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Sent on Wednesday, 2010 Nov 17Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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PubMed Results |
1. | Geospat Health. 2010 Nov;5(1):71-77.Ecological study and risk mapping of visceral leishmaniasis in an endemic area of Iran based on a geographical information systems approach.Salahi-Moghaddam A, Mohebali M, Moshfae A, Habibi M.Department of Pathobiology, Bandar Abbas Faculty of Medicine, Hormozgan University of Medical Sciences (HUMS), Iran. AbstractBetween 1998 and 2001, a total of 1,062 human cases of visceral leishmaniasis were reported from the rural district of Meshkin-Shahr in the mountainous, north-western Iranian province of Ardabil. In the summer of 2008, a cross-sectional study of dogs was conducted in this endemic area by randomly selecting 384 animals from 21 villages and testing them serologically for leishmaniasis. Villages, in which more than 10% of investigated dogs showed anti- Leishmania titres ≥1/320, were considered to be high-risk environments. Regression analysis showed no statistically significant correlation between topographic conditions and the prevalence of positive cases. However, when the results were compared with past meteorological records, a statistically significant positive correlation (P = 0.007) was found between the number of infected dogs with anti-Leishmania titres ≥1/640 and the number of days in a year with temperatures below 0 °C. While humidity showed an inverse correlation (P = 0.009) with the anti-Leishmania titres, a positive correlation (P <0.001) was found in relation to the amount of rainfall. Mapping of the areas at risk for kala-azar in the Meshkin-Shahr district supports the impression that the low temperatures prevalent in the Ardebil province constitute an important factor influencing the distribution of leishmaniasis there. |
PMID: 21080322 [PubMed - as supplied by publisher] | |
2. | Geospat Health. 2010 Nov;5(1):59-69.Temperature-derived potential for the establishment of phlebotomine sandflies and visceral leishmaniasis in Germany.Fischer D, Thomas SM, Beierkuhnlein C.Department of Biogeography, University of Bayreuth, Universitätsstrasse 30, D-95447 Bayreuth, Germany. AbstractClimate change is expected to manifest in the shift of organisms to regions where they were not present in the past, potentially entailing previously unseen biological risks. However, studies evaluating these future trends are scarce. Here, an important group of vectors (sandflies) and the pathogen transmitted (Leishmania infantum complex) causing the infectious disease visceral leishmaniasis is investigated, focussing on potential establishment in Germany during the 21st century. As the most important habitat factor, temperature requirements of pathogen and vector were derived from the literature and compared with recent climate records - provided by worldclim - and climate change scenarios. Climate data from the Regional Climate Model REMO were obtained and averaged over the time periods 2011- 2040, 2041-2070 and 2071-2100. Projected temperature changes (based on the A1B and A2 scenarios) were correlated with the constraints of vector and pathogen. Simulated potentially suitable habitat areas for vector and pathogen were merged to generate a temperature-derived risk map of visceral leishmaniasis. Temperature conditions seem to become suitable for the vector across large swaths of Germany. Nevertheless, temperature constraints for the pathogen may defer the establishment of the parasitic disease, particularly during the first half of the 21st century. Long-lasting epidemics of visceral leishmaniasis are therefore not expected in Germany during the next few decades, although during extremely warm years an increase in autochthonous cases of leishmaniasis may occur. The southwest (Upper Rhine Valley) and west (Cologne Bight) of Germany are identified as risk areas. The time of potential establishment and corresponding rise in biological risk varies between scenarios, due to differences in the predicted rate of temperature increase. |
PMID: 21080321 [PubMed - as supplied by publisher] | |
3. | Iran Biomed J. 2010 Jul;14(3):97-102.Molecular Cloning, Expression and Enzymatic Assay of Pteridine Reductase 1 from Iranian Lizard Leishmania.Kazemi B, Tohidi F, Bandehpour M, Yarian F.Cellular and Molecular Biology Research Center, Shahid Beheshti University, Tehran, Iran. kazemi@sbmu.ac.ir. AbstractBackground: Currently, there are no effective vaccines against leishmaniasis, and treatment using pentavalent antimonial drugs is occasionally effective and often toxic for patients. The PTR1 enzyme, which causes antifolate drug resistance in Leishmania parasites encoded by gene pteridine reductase 1 (ptr1). Since Leishmania lacks pteridine and folate metabolism, it cannot synthesize the pteridine moiety from guanine triphosphate. Therefore, it must produce pteridine using PTR1, an essential part of the salvage pathway that reduces oxidized pteridines. Thus, PTR1 is a good drug-target candidate for anti-Leishmania chemotherapy. The aim of this study was the cloning, expression, and enzymatic assay of the ptr1 gene from Iranian lizard Leishmania as a model for further studies on Leishmania. Methods: Promastigote DNA was extracted from the Iranian lizard Leishmania, and the ptr1 gene was amplified using specific primers. The PCR product was cloned, transformed into Escherichia coli strain JM109, and expressed. The recombinant protein (PTR1 enzyme) was then purified and assayed. Results: ptr1 gene was successfully amplified and cloned into expression vector. Recombinant protein (PTR1 enzyme) was purified using affinity chromatography and confirmed by Western-blot and dot blot using anti-Leishmania major PTR1 antibody and anti-T7 tag monoclonal antibody, respectively. The enzymatic assay was confirmed as PTR1 witch performed using 6-biopterin as a substrate and nicotinamide adenine dinucleotide phosphate as a coenzyme. Conclusion: Iranian lizard Leishmania ptr1 was expressed and enzymatic assay was performed successfully. |
PMID: 21079660 [PubMed - as supplied by publisher] | |
4. | Antimicrob Agents Chemother. 2010 Nov 15. [Epub ahead of print]High mortality among older patients treated with pentavalent antimonials for visceral leishmaniasis in East Africa and rationale for switch to liposomal amphotericin B.Chappuis F, Alirol E, Worku DT, Mueller Y, Ritmeijer K.Médecins Sans Frontières, 78 rue de Lausanne, 1211 Geneva 21, Geneva, Switzerland; Médecins Sans Frontières, Plantage Middenlaan 14, 1018 DD Amsterdam, Amsterdam, The Netherlands. AbstractVisceral leishmaniasis (VL; kala azar), a fatal disease if left untreated, is one of the most neglected tropical diseases.... |
PMID: 21078947 [PubMed - as supplied by publisher] | |
5. | J Antimicrob Chemother. 2010 Nov 14. [Epub ahead of print]Symmetrical choline-derived dications display strong anti-kinetoplastid activity.Ibrahim HM, Al-Salabi MI, El Sabbagh N, Quashie NB, Alkhaldi AA, Escale R, Smith TK, Vial HJ, de Koning HP.Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8TA, UK. AbstractObjectives To investigate the anti-kinetoplastid activity of choline-derived analogues with previously reported antimalarial efficacy. Methods From an existing choline analogue library, seven antimalarial compounds, representative of the first-, second- and third-generation analogues previously developed, were assessed for activity against Trypanosoma and Leishmania spp. Using a variety of techniques, the effects of choline analogue exposure on the parasites were documented and a preliminary investigation of their mode of action was performed. Results The activities of choline-derived compounds against Trypanosoma brucei and Leishmania mexicana were determined. The compounds displayed promising anti-kinetoplastid activity, particularly against T. brucei, to which 4/7 displayed submicromolar EC(50) values for the wild-type strain. Low micromolar concentrations of most compounds cleared trypanosome cultures within 24-48 h. The compounds inhibit a choline transporter in Leishmania, but their entry may not depend only on this carrier; T. b. brucei lacks a choline carrier and the mode of uptake remains unclear. The compounds had no effect on the overall lipid composition of the cells, cell cycle progression or cyclic adenosine monophosphate production or short-term effects on intracellular calcium levels. However, several of the compounds, displayed pronounced effects on the mitochondrial membrane potential; this action was not associated with production of reactive oxygen species but rather with a slow rise of intracellular calcium levels and DNA fragmentation. Conclusions The choline analogues displayed strong activity against kinetoplastid parasites, particularly against T. b. brucei. In contrast to their antimalarial activity, they did not act on trypanosomes by disrupting choline salvage or phospholipid metabolism, instead disrupting mitochondrial function, leading to chromosomal fragmentation. |
PMID: 21078603 [PubMed - as supplied by publisher] | |
6. | Acta Trop. 2010 Nov 12. [Epub ahead of print]Antileishmanial activity of benzocycloalkyl azole oximino ethers: The conformationally constraint analogues of oxiconazole.Verma A, Srivastava S, Marrapu VK, Srinivas N, Yadav M, Bhandari K, Gupta S.Division of Parasitology, Central Drug Research Institute, CSIR, Lucknow 226001, India. AbstractAntileishmanial activities of 16 synthetic oximino benzocycloalkyl azoles against Leishmania donovani were evaluated in vitro against extracellular promastigotes and intracellular amastigotes. Based on SI (Selectivity Index), 5 compounds were tested further in vivo in hamster model. Out of these, three compounds have shown medium activity (53-58%) and one has shown significant inhibition of parasite multiplication (70%). Despite the fact that these compounds were better than the existing antileishmanials in respect to IC(50) and SI values, they were less active than miltefosine in vivo. The present study has helped us in identifying a new lead that could be exploited as a potential antileishmanial agent. Copyright © 2010 Elsevier B.V. All rights reserved. |
PMID: 21078278 [PubMed - as supplied by publisher] | |
7. | Parasitology. 2010 Nov 16:1-21. [Epub ahead of print]Molecular approaches for a better understanding of the epidemiology and population genetics of Leishmania.Schönian G, Kuhls K, Mauricio IL.Institute of Microbiology and Hygiene, Charité University Medicine Berlin, Dorotheenstrasse 96, D-10117 Berlin, Germany. AbstractSUMMARYMolecular approaches are being used increasingly for epidemiological studies of visceral and cutaneous leishmaniases. Several molecular markers resolving genetic differences between Leishmania parasites at species and strain levels have been developed to address key epidemiological and population genetic questions. The current gold standard, multilocus enzyme typing (MLEE), needs cultured parasites and lacks discriminatory power. PCR assays identifying species directly with clinical samples have proven useful in numerous field studies. Multilocus sequence typing (MLST) is potentially the most powerful phylogenetic approach and will, most probably, replace MLEE in the future. Multilocus microsatellite typing (MLMT) is able to discriminate below the zymodeme level and seems to be the best candidate for becoming the gold standard for distinction of strains. Population genetic studies by MLMT revealed geographical and hierarchic population structure in L. tropica, L. major and the L. donovani complex. The existence of hybrids and gene flow between Leishmania populations suggests that sexual recombination is more frequent than previously thought. However, typing and analytical tools need to be further improved. Accessible databases should be created and sustained for integrating data obtained by different researchers. This would allow for global analyses and help to avoid biases in analyses due to small sample sizes. |
PMID: 21078222 [PubMed - as supplied by publisher] | |
8. | Parasitology. 2010 Nov 16:1-11. [Epub ahead of print]A global sensitivity analysis for African sleeping sickness.Davis S, Aksoy S, Galvani A.Yale School of Public Health, 60 College Street, P.O. Box 208034, New Haven, CT 06520 USA. AbstractSUMMARYAfrican sleeping sickness is a parasitic disease transmitted through the bites of tsetse flies of the genus Glossina. We constructed mechanistic models for the basic reproduction number, R0, of Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense, respectively the causative agents of West and East African human sleeping sickness. We present global sensitivity analyses of these models that rank the importance of the biological parameters that may explain variation in R0, using parameter ranges based on literature, field data and expertize out of Uganda. For West African sleeping sickness, our results indicate that the proportion of bloodmeals taken from humans by Glossina fuscipes fuscipes is the most important factor, suggesting that differences in the exposure of humans to tsetse are fundamental to the distribution of T. b. gambiense. The second ranked parameter for T. b. gambiense and the highest ranked for T. b. rhodesiense was the proportion of Glossina refractory to infection. This finding underlines the possible implications of recent work showing that nutritionally stressed tsetse are more susceptible to trypanosome infection, and provides broad support for control strategies in development that are aimed at increasing refractoriness in tsetse flies. We note though that for T. b. rhodesiense the population parameters for tsetse - species composition, survival and abundance - were ranked almost as highly as the proportion refractory, and that the model assumed regular treatment of livestock with trypanocides as an established practice in the areas of Uganda experiencing East African sleeping sickness. |
PMID: 21078220 [PubMed - as supplied by publisher] | |
9. | Stroke. 2010 Nov;41(11):2477-82. Epub 2010 Sep 23.Chagas disease predicts 10-year stroke mortality in community-dwelling elderly: the Bambui cohort study of aging.Lima-Costa MF, Matos DL, Ribeiro AL.Centro de Pesquisas Rene Rachou, Fundação Oswaldo Cruz, Belo Horizonte, Minas Gerais, Brasil. lima-costa@cpqrr.fiocruz.br Comment in: AbstractBACKGROUND AND PURPOSE: Previous case-control studies have suggested a causal link between Chagas disease, which is caused by the protozoan Trypanosoma cruzi, and stroke. We investigated the relationship between Chagas disease and long-term stroke mortality in a large community-based cohort of older adults. METHODS: Participants were 1398 (80.3% from total) residents aged ≥ 60 years in Bambuí City, Brazil. The end point was death from stroke. Potential confounding variables included age, sex, conventional stroke risk factors, and high sensitive C-reactive protein. RESULTS: Participants of this study were followed from 1997 to 2007 leading to 9740 person-years of observation. The baseline prevalence of T. cruzi infection was 37.5% and the overall mortality rate from stroke was 4.62 per 1000 person-years. The risk of death from stroke among T. cruzi-infected participants was twice that of those noninfected (adjusted hazard ratio, 2.36; 95% CI, 1.25 to 4.44). A B-type natriuretic peptide level in the top quartile was a strong and independent predictor of stroke mortality among those infected (adjusted hazard ratio, 2.72; 95% CI, 1.25 to 5.91). The presence of both a high B-type natriuretic peptide level and electrocardiographic atrial fibrillation increased the risk of stroke mortality by 11.49 (95% CI, 3.19 to 41.38) in these individuals. CONCLUSIONS: This study provides new evidence supporting a causal link between Chagas disease and stroke. The results also showed that B-type natriuretic peptide alone or in association with atrial fibrillation has prognostic value for stroke mortality in T. cruzi chronically infected older adults. |
PMID: 20864663 [PubMed - indexed for MEDLINE] | |
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10. | Stroke. 2010 Nov;41(11):2453-4. Epub 2010 Sep 23.Chagas disease: 101 years of solitude! Tim e for action.Armaganijan L, Morillo CA.Comment on: |
PMID: 20864660 [PubMed - indexed for MEDLINE] | |
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