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Relevant bibliographies by topics / Sulfadoxine

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Academic literature on the topic 'Sulfadoxine'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Sulfadoxine"

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&NA;. "Sulfadoxine see Pyrimethamine + sulfadoxine." Reactions Weekly &NA;, no. 294 (March 1990): 12. http://dx.doi.org/10.2165/00128415-199002940-00050.

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&NA;. "Sulfadoxine see Pyrimethamine + sulfadoxine." Reactions Weekly &NA;, no. 296 (April 1990): 7. http://dx.doi.org/10.2165/00128415-199002960-00031.

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&NA;. "Sulfadoxine see Pyrimethamine + sulfadoxine." Reactions Weekly &NA;, no. 340 (March 1991): 7. http://dx.doi.org/10.2165/00128415-199103400-00029.

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&NA;. "Pyrimethamine + sulfadoxine." Reactions Weekly &NA;, no. 294 (March 1990): 12. http://dx.doi.org/10.2165/00128415-199002940-00047.

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&NA;. "Pyrimethamine + sulfadoxine." Reactions Weekly &NA;, no. 296 (April 1990): 7. http://dx.doi.org/10.2165/00128415-199002960-00027.

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&NA;. "Pyrimethamine/sulfadoxine." Reactions Weekly &NA;, no. 1043 (March 2005): 17. http://dx.doi.org/10.2165/00128415-200510430-00057.

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&NA;. "Pyrimethamine + sulfadoxine." Reactions Weekly &NA;, no. 340 (March 1991): 7. http://dx.doi.org/10.2165/00128415-199103400-00027.

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&NA;. "Pyrimethamine/sulfadoxine." Reactions Weekly &NA;, no. 1401 (May 2012): 32. http://dx.doi.org/10.2165/00128415-201214010-00121.

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Korsinczky, Michael, Katja Fischer, Nanhua Chen, Joanne Baker, Karl Rieckmann, and Qin Cheng. "Sulfadoxine Resistance in Plasmodium vivax Is Associated with a Specific Amino Acid in Dihydropteroate Synthase at the Putative Sulfadoxine-Binding Site." Antimicrobial Agents and Chemotherapy 48, no. 6 (June 2004): 2214–22. http://dx.doi.org/10.1128/aac.48.6.2214-2222.2004.

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ABSTRACT Sulfadoxine is predominantly used in combination with pyrimethamine, commonly known as Fansidar, for the treatment of Plasmodium falciparum. This combination is usually less effective against Plasmodium vivax, probably due to the innate refractoriness of parasites to the sulfadoxine component. To investigate this mechanism of resistance by P. vivax to sulfadoxine, we cloned and sequenced the P. vivax dhps (pvdhps) gene. The protein sequence was determined, and three-dimensional homology models of dihydropteroate synthase (DHPS) from P. vivax as well as P. falciparum were created. The docking of sulfadoxine to the two DHPS models allowed us to compare contact residues in the putative sulfadoxine-binding site in both species. The predicted sulfadoxine-binding sites between the species differ by one residue, V585 in P. vivax, equivalent to A613 in P. falciparum. V585 in P. vivax is predicted by energy minimization to cause a reduction in binding of sulfadoxine to DHPS in P. vivax compared to P. falciparum. Sequencing dhps genes from a limited set of geographically different P. vivax isolates revealed that V585 was present in all of the samples, suggesting that V585 may be responsible for innate resistance of P. vivax to sulfadoxine. Additionally, amino acid mutations were observed in some P. vivax isolates in positions known to cause resistance in P. falciparum, suggesting that, as in P. falciparum, these mutations are responsible for acquired increases in resistance of P. vivax to sulfadoxine.

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&NA;. "Antiretrovirals/pyrimethamine/sulfadoxine." Reactions Weekly &NA;, no. 1318 (September 2010): 11. http://dx.doi.org/10.2165/00128415-201013180-00031.

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Dissertations / Theses on the topic "Sulfadoxine"

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Badenhorst, Liezl. "The dissolution analysis of sulfadoxine/pyrimethamine combination tablets / Liezl Badenhorst." Thesis, North-West University, 2007. http://hdl.handle.net/10394/1791.

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Obua, Celestino. "Fixed-dose chloroquine and sulfadoxine/pyrimethamine treatment of malaria : outcome and pharmacokinetic aspects /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-144-9/.

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Gillet, Philippe. "Hepatite medicamenteuse au fansidar : a propos d'un cas et revue de la litterature." Amiens, 1992. http://www.theses.fr/1992AMIEM024.

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Manoir, Milena du. "Résistance de Plasmodium falciparum à la sulfadoxine-pyriméthamine : données épidémiologiques et modélisation." Thesis, Toulouse 3, 2018. http://www.theses.fr/2018TOU30147.

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En 2016, 216 millions de cas et 445000 décès liés au paludisme ont été reportés par l'Organisation Mondiale de la Santé (OMS), 90 % de ces cas ont eu lieu sur le continent africain, très majoritairement causés par Plasmodium falciparum. Chez les femmes enceintes le paludisme peut avoir de lourdes conséquences en termes de morbidité et de mortalité aussi bien pour la mère que pour l'enfant à venir. Outre l'utilisation de moustiquaires imprégnées, l'OMS recommande l'utilisation d'un traitement préventif intermittent par sulfadoxine-pyriméthamine (SP) pour les femmes enceintes des zones endémiques d'Afrique sub-saharienne. La résistance du parasite à la SP est un réel problème en l'absence d'alternative thérapeutique et le niveau de résistance est déjà très élevé dans certaines régions d'Afrique. Cette résistance est causée par différents polymorphismes nucléotidiques simples (SNPs) sur les gènes codant pour DHPS et DHFR. Ces mutations modifient la structure 3D de ces enzymes, diminuant leur liaison à la SP. Ce travail s'est attaché à faire un état des lieux récent de la prévalence des mutations des gènes pfdhfr et pfdhps à travers 7 sites d'Afrique Centrale. Un octuple mutant combinant trois mutations sur le gène pfdhfr et cinq mutations sur le gène pfdhps (CirnI + vagKgs) a été découvert à Yaoundé en 2015 ; nous l'avons retrouvé au Nigeria et au Cameroun mais pour la première fois à un haut niveau de prévalence à Maroua (52,2%). Sur plusieurs sites d'Afrique Centrale, nous décrivons l'augmentation de la prévalence de la mutation K540E, typique des parasites résistants de l'Afrique de l'Est et sur laquelle se base l'implémentation de la SP par l'OMS. D'autre part, à partir d'un modèle d'homologie de pfDHPS, nous avons utilisé des techniques de dynamique moléculaire pour mieux comprendre les modifications de la structure 3D liées à différents haplotypes d'intérêts retrouvés en Afrique Centrale. Cette partie de l'étude propose une autre approche pour évaluer et visualiser l'effet structurel des mutations, élément supplémentaire à la compréhension de leur impact sur la résistance à la SP
Malaria was responsible for 445 000 death and 216 million new cases worldwide in 2016, 90% of these cases occurred in Africa. Pregnant women are particularly susceptible to malaria, resulting in medical consequences on both mother and child. In the endemic countries of sub Saharan Africa, in addition to the use of insecticidal nets, the World Health Organization (WHO) recommends a preventive treatment against Plasmodium falciparum malaria in pregnancy using Sulfadoxine Pyrimethamine (SP). Resistance of the parasite to SP is a significant problem in the absence of alternative treatment and the level of resistance is very high in some regions of Africa. This resistance is mediated by several single nucleotide polymorphisms (SNPs) in the genes coding for DHPS and DHFR, changing the 3D structure of the two target proteins and decreasing drug binding. This study offers an updated view of the epidemiology of these mutations throughout Central Africa. We identified for the first time the octuple mutant combining 3 mutations on pfdhfr gene and 5 mutations on pfdhps gene (CirnI + vagKgs), discovered in 2015 in Yaoundé, as the major haplotype in Maroua, northern Cameroon (52,2%). On several Central-African sites, we describe the increase of the prevalence of the typically East-African K540E mutation on which is based the implementation of SP by the WHO. Knowledge of the prevalence of resistance markers is crucial for the adaptation of SP recommendation in Central Africa. This study also explores the changes occurring in the 3D structure of the most common mutated pfDHPS haplotypes identified in our epidemiology study, using molecular dynamics on a homology model of the protein. It offers a new vision of the effect of the mutations on the structure, a further step to understanding the impact of mutations in resistance

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Cisse, Badara. "Seasonal preventive treatment with artesunate and sulfadoxine pyrimethamine prevents malaria in Senegalese children." Thesis, London School of Hygiene and Tropical Medicine (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.421682.

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Letillois, Claire. "Suivi clinique et immunologique de 71 cas de toxoplasmose congenitale traites." Reims, 1994. http://www.theses.fr/1994REIMM010.

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Bojang, Kalifa Abubakr. "Chemoprophylaxis with sulfadoxine-pyrimethamine to prevent morbidity in Gambian children treated for severe anaemia." Thesis, London School of Hygiene and Tropical Medicine (University of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500046.

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GRAUBY, SAINT-LEBE MARIE-NOELLE. "Chimio-resistances de plasmodium falciparum : cas de la sulfadoxine-pyrimethamine et de la quinine." Aix-Marseille 2, 1993. http://www.theses.fr/1993AIX20113.

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Silveira, Quelhas Diana Iris. "Immune responses to "Plasmodium falciparum" in Mozambican infants receiving Intermittent Preventive Treatment with Sulfadoxine Pyrimethamine." Doctoral thesis, Universitat de Barcelona, 2011. http://hdl.handle.net/10803/51637.

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Malaria has a high toll on the lives of infants and children under the age of five in endemic areas. Control, and more recently, elimination agendas consist on implementing several measures simultaneously, including vector control, vaccines and drugs. The current Millenium Development Goals aim at reducing malaria mortality and morbidity in the two most vulnerable groups: pregnant women and children. Intermittent Preventive Treatment in Infants with Sulphadoxine‐Pyrimethamine (IPTi-SP) delivered through routine EPI vaccination programs has shown to be efficacious in different transmission settings and the WHO has recently recommended its implementation as a malaria control tool. However, one of the main concerns has been the potential impairment of acquisition of naturally acquired immunity, and this could be a concern regarding IPTi. This thesis reports on a series of studies conducted in a malaria endemic area of Manhiça, Mozambique, to assess the impact of IPTi‐SP on the development of immune responses to the Plasmodium falciparum parasite. In this work, we measured antibody and cellular immune parameters considered to be the most appropriate markers of protective immunity against malaria identified to date. The most consistent finding was that IPTi-SP does not modify the magnitude of the immune responses acquired over the first two years of age in Mozambican children. In addition, we described the factors that affect the antibody and cellular immune responses, and reported those that correlated with prospective malaria incidence. Based on the studies presented herein, we can conclude that IPTi‐SP does not interfere with immune responses that are considered major contributors to the acquisition of protective immunity to malaria in early infancy. In summary, this thesis contributes to a more complete assessment of IPTi as a control measure that will possibly be implemented in the near future in malaria endemic areas of Africa and of the world. In addition, it aims to contribute to advance the knowledge on the acquisition of natural immunity in infancy which is poorly understood. Furthermore, this information will help to understand the factors that should be taken into account when designing and deploying other control measures for this age group.

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Billi, Borchert Lea. "Wirksamkeit und Verträglichkeit von IPTi mit Sulfadoxine-Pyrimethamine zur Prophylaxe gegen Anämie und Malaria in Gabun im ersten Lebensjahr /." Tübingen, 2009. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000276774.

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Book chapters on the topic "Sulfadoxine"

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Mehlhorn, Heinz. "Sulfadoxine Pyrimethamine Resistance." In Encyclopedia of Parasitology, 2582. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_4358.

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Mehlhorn, Heinz. "Sulfadoxine Pyrimethamine Resistance." In Encyclopedia of Parasitology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_4358-1.

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Nzila, M. A. "Molecular Mechanisms of Resistance to Antimalarial Antifolate Drug Pyrimethamine-Sulfadoxine." In Chemistry and Biology of Pteridines and Folates, 457–60. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0945-5_77.

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Kollaritsch, H., H. Stemberger, H. Mailer, R. Kollaritsch, R. Leimer, and G. Wiedermann. "Long-Term Tolerance of the Triple-Combination Fansimef™ (Mefloquine+Sulfadoxine+Pyrimethamine): Results of a Double-blind Field Trial in Nigeria." In Travel Medicine, 147–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73772-5_24.

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Scholar, Eric. "Sulfadoxine." In xPharm: The Comprehensive Pharmacology Reference, 1–5. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.62691-1.

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Kapoor, Vijay K. "Sulfadoxine." In Analytical Profiles of Drug Substances, 571–605. Elsevier, 1988. http://dx.doi.org/10.1016/s0099-5428(08)60226-9.

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"SULFADOXINE." In Litt's Drug Eruption and Reaction Manual, 331. CRC Press, 2015. http://dx.doi.org/10.1201/b17996-121.

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Chevrel, Guillaume, and Virginie Dessus. "sulfadoxine/pyriméthamine." In 300 médicaments injectables, 398–99. Elsevier, 2009. http://dx.doi.org/10.1016/b978-2-294-70698-1.50159-8.

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Hodoameda, Peter. "P. falciparum and Its Molecular Markers of Resistance to Antimalarial Drugs." In Plasmodium Species and Drug Resistance [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98372.

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The use of molecular markers of resistance to monitor the emergence, and the spread of parasite resistance to antimalarial drugs is a very effective way of monitoring antimalarial drug resistance. The identification and validation of molecular markers have boosted our confidence in using these tools to monitor resistance. For example, P. falciparum chloroquine resistance transporter (PfCRT), P. falciparum multidrug resistance protein 1 (PfMDR1), P. falciparum multidrug kelch 13 (pfk13), have been identified as molecular markers of resistance to chloroquine, lumefantrine, and artemisinin respectively. The mechanism of resistance to antimalarial drugs is mostly by; (1) undergoing mutations in the parasite genome, leading to expelling the drug from the digestive vacuole, or (2) loss of binding affinity between the drug and its target. Increased copy number in the pfmdr1 gene also leads to resistance to antimalarial drugs. The major cause of the widespread chloroquine and sulfadoxine-pyrimethamine resistance globally is the spread of parasites resistant to these drugs from Southeast Asia to Africa, the Pacific, and South America. Only a few mutations in the parasite genome lead to resistance to chloroquine and sulfadoxine-pyrimethamine arising from indigenous parasites in Africa, Pacific, and South America.

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Tsegaye Tseha, Sintayehu. "Plasmodium Species and Drug Resistance." In Plasmodium Species and Drug Resistance [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98344.

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Malaria is a leading public health problem in tropical and subtropical countries of the world. In 2019, there were an estimated 229 million malaria cases and 409, 000 deaths due malaria in the world. The objective of this chapter is to discuss about the different Plasmodium parasites that cause human malaria. In addition, the chapter discusses about antimalarial drugs resistance. Human malaria is caused by five Plasmodium species, namely P. falciparum, P. malariae, P. vivax, P. ovale and P. knowlesi. In addition to these parasites, malaria in humans may also arise from zoonotic malaria parasites, which includes P. inui and P. cynomolgi. The plasmodium life cycle involves vertebrate host and a mosquito vector. The malaria parasites differ in their epidemiology, virulence and drug resistance pattern. P. falciparum is the deadliest malaria parasite that causes human malaria. P. falciparum accounted for nearly all malarial deaths in 2018. One of the major challenges to control malaria is the emergence and spread of antimalarial drug-resistant Plasmodium parasites. The P. vivax and P. falciparum have already developed resistance against convectional antimalarial drugs such as chloroquine, sulfadoxine-pyrimethamine, and atovaquone. Chloroquine-resistance is connected with mutations in pfcr. Resistance to Sulfadoxine and pyrimethamine is associated with multiple mutations in pfdhps and pfdhfr genes. In response to the evolution of drug resistance Plasmodium parasites, artemisinin-based combination therapies (ACTs) have been used for the treatment of uncomplicated falciparum malaria since the beginning of 21th century. However, artemisinin resistant P. falciparum strains have been recently observed in different parts of the world, which indicates the possibility of the spread of artemisinin resistance to all over the world. Therefore, novel antimalarial drugs have to be searched so as to replace the ACTs if Plasmodium parasites develop resistance to ACTs in the future.

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