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Relevant bibliographies by topics / Erythrocytes Malaria Plasmodium falciparum

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Academic literature on the topic 'Erythrocytes Malaria Plasmodium falciparum'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Erythrocytes Malaria Plasmodium falciparum"

1

Haldar, Kasturi, and Narla Mohandas. "Malaria, erythrocytic infection, and anemia." Hematology 2009, no. 1 (January 1, 2009): 87–93. http://dx.doi.org/10.1182/asheducation-2009.1.87.

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Abstract Malaria is a major world health problem. It results from infection of parasites belonging to the genus Plasmodium. Plasmodium falciparum and Plasmodium vivax cause the major human malarias, with P falciparum being the more virulent. During their blood stages of infection, both P falciparum and P vivax induce anemia. Severe malarial anemia caused by P falciparum is responsible for approximately a third of the deaths associated with disease. Malarial anemia appears to be multi-factorial. It involves increased removal of circulating erythrocytes as well as decreased production of erythrocytes in the bone marrow. The molecular mechanisms underlying malarial anemia are largely unknown. Over the last five years, malaria parasite ligands have been investigated for their remodeling of erythrocytes and possible roles in destruction of mature erythrocytes. Polymorphisms in cytokines have been associated with susceptibility to severe malarial anemia: these cytokines and malaria “toxins” likely function by perturbing erythropoiesis. Finally a number of co-infections increase susceptibility to malarial anemia, likely because they exacerbate inflammation caused by malaria. Because of the complexities involved, the study of severe malarial anemia may need a “systems approach” to yield comprehensive understanding of defects in both erythropoiesis and immunity associated with disease. New and emerging tools such as (i) mathematical modeling of the dynamics of host control of malarial infection, (ii) ex vivo perfusion of human spleen to measure both infected and uninfected erythrocyte retention, and (iii) in vitro development of erythroid progenitors to dissect responsiveness to cytokine imbalance or malaria toxins, may be especially useful to develop integrated mechanistic insights and therapies to control this major and fatal disease pathology.

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Klotz, F. W., J. D. Chulay, W. Daniel, and L. H. Miller. "Invasion of mouse erythrocytes by the human malaria parasite, Plasmodium falciparum." Journal of Experimental Medicine 165, no. 6 (June 1, 1987): 1713–18. http://dx.doi.org/10.1084/jem.165.6.1713.

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Plasmodium falciparum malaria merozoites require erythrocyte sialic acid for optimal invasion of human erythrocytes. Since mouse erythrocytes have the form of sialic acid found on human erythrocytes (N-acetyl neuraminic acid), mouse erythrocytes were tested for invasion in vitro. The Camp and 7G8 strains of P. falciparum invaded mouse erythrocytes at 17-45% of the invasion rate of human erythrocytes. Newly invaded mouse erythrocytes morphologically resembled parasitized human erythrocytes as shown on Giemsa-stained blood films and by electron microscopy. The rim of parasitized mouse erythrocytes contained the P. falciparum 155-kD protein, which is on the rim of ring-infected human erythrocytes. Camp but not 7G8 invaded rat erythrocytes, indicating receptor heterogeneity. These data suggest that it may be possible to adapt the asexual erythrocytic stage of P. falciparum to rodents. The development of a rodent model of P. falciparum malaria could facilitate vaccine development.

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Kirchgatter, Karin, and Hernando A. Del Portillo. "Clinical and molecular aspects of severe malaria." Anais da Academia Brasileira de Ciências 77, no. 3 (September 2005): 455–75. http://dx.doi.org/10.1590/s0001-37652005000300008.

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The erythrocytic cycle of Plasmodium falciparum presents a particularity in relation to other Plasmodium species that infect man. Mature trophozoites and schizonts are sequestered from the peripheral circulation due to adhesion of infected erythrocytes to host endothelial cells. Modifications in the surface of infected erythrocytes, termed knobs, seem to facilitate adhesion to endothelium and other erythrocytes. Adhesion provides better maturation in the microaerophilic venous atmosphere and allows the parasite to escape clearance by the spleen which recognizes the erythrocytes loss of deformability. Adhesion to the endothelium, or cytoadherence, has an important role in the pathogenicity of the disease, causing occlusion of small vessels and contributing to failure of many organs. Cytoadherence can also describe adhesion of infected erythrocytes to uninfected erythrocytes, a phenomenon widely known as rosetting. Clinical aspects of severe malaria, as well as the host receptors and parasite ligands involved in cytoadherence and rosetting, are reviewed here. The erythrocyte membrane protein 1 of P. falciparum (PfEMP1) appears to be the principal adhesive ligand of infected erythrocytes and will be discussed in more detail. Understanding the role of host receptors and parasite ligands in the development of different clinical syndromes is urgently needed to identify vaccination targets in order to decrease the mortality rates of this disease.

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Willimann, K., H. Matile, N. A. Weiss, and B. A. Imhof. "In vivo sequestration of Plasmodium falciparum-infected human erythrocytes: a severe combined immunodeficiency mouse model for cerebral malaria." Journal of Experimental Medicine 182, no. 3 (September 1, 1995): 643–53. http://dx.doi.org/10.1084/jem.182.3.643.

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Cerebral malaria is a fatal complication of infection by Plasmodium falciparum in man. The neurological symptoms that characterize this form of malarial disease are accompanied by the adhesion of infected erythrocytes to the vasculature of the brain. To study this phenomenon in vivo, an acute phase severe combined immunodeficiency (SCID) mouse model was developed in which sequestration of P. falciparum-infected human erythrocytes took place. During acute cerebral malaria in humans, the expression of intercellular adhesion molecule-1 (ICAM-1) is induced in vascular endothelium by inflammatory reactions. Acute phase ICAM-1 expression can also be obtained in SCID mice. The endothelium of the midbrain region was the most responsive to such inflammatory stimulus. It is noteworthy that the reticular formation in the midbrain controls the level of consciousness, and loss of consciousness is a symptom of cerebral malaria. We found that infected human erythrocytes were retained 24 times more than normal erythrocytes in ICAM-1-positive mouse brain. Sequestration to the brain was reduced by anti-ICAM-1 antibodies. These in vivo results were confirmed by the binding of P. falciparum-infected erythrocytes to the ICAM-1-positive endothelium in tissue sections of mouse brain. We conclude that the SCID mouse serves as a versatile in vivo model that allows the study of P. falciparum-infected erythrocyte adhesion as it occurs in human cerebral malaria. Upregulation of ICAM-1 expression in the region of the midbrain correlates with increased retention of malaria-infected erythrocytes and with the symptoms of cerebral malaria.

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Kaur, Prabhjot, Arun Bhatia, Kanav Midha, and Mampi Debnath. "Malaria: A Cause of Anemia and Its Effect on Pregnancy." World Journal of Anemia 1, no. 2 (2017): 51–62. http://dx.doi.org/10.5005/jp-journals-10065-0012.

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ABSTRACT Malaria is one of the major health problems in the world. It remains an important cause of very high human morbidity and mortality, especially, among children and pregnant women. It results from the infection of parasites belonging to the genus Plasmodium. Plasmodium falciparum and Plasmodium vivax are the major pathogens responsible for causing human malaria. Approximately 75% of cases are caused by P. falciparum and associated with the mortality rate of approximately 0.5 to 1.0%. Both P. falciparum and P. vivax induce anemia during their erythrocytic stages of infection. Most of the malarial infections are related to some degree of anemia, the severity of which depends upon patient-specific characteristics (e.g., age, innate and acquired resistance, comorbid features, etc.) as well as parasite-specific characteristics (e.g., species, adhesive, and drug-resistant phenotype, etc.). Malarial anemia encompasses reduced production of erythrocytes as well as increased removal of circulating erythrocytes in the bone marrow. Susceptibility to severe malarial anemia is associated with the polymorphisms of the cytokines, which are likely to function by perturbing erythropoiesis. This article reviews the epidemiology, pathophysiology, clinical features, treatment, and various complications occurring due to malarial anemia. The second part of this article also focuses on the effect of malaria during pregnancy. Some significant effects of malaria during pregnancy include spontaneous abortion, preterm delivery, low birthweight, stillbirth, congenital infection, and maternal death. How to cite this article Saxena R, Bhatia A, Midha K, Debnath M, Kaur P. Malaria: A Cause of Anemia and Its Effect on Pregnancy. World J Anemia. 2017;1(2):51-62.

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Muniz-Junqueira, Maria Imaculada, and Carlos Eduardo Tosta. "Stages of in vitro phagocytosis of Plasmodium falciparum-infected erythrocytes by human monocytes." Revista da Sociedade Brasileira de Medicina Tropical 42, no. 2 (April 2009): 103–6. http://dx.doi.org/10.1590/s0037-86822009000200001.

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Monocytes/macrophages play a critical role in the defense mechanisms against malaria parasites, and are the main cells responsible for the elimination of malaria parasites from the blood circulation. We carried out a microscope-aided evaluation of the stages of in vitro phagocytosis of Plasmodium falciparum-infected erythrocytes, by human monocytes. These cells were obtained from healthy adult individuals by means of centrifugation through a cushion of Percoll density medium and were incubated with erythrocytes infected with Plasmodium falciparum that had previously been incubated with a pool of anti-plasmodial immune serum. We described the stages of phagocytosis, starting from adherence of infected erythrocytes to the phagocyte membrane and ending with their destruction within the phagolisosomes of the monocytes. We observed that the different erythrocytic forms of the parasite were ingested by monocytes, and that the process of phagocytosis may be completed in around 30 minutes. Furthermore, we showed that phagocytosis may occur continuously, such that different phases of the process were observed in the same phagocyte.

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Kesely, Kristina, Panae Noomuna, Michal Vieth, Philip Hipskind, Kasturi Haldar, Antonella Pantaleo, Francesco Turrini, and Philip S. Low. "Identification of tyrosine kinase inhibitors that halt Plasmodium falciparum parasitemia." PLOS ONE 15, no. 11 (November 12, 2020): e0242372. http://dx.doi.org/10.1371/journal.pone.0242372.

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Although current malaria therapies inhibit pathways encoded in the parasite’s genome, we have looked for anti-malaria drugs that can target an erythrocyte component because development of drug resistance might be suppressed if the parasite cannot mutate the drug’s target. In search for such erythrocyte targets, we noted that human erythrocytes express tyrosine kinases, whereas the Plasmodium falciparum genome encodes no obvious tyrosine kinases. We therefore screened a library of tyrosine kinase inhibitors from Eli Lilly and Co. in a search for inhibitors with possible antimalarial activity. We report that although most tyrosine kinase inhibitors exerted no effect on parasite survival, a subset of tyrosine kinase inhibitors displayed potent anti-malarial activity. Moreover, all inhibitors found to block tyrosine phosphorylation of band 3 specifically suppressed P. falciparum survival at the parasite egress stage of its intra-erythrocyte life cycle. Conversely, tyrosine kinase inhibitors that failed to block band 3 tyrosine phosphorylation but still terminated the parasitemia were observed to halt parasite proliferation at other stages of the parasite’s life cycle. Taken together these results suggest that certain erythrocyte tyrosine kinases may be important to P. falciparum maturation and that inhibitors that block these kinases may contribute to novel therapies for P. falciparum malaria.

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Fujioka, H., and M. Aikawa. "Molecular Pathogenesis of Cerebral Malaria." Microscopy and Microanalysis 3, S2 (August 1997): 39–40. http://dx.doi.org/10.1017/s143192760000708x.

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Plasmodium falciparum, the most malignant human malaria, is responsible for 2-3 million deaths annually. These infections often involve blockage of the cerebral microvasculature by P. falciparum-infected erythrocytes (Fig. 1). This aspect is considered the major factor in the pathogenesis of cerebral malaria.Upon invasion of the erythrocyte, P. falciparum immediately begins to remodel the infected erythrocyte. The adherence points of infected erythrocytes, termed knobs (Fig. 2 and 3), contain antigenically diverse 200-350kDa surface proteins (PfEMPl; Fig. 4). The PfEMPl variant surface proteins are encoded by a large and extremely diverse family of genes (var), and switches in the expression of var genes account for rapid changes in the antigenic and adhesive properties of P. falciparum-inkcted erythrocytes (2.4% per generation). Switches in the PfEMPl expression may not only affect the phenotype of the parasite strain but may also change its sequestration to endothelial cells. Genetic reorganization in this protein can lead to binding any of the following endothelial cell receptors; ICAM-1, CD36, thrombospondin, chondroitin sulfate (Fig. 5),2 ELAM-1, or VCAM-1.

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Murphy, Sean C., Souvik Bhattacharjee, Travis Harrison, and Kasturi Haldar. "Accessing the Erythrocyte Cytoplasm: A Method for Manipulating the Intracellular Environment of Erythrocytes for the Study of Malaria Invasion, Trafficking and Growth." Blood 104, no. 11 (November 16, 2004): 3688. http://dx.doi.org/10.1182/blood.v104.11.3688.3688.

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Abstract Invasion of erythrocytes by malaria parasites requires participation of both parasite ligands and host determinants. Further recent studies show that erythrocyte G protein signaling regulates malarial infection. Many of the Gs-associated signaling components reside on the cytoplasmic leaflet of the erythrocyte plasma membrane, rendering them inaccessible to most extracellular probes. Since erythrocytes are enucleated and terminally differentiated, they cannot be transfected to express exogenous transgenes. We have modified methods of hypotonic lysis and isotonic resealing to generate loaded erythrocyte ghosts that can be efficiently infected by Plasmodium falciparum and sustain normal levels of intraerythrocytic parasite growth and replication. Further, we show that these ghosts can be filled with various membrane-impermeable peptides or other proteinaceous cargoes for studying signaling and transport events inside the erythrocyte. Resealed ghosts morphologically resemble normal erythrocytes, albeit with reduced hemoglobin content. Other measures of erythrocyte function and malarial infection are being investigated. Studies will be presented on the use of ‘reconstituted’ erythrocytes in elucidating mechanisms parasite invasion as well as parasite protein trafficking in erythrocytes infected by P. falciparum.

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López, José A. "Malignant malaria and microangiopathies: merging mechanisms." Blood 115, no. 7 (February 18, 2010): 1317–18. http://dx.doi.org/10.1182/blood-2009-12-254060.

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Abstract In this issue of Blood, Bridges and colleagues report that Plasmodium falciparum–infected erythrocytes are able to attach to the endothelial surface by binding platelet-decorated VWF strands in a CD36-dependent fashion, revealing a new mechanism for erythrocyte cytoadherence in malaria.1

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Dissertations / Theses on the topic "Erythrocytes Malaria Plasmodium falciparum"

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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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Jones, Matthew L. "Erythrocyte invasion by Plasmodium falciparum." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2009r/jonesm.pdf.

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Cranmer, Susan Louise. "Characterisation of altered monocarboxylate transport in erythrocytes parasitised by Plasmodium falciparum." Thesis, University of Bristol, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.358773.

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Pettersson, Fredrik. "Sequestration, virulence and future interventions in Plasmodium falciparum malaria." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-568-2/.

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Vogt, Anna. "Heparan sulfate dependent sequestration during Plasmodium falciparum malaria /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-994-3/.

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Scholander, Carin. "Immunoglobulins in the adhesion of Plasmodium falciparum-infected erythrocytes in malaria /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4235-8/.

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Gardner, Jason Paul. "Surface changes to human erythrocytes on infection by Plasmodium falciparum malaria." Thesis, University of Oxford, 1994. http://ora.ox.ac.uk/objects/uuid:5ecd0f5c-8189-4731-a643-d6cf9463e4e5.

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Of the four Plasmodium species which cause malaria in humans, P. falciparum is responsible for the majority of the morbidity and mortality associated with this disease. The surface expression of parasite-derived proteins in the middle of the asexual cycle coincides with two important modifications of the host erythrocyte. First, a protective immune response is directed against a family of variant antigens, known as P. falciparum Erythrocyte Membrane Protein-1 (PfEMPl). Second, ligands are detected at the surface which mediate the specific cytoadherence of infected erythrocytes to vascular endothelium, such that infected cells are sequestered away from the peripheral circulation in deep vascular beds. The potentially fatal syndrome known as cerebral malaria can ensue when infected cells sequester at high density in the brain. Indirect studies have shown that the antigenic and adhesive phenotypes at the surface are linked to the expression of PfEMPl. However, there is a paucity of biochemical data which relate to PfEMPl, and this problem is addressed in this thesis. This study has confirmed, at the biochemical level, inferences from serology that clonal antigenic variation occurred rapidly. Variation produced a number of novel antigenic and adhesive phenotypes which were associated with unique forms of PfEMPl. Further insights into the mechanism of sequestration were possible because of the finding that single infected erythrocytes had the capacity to bind to at least three putative endothelial cell receptors; CD36, Intercellular Adhesion Molecule-1 (ICAM1), and Thrombospondin (TSP). It was demonstrated for the first time that PfEMPl was responsible for cytoadherence to CD36 and ICAM1, but was probably not involved in adhesion to TSP. Extensive analysis with sequence-specific proteases proved that adhesive interactions with each receptor were separable properties of the surface, and facilitated the proposal of a domain model for PfEMPl. Detailed analysis of the antigenic and adhesive phenotypes of a series of clonally-derived parasites demonstrated that infected cells expressing all variant antigenic types could adhere to CD36 whereas adhesion to ICAM1 was seen in a restricted subset. This may be clinically relevant if, as current data suggests, adhesion of infected cells to ICAM1 is important in the development of cerebral malaria. Identification of all ICAM1 binding phenotypes could lead to the design of novel therapeutic strategies for this life-threatening condition.

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Corrigan, Ruth Alexandra. "Rosetting and the innate immune response to Plasmodium falciparum." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/4041.

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Rosetting is an adhesion property of malaria parasites whereby infected erythrocytes bind to two or more uninfected erythrocytes, forming a so-called rosette. Rosetting of Plasmodium falciparum is associated with disease severity and high parasitaemia in sub-Saharan Africa, although currently the function of rosetting remains unknown. An early IFNg response elicited from the innate immune system is associated with resolution of malaria infection in mice. Published data suggests that optimal IFNg production may require contact between peripheral blood mononuclear cells and P. falciparum infected erythrocytes. The first part of this thesis investigates the hypothesis that rosetting is an immune evasion strategy to hide infected erythrocytes from detection by innate immune cells. Across five laboratory strains of P. falciparum rosetting was not associated with differential IFNg production when parasites were grown in group O blood. Reappraisal of the data with respect to blood group for one strain found that rosetting significantly reduced the IFNg response to parasites grown in group A blood (P=0.022, Wilcoxon signed-rank test), where it is known that rosettes are bigger and stronger. This is consistent with the hypothesis that rosetting is an immune evasion strategy and the first study to find evidence for a function of rosetting. Further work is needed in order to generalise this finding. The cytokine response to P. falciparum varies between people and this variation may be indicative of disease progression. In mice infected with malaria it is also apparent that parasite strain can determine the cytokine response of the host. It is unclear whether P. falciparum strains vary in their ability to induce cytokines. The second part of this thesis investigates variation in cytokine induction between P. falciparum strains. Across four laboratory strains of P. falciparum, IFNg production was significantly dependent on parasite strain (F3,178= 48.49, P<0.001). Production of GM-CSF, IL-1b, IL-6, IL-10 and TNFa significantly correlated with production of IFNg (P<0.001, Pearson correlation) and followed the same strain-dependent pattern. The ratio of pro-inflammatory cytokines to IL-10 was also dependent on parasite strain. These data provide strong evidence for P. falciparum strain-dependent cytokine responses which may be an important determinant of disease outcome. Phagocytosis by splenic macrophages is proposed to be the principle mechanism of parasitaemia control in malaria infection. CD36 mediated phagocytosis may by an important mechanism of non-opsonic parasite clearance. The final part of this thesis investigates the hypothesis that rosetting is an immune evasion strategy of P. falciparum in order to evade phagocytic clearance, in particular that mediated by CD36. Overall the data obtained were inconsistent. Phagocytosis was significantly reduced in rosetting versus non-rosetting parasites in some strains (e.g. R29; P=0.048, paired T test), whereas others showed no effect (e.g. Muz12; P=0.228, paired T test) or increased versus non-rosetting parasites (e.g. HB3, P=0.004, paired T test). The relationship between CD36 binding and phagocytosis was also unclear, and anti-CD36 antibody did not effectively block phagocytosis, suggesting the involvement of alternative mechanisms. Further experiments are needed to clarify these observations. Data presented in this thesis are suggestive that rosetting in non-group O blood may be an immune evasion strategy with regard to IFNg production by innate immune cells, mechanistically linking rosetting with enhanced parasitaemia and disease severity. Furthermore, parasite strain significantly affects cytokine production and may be a determinant of disease outcome. This thesis demonstrates the importance of continued research into the effect of parasite virulence on the immune response, with particular emphasis on rosetting.

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9

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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McCormick, Christopher John. "An investigation of the interactions between Plasmodium falciparum-infected erythrocytes and endothelium." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318757.

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Books on the topic "Erythrocytes Malaria Plasmodium falciparum"

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1941-, Eaton John Wallace, Meshnick Steven R, and Brewer George J. 1930-, eds. Malaria and the red cell 2: Proceedings of the Second Workshop on Malaria and the Red Cell, held in Ann Arbor, Michigan, October 24, 1988. New York: A.R. Liss, 1989.

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Patel, Samir. CD36-mediated clearance of Plasmodium falciparum-infected erythrocytes by rodent monocytes/macrophages. Ottawa: National Library of Canada, 2003.

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Golightly, Edmond Kwashie Odartey. Interaction between nutritional deficiencies and Plasmodium Falciparum malaria in the Gambia. Uxbridge: Brunel University, 1988.

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Group, Nature Publishing, ed. Nature: Plasmodium genome : scientific achievement and medical opportunity. London]: Nature Publishing Group, 2003.

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Mills, Caroline Dawn. Characterization of ligands mediating adherence of Plasmodium falciparum-infected erythrocytes to CD36 and ICAM-1. Ottawa: National Library of Canada, 1999.

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Iqbal, M. P. Investigation of the TFIIB and fibrillarin genes in the human malaria parasite plasmodium falciparum. Manchester: UMIST, 1996.

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Malaria resistance or susceptibility in red cells disorders. Hauppauge, NY: Nova Science, 2009.

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Malaria and the red cell 2: Proceedings of the Second Workshop on Malaria and the Red Cell, held in Ann Arbor, Michigan, October 24, 1988 (Progress in clinical and biological research). A.R. Liss, 1989.

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Gregory, Bock, Cardew Gail, Novartis Foundation, and Symposium on Transport and Trafficking in the Malaria-Infected Erythrocyte (1999 : London, England), eds. Transport and trafficking in the malaria-infected erythrocyte. Chichester: John Wiley, 1999.

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Transport and Trafficking in the Malaria-Infected Erythrocyte - No. 226. John Wiley & Sons, 2000.

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Book chapters on the topic "Erythrocytes Malaria Plasmodium falciparum"

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Tan, Joshua, and Peter C. Bull. "Agglutination Assays of the Plasmodium falciparum-Infected Erythrocyte." In Malaria Vaccines, 115–29. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2815-6_10.

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Bei, Amy Kristine, and Manoj T. Duraisingh. "Measuring Plasmodium falciparum Erythrocyte Invasion Phenotypes Using Flow Cytometry." In Malaria Vaccines, 167–86. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2815-6_14.

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Teo, Andrew, Wina Hasang, Philippe Boeuf, and Stephen Rogerson. "A Robust Phagocytosis Assay to Evaluate the Opsonic Activity of Antibodies against Plasmodium falciparum-Infected Erythrocytes." In Malaria Vaccines, 145–52. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2815-6_12.

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Teo, Andrew, Wina Hasang, and Stephen Rogerson. "Evaluating IgG Antibody to Variant Surface Antigens Expressed on Plasmodium falciparum Infected Erythrocytes Using Flow Cytometry." In Malaria Vaccines, 207–13. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2815-6_17.

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Mbengue, Alassane, Laurence Berry, and Catherine Braun-Breton. "Establishment of Plasmodium falciparum Extracellular Compartments in its Host Erythrocyte." In Heat Shock Proteins of Malaria, 133–59. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7438-4_8.

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Ballou, W. R., K. E. Kester, and D. G. Heppner. "Pre-Erythrocytic Malaria Vaccines to Prevent Plasmodium falciparum Malaria." In Chemical Immunology and Allergy, 253–61. Basel: KARGER, 2002. http://dx.doi.org/10.1159/000058848.

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Baumeister, Stefan, Alexander Burgwedel, Uwe-G. Maier, and Klaus Lingelbach. "Reconstitution of Protein Transport Across the Vacuolar Membrane in Plasmodium Falciparum-Infected Permeabilized Erythrocytes." In Novartis Foundation Symposium 226 - Transport and Trafficking in the Malaria-Infected Erythrocyte, 145–56. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470515730.ch11.

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Bozdech, Zbynek, and Erwin Schurr. "Protein Transport in the Host Cell Cytoplasm and ATP-Binding Cassette Proteins in Plasmodium Falciparum-Infected Erythrocytes." In Novartis Foundation Symposium 226 - Transport and Trafficking in the Malaria-Infected Erythrocyte, 231–51. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470515730.ch16.

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Bray, Patrick G., Omar Janneh, and Stephen A. Ward. "Chloroquine Uptake and Activity is Determined by Binding to Ferriprotoporphyrin IX in Plasmodium Falciparum." In Novartis Foundation Symposium 226 - Transport and Trafficking in the Malaria-Infected Erythrocyte, 252–64. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470515730.ch17.

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Laine, Roger A. "Glycosaminoglycans and Related Structures as Potential Inhibitors for Erythrocyte Infection by Plasmodium Falciparum Malaria." In Nonanticoagulant Actions of Glycosaminoglycans, 163–70. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0371-8_12.

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Conference papers on the topic "Erythrocytes Malaria Plasmodium falciparum"

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Zoueu, J. T., S. Ouattara, A. Toure, S. Safi, and S. T. Zan. "Spectroscopic approach of multispectral imaging of plasmodium falciparum - infected human erythrocytes." In 2009 3rd ICTON Mediterranean Winter Conference (ICTON-MW 2009). IEEE, 2009. http://dx.doi.org/10.1109/ictonmw.2009.5385598.

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Yu, Xinran, Turgay Korkmaz, Timothy G. Lilburn, Hong Cai, Jianying Gu, and Yufeng Wang. "Heavy path mining reveals novel protein-protein associations in the malaria parasite plasmodium falciparum." In 2014 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2014. http://dx.doi.org/10.1109/bibm.2014.6999137.

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Valiyaveettil, Manojkumar, Rajeshwara N. Achur, Abdulnaser Alkhalil, and Rajeshwara D. Channe Gowda. "STRUCTURAL ELEMENTS OF CHONDROITIN 4-SULFATE DODECAMER INVOLVED IN THE ADHESION OF PLASMODIUM FALCIPARUM-INFECTED ERYTHROCYTES." In XXIst International Carbohydrate Symposium 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.691.

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Hawkins, K., R. Burton, and P. LaBarre. "Diagnostics to support malaria elimination: Choosing an appropriate biomarker to target the subclinical Plasmodium falciparum transmission reservoir." In 2014 IEEE Global Humanitarian Technology Conference (GHTC). IEEE, 2014. http://dx.doi.org/10.1109/ghtc.2014.6970339.

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Muhimmah, Izzati, Nani Harniawati, and Novyan Lusiyana. "Characteristics determination of infected erithrocytes by plasmodium falciparum as a diagnostic of malaria, based on microscopic images." In 2017 International Conference on Advances in Computing, Communications and Informatics (ICACCI). IEEE, 2017. http://dx.doi.org/10.1109/icacci.2017.8126113.

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John A., Adegoke, Kochan Kamila, Heraud Philip, and Wood Bayden R. "NIR “matchbox size” spectrometer can quantify and detect malaria infection in Plasmodium falciparum infected red blood cells." In Asian Spectroscopy Conference 2020. Institute of Advanced Studies, Nanyang Technological University, 2020. http://dx.doi.org/10.32655/asc_8-10_dec2020.51.

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Sabilil Muttaqin, Sahal, and Jaler Sekar Maji. "Screening of Oxamic Acid Similar 3D Structures as Candidate Inhibitor Plasmodium falciparum L-Lactate Dehydrogenase of Malaria Through Molecular Docking." In 2018 1st International Conference on Bioinformatics, Biotechnology, and Biomedical Engineering (BioMIC). IEEE, 2018. http://dx.doi.org/10.1109/biomic.2018.8610537.

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Yu, Xinran, Hao Zhang, Timothy G. Lilburn, Hong Cai, Jianying Gu, Turgay Korkmaz, and Yufeng Wang. "Just-in-time expression of influential genes in the cellular networks of the malaria parasite Plasmodium falciparum during the red blood cycle." In 2016 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2016. http://dx.doi.org/10.1109/bibm.2016.7822526.

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Ribeiro, Deborah Helen Fabiano. "MALÁRIA: NOVAS PERSPECTIVAS DE PREVENÇÃO." In I Congresso Brasileiro de Parasitologia Humana On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/713.

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Abstract:

Introdução: Em 2014 houve cerca de 214 milhões de casos de malária mundiais, com uma estimativa de 438.000 óbitos, muitos na África subsaariana. O Brasil, por seus aspectos climáticos, também sofre com a malária. Possuindo registros de programas de controle desde 1905, contextuando a durabilidade do problema. A espécie da malária com 84% dos casos nacionais é a Plasmodium vivax, diferente da maior parte do mundo que é lesada pela Plasmodium falciparum. O mosquito transmissor, do gênero Anopheles, costuma atacar em certos períodos do ano, introduzindo o parasita. Por esse fato, foi elaborada a quimioprevenção sazonal da malária (SMC), que se trata de medicamentos ministrados ao público com idade inferior aos 5 anos, o qual é o mais afetado, antes do pico de transmissão anual. O SMC, demonstrou resultados promissores com a redução de 82% dos casos no grupo. Entretanto, a aplicação dos fármacos é trabalhosa e no futuro podem acontecer casos de resistência medicamentosa, por isso são vitais novas tecnologias para conter a enfermidade. Objetivo: Discorrer acerca das novas perspectivas envolvendo a vacinação para a malária. Material e métodos: Se trata de uma revisão de literatura, com utilização da base de dados PubMed, com as palavras de busca: malaria; vaccination; brazil; Plasmodium vivax. E artigos pesquisados dos anos de 2010 a 2020. Resultados: Foram encontradas vacinas em desenvolvimento, a maior parte delas para o P. falciparum, com destaque ao modelo RTS,S/AS01, que demonstra uma alta eficácia, mas com baixa durabilidade. Outros protótipos com mecanismos divergentes também tiveram resultados positivos, fato que demonstra as possibilidades de combate ao parasita de maneiras diferentes. Já os estudos acerca da espécie P. vivax ainda surgem timidamente. Conclusão: a vacina se trata de uma possibilidade futura, mesmo com a necessidade de mais testes e metas de imunização. Se tratando de uma importante aliada ao combate da enfermidade já que imunizará mais camadas da população que o tratamento atual, além de ser capaz de auxiliar o tratamento SMS já existente, tornandoo mais eficaz.

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