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Sent on Wednesday, 2011 Jun 22Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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| PubMed Results |
| 1. | Proc Natl Acad Sci U S A. 2011 Jun 20. [Epub ahead of print]Structure of Trypanosoma brucei flagellum accounts for its bihelical motion.Koyfman AY, Schmid MF, Gheiratmand L, Fu CJ, Khant HA, Huang D, He CY, Chiu W.SourceNational Center for Macromolecular Imaging, Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX 77030. AbstractTrypanosoma brucei is a parasitic protozoan that causes African sleeping sickness. It contains a flagellum required for locomotion and viability. In addition to a microtubular axoneme, the flagellum contains a crystalline paraflagellar rod (PFR) and connecting proteins. We show here, by cryoelectron tomography, the structure of the flagellum in three bending states. The PFR lattice in straight flagella repeats every 56 nm along the length of the axoneme, matching the spacing of the connecting proteins. During flagellar bending, the PFR crystallographic unit cell lengths remain constant while the interaxial angles vary, similar to a jackscrew. The axoneme drives the expansion and compression of the PFR lattice. We propose that the PFR modifies the in-plane axoneme motion to produce the characteristic trypanosome bihelical motility as captured by high-speed light microscope videography. |
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| 2. | Dermatol Ther. 2011 May;24(3):378-9. doi: 10.1111/j.1529-8019.2011.01424.x.Lupoid leishmaniasis of the nose responding well to cryotherapy.Benmously Mlika R, Hammami H, Sioud A, Mokhtar I, Fenniche S.SourceDepartment of Dermatology, Habib Thameur Hospital, Montfleury Tunis, Montfleury, Tunisia. |
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| 3. | J Parasitol. 2011 Apr;97(2):338-43. Epub 2010 Oct 21.Do commercial serologic tests for Trypanosoma cruzi infection detect Mexican strains in women and newborns?Gamboa-León R, Gonzalez-Ramirez C, Padilla-Raygoza N, Sosa-Estani S, Caamal-Kantun A, Buekens P, Dumonteil E.SourceLaboratorio de Parasitología, Centro de Investigaciones Regionales "Dr. Hideyo Noguchi", Universidad Autónoma de Yucatán, Ave. Itzaes 490 x 59A, 97000 Mérida, Yucatán, México. gleon@uady.mx AbstractWe sought to determine the serological test that could be used for Trypanosoma cruzi seroprevalence studies in Mexico, where lineage I predominates. In a previous study among pregnant women and their newborns in the states of Yucatan and Guanajuato, we reported a 0.8-0.9% of prevalence for T. cruzi -specific antibodies by Stat-Pak and Wiener ELISA. We have expanded this study here by performing an additional non-commercial ELISA and confirming the seropositives with Western blot, using whole antigens of a local parasite strain. We found a seroprevalence of 0.6% (3/500) in Merida and 0.4% in Guanajuato (2/488). The 5 seropositive umbilical cord samples reacted to both non-commercial ELISA and Western blot tests, and only 1 of the maternal samples was not reactive to non-commercial ELISA. A follow-up of the newborns at 10 mo was performed in Yucatan to determine the presence of T. cruzi antibodies in children as evidence of congenital infection. None of the children was seropositive. One newborn from an infected mother died at 2 wk of age of cardiac arrest, but T. cruzi infection was not confirmed. The T. cruzi seroprevalence data obtained with both commercial tests (Stat-Pak and ELISA Wiener) are similar to those from non-commercial tests using a local Mexican strain of T. cruzi. |
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| 4. | PLoS Negl Trop Dis. 2011 Mar 29;5(3):e1000.Trypanosoma cruzi in the chicken model: Chagas-like heart disease in the absence of parasitism.Teixeira AR, Gomes C, Nitz N, Sousa AO, Alves RM, Guimaro MC, Cordeiro C, Bernal FM, Rosa AC, Hejnar J, Leonardecz E, Hecht MM.SourceChagas Disease Multidisciplinary Research Laboratory, Faculty of Medicine, University of Brasilia, Brasilia, Federal District, Brazil. ateixeir@unb.br AbstractBACKGROUND:The administration of anti-trypanosome nitroderivatives curtails Trypanosoma cruzi infection in Chagas disease patients, but does not prevent destructive lesions in the heart. This observation suggests that an effective treatment for the disease requires understanding its pathogenesis. METHODOLOGY/PRINCIPAL FINDINGS:To understand the origin of clinical manifestations of the heart disease we used a chicken model system in which infection can be initiated in the egg, but parasite persistence is precluded. T. cruzi inoculation into the air chamber of embryonated chicken eggs generated chicks that retained only the parasite mitochondrial kinetoplast DNA minicircle in their genome after eight days of gestation. Crossbreeding showed that minicircles were transferred vertically via the germ line to chicken progeny. Minicircle integration in coding regions was shown by targeted-primer thermal asymmetric interlaced PCR, and detected by direct genomic analysis. The kDNA-mutated chickens died with arrhythmias, shortness of breath, cyanosis and heart failure. These chickens with cardiomyopathy had rupture of the dystrophin and other genes that regulate cell growth and differentiation. Tissue pathology revealed inflammatory dilated cardiomegaly whereby immune system mononuclear cells lyse parasite-free target heart fibers. The heart cell destruction implicated a thymus-dependent, autoimmune; self-tissue rejection carried out by CD45(+), CD8γδ(+), and CD8α lymphocytes. CONCLUSIONS/SIGNIFICANCE:These results suggest that genetic alterations resulting from kDNA integration in the host genome lead to autoimmune-mediated destruction of heart tissue in the absence of T. cruzi parasites. |
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| 5. | PLoS Negl Trop Dis. 2011 Mar 29;5(3):e943.Vaccines for the leishmaniases: proposals for a research agenda.Working Group on Research Priorities for Development of Leis hmaniasis Vaccines, Costa CH, Peters NC, Maruyama SR, de Brito EC Jr, Santos IK.Collaborators: Ali N, de Brito EC Jr, Brodskyn C, Campos-Neto A, Carvalho EM, Chang KP, Costa CH, Fernandes AP, Fujiwara R, Gazzinelli R, Goto H, Grimaldi G, Kaye P, Kedzierski L, Khamesipour A, Maia C, Maruyama SR, McMaster WR, Mendonça SC, de Janeiro R, Nakhasi HL, Peters NC, Piazza F, Quinnell R, Reis AB, Santos IK, Santos M, Santos-Gomes G, Shaw J, Valenzuela J, Walden P, Werneck G. |
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| 6. | PLoS Negl Trop Dis. 2011 Mar 8;5(3):e976.Genetic and functional role of TNF-alpha in the development Trypanosoma cruzi infection.Pissetti CW, Correia D, de Oliveira RF, Llaguno MM, Balarin MA, Silva-Grecco RL, Rodrigues V Jr.SourceLaboratory of Immunology, Universidade Federal do Triângulo Mineiro, Uberaba, Minas Gerais, Brazil. AbstractTNF-alpha plays an important role in trypanocidal mechanisms and is related to tissue injury. This cytokine has been detected in the heart of human chagasic patients where it is associated with tissue damage. This study investigated whether TNF-alpha levels and the presence of genetic polymorphisms are associated with the presence of T. cruzi infection and/or with the development of the cardiac form in chronic chagasic patients. Genomic DNA of 300 subjects from an endemic area was extracted and analyzed by PCR using specific primers. TNF-alpha was assayed in culture supernatants by ELISA. An association was observed between the absence of the TNF-238A allele and negative serology. Furthermore, seropositive individuals carrying the TNF-238A allele produced significantly higher TNF-alpha levels without stimulation (p=0.04) and after stimulation with LPS (p=0.007) and T. cruzi antigens (p=0.004). The present results suggest that the polymorphism at position -238 influences susceptibility to infection and that this allele is associated with higher TNF-alpha production in seropositive individuals. |
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| 7. | Eur J Heart Fail. 2010 Aug;12(8):782-4.Exercise training in Chagas' cardiomyopathy: trials are welcome for this neglected heart disease.Bocchi EA.Comment on |
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