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Relevant bibliographies by topics / Malaria – Pathogenesis

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Academic literature on the topic 'Malaria – Pathogenesis'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 September 2023

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Journal articles on the topic "Malaria – Pathogenesis"

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Milner, Danny A. "Malaria Pathogenesis." Cold Spring Harbor Perspectives in Medicine 8, no. 1 (May 22, 2017): a025569. http://dx.doi.org/10.1101/cshperspect.a025569.

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Miller, L., M. Good, and G. Milon. "Malaria pathogenesis." Science 264, no. 5167 (June 24, 1994): 1878–83. http://dx.doi.org/10.1126/science.8009217.

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Amoako-Sakyi, Daniel, Selorme Adukpo, Kwadwo A. Kusi, Daniel Dodoo, Michael F. Ofori, George O. Adjei, Dominic E. Edoh, et al. "A STAT6 Intronic Single-Nucleotide Polymorphism is Associated with Clinical Malaria in Ghanaian Children." Genetics & Epigenetics 8 (January 2016): GEG.S38307. http://dx.doi.org/10.4137/geg.s38307.

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Malaria pathogenesis may be influenced by IgE responses and cytokine cross-regulation. Several mutations in the IL-4/STAT6 signaling pathway can alter cytokine cross-regulation and IgE responses during a Plasmodium falciparum malarial infection. This study investigated the relationship between a STAT6 intronic single-nucleotide polymorphism (rs3024974), total IgE, cytokines, and malaria severity in 238 Ghanaian children aged between 0.5 and 13 years. Total IgE and cytokine levels were measured by ELISA, while genotyping was done by polymerase chain reaction-restriction fragment length polymorphism (RFLP). Compared with healthy controls, heterozygosity protected against clinical malaria: uncomplicated malaria (odds ratios [OR] = 0.13, P < 0.001), severe malarial anemia (OR = 0.18, P < 0.001), and cerebral malaria (OR = 0.39, P = 0.022). Levels of total IgE significantly differed among malaria phenotypes (P = 0.044) and rs3024974 genotypes (P = 0.037). Neither cytokine levels nor IL-6/IL-10 ratios were associated with malaria phenotypes or rs3024974 genotypes. This study suggests a role for rs3024974 in malaria pathogenesis and offers further insights into an IL-4/STAT6 pathway mutation in malaria pathogenesis.

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John, Chandy C. "Cerebral Malaria Pathogenesis." American Journal of Pathology 171, no. 6 (December 2007): 1729–32. http://dx.doi.org/10.2353/ajpath.2007.070917.

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Clark, I. A., and L. Schofield. "Pathogenesis of Malaria." Parasitology Today 16, no. 10 (October 2000): 451–54. http://dx.doi.org/10.1016/s0169-4758(00)01757-9.

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Mideo, Nicole, Troy Day, and Andrew F. Read. "Modelling malaria pathogenesis." Cellular Microbiology 10, no. 10 (October 2008): 1947–55. http://dx.doi.org/10.1111/j.1462-5822.2008.01208.x.

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O’Sullivan, Jamie M., and James S. O’Donnell. "Platelets in malaria pathogenesis." Blood 132, no. 12 (September 20, 2018): 1222–24. http://dx.doi.org/10.1182/blood-2018-08-865618.

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Dasari, Prasad, and Sucharit Bhakdi. "Pathogenesis of malaria revisited." Medical Microbiology and Immunology 201, no. 4 (September 7, 2012): 599–604. http://dx.doi.org/10.1007/s00430-012-0265-y.

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Meshnick, Steven R., and Stephen J. Rogerson. "Pathogenesis of malaria in pregnancy." Microbiology Australia 29, no. 4 (2008): 204. http://dx.doi.org/10.1071/ma08204.

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Even though we have good tools to prevent and treat malaria, it remains a tragically common disease in poor countries, especially in Africa. Pregnant women are particularly susceptible to malaria, causing anaemia and poor birth outcomes. There is marked sequestration of Plasmodium falciparum-infected erythrocytes (IEs) in the placenta, but the pathogenesis of malaria in pregnancy is still incompletely understood. Both intermittent preventive therapy and insecticide-impregnated bed nets are effective protective measures, but new measures are also needed.

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Moxon, Christopher A., Matthew P. Gibbins, Dagmara McGuinness, Danny A. Milner, and Matthias Marti. "New Insights into Malaria Pathogenesis." Annual Review of Pathology: Mechanisms of Disease 15, no. 1 (January 24, 2020): 315–43. http://dx.doi.org/10.1146/annurev-pathmechdis-012419-032640.

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Malaria remains a major public health threat in tropical and subtropical regions across the world. Even though less than 1% of malaria infections are fatal, this leads to about 430,000 deaths per year, predominantly in young children in sub-Saharan Africa. Therefore, it is imperative to understand why a subset of infected individuals develop severe syndromes and some of them die and what differentiates these cases from the majority that recovers. Here, we discuss progress made during the past decade in our understanding of malaria pathogenesis, focusing on the major human parasite Plasmodium falciparum.

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Dissertations / Theses on the topic "Malaria – Pathogenesis"

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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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Chang, Kai-Hsin 1974. "Erythropoietin, erythropoiesis, and malarial anemia : the mechanisms and implications of insufficient erythropoiesis during murine blood-stage malaria." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84490.

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Severe anemia is a major life-threatening complication of malaria. Inappropriately low reticulocytosis in malaria patients with anemia suggests insufficient erythropoiesis, of which the mechanisms and implications are not clear. The principle growth factor that promotes erythropoiesis is erythropoietin (Epo). Studies determining the serum level of Epo in malaria infected patients have been inconclusive. Furthermore, the role of Epo and the erythropoietic response to Epo stimulation during malaria have never been examined. The purpose of the experiments performed in this thesis was, thus, to investigate the role of Epo and erythropoiesis in relation to anemia during blood-stage malaria using the murine model of Plasmodium chabaudi AS. A murine Epo specific ELISA, which was determined to be less biased by the presence of other cytokines in the samples as compared to the conventional Epo bioassay, was first developed to facilitate the research. The kinetics of Epo production in the kidney and the levels in the serum were characterized. It was demonstrated that Epo production during blood-stage malaria is mainly regulated by the degree of anemia and that renal cytokines may have only a minor effect on this response. Next, the roles of Epo and erythropoiesis during blood-stage malaria were investigated by neutralization of endogenous Epo or by administration of exogenous Epo. Timely onset of Epo-induced reticulocytosis was shown to be important for the alleviation of malarial anemia and survival. However, reticulocytosis in response to Epo stimulation is severely suppressed by infection with malaria. Dissection of the upstream events of erythropoiesis demonstrated that blood-stage malaria compromises the generation of reticulocytes by suppressing the proliferation, differentiation, and maturation of erythroid-lineage cells at various stages of erythroid development. Taken together, our data provide important insights for understanding the patho

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Okrinya, Aniayam. "Mathematical modelling of malaria transmission and pathogenesis." Thesis, Loughborough University, 2015. https://dspace.lboro.ac.uk/2134/17160.

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In this thesis we will consider two mathematical models on malaria transmission and patho- genesis. The transmission model is a human-mosquito interaction model that describes the development of malaria in a human population. It accounts for the various phases of the disease in humans and mosquitoes, together with treatment of both sick and partially im- mune humans. The partially immune humans (termed asymptomatic) have recovered from the worst of the symptoms, but can still transmit the disease. We will present a mathematical model consisting of a system of ordinary differential equations that describes the evolution of humans and mosquitoes in a range of malarial states. A new feature, in what turns out to be a key class, is the consideration of reinfected asymptomatic humans. The analysis will include establishment of the basic reproduction number, R0, and asymptotic analysis to draw out the major timescale of events in the process of malaria becoming non-endemic to endemic in a region following introduction of a few infected mosquitoes. We will study the model to ascertain possible time scale in which intervention programmes may yield better results. We will also show through our analysis of the model some evidence of disease control and possible eradication. The model on malaria pathogenesis describes the evolution of the disease in the human host. We model the effect of immune response on the interaction between malaria parasites and erythrocytes with a system of delay differential equations in which there is time lag between the advent of malaria merozoites in the blood and the training of adaptive immune cells. We will study the model to ascertain whether or not a single successful bite of an infected mosquito would result in death in the absence of innate and adaptive immune response. Stability analysis will be carried out on the parasite free state in both the immune and non immune cases. We will also do numerical simulations on the model to track the development of adaptive immunity and use asymptotic methods, assuming a small delay to study the evolution of the disease in a naive individual following the injection of small amount of merozoites into the blood stream. The effect of different levels of innate immune response to the pathogenesis of the disease will be considered in the simulations to elicit a possible immune level that can serve as a guide to producing a vaccine with high efficacy level.

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Weiser, Silvia. "In vitro studies on the pathogenesis of cerebral malaria." Thesis, The University of Sydney, 2007. https://hdl.handle.net/2123/28140.

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Malaria is caused by infection with the protozoan Plasmodium. About 40% of the world’s population is at risk, nearly all of them living in the least developed countries. While 300-500 million cases are reported per year, about 2 million people die annually. Most of the fatal cases develop severe malaria, which is a complication of Plasmodium fulciparum infection. Symptoms can include multi-organ dysfunction, anaemia, lung complications and cerebral malaria (CM). Although the pathogenesis is controversial, there are two main theories to explain the aetiology of CM: sequestration of parasitised red blood cells (pRBC) and leukocytes in the vasculature, and an over-reaction of the immune system. In the latter case, enhanced production of deleterious immune effectors such as cytokines is involved. Experimental models of CM (in vitro and in vivo) have been developed because clinical studies are hampered by ethical constraints and post-mortem human tissue is hard to obtain. CBA or C57BL/6 mice infected with Plasmodium berghei ANKA (PbA) succumb to murine CM and show progressive behavioural, histopathological and immunological changes. In contrast, Plasmodium berghei K173 (PbK)-infected C57BL/6 mice die due to anaemia and hyperparasitaemia, but without neurological symptoms. Although it is important to study the disease in the whole animal, in vitro studies are helpful to elucidate mechanisms at the cellular level. It is known that various cell types contribute to the pathogenesis of CM. In particular, endothelial cells lining the cerebral microvasculature are involved in the development of CM. They form part of the blood-brain barrier (BBB) which tightly regulates the traffic of substances and cells into the brain parenchyma to protect cerebral cells and to maintain the intemeuronal milieu. The permeability of the BBB is increased early after infection (day 3-4 p.i.) in the murine experimental model of CM. This might lead to an influx of deleterious substances into the cerebral parenchyma, causing the neurological symptoms observed. Changes at the microvascular endothelium are thought to contribute to the leakage of the BBB. In response to various stimulants ECs increase the expression of cellular adhesion molecules (CAM) on their surface. Cells such as leucocytes (in murine CM) and pRBCs (in human CM) adhere to the vessels, recruiting an immune response to the area.

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Knackstedt, Sebastian Lorenz. "Neutrophil extracellular traps drive inflammatory pathogenesis in malaria." Doctoral thesis, Humboldt-Universität zu Berlin, 2019. http://dx.doi.org/10.18452/19767.

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Malaria ist die Erkrankung, die durch Infektion eines Säugetiers mit dem eukaryotischen Parasiten Plasmodium entsteht. Die Symptome dieser Erkrankungen reichen von Fieber und Gelenkschmerzen bis zu schweren Organschäden in Hirn, Lunge, Niere und Leber bei einem geringen Teil der Erkrankten. Diese klinischen Symptome treten nur auf, während der Parasit sich asexuell in roten Blutzellen vermehrt. Die Zerstörung von Erythrozyten und die daraus resultierende Freisetzung von Zytokinen sind die Verursacher der malariatypischen wiederkehrenden Fieberzyklen. Der Mechanismus, der zur Entstehung von Gewebsschäden führt, ist hingegen nur unzureichend bekannt. Eine notwendige Bedingung für das Auftreten von Gewebeschäden ist, dass infizierte rote Blutzellen an das Endothel der Mikrovaskulatur bin. Die Schwere der Erkrankung ist direkt mit dem extrazellulären Auftreten von Stoffen verbunden, die normalerweise von neutrophilen Granulozyten im Zellinnern gespeichert werden. Neutrophile sind dafür bekannt sind, ein ganzes Arsenal an Waffen bereitwillig durch Degranulierung oder programmierten Zelltod einzusetzen. In dieser Studie berichten wir von einem direkten kausalen Zusammenhang zwischen dem aktiven inflammatorischen Zelltod (NETose) von Neutrophilen und der Entstehung von Organschäden bei einer Plasmodium-Infektion. Wir zeigen, dass NETs in Zirkulation freigesetzt und von extrazellulären DNase verdaut werden. Dadurch werden systemisch Aktivierungssignale für eine weitere Immunantwort zur Verfügung gestellt und es kommt zur Freisetzung von Zytokinen, Notfallgranulopoese und der Hochregulierung von zellulären Adhäsionsmarkern auf Endothelzellen. Dies erlaubt das Binden von infizierten Erythrozyten und Immunzellen an die Mikrovaskulatur bestimmter Organe. Wir zeigen außerdem, dass eine Intervention mit der Entstehung von NETs oder der Freisetzung neuer Neutrophiler diesen Prozess unterbindet und einen vielversprechenden therapeutischen Ansatz darstellt.
Malaria is the disease caused by an infection of a mammalian host by the mosquito borne eukaryotic parasite Plasmodium. The symptoms of the disease are diverse, ranging from fever and rigor in most patients to severe damage in solid organs such as brain, lung, kidney and liver in a small fraction of the afflicted. Clinical symptoms of the disease only occur when the parasite undergoes asexual replication within the red blood cells of the host. Destruction of these cells and subsequent release of cytokines are responsible for the recurring fever cycles of mild malaria. The mechanism underlying the occurrence of tissue damage however, remain mostly elusive. The adhesion of infected red blood cells to the endothelial wall of the microvasculature in the affected organs is a necessary requirement and pathology is associated with the activation of specific immune cells residing within the blood stream. Severity of disease is linked to extracellular accumulation of neutrophil proteins. Neutrophils are abundant white blood cells, known to readily deploy an arsenal of weaponry either by degranulation or by externalization of chromatin. In this study we report a direct causal relationship between the active inflammatory neutrophil cell death (NETosis) and the development of organ damage during a Plasmodium infection. We show that NETs are released in circulation, digested by extracellular DNase and thereby supply immune activation signals that drive inflammation. The systemic dissemination of these factors leads to the release of cytokines, emergency granulopoiesis and upregulation of cellular adhesion markers on endothelial cells thereby allowing for the binding of both infected red blood cells and immune cells to the microvasculature of specific organs. Furthermore we supply evidence, that repression of NETosis or inhibition of granulopoiesis abrogate these processes and present promising therapeutic strategies.

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Bakmiwewa, Supun Madushani. "The Astrocyte: a Crossroads in Cerebral Malaria Pathogenesis." Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/14952.

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Cerebral malaria (CM) is a severe complication of malaria, and involves the central nervous system (CNS). Despite the significant negative impact of CM, its pathogenesis is not fully understood. Two theories, namely cerebral hypoxia and cytokine expression, are considered to be involved in the process. The present study investigated the potential interaction of these two theories in driving the development of CM. Astrocytes can be a major determinant of the outcome of CNS diseases, and we hypothesised that astrocytes, by responding to the pathways involved in the two theories, would drive the development of CM. The cytokines interferon-gamma (IFN-γ) and lymphotoxin-alpha (LT-α) are essential for the development of experimental CM in a murine model. The chemokine C-X-C motif ligand 10 (CXCL10) also is implicated in this process. Both Malawian paediatric and mouse CM brain samples showed increased cytokine expression and astrocyte activation. Furthermore, by the use of Ifnγ-/- mice, it was shown that IFN-γ was involved in this CM-associated astrocyte activation. Cultured human primary astrocytes were directly activated by IFN-γ and LT-α to produce synergistic levels of CXCL10. This finding provides a potential mechanism by which astrocytes could be involved in the pathogenesis of CM, and sheds light on the possible role of LT-α in CM. Hypoxia had an effect on astrocytes, but their response to cytokines was not altered by hypoxia. However, oxygen-glucose deprivation resulted in a decline in cytokine-induced CXCL10 release by cultured astrocytes. Decreased production of CXCL10 has the potential to translate into less blood brain barrier damage. Thus, the mechanisms underlying these two theories do interact at the astrocyte level, but astrocytes show both protective and pathological features as a result of this interaction. The present thesis shows that it is unlikely that the two mechanisms act together to reinforce the astrocytes’ pathological effects to cause CM.

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Contreras, Ana Paulina. "Modulation of macrophage nitric oxide production by hemozoin." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=100786.

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Malaria is one of the most serious human infectious diseases. To date, the collection of studies suggest that the disease is determined by transmission dynamics and host age altogether with host genetics and immunological responses. The precise and direct contribution of parasite components to the activation of such immunological responses has not been fully unravelled. In addition to a role proposed for plasmodial GPI, different lines of evidence suggest that hemozoin (HZ) could also be a potential inflammatory agent. The role of HZ in the modulation of immune responses has remained a polemic subject, making it difficult to describe the contribution of this molecule in pathogenesis of malaria. However, our previous laboratory studies, suggest that HZ has a pro-inflammatory role. For this reason, our study was designed to further define the contribution of HZ to the pro-inflammatory events related to malaria immunopathology, and to identify the intracellular signals underlying the up-regulatory effects of HZ in the macrophage, one of the major sources of inflammatory mediators in malaria. In order to do that, we used a chemically characterized synthetic version of the native PfHZ, rcHZ; and evaluated its effects on macrophage nitric oxide (NO) production. Our first approach was to compare the effects of rcHZ with other morphologically different versions of this molecule (aHZ and scHZ) alone or in combination with IFN-gamma on macrophage NO production. In a second approach, we evaluated if the presence of serum proteins plays a role in the increased IFN-gamma induced-NO production by rcHZ. In the third part of our study, we explored if rcHZ is able to increase NO production by macrophages when incubated in combination with a molecule from another pathogen, such as gram-negative bacteria lipopolysaccaride (LPS). The present study is a functional study that uses a synthetic and morphologically identical version of the native PfHZ. Our results suggests that intrinsic physical characteristics, such as shape and size; presence of host serum proteins, and presence of other pathogenic molecules, are important determinants for the macrophage response to HZ in the context of NO production. Besides, it describes part of the signaling pathways that are involved, which may contribute in the future, not only to understand mechanisms of regulation; but also, to find new therapeutic targets against malaria.

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Cohen, Amy. "Cellular, subcellular, and molecular elements of cerebral malaria pathogenesis." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/18112.

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A complex network of elements is responsible for cerebral malaria (CM) development, but interactions between these elements are still being explored. Annually, there are 212 million cases of malaria with 1-2% progressing to CM. Plasma microvesicles (MV) are increased in patients and mice with CM and blocking their release protects against CM. The miRNA content of circulating plasma MV and brain tissue during murine CM and non-CM was assessed using microarray and RT-qPCR techniques. Following infection, MV and brain miRNA were altered in CM mice, coinciding with neurological syndrome onset. Particularly, miR-146a and miR-193b were dysregulated in plasma MV from CM mice and play roles in apoptosis, cytokine regulation and inflammatory cell recruitment. Several other miRNA were dysregulated in the brains of CM mice and play roles in TGF- signalling, endocytosis, FoxO signalling and adherens junctions. Using confocal microscopy, we investigated monocyte, platelet, T cell, parasite and ICAM-1-positive cell accumulation in CM brains. These cells accumulate at vessel branch points, associated with haemorrhaging and the development of tissue hypoxia, consistent with previous findings. As monocytes were the most numerous cells in the brains of CM mice, we targeted them therapeutically. Treatment in vivo with immuno-modulatory particles and artesunate resulted in 88% protection when administered at CM onset, while monotherapies resulted in greatly reduced protection. All successfully treated mice displayed reduced clinical signs of CM and monocyte and MV numbers, and were immune to reinfection. This thesis reinforces existing findings regarding CM pathogenesis and highlights several novel candidates as players in CM development. We explore the potential of miRNA as biomarkers of the neurological syndrome. We show that monocytes displaying a Ly6Clo phenotype aggravate CM development and that therapy targeting this cell subset is a novel strategy to abrogate late-stage CM.

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Nunes, da Silva Ana Sofia. "Characterization of the molecular mechanisms involved in severe malaria pathogenesis." Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCC065.

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L'importante virulence de P. Falciparum a été reliée à la capacité du parasite à adhérer aux cellules endothéliales de la microvasculature ou aux syncytiotrophoblastes placentaires. La séquestration de globules rouges infectés dans différents organes conduit à l'apparition des symptômes cliniques de la maladie. Les protéines variables PfEMP1, exprimées à la surface des hématies parasitées, sont les ligands parasitaires majeurs responsables de la cytoadhérence. PfEMP1-VAR2CSA est le candidat vaccinal le plus prometteur pour lutter contre le paludisme gestationnel. Afin de mieux caractériser les interactions entre la protéine VAR2CSA et son ligand naturel, la CSA, nous avons généré des VEIH contre VAR2CSA. Nous avons obtenu 19 VHHs, en grand partie dirigés contre le domaine DBLIX. Quatre VHHs contre DBL1X étaient capable d'inhiber les interactions entre les hématies parasitées et la CSA, montrant que le domaine DBL1X fait partie ou est localisé très proche du site de liaison au récepteur. Le paludisme sévère a été associé la séquestration des hématies parasitées, exprimant les cassettes de domaines DC8 ou DC13, au récepteur endothélial de la protéine C (EPCR) exprimé à l'endothélium vasculaire. Dans cette étude nous avons montré que la cassette DC8 de IT4VAR19 adhère avec une plus grande affinité à l'EPCR et HBEC5i que le domaine CIDRŒ I. 1 seul. Nous avons observé que, même si IT4VAR19 est le variant préférentiellement exprimé par la souche IT4 après sélection à l'EPCR, l'immunité humorale contre IT4VAR19-DC8 cassette et IT4VAR19-CIDR n'est pas stimulé pendant un épisode de paludisme pédiatrique sévère au Bénin. En conclusion, ce projet de thèse permet de mieux comprendre les interactions moléculaires impliquées dans l'adhérence des globules rouges parasités aux cellules endothéliales de l'hôte et contribuera à l'élaboration d'approches vaccinales ou thérapeutiques visant à protéger les patients des symptômes cliniques du paludisme sévère
Sequestration of infected erythrocytes (IEs) is the prime mediator of disease and is mediated by members of the highly diverse PfEMP1. The aim of this thesis was to characterize the molecular mechanisms associated to pregnancy associated malaria (PAM) and severe malaria, in order to design new intervention strategies to protect patients against severe malaria clinical symptoms. PfEMP 1 -VAR2CSA stands today as the leading vaccine candidate aiming to protect future pregnant women against the severe clinical outcomes of PAM. In order to better characterize the interactions between PfEMPI-VAR2CSA and its receptor CSA, we generated VAR2CSA specific nanobodies. Following immunization of a Ilama with the full-length VAR2CSA recombinant protein, we obtained 19 nanobodies, mainly targeting the DBL1X. Four nanobodies targeting DBL1X reproducibly inhibited CSA adhesion of erythrocytes infected with the homologous NF54-CSA parasite strain, providing evidences that DBL1X domain is part or close to the CSA binding site. Severe malaria was recently associated with binding of IEs, expressing domain cassettes DC8 and DC13, to Endothelial Protein C Receptor (EPCR) pr'sent in the host endothelium. In this study we demonstrated that the IT4VAR19-DC8 binds to EPCR with a greater affinity than the CIDRa1. L domain alone and also the binding to EPCR-expressing endothélial cell line (HBEC5i) is more pronounced. We observed that although IT4VAR19 is the preferentially selected EPCR-binding variant from IT4 strain, the humoral immunity against the EPCR binding IT4VAR19-DC8 cassette or the CIDRa1. 1 domain is not boosted during a severe pediatric malaria episode in Benin. In conclusion, this thesis provide new insights on the molecular mechanisms underlying the binding of P. Falciparum infected erythrocytes to the host endothelium that will help in the development of anti-adhesive strategies to protect patients against severe malaria clinical outcomes

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Ariyoshi, Koya. "The role of viral load in the pathogenesis of HIV-2 infection." Thesis, Open University, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262968.

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Books on the topic "Malaria – Pathogenesis"

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Peterson, Anna Margrét, and Gerald E. Calamandrei. Malaria: Etiology, pathogenesis, and treatments. New York: Nova Science Publishers, 2011.

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Stoute, José A., ed. Complement Activation in Malaria Immunity and Pathogenesis. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77258-5.

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P, Waters Andrew, and Janse Chris J, eds. Malaria parasites, genomes and molecular biology. Wymondham, Norfolk, England: Caister Academic Press, 2004.

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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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Kelty, Christopher M. Ebola's ecologies. California]: Creative Commons, 2015.

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Tsuyoshi, Ishii, Allsop David, Selkoe Dennis J, and International Congress of Neuropathology (11th : 1990 : Kyoto, Japan), eds. Frontiers of Alzheimer research: Proceedings of the 5th International Symposium of the Psychiatric Research Institute of Tokyo (PRIT), Tokyo, 10-12 September 1990. Amsterdam: Excerpta Medica, 1991.

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Khalid, Iqbal, and International Conference on Alzheimer's Disease and Related Disorders (4th : 1994 : Minneapolis, Minn.), eds. Research advances in Alzheimer's disease and related disorders. Chichester: Wiley, 1995.

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Lester, Packer, Prilipko L. 1945-, and Christen Yves, eds. Free radicals in the brain: Aging, neurological, and mental disorders. Berlin: Springer-Verlag, 1992.

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J, Epstein Charles, Nadel Lynn, and National Down Syndrome Society (U.S.), eds. Down syndrome and Alzheimer disease: Proceedings of the National Down Syndrome Society Conference on Down Syndrome and Alzheimer Disease, held in New York, January 16 and 17, 1992. New York: Wiley-Liss, 1992.

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Uehara Memorial Foundation Symposium on Common Disease (1999 Tokyo). Common disease: Genetic and pathogenetic aspects of multifactorial diseases, proceedings of the Uehara Memorial Foundation Symposium on Common Disease, Tokyo on June 30-July 2, 1999. Edited by Imura Hiroo, Kasuga Masato, and Nakao Kazuwa 1948-. Amsterdam: Elsevier Science B.V., 1999.

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Book chapters on the topic "Malaria – Pathogenesis"

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Gonçalves, Bronner P., Michal Fried, and Patrick E. Duffy. "Malaria pathogenesis." In Advances in Malaria Research, 427–64. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118493816.ch16.

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Ferluga, Janez, Iesha Singh, Sashmita Rout, Ahmed Al-Qahtani, Hadida Yasmin, and Uday Kishore. "Immune Responses in Malaria and Vaccine Strategies." In Microbial Pathogenesis, 273–91. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-67452-6_12.

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Amaratunga, Chanaki, Tatiana M. Lopera-Mesa, Jeanette G. Tse, Neida K. Mita-Mendoza, and Rick M. Fairhurst. "Pathology and Pathogenesis of Malaria." In The Immune Response to Infection, 361–81. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816872.ch29.

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Weckman, Andrea, Vanessa Tran, and Kevin C. Kain. "Complement and Malaria in Pregnancy." In Complement Activation in Malaria Immunity and Pathogenesis, 91–105. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77258-5_5.

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Grau, Georges Emile Raymond, and Nicholas Henry Hunt. "Cytokines and Some of Their Effector Mechanisms in Cerebral Malaria Pathogenesis." In Encyclopedia of Malaria, 1–11. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8757-9_94-1.

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Taylor, Ronald P., José A. Stoute, and Margaret A. Lindorfer. "Mechanisms of Complement Activation in Malaria." In Complement Activation in Malaria Immunity and Pathogenesis, 31–49. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77258-5_2.

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Schein, Theresa N., and Scott R. Barnum. "Role of Complement in Cerebral Malaria." In Complement Activation in Malaria Immunity and Pathogenesis, 65–90. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77258-5_4.

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Stoute, José A. "Role of Complement in Immunity Against Malaria." In Complement Activation in Malaria Immunity and Pathogenesis, 125–37. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77258-5_7.

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Biryukov, Sergei, and José A. Stoute. "The Complement System." In Complement Activation in Malaria Immunity and Pathogenesis, 1–29. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77258-5_1.

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Stoute, José A. "Role of Complement in Severe Malarial Anemia." In Complement Activation in Malaria Immunity and Pathogenesis, 51–64. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77258-5_3.

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Conference papers on the topic "Malaria – Pathogenesis"

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Meissner, PeterE. "Malaria – Pathogenese, Klinik und Therapie." In 8. Symposium HÄMATOLOGIE HEUTE. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0042-1744089.

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Younis, Khansa Mohammed, Gires Usup, and Asmat Ahmad. "A prospective study on evaluation of pathogenesis, biofilm formation, antibiotic susceptibility of microbial community in urinary catheter." In THE 2015 UKM FST POSTGRADUATE COLLOQUIUM: Proceedings of the Universiti Kebangsaan Malaysia, Faculty of Science and Technology 2015 Postgraduate Colloquium. AIP Publishing LLC, 2015. http://dx.doi.org/10.1063/1.4931227.

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Reports on the topic "Malaria – Pathogenesis"

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Oakley, Miranda S. Molecular Factors and Biological Pathways Associated with Malaria Fever and the Pathogenesis of Cerebral Malaria. Fort Belvoir, VA: Defense Technical Information Center, March 2007. http://dx.doi.org/10.21236/ad1014029.

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