What's new for 'Trypanosomatids' in PubMed

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Sent on Tuesday, 2011 Feb 15
Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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PubMed Results

Items 1 - 8 of 8

1.	Methods Mol Biol. 2011;720:309-26. Genetic and biochemical analysis of protozoal polyamine transporters. Hasne MP, Ullman B. Department of Biochemistry and Molecular Biology, Oregon Health and Science University, Portland, OR, USA. Abstract Polyamines are aliphatic polycations that function in key cellular processes such as growth, differentiation, and macromolecular biosynthesis. Intracellular polyamines pools are maintained from de novo synthesis and from transport of polyamines from the extracellular milieu. This acquisition of exogenous polyamines is mediated by cell surface transporter proteins. Protozoan parasites are the etiologic agents of a plethora of devastating and often fatal diseases in humans and their domestic animals. These pathogens accommodate de novo and/or salvage mechanisms for polyamine acquisition. Because of its therapeutic relevance, the polyamine biosynthetic pathway has been thoroughly investigated in many genera of protozoan parasites, but the polyamine permeation pathways have generally been ignored. Our group has now identified at the molecular level polyamine transporters from two species of protozoan parasites, Leishmania major and Trypanosoma cruzi, characterized these polytopic proteins with respect to ligand specificities and affinities, and determined the subcellular environments in which these transporters reside.
	PMID: 21318882 [PubMed - in process]
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2.	Int J Environ Res Public Health. 2010 Dec;7(12):4267-77. Epub 2010 Dec 20. Antimony toxicity. Sundar S, Chakravarty J. Department of Medicine, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221 005, India; E-Mail: tapadar@gmail.com. Abstract Antimony toxicity occurs either due to occupational exposure or during therapy. Occupational exposure may cause respiratory irritation, pneumoconiosis, antimony spots on the skin and gastrointestinal symptoms. In addition antimony trioxide is possibly carcinogenic to humans. Improvements in working conditions have remarkably decreased the incidence of antimony toxicity in the workplace. As a therapeutic, antimony has been mostly used for the treatment of leishmaniasis and schistosomiasis. The major toxic side-effects of antimonials as a result of therapy are cardiotoxicity (~9% of patients) and pancreatitis, which is seen commonly in HIV and visceral leishmaniasis co-infections. Quality control of each batch of drugs produced and regular monitoring for toxicity is required when antimonials are used therapeutically.
	PMID: 21318007 [PubMed - in process]
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3.	J Proteomics. 2011 Feb 10. [Epub ahead of print] Transcriptomics and Proteomics in Human African Trypanosomiasis: current status and perspectives. Geiger A, Simo G, Grébaut P, Peltier JB, Cuny G, Holzmuller P. UMR 177, IRD-CIRAD, CIRAD TA A-17/G, Campus International de Baillarguet, 34398 Montpellier Cedex 5, France. Abstract Human African trypanosomiasis, or sleeping sickness, is a neglected vector-borne parasitic disease caused by protozoa of the species Trypanosoma brucei sensu lato. Within this complex species, T. b. gambiense is responsible for the chronic form of sleeping sickness in Western and Central Africa, whereas T. b. rhodesiense causes the acute form of the disease in East Africa. Presently, 1.5 million disability-adjusted life years (DALYs) per year are lost due to sleeping sickness. In addition, on the basis of the mortality, the disease is ranked ninth out of 25 human infectious and parasitic diseases in Africa. Diagnosis is complex and needs the intervention of a specialized skilled staff; treatment is difficult and expensive and has potentially life-threatening side effects. The use of transcriptomic and proteomic technologies, currently in rapid development and increasing in sensitivity and discriminating power, is already generating a large panel of promising results. The objective of these technologies is to significantly increase our knowledge of the molecular mechanisms governing the parasite establishment in its vector, the development cycle of the parasite during the parasite's intra-vector life, its interactions with the fly and the other microbial inhabitants of the gut, and finally human host-trypanosome interactions. Such fundamental investigations are expected to provide opportunities to identify key molecular events that would constitute accurate targets for further development of tools dedicated to field work for early, sensitive, and stage-discriminant diagnosis, epidemiology, new chemotherapy, and potentially vaccine development, all of which will contribute to fighting the disease. The present review highlights the contributions of the transcriptomic and proteomic analyses developed thus far in order to identify potential targets (genes or proteins) and biological pathways that may constitute a critical step in the identification of new targets for the development of new tools for diagnostic and therapeutic purposes. Copyright © 2010. Published by Elsevier B.V.
	PMID: 21316496 [PubMed - as supplied by publisher]
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4.	J Am Acad Dermatol. 2011 Mar;64(3):606-8. Superior efficacy of oral fluconazole 400 mg daily versus oral fluconazole 200 mg daily in the treatment of cutaneous leishmania major infection: A randomized clinical trial. Emad M, Hayati F, Fallahzadeh MK, Namazi MR. Shiraz Skin Research Center, Shiraz University of Medical Sciences; Shiraz, Iran.
	PMID: 21315963 [PubMed - in process]
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5.	FEBS Lett. 2011 Feb 9. [Epub ahead of print] Ubiquitination of mRNA cycling sequence binding protein from Leishmania donovani (LdCSBP) modulates the RNA endonuclease activity of its Smr domain. Bhandari D, Guha K, Bhaduri N, Saha P. Crystallography and Molecular Biology Division, Saha Institute of Nuclear Physics, Kolkata 700064, India. Abstract In trypanosomatid parasites, an octanucleotide sequence (C/A)AUAGAA(G/A) in the UTRs primarily determines the stability of S-phase specific mRNAs. A multi-domain protein LdCSBP from Leishmania donovani interacts with the UTR of an S-phase RNA containing the octanucleotide sequence through its unique CCCH-type Zn-finger motifs. Interestingly, the RNA binding protein contains a previously characterized DNA endonuclease domain - Smr. It has been demonstrated here that the LdCSBP Smr domain independently possesses both DNA and RNA endonuclease activities, but the full-length LdCSBP exhibits only riboendonuclease activity. Moreover, LdCSBP protein has been shown to be ubiquitinated, resulting in the down-regulation of its riboendonuclease activity. In conclusion, the results described here suggest a novel regulatory mechanism of mRNA degradation through ubiquitination in eukaryotes. Copyright © 2011. Published by Elsevier B.V.
	PMID: 21315716 [PubMed - as supplied by publisher]
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6.	Bioorg Med Chem. 2011 Jan 21. [Epub ahead of print] Huprines as a new family of dual acting trypanocidal-antiplasmodial agents. Defaux J, Sala M, Formosa X, Galdeano C, Taylor MC, Alobaid WA, Kelly JM, Wright CW, Camps P, Muñoz-Torrero D. Laboratori de Química Farmacèutica (Unitat Associada al CSIC), Facultat de Farmàcia, and Institut de Biomedicina (IBUB), Universitat de Barcelona, Av. Diagonal, 643, 08028 Barcelona, Spain. Abstract A series of 19 huprines has been evaluated for their activity against cultured bloodstream forms of Trypanosoma brucei and Plasmodium falciparum. Moreover, cytotoxicity against rat myoblast L6 cells was assessed for selected huprines. All the tested huprines are moderately potent and selective trypanocidal agents, exhibiting IC(50) values against T. brucei in the submicromolar to low micromolar range and selectivity indices for T. brucei over L6 cells of approximately 15, thus constituting interesting trypanocidal lead compounds. Two of these huprines were also found to be active against a chloroquine-resistant strain of P. falciparum, thus emerging as interesting trypanocidal-antiplasmodial dual acting compounds, but they exhibited little selectivity for P. falciparum over L6 cells. Copyright © 2011 Elsevier Ltd. All rights reserved.
	PMID: 21315611 [PubMed - as supplied by publisher]
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7.	J Proteomics. 2010 Nov 10;73(12):2306-15. Epub 2010 Jul 16. A proteomic analysis of the mechanism of action of naphthoimidazoles in Trypanosoma cruzi epimastigotes in vitro. Menna-Barreto RF, Beghini DG, Ferreira AT, Pinto AV, De Castro SL, Perales J. Laboratório de Biologia Celular, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz, Rio de Janeiro, RJ, 21040-360, Brazil. Abstract Chagas' disease, caused by the protozoan Trypanosoma cruzi, is endemic in Latin America, which current treatment presents variable efficacy and serious side effects. A previous screening of naphthoquinone derivatives pointed to the naphthoimidazoles N1, N2 and N3 as the most active compounds against T. cruzi. In this study, a proteomic approach was employed to identify proteins involved in the N1, N2 and N3 trypanocidal activity. In epimastigotes, the naphthoimidazoles are involved in multiple mechanisms: (a) redox metabolism; (b) energy production; (c) ergosterol biosynthesis; (d) cytoskeleton assembly; (e) protein metabolism and biosynthesis; and (f) chaperones modulation. They induce an imbalance in crucial pathways of the parasite, leading to the loss of metabolic homeostasis and T. cruzi death. Copyright © 2010 Elsevier B.V. All rights reserved.
	PMID: 20621210 [PubMed - indexed for MEDLINE]
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8.	Parasitology. 2010 Dec;137(14):1995-2006. Epub 2009 Dec 23. Trypanosomiasis and the brain. Rodgers J. Institute of Comparative Medicine, Faculty of Veterinary Medicine, University of Glasgow, Bearsden Road, Glasgow. Jean.Rodgers@vet.gla.ac.uk Abstract Neurological involvement following trypanosome infection has been recognised for over a century. However, there are still many unanswered questions concerning the mechanisms used by the parasite to gain entry to the CNS and the pathogenesis of the resulting neuroinflammatory reaction. There is a paucity of material from human cases of the disease therefore the majority of current research relies on the use of animal models of trypanosome infection. This review reports contemporary knowledge, from both animal models and human samples, regarding parasite invasion of the CNS and the neuropathological changes that accompany trypanosome infection and disease progression. The effects of trypanosomes on the blood-brain barrier are discussed and possible key molecules in parasite penetration of the barrier highlighted. Changes in the balance of CNS cytokines and chemokines are also described. The article closes by summarising the effects of trypanosome infection on the circadian sleep-wake cycle, and sleep structure, in relation to neuroinflammation and parasite location within the CNS. Although a great deal of progress has been made in recent years, the advent and application of sophisticated analysis techniques, to decipher the complexities of HAT pathogenesis, herald an exciting and rewarding period for advances in trypanosome research.
	PMID: 20028610 [PubMed - indexed for MEDLINE]
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