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Sent on Thursday, 2011 December 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. | Mol Biol Rep. 2011 Dec 21. [Epub ahead of print]Gene expression profiles of prohibitin in testes of Octopus tankahkeei (ot-phb) revealing its possible role during spermiogenesis.Mao HT, Wang DH, Lan Z, Zhou H, Yang WX.SourceThe Sperm Laboratory, College of Life Sciences, Zhejiang University, 866 Yu Hang Tang Road, Hangzhou, 310058, Zhejiang, China. AbstractProhibitin is essential for intracellular homeostasis and stabilization of mitochondrial respiratory chain complexes. To explore its functions during spermiogenesis of Octopus tankahkeei (O. tankahkeei), we have cloned and sequenced the cDNA of this mammalian PHB homologue (termed ot-PHB) from the testes of O. tankahkeei. The 1165 bp ot-phb cDNA contains a 100 bp 5' UTR, a 882 bp open reading frame and a 183 bp 3' UTR. The putative ot-PHB protein owns a transmembrane domain from 6 to 31 amino acid (aa) and a putative PHB domain from 26 to 178 aa. Protein alignment demonstrated that ot-PHB had 73.3, 73.6, 74.0, 75.1, and 45.4% identity with its homologues in Homo sapiens, Mus muculus, Danio rerio, Xenopus tropicalis and Trypanosoma brucei, respectively. Tissue distribution profile analysis revealed its presence in all the tissues examined. In situ hybridization in spermiogenic cells demonstrated that ot-phb was expressed moderately at the beginning of the spermiogenesis. The abundance of transcripts increased in intermediate spermatids and in drastically remodeling final spermatids. In mature spermatozoa, the residuary transcripts concentrated around the chondriosomal mantle where mitochondria assemble around. In summary, the expression of ot-phb during spermiogenesis implicates a potential function of this protein during mitochondrial ubiquitination. It is the first time to implicate the role of prohibitin in cephalopod spermiogenesis. |
| 2. | Rev Neurol. 2012 Jan 1;54(1):49-58.[Gustavo Pittaluga and the expedition to study sleeping sickness in the Spanish territories of the Gulf of Guinea (1909)]. [Article in Spanish] Corral-Corral I, Quereda Rodriguez-Navarro C.SourceHospital Universitario Ramon y Cajal, 28034 Madrid, Espana. AbstractINTRODUCTION. Sleeping sickness, or human African trypanosomiasis, caused an important mortality at the beginnings of the twentieth century. For this reason the European colonial countries organized several scientific expeditions which contributed decisively to the knowledge of the disease. AIM. To study the first investigation performed in Spain on African trypanosomiasis and in the field of tropical medicine, which was accomplished by a scientific expedition to the Spanish territories in the Gulf of Guinea organized by Cajal in 1909. DEVELOPMENT. The parasitologist Gustavo Pittaluga, who became one of the most outstanding figures in Spanish medicine and public health during the first third of the twentieth century, commanded the expedition. Other members were Luis Rodriguez Illera and Jorge Ramon Fananas, Cajal's son. Along four months they travelled through the Spanish territories of Guinea, collecting clinical and epidemiological information on sleeping sickness and other diseases, and examining a great number of patients, who had hematological and parasitological studies performed. In the clinical description of the 14 cases of trypanosomiasis studied we have found the first description of the opsoclonus-myoclonus syndrome. A pathological study of the brain was performed in one case. In addition, important entomological studies and experimental investigations on trypanosomiasis were also performed. CONCLUSIONS. This expedition took place in the context of the impulse of renovation of Spanish science headed by Cajal through the Junta de Ampliacion de Estudios, recently created. In the investigations performed in Guinea, Pittaluga demonstrated a high scientific standard in the fields of clinical medicine, hygiene, parasitology and entomology, comparable with other contemporary European studies. |
| 3. | Protist. 2011 Dec 18. [Epub ahead of print]A Trypanosoma brucei Protein Required for Maintenance of the Flagellum Attachment Zone and Flagellar Pocket ER Domains.Lacomble S, Vaughan S, Deghelt M, Moreira-Leite FF, Gull K.SourceSir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom. AbstractTrypanosomes and Leishmanias are important human parasites whose cellular architecture is centred on the single flagellum. In trypanosomes, this flagellum is attached to the cell along a complex flagellum attachment zone (FAZ), comprising flagellar and cytoplasmic components, the integrity of which is required for correct cell morphogenesis and division. The cytoplasmic FAZ cytoskeleton is conspicuously associated with a sheet of endoplasmic reticulum termed the 'FAZ ER'. In the present work, 3D electron tomography of bloodstream form trypanosomes was used to clarify the nature of the FAZ ER. We also identified TbVAP, a T. brucei protein whose knockdown by RNAi in procyclic form cells leads to a dramatic reduction in the FAZ ER, and in the ER associated with the flagellar pocket. TbVAP is an orthologue of VAMP-associated proteins (VAPs), integral ER membrane proteins whose mutation in humans has been linked to familial motor neuron disease. The localisation of tagged TbVAP and the phenotype of TbVAP RNAi in procyclic form trypanosomes are consistent with a function for TbVAP in the maintenance of sub-populations of the ER associated with the FAZ and the flagellar pocket. Nevertheless, depletion of TbVAP did not affect cell viability or cell cycle progression. Copyright © 2011 Elsevier GmbH. All rights reserved. |
| 4. | Protist. 2011 Dec 18. [Epub ahead of print]Quantification of Individual Flagellate - Bacteria Interactions within Semi-natural Biofilms.Erken M, Farrenschon N, Speckmann S, Arndt H, Weitere M.SourceHelmholtz Centre for Environmental Research - UFZ, Department River Ecology, Brückstraße 3a, 39114 Magdeburg, Germany; University of Cologne, Cologne Biocenter, Zoological Institute, Department General Ecology, Zülpicher Straße 47b, D-50674 Köln, Germany. AbstractHere we present a new approach to quantify food-web interactions within semi-natural biofilms by combining the establishment of biofilms from natural rivers in flow cells with video microscopy. In a first application of this approach, we focused on the surface-gliding heterotrophic flagellates (HF) Neobodo designis, Rhynchomonas nasuta and Planomonas sp. It was shown that the three HF generally ingested single biofilm-associated bacteria whereas bacteria within microcolonies were attacked but not ingested. However, grazing strategies differed considerably. While the kinetoplastids N. designis and R. nasuta displayed long search and short handling times, Planomonas sp. showed the opposite grazing characteristics. The latter behaviour resulted in a high relative predation success of 80% (precent of attacked prey ingested), whereas the relative predation success of the two kinetoplastids was only 20%. However, the two contrasting strategies resulted in similar ingestion rates for Planomonas sp. and N. designis of 0.5 to 0.6 ingestions flagellates(-1) minute(-1), respectively. Our results showed distinct differences in the feeding behaviour of three flagellates having similar life forms and provide direct evidence that microcolony formation in biofilms protects bacteria from grazing by HF in situ. The new approach provides individual-based insights into the complex food web interactions within biofilms. Copyright © 2011 Elsevier GmbH. All rights reserved. |
| 5. | Ann Trop Med Parasitol. 2011 Oct;105(7):485-91.First microscopical and molecular-based characterization of Leishmania major within naturally infected Phlebotomus salehi (Diptera; Psychodidae) in Fars province, southern Iran.Davami MH, Motazedian MH, Kalantari M, Asgari Q, Badzohre A, Mohammadpour I.SourceDepartment of Medical Microbiology, School of Medicine, Jahrom University of Medical Sciences, Jahrom, Iran. AbstractZoonotoc cutaneous leishmaniasis is endemic in several parts of Iran. Jahrom district is one of the most important endemic foci of leishmaniasis located in Fars province, southern Iran. To identify the vectors of leishmaniasis in this area, a total of 349 sandflies were collected during May to August 2009. They were caught from outdoors in five regions of Jahrom district including villages of Mousavieh, Ghotb-Abad, Heydar-Abad, Fath-Abad and Jahrom County. Eleven species of Phlebotomine (three Phlebotomus spp. and eight Sergentomyia spp.) were detected. To determine the sandflies naturally infected by Leishmania spp., 122 female sandflies were dissected and evaluated microscopically using Giemsa-stained slides. Natural infection of 2 out of 38 (5·26%) P. papatasi and 1 out of 8 (12·5%) P. salehi to Leishmania major was confirmed in the region. Sequencing and nested polymerase chain reaction-based detection of Leishmania were carried out to confirm the microscopic findings. Five (13·16%) P. papatasi and two (25%) P. salehi were positive in nested polymerase chain reaction assay. All positive samples were shown 72-76% similarity with L. major Friedlin. On the basis of our knowledge, this is the first molecular detection of L. major within naturally infected P. salehi in this region in southern Iran. |
| 6. | Adv Parasitol. 2011;76:235-50. doi: 10.1016/B978-0-12-385895-5.00010-4.Adipose tissue, diabetes and Chagas disease.Tanowitz HB, Jelicks LA, Machado FS, Esper L, Qi X, Desruisseaux MS, Chua SC, Scherer PE, Nagajyothi F.SourceDepartment of Pathology, Albert Einstein College of Medicine, Bronx, New York, USA. AbstractAdipose tissue is the largest endocrine organ in the body and is composed primarily of adipocytes (fat cells) but also contains fibroblasts, endothelial cells, smooth muscle cells, macrophages and lymphocytes. Adipose tissue and the adipocyte are important in the regulation of energy metabolism and of the immune response. Adipocytes also synthesize adipokines such as adiponectin which is important in the regulation of insulin sensitivity and inflammation. Infection of mice with Trypanosoma cruzi results in an upregulation of inflammation in adipose tissue that begins during the acute phase of infection and persists into the chronic phase. The adipocyte is both a target of infection and a reservoir for the parasite during the chronic phase from which recrudescence of the infection may occur during periods of immunosuppression. Copyright © 2011 Elsevier Ltd. All rights reserved. |
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| 7. | Adv Parasitol. 2011;76:195-233. doi: 10.1016/B978-0-12-385895-5.00009-8.Neurodegeneration and neuroregeneration in Chagas disease.Chuenkova MV, Pereiraperrin M.SourceDepartment of Pathology and Sackler School of Graduate Students, Tufts University School of Medicine, Boston, Massachusetts, USA. AbstractAutonomic dysfunction plays a significant role in the development of chronic Chagas disease (CD). Destruction of cardiac parasympathetic ganglia can underlie arrhythmia and heart failure, while lesions of enteric neurons in the intestinal plexuses are a direct cause of aperistalsis and megasyndromes. Neuropathology is generated by acute infection when the parasite, though not directly damaging to neuronal cells, elicits immune reactions that can become cytotoxic, inducing oxidative stress and neurodegeneration. Anti-neuronal autoimmunity may further contribute to neuropathology. Much less clear is the mechanism of subsequent neuronal regeneration in patients that survive acute infection. Morphological and functional recovery of the peripheral neurons in these patients correlates with the absence of CD clinical symptoms, while persistent neuronal deficiency is observed for the symptomatic group. The discovery that Trypanosoma cruzi trans-sialidase can moonlight as a parasite-derived neurotrophic factor (PDNF) suggests that the parasite might influence the balance between neuronal degeneration and regeneration. PDNF functionally mimics mammalian neurotrophic factors in that it binds and activates neurotrophin Trk tyrosine kinase receptors, a mechanism which prevents neurodegeneration. PDNF binding to Trk receptors triggers PI3K/Akt/GSK-3β and MAPK/Erk/CREB signalling cascades which in neurons translates into resistance to oxidative and nutritional stress, and inhibition of apoptosis, whereas in the cytoplasm of infected cells, PDNF represents a substrate-activator of the host Akt kinase, enhancing host-cell survival until completion of the intracellular cycle of the parasite. Such dual activity of PDNF provides sustained activation of survival mechanisms which, while prolonging parasite persistence in host tissues, can underlie distinct outcomes of CD. Copyright © 2011 Elsevier Ltd. All rights reserved. |
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| 8. | Adv Parasitol. 2011;76:171-94. doi: 10.1016/B978-0-12-385895-5.00008-6.Inflammation and Chagas disease some mechanisms and relevance.Talvani A, Teixeira MM.SourceLaboratório de doença de Chagas, Departamento de Ciências Biológicas & NUPEB, Universidade Federal de Ouro Preto, Minas Gerais, Brazil. AbstractChagas cardiomyopathy is caused by infection with flagellated protozoan Trypanosoma cruzi. In patients, there is a fine balance between control of the replication and the intensity of the inflammatory response so that the host is unable to eliminate the parasite resulting in the parasite persisting as a lifelong infection in most individuals. However, the parasite persists in such a way that it causes no or little disease. This chapter reviews our understanding of many of the mediators of inflammation and cells which are involved in the inflammatory response of mammals to T. cruzi infection. Particular emphasis is given to the role of chemokines, endothelin and lipid mediators. Understanding the full range of mediators and cells present and how they interact with each other in Chagas disease may shed light on how we modulate disease pathogenesis and define new approaches to treat or prevent the disease. Copyright © 2011 Elsevier Ltd. All rights reserved. |
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| 9. | Adv Parasitol. 2011;76:153-70. doi: 10.1016/B978-0-12-385895-5.00007-4.ROS signalling of inflammatory cytokines during Trypanosoma cruzi infection.Gupta S, Dhiman M, Wen JJ, Garg NJ.SourceDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, USA. AbstractInflammation is a host defence activated by exogenous (e.g. pathogen-derived, pollutants) or endogenous (e.g. reactive oxygen species-ROS) danger signals. Mostly, endogenous molecules (or their derivatives) have well-defined intracellular function but become danger signal when released or exposed following stress or injury. In this review, we discuss the potential role of ROS in chronic evolution of inflammatory cardiovascular diseases, using our experiences working on chagasic cardiomyopathy as a focus-point. Copyright © 2011 Elsevier Ltd. All rights reserved. |
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| 10. | Adv Parasitol. 2011;76:129-52. doi: 10.1016/B978-0-12-385895-5.00006-2.Autoimmunity.Cunha-Neto E, Teixeira PC, Nogueira LG, Kalil J.SourceLaboratório de Imunologia, Instituto do Coração, Hospital das Clínicas, Universidade de São Paulo, Brazil. AbstractThe scarcity of Trypanosoma cruzi in inflammatory lesions of chronic Chagas disease led early investigators to suggest that tissue damage had an autoimmune nature. In spite of parasite persistence in chronic Chagas disease, several reports indicate that inflammatory tissue damage may not be correlated to the local presence of T. cruzi. A significant number of reports have described autoantibodies and self-reactive T cells, often cross-reactive with T. cruzi antigens, both in patients and in animal models. Evidence for a direct pathogenetic role of autoimmunity was suggested by the development of lesions after immunization with T. cruzi antigens or passive transfer of lymphocytes from infected animals, and the amelioration of chronic myocarditis in animals made tolerant to myocardial antigens. Autoimmune and T. cruzi-specific innate or adaptative responses are not incompatible or mutually exclusive, and it is likely that a combination of both is involved in the pathogenesis of chronic Chagas disease cardiomyopathy. The association between persistent infection and autoimmune diseases-such as multiple sclerosis or diabetes mellitus-suggests that post-infectious autoimmunity may be a frequent finding. Here, we critically review evidence for autoimmune phenomena and their possible pathogenetic role in human Chagas disease and animal models, with a focus on chronic Chagas disease cardiomyopathy. Copyright © 2011 Elsevier Ltd. All rights reserved. |
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