Littérature scientifique sur le sujet « Metabolism in Toxoplasma Gondii »
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Articles de revues sur le sujet "Metabolism in Toxoplasma Gondii"
Krug, E. C., J. J. Marr et R. L. Berens. « Purine Metabolism in Toxoplasma gondii ». Journal of Biological Chemistry 264, no 18 (juin 1989) : 10601–7. http://dx.doi.org/10.1016/s0021-9258(18)81663-5.
Texte intégralChang, Hernán R., et Jean-Claude Pechère. « Macrophage oxidative metabolism and intracellular Toxoplasma gondii ». Microbial Pathogenesis 7, no 1 (juillet 1989) : 37–44. http://dx.doi.org/10.1016/0882-4010(89)90109-5.
Texte intégralChen, Min, Lijuan Zhou, Shengmin Li, Hiaxia Wei, Jiating Chen, Pei Yang et Hongjuan Peng. « Toxoplasma gondii DNA methyltransferases regulate parasitic energy metabolism ». Acta Tropica 229 (mai 2022) : 106329. http://dx.doi.org/10.1016/j.actatropica.2022.106329.
Texte intégralPrandovszky, Emese, Elizabeth Gaskell, Heather Martin, J. P. Dubey, Joanne P. Webster et Glenn A. McConkey. « The Neurotropic Parasite Toxoplasma Gondii Increases Dopamine Metabolism ». PLoS ONE 6, no 9 (21 septembre 2011) : e23866. http://dx.doi.org/10.1371/journal.pone.0023866.
Texte intégralSonda, Sabrina, Giusy Sala, Riccardo Ghidoni, Andrew Hemphill et Jean Pieters. « Inhibitory Effect of Aureobasidin A on Toxoplasma gondii ». Antimicrobial Agents and Chemotherapy 49, no 5 (mai 2005) : 1794–801. http://dx.doi.org/10.1128/aac.49.5.1794-1801.2005.
Texte intégralMageed, Sarmad N., Fraser Cunningham, Alvin Wei Hung, Hernani Leonardo Silvestre, Shijun Wen, Tom L. Blundell, Chris Abell et Glenn A. McConkey. « Pantothenic Acid Biosynthesis in the Parasite Toxoplasma gondii : a Target for Chemotherapy ». Antimicrobial Agents and Chemotherapy 58, no 11 (21 juillet 2014) : 6345–53. http://dx.doi.org/10.1128/aac.02640-14.
Texte intégralel Kouni, Mahmoud. « Adenosine Metabolism in Toxoplasma gondii : Potential Targets for Chemotherapy ». Current Pharmaceutical Design 13, no 6 (1 février 2007) : 581–97. http://dx.doi.org/10.2174/138161207780162836.
Texte intégralWeilhammer, Dina R., Anthony T. Iavarone, Eric N. Villegas, George A. Brooks, Anthony P. Sinai et William C. Sha. « Host metabolism regulates growth and differentiation of Toxoplasma gondii ». International Journal for Parasitology 42, no 10 (septembre 2012) : 947–59. http://dx.doi.org/10.1016/j.ijpara.2012.07.011.
Texte intégralWu, Liang, Lipei Wu, Chenyu Tang, Jiajian Wang, Xiaoling Jin, Xugan Jiang et Shengxia Chen. « Induction of FAS II Metabolic Disorders to Cause Delayed Death of Toxoplasma gondii ». Journal of Nanoscience and Nanotechnology 18, no 12 (1 décembre 2018) : 8155–59. http://dx.doi.org/10.1166/jnn.2018.16396.
Texte intégralLi, Meiqi, Xiaoyu Sang, Xiaohan Zhang, Xiang Li, Ying Feng, Na Yang et Tiantian Jiang. « A Metabolomic and Transcriptomic Study Revealed the Mechanisms of Lumefantrine Inhibition of Toxoplasma gondii ». International Journal of Molecular Sciences 24, no 5 (3 mars 2023) : 4902. http://dx.doi.org/10.3390/ijms24054902.
Texte intégralThèses sur le sujet "Metabolism in Toxoplasma Gondii"
Roohi, Aysha. « Toxoplasma gondii infection and the host cell metabolism ». Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648369.
Texte intégralRen, Bingjian. « Physiological importance of phospholipid biogenesis in Toxoplasma gondii ». Doctoral thesis, Humboldt-Universität zu Berlin, 2019. http://dx.doi.org/10.18452/20721.
Texte intégralToxoplasma gondii is an obligate intracellular parasite that causes Toxoplasmosis in human and livestock. Phospholipid biosynthesis is crucial for the successful intracellular survival and replication of the parasites, as the phospholipids have important roles in the biogenesis of membrane organelles, signal transduction and other cellular processes. Here, we dissected the physiological importance of two pathways accounting for the synthesis of PtdEtn and PtdIns. We demonstrated the presence of a novel PtdIns synthase (PIS) in T.gondii termed TgPIS, expressing a functional enzyme with a catalytically vital CDP-alcohol phosphotransferase motif, which resides exclusively in the Golgi body. The parasite imports myo-inositol from milieu, and co-utilizes de novo-synthesized CDP-diacylglycerol to produce PtdIns. An auxin-inducible conditional repression of TgPIS abrogated the lytic cycle of the parasite in mammalian cells due to defects in the replication, motility and egress. Lipidomic profiling of the PIS mutant demonstrated selective reduction of certain PtdIns and PtdThr species, whereas selected PtdGro, PtdSer and BMP species were increased, which suggested a tight inter-regulation and homeostasis of anionic phospholipids to maintain the membrane integrity. In addition, we identified an ethanolamine cytidyltransferase (TgECT), the rate-limiting enzyme of Kennedy pathway, which is localized in the cytosol. The enzyme is clearly essential for the lytic cycle as its genetic ablation was not feasible, and auxin-meditated conditional knockdown severely impaired the parasite growth in plaque assays. Similarly, lipidomic analysis of the mutant identified an important role in the biogenesis of selected species of PtdEtn, PtdSer and PtdThr. Moreover, we discovered that TgECT is required for the generation of ethanolamine-phosphory ceramide (EPC), a rare sphingolipid present only a limited number of organisms.
Nitzsche, Richard. « Genetic dissection of the central carbon metabolism in the intracellular parasite Toxoplasma gondii ». Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2017. http://dx.doi.org/10.18452/17744.
Texte intégralToxoplasma gondii is a widespread protozoan parasite, infecting nearly all warm-blooded organisms. Asexual reproduction of the parasite within its host cells is achieved by consecutive lytic cycles, which necessitates biogenesis of significant energy and biomass. This work shows that glucose and glutamine are the two major physiologically important nutrients used for the synthesis of macromolecules (ATP, nucleic acid, proteins and lipids) in T. gondii, and either of them is sufficient to ensure the parasite survival. The parasite can counteract genetic ablation of its glucose transporter by increasing the flux of glutamine-derived carbon through the TCA cycle and by concurrently activating gluconeogenesis, which guarantee a continued biogenesis of ATP and biomass for host-cell invasion and parasite replication, respectively. Growth defect in the glycolysis-impaired mutant is caused by a compromised synthesis of lipids, which cannot be counterbalanced by glutamine, but can be restored by acetate. Consistently, supplementation of parasite cultures with exogenous acetate can amend the lytic cycle of the glucose transport mutant. Furthermore, this work revealed two discrete phosphoenolpyruvate carboxykinase (PEPCK) enzymes in the parasite, one of which resides in the mitochondrion (TgPEPCKmt), whereas the other protein is not expressed in tachyzoites (TgPEPCKnet). Parasites with an intact glycolysis can tolerate genetic deletions of TgPEPCKmt as well as of TgPEPCKnet, indicating their nonessential roles for the tachyzoite survival. TgPEPCKnet can also be ablated in glycolysis-deficient mutant, whereas TgPEPCKmt is refractory to deletion. In accord, the lytic cycle of a conditional mutant of TgPEPCKmt in the glycolysis-impaired strain was aborted upon induced repression of the mitochondrial isoform, demonstrating its essential role for the glucose-independent survival of tachyzoites.
Sampels, Vera. « Plasticity of the phosphatidylcholine biogenesis in the obligate intracellular Parasite Toxoplasma gondii ». Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2012. http://dx.doi.org/10.18452/16491.
Texte intégralToxoplasma gondii is an obligate intracellular apicomplexan parasite that causes life-threatening disease in neonates and in immunocompromised people. Successful replication of Toxoplasma requires substantial membrane biogenesis, which must be satisfied irrespective of the host-cell milieu. Like in other eukaryotes, the two most abundant phospholipids in the T. gondii membrane are phosphatidylcholine (PtdCho) and phosphatidylethanolamine (PtdEtn). Bioinformatics and precursor labeling analyses confirm their synthesis via the CDP-choline and CDP-ethanolamine pathway, respectively. This work shows that the 3-step CDP-choline pathway, involving the activities of TgCK, TgCCT and TgCPT, localizes to the cytosol, nucleus and ER membrane, respectively. The initial reaction is catalyzed by a dual-specificity choline kinase (TgCK, ~70-kDa), capable of phosphorylating choline as well as ethanolamine. The purified full-length TgCK displayed a low affinity for choline (Km ~0.77 mM). TgCK harbors a unique N-terminal hydrophobic peptide that is required for the formation of enzyme oligomers in the parasite cytosol but not for activity. The displacement of the TgCK promoter in a conditional mutant of T. gondii (deltatgcki) attenuated the enzyme expression by ~80%. Unexpectedly, the ?tgcki mutant was not impaired in intracellular growth, and exhibited a normal PtdCho biogenesis. To recompense for the loss of full-length TgCK, the mutant appears to make use of an alternative promoter and/or start codon, resulting in the expression of a shorter but active TgCK isoform identified by the anti-TgCK antiserum, which correlated with its persistent choline kinase activity. Accordingly, the ?tgcki showed an expected incorporation of choline into PtdCho, and susceptibility to dimethylethanolamine (a choline analog). Interestingly, the conditional mutant displayed a regular growth in off state despite a 25% decline in PtdCho content, which suggests a compositional flexibility in T. gondii membranes and insignificant salvage of host-derived PtdCho. The two-step conditional mutagenesis of TgCCT, which caused a reduced growth rate to about 50%, further substantiated this finding. The enzymatic activity of TgCCT and its role in PtdCho synthesis remain to be proven, however. Taken together, the results demonstrate that the CDP-route is likely essential in T. gondii. The competitive inhibition of choline kinase to block the parasite replication appears a potential therapeutic application.The work also reveals a remarkably adaptable membrane biogenesis in T. gondii, which may underly the evolution of Toxoplasma as a promiscuous pathogen.
Sundaram, Lalitha Sridevi. « Toxoplasma gondii-mediated host cell transcriptional changes lead to metabolic alterations akin to the Warburg effect ». Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/267958.
Texte intégralBlume, Martin. « Characterization of the differential significance of sugar Import in the apicomplexan parasites Toxoplasma gondii and Plasmodium ». Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2011. http://dx.doi.org/10.18452/16396.
Texte intégralToxoplasma gondii and Plasmodium species are obligate intracellular pathogens that utilize host sugars for energy homeostasis and macro molecular synthesis. Here, we report that the T. gondii glucose transporter, TgGT1, and of its homologs of P. falciparum and P. berghei (PfHT1 and PbHT1) transport glucose, mannose, galactose and fructose. Besides TgGT1, Toxoplasma harbours one additional surface localized putative sugar transporter (TgST2). Surprisingly both Proteins are nonessential and only the deletion of TgGT1 inflicts a mild defect in the parasite replication. The ?tggt1 mutant is unable to import glucose and consequently displays an attenuated glucose-dependent motility, which is completely rescued by glutamine. ?tggt1 performs increased glutamine metabolism that is sufficient to sustain motility and replication. The ?tggt1 strain provides a model for further investigating its adaptation to disparate host cells. In contrast to T. gondii, erythrocytic stages of Plasmodium species critically depend on glucose uptake, and the PfHT1 transporter is considered as a drug target against human malaria. Here, we report that PbHT1 (a PfHT1 homolog) is also essential for blood stage development in the rodent malaria parasite P. berghei. PbHT1 is expressed throughout the life cycle. Moreover, a PfHT1- and PbHT1-specific sugar analogue, compound 3361, can inhibit the hepatic development and ookinete formation in P. berghei. These results signify that PbHT1 and exogenous glucose are also required during the ex-erythrocytic stages of P. berghei. To permit a high-throughput screening of selective PfHT1 inhibitors and their subsequent in vivo assessment, we have established a PfHT1-expressing Saccharomyces cerevisiae mutant and generated a PfHT1-dependent ?pbht1 of P. berghei strain. This thesis underscores various previously unknown aspects of sugar metabolism in Toxoplasma and Plasmodium, and unravel their metabolic differences.
Molan, Aus. « Involvement of Toxoplasma gondii and associated inflammatory markers in the pathogenesis of type 2 diabetes mellitus ». Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2020. https://ro.ecu.edu.au/theses/2338.
Texte intégralCosta, Beatriz Guerreiro Basilio. « Estudo da modulação do metabolismo lipídico de células dendríticas humanas na infecção por Toxoplasma gondii ». Instituto Oswaldo Cruz, 2012. https://www.arca.fiocruz.br/handle/icict/7036.
Texte intégralMade available in DSpace on 2013-10-03T11:40:07Z (GMT). No. of bitstreams: 1 Beatriz Guerreiro Basilio Costa.pdf: 1448715 bytes, checksum: 9fad325ac3484b88b47961c78ef5db34 (MD5) Previous issue date: 2012
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil
A toxoplasmose é uma doença de alta prevalência no mundo, causada pelo Toxoplasma gondii, um parasita intracelular obrigatório. O T. gondii possui mecanismos de modulação do metabolismo do seu hospedeiro que garantem sua sobrevivência e a instalação da infecção crônica. Um dos tipos celulares mais permissivos à infecção e multiplicação do T. gondii são as células dendríticas (DC), paradoxalmente as células apresentadoras de antígeno mais eficazes, com capacidade de deflagrar uma resposta imune protetora eficaz e duradoura. Neste trabalho, estudamos a modulação do metabolismo lipídico de células dendríticas humanas na infecção por T. gondii. Mostramos que o parasita induziu a maturação da célula e um padrão misto de resposta inflamatória, com altas concentrações das citocinas pró-inflamatórias IL-6 e TNF- e da citocina antiinflamatória IL-10. Após 3 horas de infecção, verificamos que T. gondii induziu a expressão gênica de ciclooxigenase-2 (COX-2). De forma importante, observamos por qRT-PCR que a infecção com T. gondii regulou positivamente a expressão do gene do receptor nuclear (RN) regulado por lipídios PPAR, mas não do LXR. Já a expressão do mRNA das moléculas envolvidas no transporte e estoque de lipídios, FABP4 e ADRP, alvos do PPAR, e ABCA1, alvo do LXR, foram aumentadas pela infecção de 3 horas com o parasita. Utilizando duas técnicas distintas (BODIPY e coloração com ósmio) avaliamos a biogênese de corpúsculos lipídicos (CL) após infecção com o T. gondii e constatamos que essas organelas não foram induzidas após 3 horas de infecção. Entretanto, após 24 horas, 90% das DC apresentaram CL e o número de CL por DC foi estatisticamente maior. Observamos a presença de CL em DC não infectadas pelo parasita, mostrando que a indução da biogênese de CL é um fenômeno parácrino, não dependente da infecção celular. Avaliamos também a importância do PPAR na infecção por T. gondii, através do tratamento das DC com seu agonista ou antagonista. Após 3 horas, apenas os genes ADRP, FABP4 e ABCA1, alvos dos receptores nucleares, foram modulados. Por último, investigamos a influência do T. gondii na expressão das moléculas apresentadoras de antígenos lipídicos. Por citometria de fluxo, constatamos que não há alteração na expressão de membrana dessas moléculas. Contudo, por qRT-PCR, observamos que o T. gondii regula negativamente a expressão dos genes cd1d e cd1e. Em conclusão, mostramos que T. gondii foi capaz de regular positivamente o metabolismo lipídico das DC e negativamente as moléculas apresentadoras de lipídios CD1, sem a participação essencial de PPAR nesses processos.
Toxoplasmosis is a worldwide high prevalence disease caused by Toxoplasma gondii, an obligate intracellular parasite. T. gondii developed mechanisms for modulating the metabolism of its host, ensuring their survival and the chronic infection. Dendritic cells (DC) are one of the most permissive cell types to T. gondii infection and replication and are, paradoxically, considered the most effective antigen presenting cells, triggering an effective and long-lasting protective immune response. In this work, we studied the modulation of lipid metabolism in human dendritic cells infected with T. gondii. We showed that the parasite induced cell maturation, and a mixed pattern of inflammatory response with high levels of proinflammatory cytokines IL-6 and TNF-, and anti-inflammatory cytokine IL-10. After 3h of infection, we found that T. gondii induced increased gene expression of cyclooxygenase-2 (COX-2). Importantly, we observed by qRT-PCR that T. gondii infection upregulated the nuclear receptor (RN) PPAR gene expression, while the levels of LXR were unchanged. Furthermore, the mRNA expression of molecules involved in the transport and storage of lipids, FABP4 and ADRP, PPARtargets, and ABCA1, LXR target, were also increased at 3h of infection with the parasite. In parallel, using two different techniques, (BODIPY and osmium staining), we evaluated the biogenesis of lipid droplets (LD) after infection with T. gondii, and observed that these organelles were not induced after 3 hours of infection. However, after 24 hours, 90% of DC showed LD and the number of LD per DC was statistically enhanced. We observed the presence of LD in DC not infected with the parasite, showing that induction of biogenesis of LD is a paracrine phenomenon not dependent on cell infection. We also evaluated the role of PPAR in T. gondii infection by treating DC with its agonist or antagonist. After 3 hours of infection only the nuclear receptor target genes ADRP, FABP4 and ABCA1 were modulated. Finally, we investigated the influence of T. gondii in the expression of lipid antigens presenting molecules. By flow cytometry, we observed no variation in expression of these molecules in cell membrane. However, by qRT-PCR, we found that the T. gondii downregulated gene expression of cd1d and cd1e. In conclusion, we showed that T. gondii was able to upregulate the DC lipid metabolism, and downregulate CD1 lipid presentation. Apparently, the RN PPAR has no essential role in this process.
Silva, Camila Luna da. « Estudo do metabolismo mitocondrial e da resposta anti-apoptótica de células endoteliais humanas durante a evolução da infecção por taquizoítos de Toxoplasma gondii ». Universidade do Estado do Rio de Janeiro, 2013. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=8172.
Texte intégralA toxoplasmose é uma zoonose amplamente distribuída que afeta mais de um terço da população mundial e de grande importância na saúde pública. A maioria das infecções em humanos por Toxoplasma gondii é assintomática. A toxoplasmose é amplamente investigada visto que se apresenta como uma doença grave em pessoas imunodeprimidas (portadores da síndrome da imunodeficiência adquirida (SIDA), não tratados, indivíduos transplantados, paciente em tratamento quimioterápico ou em uso de drogas supressoras e gestantes). A toxoplasmose congênita frequentemente pode levar ao aborto espontâneo ou até mesmo resultar na formação de crianças com algum grau de atraso no desenvolvimento mental e/ou físicos, deste modo, a transmissão congênita pode ser muito mais importante do que se pensava, pois os parasitos encontrados na circulação sanguinea são capazes de infectar as células endoteliais dos vasos e os tecidos circunjacentes, podendo resultar no encistamento do T. gondii. Atualmente a toxoplasmose vem sendo investigada devido a sua associação a inúmeras outras doenças, assim, estudos sobre a evolução da infecção por T. gondii em diferentes tipos de células hospedeiras se fazem necessários para uma abordagem terapêutica adequada. Ao invadir a célula hospedeira o parasito possui a capacidade de recrutar as mitocôndrias promovendo mudanças na organização mitocondrial ao longo da progressão da infecção, garantindo um ambiente favorável a sua multiplicação. Diante disso, investigamos se o parasito possui a capacidade de interferir no metabolismo mitocondrial e na resposta apoptótica da célula endotelial. O presente trabalho teve como objetivo analisar o metabolismo mitocondrial através da respirometria de alta-resolução e da resposta apoptótica através do western blotting das células endoteliais da veia umbilical humana (HUVEC) infectadas por 2, 6 e 20 horas por taquizoítos de T. gondii. A respirometria de alta-resolução revelou que o parasito interfere no metabolismo energético da célula hospedeira. A análise do conteúdo de proteínas da família Bcl-2 por western blotting revelou maior estímulo apoptótico no tempo inicial de infecção, quando comparado aos demais tempos. Os resultados dos conteúdos de caspase 3, proteína efetora da apoptose, não demonstrou diferença nos tempos iniciais de infecção Entretanto, em tempos mais tardios, o conteúdo de caspase 3 mostrou-se significativamente aumentado quando comparado às HUVEC não infectadas. A dinâmica de replicação do parasito foi observada através do monitoramento pelo sistema Time-Lapse Nikon BioStation IMQ em tempo real das células infectadas por T.gondii. Portanto, nossos resultados sugerem que o protozoário ao recrutar as mitocôndrias da célula hospedeira interfere no metabolismo mitocondrial e na modulação da apoptose para garantir um ambiente favorável a sua multiplicação.
Toxoplasmosis is a widespread zoonosis that affects more than a third of the world population and of great public health importance. Most human infections with Toxoplasma gondii are asymptomatic. Toxoplasmosis is widely investigated since it presents itself as a serious disease in immunocompromised persons (holders of acquired immunodeficiency syndrome (AIDS), untreated, transplant recipients, patients undergoing chemotherapy or suppressing drugs and pregnant). Congenital toxoplasmosis can often lead to miscarriage or even result in the formation of children with some degree of developmental delay mental and / or physical, thus congenital transmission may be much more important than previously thought, because the parasites found In the bloodstream are able to infect endothelial cells of blood vessels and surrounding tissues, which may result in encystment T. gondii. Currently toxoplasmosis has been investigated because of their association with other diseases, so, studies of the evolution of T.gondii infection in different types of host cells are necessary for an adequate therapeutic approach. To invade the host cell, the parasite has the ability to recruit mitochondria promoting changes in mitochondrial organization along the progression of infection, ensuring a favorable environment for their multiplication. Therefore, we investigated whether the parasite has the ability to interfere with mitochondrial metabolism and apoptotic response of endothelial cells. This study aimed to analyze the mitochondrial metabolism by high-resolution respirometry and apoptotic response by western blotting of endothelial cells of human umbilical vein (HUVEC) infected for 2, 6 and 20 hours per tachyzoites of T. gondii. The high-resolution respirometry revealed that the parasite interferes with the energy metabolism of the host cell. The analysis of the family protein content of Bcl-2 by western blotting revealed higher apoptotic stimulus at the initial time of infection, as compared to other times. The results of the contents of caspase 3 protein effector of apoptosis, showed no difference in the initial days of infection However, in more recent times, the content of caspase 3 was significantly increased when compared to non-infected HUVEC. The dynamics of parasite replication was observed by monitoring the system Time-Lapse Nikon BioStation IMQ in real time from infected cells by T. gondii. Therefore, our findings suggest that mitochondria in recruiting protozoan host cell interfere with mitochondrial metabolism and in the modulation of apoptosis to ensure a favorable environment for multiplication.
HIRAMOTO, ROBERTO M. « Efeitos da radiacao ionizante sobre a estrutura, metabolismo e infecciosidade de um protozoario patogenico, Toxoplasma gondii (Nicolle and Manceaux, 1908) ». reponame:Repositório Institucional do IPEN, 1998. http://repositorio.ipen.br:8080/xmlui/handle/123456789/10660.
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Instituto de Pesquisas Energeticas e Nucleares - IPEN/CNEN-SP
Livres sur le sujet "Metabolism in Toxoplasma Gondii"
Gross, Uwe, dir. Toxoplasma gondii. Berlin, Heidelberg : Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-51014-4.
Texte intégralTonkin, Christopher J., dir. Toxoplasma gondii. New York, NY : Springer US, 2020. http://dx.doi.org/10.1007/978-1-4939-9857-9.
Texte intégralPashley, T. V. Molecular genetic analysis of toxoplasma gondii. Manchester : UMIST, 1996.
Trouver le texte intégralToxoplasma gondii : The model apicomplexan : perspectives and methods. Amsterdam : Elsevier/Academic Press, 2007.
Trouver le texte intégral1949-, Aosai Fumie, et Norose Kazumi 1952-, dir. Nihon ni okeru Tokisopurazuma-shō. Fukuoka-shi : Kyūshū Daigaku Shuppankai, 2007.
Trouver le texte intégralUggla, Arvid. Toxoplasma Gondii in farm animals : Some immunodiagnostic methods and their potential. Uppsala : Sveriges Lantbruksuniversitet, 1986.
Trouver le texte intégralFlegr, Jaroslav. Pozor, Toxo ! : Tajná učebnice praktické metodologie vědy. Praha : Academia, 2011.
Trouver le texte intégralLantbruksuniversitet, Sveriges, dir. Toxoplasma gondii infection in sheep : Studies on epidemiology, food hygiene and vaccination. Uppsala : Sveriges Lantbruksuniversitet, 1994.
Trouver le texte intégralStrachan, Dina D. Construction of an epitope-tagged clone of GRA3 for electroporation into Toxoplasma Gondii. [New Haven, Conn : s.n.], 1994.
Trouver le texte intégralAegerter, Mary. Food safety during your pregnancy. [Pullman, Wash.] : Cooperative Extension, Washington State University, 2000.
Trouver le texte intégralChapitres de livres sur le sujet "Metabolism in Toxoplasma Gondii"
Cioffi, William G., Michael D. Connolly, Charles A. Adams, Mechem C. Crawford, Aaron Richman, William H. Shoff, Catherine T. Shoff et al. « Toxoplasma gondii ». Dans Encyclopedia of Intensive Care Medicine, 2244. Berlin, Heidelberg : Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_3339.
Texte intégralCoia, John, et Heather Cubie. « Toxoplasma gondii ». Dans The Immunoassay Kit Directory, 918–70. Dordrecht : Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-009-0359-3_36.
Texte intégralStöcker, W. « Toxoplasma gondii ». Dans Springer Reference Medizin, 2327–28. Berlin, Heidelberg : Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_3074.
Texte intégralStöcker, W. « Toxoplasma gondii ». Dans Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg : Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_3074-1.
Texte intégralRingelmann, R., et Beate Heym. « Toxoplasma gondii ». Dans Parasiten des Menschen, 243–45. Heidelberg : Steinkopff, 1991. http://dx.doi.org/10.1007/978-3-642-85397-5_90.
Texte intégralMehlhorn, Heinz. « Toxoplasma gondii ». Dans Encyclopedia of Parasitology, 2766–72. Berlin, Heidelberg : Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_3207.
Texte intégralMehlhorn, Heinz. « Toxoplasma gondii ». Dans Encyclopedia of Parasitology, 1–9. Berlin, Heidelberg : Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_3207-2.
Texte intégralLiesenfeld, Oliver. « Toxoplasma gondii ». Dans Lexikon der Infektionskrankheiten des Menschen, 800–803. Berlin, Heidelberg : Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-39026-8_1082.
Texte intégralKissinger, Jessica C., Michael J. Crawford, David S. Roos et James W. Ajioka. « Toxoplasma gondii ». Dans Pathogen Genomics, 255–79. Totowa, NJ : Humana Press, 2002. http://dx.doi.org/10.1007/978-1-59259-172-5_17.
Texte intégralJeoffreys, Neisha. « Toxoplasma gondii ». Dans PCR for Clinical Microbiology, 389–92. Dordrecht : Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9039-3_68.
Texte intégralActes de conférences sur le sujet "Metabolism in Toxoplasma Gondii"
Eassa, Souzan, Chhanda Bose, Pierre Alusta, Olga Tarasenko et Olga Tarasenko. « DETECTION METHOD OF TOXOPLASMA GONDII TACHYZOITES ». Dans BIOLOGY, NANOTECHNOLOGY, TOXICOLOGY, AND APPLICATIONS : Proceedings of the 5th BioNanoTox and Applications International Research Conference. AIP, 2011. http://dx.doi.org/10.1063/1.3587472.
Texte intégralPires, Sara M., Heidi Enemark, Thomas Rosendal, Anna Lundén, Pikka Jokelainen et Lis Alban. « Toxoplasma gondii and the role of pork ». Dans Safe Pork 2015 : Epidemiology and control of hazards in pork production chain. Iowa State University, Digital Press, 2017. http://dx.doi.org/10.31274/safepork-180809-396.
Texte intégralFazli, Mojtaba S., Stephen A. Velia, Silvia N. J. Moreno et Shannon Quinn. « Unsupervised discovery of toxoplasma gondii motility phenotypes ». Dans 2018 IEEE 15th International Symposium on Biomedical Imaging (ISBI 2018). IEEE, 2018. http://dx.doi.org/10.1109/isbi.2018.8363735.
Texte intégralPyburn, David G., S. Patton, J. J. Zimmerman, James D. McKean, R. B. Evans, Annette M. O'Connor, K. L. Smedley, C. T. Faulkner, E. M. Zhou et E. M. Zhou. « Risk Factors for Swine Infection with Toxoplasma gondii ». Dans Fourth International Symposium on the Epidemiology and Control of Salmonella and Other Food Borne Pathogens in Pork. Iowa State University, Digital Press, 2003. http://dx.doi.org/10.31274/safepork-180809-228.
Texte intégralLudewig, M., K. de Buhr et K. Fehlhaber. « Seroprevalence of Toxoplasma gondii in German swine herds ». Dans First International Symposium on the Ecology of Salmonella in Pork Production. Iowa State University, Digital Press, 2007. http://dx.doi.org/10.31274/safepork-180809-43.
Texte intégralHammacher, Gabriela Koh, Saulo Bueno de Azeredo, Natália Gonçalves Rengel, Gean Scherer da Silva et Fabiana Tonial. « Toxoplasma gondii NA GESTAÇÃO - DANOS NO DESENVOLVIMENTO FETAL ». Dans I Congresso Brasileiro de Parasitologia Humana On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/704.
Texte intégralSilva, Keyla Cristina Pereira Ponciano, et MELISSA DA SILVA PAES. « TOXOPLASMA GONDII EM ROEDORES SILVESTRES NO BRASIL : RESUMO ». Dans I Congresso Brasileiro On-line de Clínica Médica Veterinária. Revista Multidisciplinar em Saúde, 2023. http://dx.doi.org/10.51161/convet/16222.
Texte intégralWarid MAYA, Rana, Nesreen Ahmed NASSER et Anas H. SADEK. « CORRELATION BETWEEN TOXOPLASMA GONDII (T. GONDII) AND VITAMIN D3 LEVELS IN IRAQI PREGNANT WOMEN ». Dans VII. INTERNATIONAL SCIENTIFIC CONGRESSOF PURE,APPLIEDANDTECHNOLOGICAL SCIENCES. Rimar Academy, 2023. http://dx.doi.org/10.47832/minarcongress7-23.
Texte intégralBoughattas, Sonia, Aarti Sharma et Marawan Abu-Madi. « Seroprevalence of Toxoplasma Gondii Among Stray Cats in Qatar ». Dans Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2016. http://dx.doi.org/10.5339/qfarc.2016.hbpp2667.
Texte intégralVesco, Gesualdo, F. Liga, A. Vella, G. Lo Cascio et S. Villari. « Seroprevalence of Toxoplasma gondii in swine slaughtered in Sicily ». Dans Seventh International Symposium on the Epidemiology and Control of Foodborne Pathogens in Pork. Iowa State University, Digital Press, 2007. http://dx.doi.org/10.31274/safepork-180809-102.
Texte intégralRapports d'organisations sur le sujet "Metabolism in Toxoplasma Gondii"
Steinman, Richard A. The Dialogue of Metastasis-Uncovering Juxtacrine Genetic Cascades with a Toxoplasma Gondii Enzyme. Fort Belvoir, VA : Defense Technical Information Center, août 2008. http://dx.doi.org/10.21236/ada494955.
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