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Relevant bibliographies by topics / Plasmodium falciparum

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Academic literature on the topic 'Plasmodium falciparum'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 April 2025

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Journal articles on the topic "Plasmodium falciparum"

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Tokponnon, Filémon, Razak Osse, Jean Gille Egui, Gylchrist Houndjo, Zoulkifilou Sare Dabou, Festus Houessinon, Idayath Gounou Yerima, Brice Fanou, and Martin Akogbeto. "Determination of Plasmodial Species Prevalence among Patients Received at Cotonou Boni Clinic during Rainy Season in the Year 2022." International Journal of TROPICAL DISEASE & Health 44, no. 16 (September 5, 2023): 9–15. http://dx.doi.org/10.9734/ijtdh/2023/v44i161464.

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Aims: Malaria is a life-threatening disease caused by parasites transmitted by bites from infected female anopheles. It is a preventable and treatable illness. It remains a recurring disease among public health diseases that exposes many people to a risk of infection, including children under the age of 05 in Benin. Methods: To determine the prevalence of malaria and different plasmodial species at the Dr Pierre BONI Clinic, we performed venous and capillary samples on 731 patients for the realization of thick drops and blood smears between June and July 2022. Results: Three plasmodial species were identified in 228 patients (31%) as malaria of the 731 patients included in the study with 3 species of plasmodium found: Plasmodium falciparum (95.5%), Plasmodium malariae (2.85%), Plasmodium ovale (1.65%). Mixed or double species was also recorded in some patients: Plasmodium falciparum+ Plasmodium malariae and Plasmodium falciparum+ Plasmodium ovale. The majority of patients have the presence of trophozoites at Plasmodium falciparum, 95.5%. The parasitic density of P. falciparum is higher than that of P. malariae and that of P. ovale. Conclusion: Although evaluated during a period of low transmission, malaria remains a real public health problem. The distribution of the disease is closely related to the presence in the blood of plasmodial species.

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MD, Dr Tapan Biswas. "Artesunate Resistant Plasmodium Falciparum." Journal of Medical Science And clinical Research 05, no. 04 (April 8, 2017): 20025–27. http://dx.doi.org/10.18535/jmscr/v5i4.48.

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Merrick, Catherine J. "Plasmodium falciparum." Emerging Topics in Life Sciences 1, no. 6 (December 22, 2017): 517–23. http://dx.doi.org/10.1042/etls20170099.

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Plasmodium falciparum is a protozoan parasite that causes the most severe form of human malaria. Five other Plasmodium species can also infect humans — P. vivax, P. malariae, P. ovale curtisi, P. ovale wallikeri and P. knowlesi — but P. falciparum is the most prevalent Plasmodium species in the African region, where 90% of all malaria occurs, and it is this species that causes the great majority of malaria deaths. These were reported by the WHO at 438 000 in 2015 from an estimated 214 million cases; importantly, however, figures for the global burden of malaria tend to have wide margins of error due to poor and inaccurate reporting. In this Perspective, features of P. falciparum that are unique among human malaria parasites are highlighted, and current issues surrounding the control and treatment of this major human pathogen are discussed.

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Maier, Alexander G., Kai Matuschewski, Meng Zhang, and Melanie Rug. "Plasmodium falciparum." Trends in Parasitology 35, no. 6 (June 2019): 481–82. http://dx.doi.org/10.1016/j.pt.2018.11.010.

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Fayyaz Ahmed Memon, Uzma Bukhari, and Mir Mohammad Sahito. "PREVALENCE OF MALARIA AMONG THE PATIENTS LIVING IN AREAS OF DISTRICT SBA (SHAHEED BENAZIR BHUTTO) AND MIRPURKHAS." JMMC 5, no. 1 (November 26, 2014): 1–3. http://dx.doi.org/10.62118/jmmc.v5i1.345.

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Objective:Malaria is a major cause of morbidity in the tropics and about 300 million causes were reported word wide in2006 among the 100 species of genous plasmodia, the four species such as PL: falciparum, vivax, ovaule andmalaria causes malaria. The malaria is transmitted by the bite of female anopheles mosquitoes. .Methodology: This descriptive and experimental study was carried out at department of pathology, People'sUniversity of Medical & Health Science (PUMHS), Nawabshah. The cases were collected from paediatrics &Medical outpatients departments of PUMHS Hospital Nawabshah and also from Muhammad Medical College(MMC) Hospital & Civil hospital Mirpurkhas (CHM) from January 2010 to December 2011. A total of 1200 patientswere included. The prevalence of malaria on the basis of age, sex, areas of resident, and clinical finding of allpatients were recorded and blood tests performed.Results: Plasmodium Vivax in 70.8% of cases and Plasmodium Falciparum in29.2%of cases.Conclusion: In the areas (Nawabshah and Mirpurkhas), Plasmodium Vivax and Plasmodium Falciparum are thecause of Malaria.Keywords: Malaria, Plasmodium, Pakistan, Nawabshah, Mirpurkhas.

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Trasi, Reqgi First. "Plasmodium Resistance to Artemisinin Derivates due to Kelch-3 Gene Mutation." Indonesian Journal of Pharmaceutical and Clinical Research 4, no. 2 (December 30, 2021): 39–44. http://dx.doi.org/10.32734/idjpcr.v4i2.6332.

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Artemisinin class of antimalarial drugs play an important role in controlling falciparum malaria after the emergence of resistance of Plasmodium falciparum to other antimalarial drugs such as chloroquine, sulfadoxine-pyrimethamine and mefloquine. Therefore, the presence of Plasmodium falciparum resistance to this class of drugs is threat to global efforts to eliminate this disease. Resistance of Plasmodium falciparum to artemisinin recently known to be associated with mutations in the propeller domain of the kelch-13 (K13) Plasmodium falciparum gene. The incidence of Plasmodium falciparum resistance due to mutations in the K13 gene, among others, can be found in Cambodia, Laos, Vietnam, China, Myanmar, Thailand and Africa. The presence of mutations in this gene will change the response of Plasmodium falciparum against oxidative stress induced by artemisinin by involving the proteasome-ubiquitin pathway. In addition, mutation K13 will also change the levels of PI3K and PI3P in the body of Plasmodium falciparum. PI3K and PI3P are lipids that essential for the development of Plasmodium falciparum from ring stage to schizont. Resistance to artemisinin will also provide phenotypic changes in the life cycle of Plasmodium falciparum in the form of elongation at the stage ring and transient shortening in trophozoite development. This resistance incident can be overcome, among others by prolonging the duration of treatment (from a 3-day regimen to a 4-day regimen) and combining artemisinin with proteasome inhibitors.

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ARICAN ÇELİK, Aslı, Rıfat TAMALI, Gülruhsar YILMAZ, Pınar KARABACAK, and Mustafa Soner ÖZCAN. "A Rare Cause of Fever in ICU; Malaria." Acta Medica Nicomedia 5, no. 3 (October 15, 2022): 235–37. http://dx.doi.org/10.53446/actamednicomedia.1103400.

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Sıtma, anofel cinsi sivrisineklerin insanları sokması sonucu bulaşan paraziter bir hastalıktır. Plasmodium falciparum (P Falciparum) en ölümcül tabloya yol açan türüdür, ülkemizde nadir görülür ve genellikle yurtdışı kaynaklıdır. Yoğun bakımda yüksek ateş pek çok klinik durumda karşımıza çıksa da nadir görülen bir durum olan P. Falciparuma bağlı sıtma aklımızda bulunmalıdır Bu olgu sunumunda, yurt dışı seyahat öyküsü bulunan P. Falciparum sıtma tanısı konulan hastanın yoğun bakım takip ve tedavi süreci sunulmuştur.

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Umar, Khairuddin Zainuddin, Yuri P.Utami, and Muhammad A.Y. Ardi. "Antimalarial Activity of Ethanol Extract of Sampare Leaves (Glochidion sp var. Biak) Against Plasmodium falciparum In Vitro." Indonesian Journal of Pharmaceutical Science and Technology 10, no. 1 (February 28, 2023): 10. http://dx.doi.org/10.24198/ijpst.v10i1.29477.

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Malaria is one of the health problems in the world and in Indonesia. This disease is caused by theprotozoan parasite, the genus Plasmodium. Plasmodium falciparum is the most important parasiticdisease with high morbidity and mortality in the world and tropical countries such as Indonesia inparticular. This study aims to determine the activity of sampare leaf extract in inhibiting the growth ofthe FCR-3 strain of the P. falciparum parasite which causes malaria. Sampare leaves were extracted bymaceration method using 70% ethanol. Extract the results extraction were tested against P. falciparumby in vitro method. 32,67% Yield extract resulted from the extraction process. Phytochemical screeningshows the presence of alkaloid compounds, flavonoids, quinones, saponins, and tannins. The ethanolextract of sampare leaves had IC50 antimalarial activity of 0,125 μg/mL and was categorized very well.Keywords: Antimalarial, Glochidion sp var. Biak, IC50, Plasmodium falciparum.

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Ibraheem, Zaid O., R. Abd Majid, S. Mohd Noor, H. Mohd Sedik, and R. Basir. "Role of Different Pfcrt and Pfmdr-1 Mutations in Conferring Resistance to Antimalaria Drugs in Plasmodium falciparum." Malaria Research and Treatment 2014 (November 11, 2014): 1–17. http://dx.doi.org/10.1155/2014/950424.

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Emergence of drugs resistant strains of Plasmodium falciparum has augmented the scourge of malaria in endemic areas. Antimalaria drugs act on different intracellular targets. The majority of them interfere with digestive vacuoles (DVs) while others affect other organelles, namely, apicoplast and mitochondria. Prevention of drug accumulation or access into the target site is one of the mechanisms that plasmodium adopts to develop resistance. Plasmodia are endowed with series of transporters that shuffle drugs away from the target site, namely, pfmdr (Plasmodium falciparum multidrug resistance transporter) and pfcrt (Plasmodium falciparum chloroquine resistance transporter) which exist in DV membrane and are considered as putative markers of CQ resistance. They are homologues to human P-glycoproteins (P-gh or multidrug resistance system) and members of drug metabolite transporter (DMT) family, respectively. The former mediates drifting of xenobiotics towards the DV while the latter chucks them outside. Resistance to drugs whose target site of action is intravacuolar develops when the transporters expel them outside the DVs and vice versa for those whose target is extravacuolar. In this review, we are going to summarize the possible pfcrt and pfmdr mutation and their role in changing plasmodium sensitivity to different anti-Plasmodium drugs.

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Maslachah, Lilik, Yoes Prijatna Dachlan, Chairul A. Nidom, and Loeki Enggar Fitr. "Experimental Models Point Mutations In Plasmodium falciparum pfatpase6 Gene Exposed to Recuring Artemisinin In Vitro." KnE Life Sciences 3, no. 6 (December 3, 2017): 422. http://dx.doi.org/10.18502/kls.v3i6.1151.

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The aims of this research to prove that repeated exposure of artemisinin can cause pfatpase6 gene mutation on Plasmodium falciparum in vitro. The research methods used culture In Vitro Plasmodium falciparum of strain 2300 IC50 value determination test artemisinin, artemisinin repeated exposure test (PO1, PO2, PO3 dan PO4) dose IC50, DNA extraction, gene amplification of pfatpase6 using Polymerase Chain Reaction (PCR) technique, electrophoresis, PCR product purification, labeling DNA from PCR results, DNA precipitation of PCR product, application of product labeling on the sequencing machines, analysis of the results of sequencing, and Data Analysis. The results of PCR pfatpase6 gene amplification include region 6 – 3216 for codon 89-1031 located in exon 1 and 2 Plasmodium falciparum 2300 by using five pairs of primers. Primer pair 1FR produce a long amplicon of 737 bp which covers of codon 89; primer pair 2FR produce a long amplicon of 813 bp which covers of codon 263, 431; primer pair 4FR produce a long amplicon of 700 bp which covers of codon 460, 465, 623; primer pair 5FR produce a long amplicon of 550 bp which includes of codon 683, 769; and primer pair 6FR produce a long amplicon of 876 bp which covers of codon 898, 1031.Multialigment pfatpase6 gene Plasmodium falciparum of strains Papua 2300 point mutations are obtained in the form of transition and transversion in treatment groups at the same nucleotide region 123, 2035, 2043, 2138 dan 2148. Conclusion of this research Artemisinin repeated exposure can cause point mutations in pfatpase6 genes Plasmodium falciparum of strains 2300 in vitro Keyword: Artemisinin, Plasmodium falciparumof strain Papua 2300, pfatpase6 gene, point mutation

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Dissertations / Theses on the topic "Plasmodium falciparum"

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Krishna, S. "Cation atpases in Plasmodium falciparum." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293442.

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Holland, Zoe. "Plasmodium falciparum protein kinase CK2." Thesis, University of Glasgow, 2008. http://theses.gla.ac.uk/606/.

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Malaria, caused by infection with intracellular protozoan parasites of the genus Plasmodium, is responsible for 300 to 600 million clinical cases annually (Snow et al., 2005), resulting in the deaths of up to three million people every year (Breman, 2001, Breman et al., 2004). There is a clear need for further research aimed at identifying novel drug targets (Ridley, 2002). Reversible phosphorylation of proteins is a major regulatory mechanism in most cellular processes, and protein kinases are considered promising drug targets, comprising as much as 30% of all protein targets under investigation (Cohen, 2002). The divergences between human and plasmodial protein kinases suggest that specific inhibition of the latter is an achievable goal (Doerig, 2004, Doerig and Meijer, 2007). This study investigates protein kinase CK2 of Plasmodium falciparum, seeking to establish by reverse genetics and biochemical approaches whether it represents a possible antimalarial drug target. Protein-kinase CK2, formerly known as Casein Kinase II, is a dual-specificity (Serine/Threonine and Tyrosine) protein kinase ubiquitously expressed in eukaryotes. It has over 300 cellular substrates catalogued to date (Meggio and Pinna, 2003). Consistent with its multiple substrates, the enzyme plays a crucial role in many cellular processes, and is essential to viability in yeast and slime mould (Padmanabha et al., 1990, Kikkawa et al., 1992). The human CK2 holoenzyme consists of two catalytic a or a’ subunits and two regulatory b subunits, and recent evidence indicates that the latter interact with several protein kinases in addition to CK2a (reviewed in (Bibby and Litchfield, 2005)), pointing to a likely role in the integration of numerous signalling pathways. A putative CK2a orthologue and two predicted CK2b subunits were identified in the P. falciparum genome (Ward et al., 2004, Anamika et al., 2005). Here we present the biochemical characterisation of the PfCK2a orthologue and both PfCK2b orthologues, and demonstrate by using a reverse genetics approach that each of the three subunits is essential for completion of the erythrocytic asexual cycle of the parasite, thereby validating the enzyme as a possible drug target. Recombinant PfCK2a possesses protein kinase activity, exhibits similar substrate and co-substrate preferences to those of CK2a subunits from other organisms, and interacts with both of the PfCK2b subunits in vitro. PfCK2a is amenable to inhibitor screening, and we report differential susceptibility between the human and P. falciparum CK2a enzymes to a small molecule inhibitor. Taken together, the data indicate that PfCK2a is an attractive, validated target for antimalarial chemotherapeutic intervention.

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Patzewitz, Eva-Maria. "Glutathione metabolism of Plasmodium falciparum." Thesis, University of Glasgow, 2009. http://theses.gla.ac.uk/913/.

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Apicomplexan parasites of the genus Plasmodium are the causative agent of malaria, one of the most prevalent infectious diseases worldwide. Five different Plasmodium species can cause malaria in humans, leading to a total of approximately 500 million cases each year and of these, P. falciparum causes the most deadly form of the disease and is responsible for more than 1 million deaths annually. A major problem in the global fight against malaria is the widespread resistance of the parasites against the currently available drugs. It is of great importance to identify new drug target as well as to understand the mechanisms that lead to drug resistance in the first instance in order to potentially reverse the resistant phenotypes and to avoid the development of resistance in the future. The tripeptide glutathione (GSH) or γ-glutamylcysteinyl-glycine is the most abundant low molecular weight thiol in most eukaryotic organisms and serves a number of important functions as sulfhydryl-buffer, cofactor for enzymes and for the detoxification of xenobiotics and drugs. GSH is an important component of the antioxidant machinery and because malaria parasites live in an environment rich in iron and oxygen and thus increased oxidative stress, they depend on functional antioxidant systems. The biosynthesis pathway for GSH, consisting of γ-glutamylcysteine synthetase (γGCS) and glutathione synthetase (GS) is present in malaria parasites as well as in their host cells. Previous studies have shown that depletion of GSH has an antimalarial effect, but it remained unclear whether parasites were killed directly or died because their host cell could not survive the depletion of GSH. To address this question, the knockout of both genes encoding the enzymes of the GSH biosynthesis pathway in P. falciparum was attempted. While both gene loci were targeted by control constructs, the knockout of either pfγgcs or pfgs was impossible, indicating both genes are essential for parasite survival in the erythrocytic stages. To analyse the localization of γGCS and GS, GFP-tagged recombinant fusion proteins were expressed in the parasites and showed that GSH biosynthesis is cytosolic. Apart form its other functions GSH has previously been suggested to be involved in resistance to the antimalarial drug chloroquine (CQ). CQ was for a long time the first line antimalarial drug due to its high efficiency, low cost and low toxicity, but is now widely inefficient in the treatment of the disease. CQ resistance is associated with mutations in the CQ resistance transporter (PfCRT), a membrane protein of the digestive vacuole that allows the efflux of the drug form its site of action. However, PfCRT mutations alone cannot explain the full array of phenotypes found in resistant parasites. GSH is able to degrade heme, the target of CQ, in vitro and it has been suggested that elevated GSH levels contribute to CQ resistance. However, analyses of isogenic parasite lines bearing different forms of PfCRT in this study revealed lower GSH levels and higher susceptibility to inhibition of GSH biosynthesis in the CQ resistant lines. These changes did not correlate with changes in the expression of enzymes involved in the de novo biosynthesis or consumption of GSH. However, the cellular accumulation ratio for CQ indicated a decrease of free heme in the resistant parasites. Mutant forms of PfCRT expressed in oocytes of Xenopus laevis were able to transport GSH, while the sensitive wild-type form did not transport the tripeptide. The findings of this study suggest that in parasites bearing mutant PfCRT, GSH is transported into the digestive vacuole where it is able to contribute to resistance by degrading heme, before the tripeptide itself is degraded by peptidases inside the vacuole, consistent with the overall reduction of GSH levels in CQ resistant parasites.

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Quashie, Neils Benjamin. "Purine transport in plasmodium falciparum." Thesis, Thesis restricted. Connect to e-thesis to view abstract, 2008. http://theses.gla.ac.uk/165/.

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Thesis (Ph.D.) -- University of Glasgow, 2008.
Ph.D. thesis submitted to the Division of Infection and Immunity, Institute of Biomedical and Life Sciences, University of Glasgow, 2008. Includes bibliographical references. Print version also available.

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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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Vetelet, Philippe. "Paludisme grave à plasmodium falciparum." Bordeaux 2, 1988. http://www.theses.fr/1988BOR25294.

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Mejia, Pedro. "Amélioration et utilisation d'un modèle murin des stades érythrocytaires du paludisme humain." Rouen, 2006. http://www.theses.fr/2006ROUES062.

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Paul, Richard E. L. "The genetic diversity of Plasmodium falciparum." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318788.

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Hayward, Rhian Elizabeth. "The biology of Plasmodium falciparum gametocytes." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360296.

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Beveridge, Susan Elizabeth. "Metabolite transport pathways of Plasmodium falciparum." Thesis, University of Liverpool, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.590055.

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Metabolite transport pathways of the malaria parasite, Plasmodium falciparum, are an important area for study in order to further the understanding of the parasite's biology. Identification and characterisation of the transporters involved in these pathways may also provide potential novel drug targets or drug delivery mechanisms. This is especially valuable as chemotherapy remains one of the main management strategies in the fight against malaria and the usefulness 0 f the current range 0 f antimalarial drugs is seriously threatened by the emergence and spread of resistance . .' In this thesis the Xenopus laevis oocyte heterologous expression system was used to functionally characterise a gene-specific cDNA library of 48 putative membrane proteins and the previously annotated putative amino acid transporter PFF1430c for the uptake of several amino acids. This screening failed to identify any definite amino acid transport by the cDNA library or PFF1430c, however this could have been due to the fact that uptake of a relatively narrow range of amino acids was tested and these were used at concentrations lower than found physiologically. Inherent issues with the X laevis expression system may also have been an issue, including the expression of endogenous transporters for the substrates being investigated.

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Books on the topic "Plasmodium falciparum"

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Costanzo, Marna Schutte. Constraints and trade-offs in enzyme evolution of Plasmodium falciparum. Cambridge, Mass: Harvard University, 2010.

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Tarique, Mohammed. Drug Targets for Plasmodium Falciparum: Historic to Future Perspectives. Singapore: Springer Nature Singapore, 2024. http://dx.doi.org/10.1007/978-981-19-4484-0.

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Murithi, James Muriungi. Dissecting the mechanisms of antiplasmodial resistance in Plasmodium falciparum. [New York, N.Y.?]: [publisher not identified], 2021.

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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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Iqbal, Jamshaid. Erythrocyte membrane associated Plasmodium falciparum antigens, involvement in immunity and sequestration. Stockholm: Department of Immunology, the Wenner-Gren Institute, Stockholm University, 1994.

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Chu, Yen. Rheological beheaviour[sic] of erythrocyte rosettes induced by Plasmodium falciparum in flow. Birmingham: University of Birmingham, 1995.

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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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Scanfeld, Daniel. Exploring the Plasmodium falciparum Transcriptome Using Hypergeometric Analysis of Time Series (HATS). [New York, N.Y.?]: [publisher not identified], 2013.

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Verrall, B. Expresssion of the TATA box binding protein of plasmodium falciparum in heterologous systems. Manchester: UMIST, 1997.

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Lee, Andrew Hojin. Investigating mutability and the plasmodium falciparum chloroquine resistance transporter in drug resistant malaria parasites. [New York, N.Y.?]: [publisher not identified], 2016.

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Book chapters on the topic "Plasmodium falciparum"

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Keenihan, Sarah Hudson, Robert Gramzinksi, Sutanti Ratiwayanto, Hilda Hadiputranto, Wiwi Riberu, Saraswati Soebianto, Faisal Rusjdy, et al. "Plasmodium Falciparum." In Tropical Diseases, 83–102. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0059-9_7.

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Ringelmann, R., and Beate Heym. "Plasmodium falciparum." In Parasiten des Menschen, 202–5. Heidelberg: Steinkopff, 1991. http://dx.doi.org/10.1007/978-3-642-85397-5_72.

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Mehlhorn, Heinz. "Plasmodium falciparum: Endothelial Receptors." In Encyclopedia of Parasitology, 2171–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_4778.

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Mehlhorn, Heinz. "Plasmodium falciparum: Phylogenetic Origins." In Encyclopedia of Parasitology, 2172. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_4782.

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Mehlhorn, Heinz. "Plasmodium falciparum: Endothelial Receptors." In Encyclopedia of Parasitology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_4778-1.

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Mehlhorn, Heinz. "Plasmodium falciparum: Phylogenetic Origins." In Encyclopedia of Parasitology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_4782-1.

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Rug, Melanie, and Alexander G. Maier. "Transfection of Plasmodium falciparum." In Methods in Molecular Biology, 75–98. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-026-7_6.

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Noor, Rana. "Pathogenesis of Plasmodium falciparum." In Drug Targets for Plasmodium Falciparum: Historic to Future Perspectives, 19–40. Singapore: Springer Nature Singapore, 2024. http://dx.doi.org/10.1007/978-981-19-4484-0_2.

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Petter, Michaela, and Michael F. Duffy. "Antigenic Variation in Plasmodium falciparum." In Results and Problems in Cell Differentiation, 47–90. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-20819-0_3.

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Cohen, Scott J. "Plasmodium Falciparum Malaria in Children." In Updates in Emergency Medicine, 51–55. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0155-8_10.

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Conference papers on the topic "Plasmodium falciparum"

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Quevedo, Viviana, and Bernabe Ortega-Tenezaca. "IF for the dataset of Plasmodium Falciparum." In MOL2NET 2019, International Conference on Multidisciplinary Sciences, 5th edition. Basel, Switzerland: MDPI, 2019. http://dx.doi.org/10.3390/mol2net-05-06253.

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Cai, Hong, Maribel Sanchez, Yufeng Wang, and Jianying Gu. "Putative Cell Cycle Related Genes in Plasmodium Falciparum." In 2009 International Joint Conference on Bioinformatics, Systems Biology and Intelligent Computing. IEEE, 2009. http://dx.doi.org/10.1109/ijcbs.2009.44.

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Evans, Krystal J., Dedreia Tull, Michael C. Hewitt, Malcolm J. McConville, Peter H. Seeberger, and Louis Schofield. "PURIFICATION OF THE GLYCOSYLPHOSPHATIDYLINOSITOL TOXIN OF PLASMODIUM FALCIPARUM." In XXIst International Carbohydrate Symposium 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.690.

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Yumang, Analyn N., Ericson D. Dimaunahan, Jennifer Dela Cruz, Geraldo C. Talisic, Gabriel Avelino R. Sampedro, and Maricor N. Soriano. "Real-Time Plasmodium Falciparum Parasitemia using Natural Neighbor Interpolation." In 2018 IEEE 10th International Conference on Humanoid, Nanotechnology, Information Technology,Communication and Control, Environment and Management (HNICEM). IEEE, 2018. http://dx.doi.org/10.1109/hnicem.2018.8666280.

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Rocha, Maura G. R., Rodrigo M. S. Veras, Maíla L. Claro, Laurindo S. Britto Neto, and Kelson R. T. Aires. "Análise Comparativa de Versões YOLO na Detecção e Identificação de Parasitas da Malária." In Simpósio Brasileiro de Computação Aplicada à Saúde. Sociedade Brasileira de Computação - SBC, 2021. http://dx.doi.org/10.5753/sbcas.2021.16066.

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A malária é uma doença endêmica causada pelo parasita Plasmodium que pode ser fatal em muitas regiões do mundo. Alguns pesquisadores estão utilizando conceitos de aprendizagem de máquina para detectar e classiﬁcar células infectadas pelo parasita Plasmodium. Este trabalho apresenta um estudo comparativo de três versões recentes da rede neural convolucional You Only Look Once (YOLO), são elas a: YOLOv4, Scaled-YOLOv4 e YOLOv5. Foi utilizado a base de dados MP-IDB que possui 210 imagens com o parasita Plasmodium. Os modelos alcançaram excelentes resultados, tendo o melhor resultado com mAP e precisão de 94,8% e 93,3%, respectivamente, para a classiﬁcação em dois tipos de espécies do Plasmodium falciparum e vivax.

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Fogel, Gary B., Carla Islas, and David Hecht. "Modeling the evolution of drug resistance in Plasmodium falciparum DHFR." In 2013 IEEE Congress on Evolutionary Computation (CEC). IEEE, 2013. http://dx.doi.org/10.1109/cec.2013.6557572.

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Setianingrum, Anif Hanifa, Luh Kesuma Wardhani, A. Faisal Ridwan, and Silvia F. Nasution. "Identification of Plasmodium falciparum Stages Using Support Vector Machine Method." In 2019 7th International Conference on Cyber and IT Service Management (CITSM). IEEE, 2019. http://dx.doi.org/10.1109/citsm47753.2019.8965413.

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Lawford, Nicola, and Jonathan H. Chan. "Predicting Dihydroartemisinin Resistance in Plasmodium falciparum using Pathway Activity Inference." In CSBio2020: The 11th International Conference on Computational Systems-Biology and Bioinformatics. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3429210.3429215.

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Avanci, Lorrany da Silva, Josilene Carla Ferreira de Araujo, Audrey Luiza Fonseca Nunes, Cibele do Nascimento, and Dr Saumel Rangel Cláudio. "REVISÃO DE LITERATURA DA FISIOPATOLOGIA DO FÍGADOINFECTADO PELO PLASMODIUM FALCIPARUM." In II Congresso Brasileiro de Parasitologia Humana On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/conbrapah/21.

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Introdução: O Plasmodium é o agente etiológico da malária, e a infecção no hospedeiro vertebrado ocorre envolvendo diferentes células e depende de uma complexidade de eventos celulares e bioquímicos no hospedeiro para realizar o ciclo de desenvolvimento.Os casos de malária reportado pela Organização Mundial da Saúde (OMS), ocorrem em países distribuídos ao longo da faixa intertropical do globo terrestre, são áreas com condições favoráveis à ocorrência e desenvolvimento do vetor Anopheles spp. No ano de 2019 ocorreram cerca de 229 milhões de novos casos de malária e 409 mil mortes, crianças menores de 5 anos são mais vulneráveis, representando cerca de 67% de todas as mortes no ano de 2019. Objetivo: Em vista disso, O presente estudo tem finalidade descritiva e através da análise de artigos científicos, avaliar alterações da morfologia hepática e detecção de fibrose nos hospedeiros infectados pelo Plasmodium submetidos ou não aos tratamentos com antimalaricos, observar o ciclo de vida do Plasmodium, como ocorre a infecção no humano da doença malárica, as possíveis alterações morfológicas e fisiopatológicas causadas pela hemozoína no tecido hepático e presença de fibrose. Metodologia: A metodologia utilizada é baseada em artigos científicos de revisão exploratória. Foram selecionados artigos referentes à malária, nos idiomas português e inglês. São artigos levantados por meio de consultas através dos sites acadêmicos PudMed, SciElo, Science Direct, Malaria Journal e WHO, com período de abrangência de 2015 a 2021. Resultados: As alterações fisiopatológicas no fígado do hospedeiro infectado estão relacionadas com o processo inflamatório pela hemozoína e necessitam de estudos para a compreensão da relação parasita x hospedeiro e do potencial comprometimento tecidual hepático. É observado presença de fibrose hepática, células mortas, neoplasias e quadro inflamatório tecidual hepático, desencadeado pela hemozoína, quando não há tratamento para regressão da fibrose hepática e a lesão celular continua sendo persistente, ocorre o desenvolvimento de cirrose, que pode evoluir para carcinoma hepatocelular. Conclusão: A observação das alterações hepática durante e após a infecção da malária é essencial para entender os potenciais danos teciduais hepáticos, avaliar os tratamentos disponíveis e ações preconizadas pela OMS para redução da infecção e óbitos causados pela malária.

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Silva, Saulo Brivaldo Mendonça da, Ana Bárbara Xavier da Silva, Mariana Souza Bezerra Cavalcanti, João Lucas Pessoa de Vasconcelos, Maria Clara Cavalcante Gomes, and Nathaly Bruna de Oliveira Silva. "A PROTEÍNA PfGARP COMO POSSÍVEL CANDIDATA À VACINA ANTIMALÁRICA." In XXVII Semana de Biomedicina Inovação e Ciência. Editora IME, 2021. http://dx.doi.org/10.51161/9786588884119/28.

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Introdução: A malária é uma parasitose que, apesar de antiga, continua sendo um grande risco para saúde pública com cerca de 445 mil mortes por ano ao redor do mundo(2). Apesar de possuir cinco agentes etiológicos, o Plasmodium falciparum é o principal, sendo responsável pelo maior número de mortes por malária(1,2). Uma vez que há diversos empecilhos quando se trata da erradicação da malária como resistência a inseticidas e a drogas antimaláricas, foi observada a necessidade de uma vacina contra o agravamento dessa parasitose(1). O fato de que a fase sanguínea do Plasmodium é atualmente apontada como um dos possíveis alvos para a ação de uma vacina, fez os pesquisadores enxergarem a proteína rica em ácido glutâmico do P. falciparum (PfGARP) que é encontrada na superfície das células vermelhas infectadas pelo parasita(2,3). Assim, fez-se necessária uma pesquisa com os anticorpos contra essa proteína para melhor elucidação. Objetivos: O objetivo deste resumo é observar os efeitos dos anticorpos anti-PfGARP contra trofozoítos do Plasmodium falciparum e como esses anticorpos oferecem proteção contra o agravamento da malária. Métodos: Foi realizada a procura nas plataformas científicas PubMed e Google Acadêmico e os artigos utilizados foram encontrados por meio do descritor “malaria vaccine”. Resultados: Os anticorpos anti-PfGARP presentes nos indivíduos estudados foram apontados como responsáveis pela diminuição da integridade morfológica dos parasitas, onde os mesmos apresentaram-se picnóticos, característicos de morte(3). Além disso, esses anticorpos causaram uma diminuição da integridade do vacúolo digestivo, apresentando-se com um tamanho menor ou até mesmo ausente(3). Outrossim, os parasitas sofreram alterações no potencial de membrana mitocondrial, tendo a mitocôndria perdido função após 24h(3). Por fim, os anticorpos anti-PfGARP ativaram a morte celular programada desses parasitas por meio da ativação de caspases(3). Conclusões: Com base no que foi exposto, é possível concluir que a PfGARP é uma excelente candidata para o desenvolvimento de uma vacina contra o Plasmodium falciparum por meio da morte dos parasitas. Sendo assim, é necessário que sejam realizados mais estudos com a PfGARP com o objetivo de obter mais informações acerca dos benefícios de uma vacina com essa proteína e, ainda, conhecer possíveis malefícios para que possa ser inclusa no mercado de forma eficaz e segura, diminuindo a ocorrência de malária grave e assim evitando o sofrimento de milhares de pessoas infectadas com esta parasitose ao redor do mundo.

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Reports on the topic "Plasmodium falciparum"

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สืบหลินวงศ์, ธาดา, and จุฑาพันธุ์ พิณสวัสดิ์. รูปแบบของโปรตีนใน Plasmodium falciparum โดยอิเล็คโตรฟอรีซิสสองมิติ : รายงานวิจัยฉบับสมบูรณ์. จุฬาลงกรณ์มหาวิทยาลัย, 1988. https://doi.org/10.58837/chula.res.1988.10.

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โปรตีนในแต่ละเซลล์จะถูกสังเคราะห์ขึ้นอย่างรัดกุม มีการควบคุมในระดับยีน จึงมีคุณสมบัติเฉพาะตัวสำหรับแต่ละเซลล์หรือแต่ละชนิดของสัตว์และพืช ดังนั้น การศึกษารูปแบบของโปรตีนซึ่งถือเป็น gene product จึงอาจใช้เป็น marker ของเซลล์หรือสัตว์แต่ละชนิดได้ วัตถุประสงค์ของการวิจัยครั้งนี้เพื่อนำรูปแบบโปรตันซึ่งศึกษาโดยเทคนิค 2-D electrophoresis มาเป็น marker ของแต่ละสายพันธุ์บริสุทธิ์ของ P.falciparum โดยได้ศึกษารูปแบบโปรตีนของเม็ดเลือดแดงที่ติดเชื้อ P.falciparum ในตัวอย่างที่เป็น isolate และสายพันธุ์บริสุทธิ์รวม 70 ตัวอย่าง และศึกษาโปรตีนใน P. falciparum โดยใช้ [superscript 3 5]S-methionine incorporation, 2-D electrophoresis และ autoradiography และ autoradiography นั้น ไวกว่าการย้อมด้วย Coomassie blue R โดยแยกโปรตีนของ P. falciparum ออกเป็น 14 กลุ่มและแต่ละกลุ่มยังแยกย่อย ๆออกไปอีก 1-7 ชนิดย่อย และพบว่า รูปแบบโปรตีนใน P. falciparum ซึ่งเลี้ยงในห้องปฏิบัติการเป็นเวลานานกว่า 3 ปี ยังคงที่ จึงสรุปว่าความแตกต่างในรูปแบบโปรตีนของ P. falciparum สามารถใช้เป็นเครื่องแสดงลักษณะเฉพาะประจำตัวปรสิตได้

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Rossan, Richard N. Drug Evaluation in the Plasmodium Falciparum-Aotus Model. Fort Belvoir, VA: Defense Technical Information Center, June 1989. http://dx.doi.org/10.21236/ada210494.

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Rossan, Richard N. Drug Evaluation in the Plasmodium Falciparum - Aotus Model. Fort Belvoir, VA: Defense Technical Information Center, October 1986. http://dx.doi.org/10.21236/ada211392.

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Rossan, Richard N. Drug Evaluation in the Plasmodium falciparum - Aotus Model. Fort Belvoir, VA: Defense Technical Information Center, December 1990. http://dx.doi.org/10.21236/ada232854.

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Wirth, Dyann F. New Strategies for Drug Discovery and Development for Plasmodium Falciparum. Fort Belvoir, VA: Defense Technical Information Center, January 2000. http://dx.doi.org/10.21236/ada375802.

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Piper, Robert C. Parasite Lactate Dehydrogenase for Diagnosis of Plasmodium Falciparum. Phase II. Fort Belvoir, VA: Defense Technical Information Center, April 1997. http://dx.doi.org/10.21236/adb230017.

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Obaldia, Nicanor, and III. Drug and Vaccine Evaluation in the Human-Aotus Plasmodium Falciparum Model. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada405377.

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Rollwagen, Florence M., Nancy D. Pacheco, Jr Wistar, and Richard. Proliferative Responses of Mice to a Cloned Plasmodium Falciparum Sporozoite Antigen. Fort Belvoir, VA: Defense Technical Information Center, December 1988. http://dx.doi.org/10.21236/ada205098.

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Makler, Michael T. Method for Evaluation of Drug Resistance for Plasmodium Falciparum. Phase 2. Fort Belvoir, VA: Defense Technical Information Center, July 1991. http://dx.doi.org/10.21236/adb158380.

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Obaldia, III, and Nocanor. Drug and Vaccine evaluation in the Human Aotus Plasmodium falciparum Model. Fort Belvoir, VA: Defense Technical Information Center, May 2011. http://dx.doi.org/10.21236/ada547285.

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