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Sent on Wednesday, 2011 May 25Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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| PubMed Results |
| 1. | J Nephrol. 2011 May 23. pii: DE808924-D9F2-4038-80F9-AA74A6BAAC04. doi: 10.5301/JN.2011.8343. [Epub ahead of print]Visceral leishmaniasis reactivation in transplant patients: a minireview with report of a new case.Postorino MC, Bellantoni M, Catalano C, Caridi G, De Rosa M, Seck S, Enia G.SourceNephrology, Hypertension and Renal Transplantation Unit, CNR-IBIM Clinical Epidemiology and Physiopathology of Renal Diseases and Hypertension, Ospedali Riuniti, Reggio Calabria - Italy. AbstractAn updated review of cases of reactivated visceral leishmaniasis (VL) in transplant patients is presented, with a new report of a kidney transplant patient who had VL caused by reactivation of a dormant infection contracted 21 years previously. Close to the time of disease reactivation, the patient had a primary varicella-zoster infection. |
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| 2. | J Exp Med. 2011 May 23. [Epub ahead of print]Platelet activation attracts a subpopulation of effector monocytes to sites of Leishmania major infection.Goncalves R, Zhang X, Cohen H, Debrabant A, Mosser DM.SourceDepartment of Cell Biology and Molecular Genetics and the Maryland Pathogen Research Institute, University of Maryland, College Park, MD 20782. AbstractLeishmania species trigger a brisk inflammatory response and efficiently induce cell-mediated immunity. We examined the mechanisms whereby leukocytes were recruited into lesions after Leishmania major infection of mice. We found that a subpopulation of effector monocytes expressing the granulocyte marker GR1 (Ly6C) is rapidly recruited into lesions, and these monocytes efficiently kill L. major parasites. The recruitment of this subpopulation of monocytes depends on the chemokine receptor CCR2 and the activation of platelets. Activated platelets secrete platelet-derived growth factor, which induces the rapid release of CCL2 from leukocytes and mesenchymal cells. This work points to a new role for platelets in host defense involving the selective recruitment of a subpopulation of effector monocytes from the blood to efficiently kill this intracellular parasite. |
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| 3. | Int J Infect Dis. 2011 May 22. [Epub ahead of print]Recent advances in leishmaniasis treatment.Tiuman TS, Santos AO, Ueda-Nakamura T, Filho BP, Nakamura CV.SourcePrograma de Pós-Graduação em Ciências Farmacêuticas, Universidade Estadual de Maringá, Av. Colombo 5790, 87020-900 Maringá, Paraná, Brazil; Departamento de Ciências Básicas da Saúde, Laboratório de Inovação Tecnológica no Desenvolvimento de Fármacos e Cosméticos, Universidade Estadual de Maringá, Maringá, Paraná, Brazil. AbstractAbout 1.5 million new cases of cutaneous leishmaniasis and 500 000 new cases of visceral leishmaniasis occur each year around the world. For over half a century, the clinical forms of the disease have been treated almost exclusively with pentavalent antimonial compounds. In this review, we describe the arsenal available for treating Leishmania infections, as well as recent advances from research on plants and synthetic compounds as source drugs for treating the disease. We also review some new drug-delivery systems for the development of novel chemotherapeutics. We observe that the pharmaceutical industry should employ its modern technologies, which could lead to better use of plants and their extracts, as well as to the development of synthetic and semi-synthetic compounds. New studies have highlighted some biopharmaceutical technologies in the design of the delivery strategy, such as nanoparticles, liposomes, cochleates, and non-specific lipid transfer proteins. These observations serve as a basis to indicate novel routes for the development and design of effective anti-Leishmania drugs. Copyright © 2011 International Society for Infectious Diseases. Published by Elsevier Ltd. All rights reserved. |
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| 4. | Acta Trop. 2011 May 13. [Epub ahead of print]Habitats of the sandfly vectors of Leishmania tropica and L. major in a mixed focus of cutaneous leishmaniasis in southeast Tunisia.Tabbabi A, Ghrab J, Aoun K, Ready PD, Bouratbine A.SourceLaboratoire de Parasitologie, LR 05SP03, Institut Pasteur de Tunis, 13 place Pasteur, 1002 Tunis, Tunisia; Molecular Biology Laboratory, Department of Entomology, Natural History Museum, London, UK. AbstractFrom 2009 to 2010, 3129 sandflies were caught in CDC light traps placed in various habitats in Ghomrassen, Tataouine governorate, southeast Tunisia, a mixed focus of human cutaneous leishmaniasis caused by Leishmania tropica and Leishmania major. Species diversity was quantified in anthropogenic, semi-anthropogenic and semi-natural locations. Sandflies were identified according to morphological characters and also by the comparative sequence analysis of a fragment of the mitochondrial cytochrome b gene to distinguish between two putative local vectors of L. tropica, namely Phlebotomus chabaudi and Phlebotomus riouxi. The lowest sandfly diversities were found in L. major sites, where the incriminated vector P. papatasi predominated in the burrows of the rodent reservoir hosts (Meriones) as well as inside and outside houses of human cases. In L. tropica sites, the incriminated peri-domestic vector Phlebotomus sergenti was the most abundant species inside houses, whereas P. riouxi or P. chabaudi was the dominant species in the semi-natural rocky habitats favoured by the putative rodent reservoir, Ctenodactylus gundi. All specimens of P. chabaudi identified molecularly had the diagnostic cytochrome b characters of P. riouxi, indicating either that the latter represents only a geographical variant of P. chabaudi or that these two species may sometimes hybridize. Copyright © 2011. Published by Elsevier B.V. |
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| 5. | Phytomedicine. 2010 Dec 15;18(1):36-9. Epub 2010 Oct 28.Synergistic effects of parthenolide and benznidazole on Trypa nosoma cruzi.Pelizzaro-Rocha KJ, Tiuman TS, Izumi E, Ueda-Nakamura T, Dias Filho BP, Nakamura CV.SourceDepartamento de Ciências Básicas da Saúde, Universidade Estadual de Maringá, Maringá, Paraná, Brazil. AbstractParthenolide previously isolated from Tanacetum vulgare was tested for its in vitro combinatory effect with benznidazole against Trypanosoma cruzi. Parthenolide showed a strong synergistic activity against epimastigote forms, reducing 23-fold the concentration of benznidazole necessary to inhibit 50% of cell growth (IC(50) of 1.6 to 0.07 μg/ml) when in combination with parthenolide. In addition, an additive effect against trypomastigote forms (FIC 1.06), followed by an antagonistic effect on the cytotoxicity (FIC 2.36), was observed for the combination of both drugs. Parthenolide induced morphological alterations in the body shape of trypomastigote forms, causing rounding and shortening of the parasite and loss of integrity of the plasma membrane, as previously described by other workers. Copyright © 2010 Elsevier GmbH. All rights reserved. |
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