by various channels and transporters. The central theme of this thesis is to understand the biophysics and biochemical properties of the cell membrane in relation to the cell's ability to deform and adapt to physical and chemical stress. I focus on the human red blood cell (RBC), using various cytotoxins as agents that alter membrane properties. The human RBC is a non-nucleated cell filled with haemoglobin,~ 150 g (L of whole blood)"1, which circulates around the body via the cardiovascular system, exchanging gases (oxygen and carbon dioxide) for various tissues in the human body. During circulation through narrow blood capillaries (sometimes ~2-3 µm in diameter) an RBC is able to withstand large shear stresses, which in addition to its simple cell structure, having no organelles, makes it an ideal model to study cell membrane biology. The dynamics of RBC membrane fluctuation ("flickering") are believed to be an important contribution to the cell's ability to "wiggle" through narrow capillaries. There exists a controversy as to whether flickering is thermodynamically or metabolically driven. Differential interference contrast (DIC) microscopy was used to investigate RBC flickering under various biochemical stresses. A computer model of the RBC was used to simulate flickering data for comparison with the experimental DIC results.

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Niedowicz, Dana M. "The mechanisms of hyperglycemia-induced oxidative stress in human erythrocytes." [Bloomington, Ind.] : Indiana University, 2006. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:3204307.

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Thesis (Ph. D.)--Indiana University, Dept. of Biology, 2006.
Source: Dissertation Abstracts International, Volume: 67-01, Section: B, page: 0043. Adviser: David L. Daleke. "Title from dissertation home page (viewed Feb. 21, 2007)."

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MacMeccan, Robert Miles III. "Mechanistic Effects of Erythrocytes on Platelet Deposition in Coronary Thrombosis." Diss., Georgia Institute of Technology, 2007. http://hdl.handle.net/1853/19786.

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A new lattice-Boltzmann finite-element method is used to simulate large numbers of deformable red blood cells and platelets in suspension for the investigation of stress-mediated platelet-deposition mechanisms in blood. The coupled lattice-Boltzmann finite-element method provides the novel ability to simulate hundreds of realistic and deformable red blood cells and produce continuum-scale physics at physiologic hematocrit and low arterial-shear rates. The new method is developed and shown to produce single red blood cell deformation consistent with experimental results in flow chambers. Simulations of 77 to 216 cells in unbounded shear flow produce bulk and micro-rheological behavior consistent with experimental results in viscometers and tubes, including shear-thinning behavior at various shear rates. Investigation of the local stress environment in blood indicates that, although the majority of platelets experience a time-averaged shear stress equal to the suspension stress, 25% of platelets experience a localized shear stress greater than twice the suspension stress. The lattice-Boltzmann finite-element method developed in this work has been shown capable of investigating the fundamental gap between cell-level processes and continuum-level function. The complex stress environment in whole blood has been described for simple shear flow and the methodology may be extended to more complex flow geometries and incorporate platelet-adhesion models for adhesion studies. Thus, this research fits into the greater objective of prediction and control of platelet deposition in clinical and engineering applications. Furthermore, the ability to bridge the gap between cell-level processes and continuum-level function is useful in other important cardiovascular areas including leukocyte adhesion, platelet aggregate embolization, and artheriogenesis.

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Sharma, Mana L. "Origins and consequences of mitochondrial decline in rainbow trout erythrocytes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0018/MQ53025.pdf.

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Grudzien, Simon Paul. "Exercise-induced net and unidirectional potassium transport in human erythrocytes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ56329.pdf.

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Liew, Yew Wah. "Lectins with predominant specificity for erythrocytes treated with various enzymes." Thesis, University of Portsmouth, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.292399.

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