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Sent on Tuesday, 2010 Jun 01Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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PubMed Results |
1. | Amino Acids. 2010 May 29. [Epub ahead of print]Polyamine metabolism in Leishmania: from arginine to trypanothione.Colotti G, Ilari A.Institute of Biology and Molecular Pathology, CNR, c/o Department of Biochemical Sciences, University "Sapienza", P.le A. Moro 5, 00185, Rome, Italy, Gianni.colotti@uniroma1.it. AbstractPolyamines (PAs) are essential metabolites in eukaryotes, participating in a variety of proliferative processes, and in trypanosomatid protozoa play an additional role in the synthesis of the critical thiol trypanothione. The PAs are synthesized by a metabolic process which involves arginase (ARG), which catalyzes the enzymatic hydrolysis of L: -arginine (L: -Arg) to L: -ornithine and urea, and ornithine decarboxylase (ODC), which catalyzes the enzymatic decarboxylation of L: -ornithine in putrescine. The S-adenosylmethionine decarboxylase (AdoMetDC) catalyzes the irreversible decarboxylation of S-adenosylmethionine (AdoMet), generating the decarboxylated S-adenosylmethionine (dAdoMet), which is a substrate, together with putrescine, for spermidine synthase (SpdS). Leishmania parasites and all the other members of the trypanosomatid family depend on spermidine for growth and survival. They can synthesize PAs and polyamine precursors, and also scavenge them from the microenvironment, using specific transporters. In addition, Trypanosomatids have a unique thiol-based metabolism, in which trypanothione (N1-N8-bis(glutathionyl)spermidine, T(SH)(2)) and trypanothione reductase (TR) replace many of the antioxidant and metabolic functions of the glutathione/glutathione reductase (GR) and thioredoxin/thioredoxin reductase (TrxR) systems present in the host. Trypanothione synthetase (TryS) and TR are necessary for the protozoa survival. Consequently, enzymes involved in spermidine synthesis and its utilization, i.e. ARG, ODC, AdoMetDC, SpdS and, in particular, TryS and TR, are promising targets for drug development. |
PMID: 20512387 [PubMed - as supplied by publisher] | |
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2. | Mem Inst Oswaldo Cruz. 2010 May;105(3):341-7.Kinetoplastid membrane protein-11 is present in promastigotes and amastigotes of Leishmania amazonensis and its surface expression increases during metacyclogenesis.< a href="http://www.ncbi.nlm.nih.gov/pubmed?term=%22Matos%20DC%22%5BAuthor%5D">Matos DC, Faccioli LA, Cysne-Finkelstein L, Luca PM, Corte-Real S, Armôa GR, Lemes EM, Decote-Ricardo D, Mendonça SC.Laboratório de Imunoparasitologia, Instituto de Tecnologia em Imunobiológicos, Fiocruz, Rio de Janeiro, RJ, Brasil, 21040-360. AbstractKinetoplastid membrane protein-11 (KMP-11), a protein present in all kinetoplastid protozoa, is considered a potential candidate for a leishmaniasis vaccine. A suitable leishmaniasis vaccine candidate molecule must be expressed in amastigotes, the infective stage for mammals. However, the expression of KMP-11 in Leishmania amastigotes has been a subject of controversy. We evaluated the expression of this molecule in logarithmic and stationary growth phase promastigotes, as well as in amastigotes, of Leishmania amazonensis by immunoblotting, flow cytometry and immunocytochemistry, using a monoclonal antibody against KMP-11. We found that KMP-11 is present in promastigotes and amastigotes. In both stages, the protein was found in association with membrane structures (at the cell surface, flagellar pocket and intracellular vesicles). More importantly, its surface expression is higher in amastigotes than in promastigotes and increases during metacyclogenesis. The increased expression of KMP-11 in metacyclic promastigotes, and especially in amastigotes, indicates a role for this molecule in the parasite relationship with the mammalian host. The presence of this molecule in amastigotes is consistent with the previously demonstrated immunoprotective capacity of vaccine prototypes based on the KMP-11-coding gene and the presence of humoral and cellular immune responses to KMP-11 in Leishmania-infected humans and animals. |
PMID: 20512252 [PubMed - in process] | |
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3. | Mem Inst Oswaldo Cruz. 2010 May;105(3):310-3.Polymerase chain reaction of peripheral blood as a tool for the diagnosis of visceral leishmaniasis in children.Fraga TL, Brustoloni YM, Lima RB, Dorval ME, Oshiro ET, Oliveira J, Oliveira AL, Pirmez C.Programa de Pós-graduação em Doenças Infecciosas e Parasitárias, Departamento de Patologia, Universidade Federal de Mato Grosso do Sul, Campo Grande, MS, Brasil, 79070-900. AbstractThe diagnosis of visceral leishmaniasis (VL) generally requires the use of invasive tests for the collection of infected tissue (aspirates of bone marrow, spleen, liver or lymph nodes). This difficulty has led to the search for safer and less painful techniques to confirm the occurrence of the disease in children. Polymerase chain reaction (PCR) is a method that is advantageous in that it allows the use of peripheral blood samples for diagnosis. This paper reports the utilisation of PCR on peripheral blood samples to diagnose VL in 45 children in Mato Grosso do Sul, Brazil. This technique is compared with methods carried out using tissue collected by invasive procedures, including direct microscopy, culture and detection of Leishmania DNA by PCR in bone marrow aspirates. The results show that PCR of peripheral blood provides great sensitivity (95.6%) that is similar to that from the PCR of bone marrow aspirates (91.1%) and higher than that achieved with microscopy (80%) or culture (26.7%) methods. PCR of peripheral blood proved to be a suitable tool for the diagnosis of VL in children because it is highly sensitive and safe, with tissue collection being less invasive than in traditional tests. |
PMID: 20512245 [PubMed - in process] | |
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4. | Cad Saude Publica. 2010 Apr;26(4):644-5.[Geographic spread of visceral leishmaniasis in Brazil.][Article in Portuguese] Werneck GL.Escola Nacional de Saúde Pública Sergio Arouca, Fundação Oswaldo Cruz, Rio de Janeiro, Brasil. |
PMID: 20512199 [PubMed - in process] | |
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5. | J Clin Rheumatol. 2010 Jun;16(4):203-4.Visceral leishmaniasis mimicking systemic lupus erythematosus.Arlet JB, Capron L, Pouchot J.Service de Médecine Interne Faculté de Médecine Paris Descartes et Assistance Publique Hôpitaux de Paris, Hôpital Européen Georges Pompidou Paris, France. |
PMID: 20511988 [PubMed - in process] | |
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6. | Lancet Infect Dis. 2010 Jun;10(6):433-439.Molecular diagnostics for sleeping sickness: what is the benefit for the patient?Deborggraeve S, Büscher P.Department of Parasitology, Institute of Tropical Medicine, Antwerp, Belgium; Rega Institute for Medicinal Research, Catholic University of Leuven, Leuven, Belgium. AbstractSleeping sickness, or human African trypanosomiasis, is a vector-borne disease caused by two subspecies of the protozoan parasite Trypanosoma brucei, and is geographically restricted to sub-Saharan Africa. Although the disease causes major public-health and socioeconomic problems among affected populations, sleeping sickness is one of the world's most neglected diseases. Within the rapidly evolving field of biotechnology, many molecular diagnostics have been developed to detect the parasite. These range from conventional, high-tech, and low-tech PCR formats (eg, isothermal nucleic-acid-amplification techniques), to direct visualisation of the parasite's nucleic acids by fluorescent probes. Besides reviewing the most important molecular diagnostics available, we discuss their current role in diagnosis and disease control. Although powerful, molecular diagnostics are confined to research settings and do not reach the patient or national control programmes. The current formats are not applicable to field conditions, and simplification, standardisation, and proper test evaluation in the target setting should be the main focus for future development. Copyright © 2010 Elsevier Ltd. All rights reserved. |
PMID: 20510283 [PubMed - as supplied by publisher] | |
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