This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
Do not reply directly to this message.
Sender's message:
Sent on Wednesday, 2011 Jun 15Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
Click here to view complete results in PubMed. (Results may change over time.)
To unsubscribe from these e-mail updates click here.
| PubMed Results |
| 1. | Diagn Cytopathol. 2011 Jun 10. doi: 10.1002/dc.21747. [Epub ahead of print]Role of fine-needle aspiration cytology in the prompt diagnosis of recurrence of visceral leishmaniasis presented as isolated cervical leishmanial lymphadenopathy.Kumar B, Verma P.SourceDepartment of Pathology, B. P. Koirala Institute of Health Sciences, Dharan, Nepal. bipinkumar31@yahoo.co.in. AbstractWe report a case of isolated cervical leishmanial lymphadenopathy diagnosed by fine-needle aspiration cytology (FNAC) in apparently cured case of visceral leishmaniasis. A 28-year-old female presented with cervical lymphnode enlargement to surgery outpatient department and was subjected for FNAC. Smear showed numerous Leishmania donovani bodies in the cytoplasm of macrophages and giant cells, and extracellular spaces. She was treated by Amphotericin B for alternate 14 days and the size of the lymphnode regressed. She was found asymptomatic for 1 year of follow-up. Diagn. Cytopathol. 2011; © 2011 Wiley-Liss, Inc. Copyright © 2011 Wiley-Liss, Inc. |
| Related citations | |
| 2. | Braz J Infect Dis. 2011 Jun;15(3):204-10.Comparison of different primes for PCR-based diagnosis of cutaneous leishmaniasis.Oliveira DM, Lonardoni MV, Teodoro U, Silveira TG.SourceUniversidade Estadual de Maringá, PR, Brazil. AbstractOBJECTIVE:The objective of this study was to analyze different primers that are commonly used in epidemiological studies for the detection of Leishmania DNA by PCR, and to compare them to the conventional direct parasite search for American cutaneous leishmaniasis (ACL) diagnosis. MATERIAL AND METHODS:Five pairs of primers, four of them derived from Leishmania kDNA sequences (MP3H-MP1L; B1-B2; LBF1-LBR1; 13A-13B), and one derived from the SL RNA (mini-exon) gene repeat (LU5A-LB3C), reported previously, were used. RESULTS:The MP3H-MP1L primers were the best at amplifying the DNA, detecting 2 fg of Leishmania spp. DNA. The 13A-13B primers presented the worst performance, detecting 512 x 10³ fg of DNA. CONCLUSION:The wide variation in the analytical sensitivity of the primers used in the PCR, and the significant differences from the conventional method of ACL diagnosis found in this study, emphasize the importance of standardizing the PCR technique, analyzing sensitivity, and selecting suitable oligonucleotide primers. |
| Related citations | |
| 3. | Antimicrob Agents Chemother. 2011 Jun 13. [Epub ahead of print]The 8-aminoquinoline analogue sitamaquine causes oxidative stress in Leishmania donovani promastigotes by targeting succinate dehydrogenase.Carvalho L, Luque-Ortega JR, López-Martín C, Castanys S, Rivas L, Gamarro F.SourceInstituto de Parasitología y Biomedicina "López-Neyra", CSIC (IPBLN-CSIC), Parque Tecnológico de Ciencias de la Salud, Avd. del Conocimiento s/n, 18100-Armilla (Granada), Spain. AbstractThe 8-aminoquinoline analogue sitamaquine (SQ) is an oral antileishmanial drug currently undergoing phase 2b clinical trials for the treatment of visceral leishmaniasis. In this work, we have studied the mechanism of action of this drug in Leishmania donovani promastigotes. SQ causes a dose-dependent inhibition of complex II (succinate dehydrogenase) of the respiratory chain in digitonin-permeabilized promastigotes together with a drop in intracellular ATP levels and a decrease of the mitochondrial electrochemical potential. This is associated with an increase of ROS and intracellular Ca(2+) levels, a higher percentage of the sub-G(1) DNA content population and exposure of phosphatidylserine. Taken together, these results support a lethal mechanism for SQ that involves inhibition of the respiratory chain complex II, which in turn triggers oxidative stress and finally an apoptosis-like death of Leishmania parasites. |
| Related citations | |
| 4. | Cell Host Microbe. 2011 Jun 16;9(6):463-71.Leishmania Promotes Its Own Virulence by Inducing Expression of the Host Immune Inhibitory Ligand CD200.Cortez M, Huynh C, Fernandes MC, Kennedy KA, Aderem A, Andrews NW.SourceDepartment of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742, USA; Section of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06510, USA. AbstractLeishmania parasites infect macrophages, cells normally involved in innate defense against pathogens. Leishmania amazonensis and Leishmania major cause severe or mild disease, respectively, consistent with each parasite's ability to survive within activated macrophages. The mechanisms underlying increased virulence of L. amazonensis are mostly unknown. We show that L. amazonensis promotes its own survival by inducing expression of CD200, an immunoregulatory molecule that inhibits macrophage activation. L. amazonensis does not form typical nonhealing lesions in CD200(-/-) mice and cannot replicate in CD200(-/-) macrophages, an effect reversed by exogenous administration of soluble CD200-Fc. The less virulent L. major does not induce CD200 expression and forms small, self-healing lesions in both wild-type and CD200(-/-) mice. Notably, CD200-Fc injection transforms the course of L. major infection to one resembling L. amazonensis, with large, nonhealing lesions. CD200-dependent iNOS inhibition allows parasite growth in macrophages, identifying a mechanism for the increased virulence of L. amazonensis. Copyright © 2011 Elsevier Inc. All rights reserved. |
| Related citations | |
| 5. | Chem Biol Drug Des. 2011 Jun 11. doi: 10.1111/j.1747-0285.2011.01156.x. [Epub ahead of print]High Throughput Analysis of an RNAi Library Identifies Novel Kinase targets in Trypanosoma brucei.< /a>Mackey ZB, Koupparis K, Nishino M, McKerrow JH.SourceDepartment of Pathology, University of California, San Francisco, and Sandler Center for Drug Discovery BMS Graduate Program TETRAD Graduate Program. AbstractNew drugs are needed to treat Human African Trypanosomiasis because the currently approved treatments are toxic or limited in efficacy. One strategy for developing new drugs involves discovering novel genes whose products can be targeted for modulation by small molecule chemotherapeutic agents. The Trypanosoma brucei genome contains many genes with the potential to become such targets. Kinases represent one group of genes that regulate many important cell functions and can be modulated by small molecules, thus represent a promising group of enzymes to screen for potential therapeutic targets. RNAi screens could help identify the most promising kinase targets, but the lack of suitable assays represents a barrier for optimizing the use of this technology in T. brucei. Here we describe an RNAi screen of a small RNAi library targeting 30 members of the T. brucei kinome utilizing a luciferase-based assay. This screen both validated the luciferase-based assay as a suitable method for conducting RNAi screens in T. brucei, and also identified 2 kinases (CRK12 and ERK8) that are essential for normal proliferation by the parasite. © 2011 John Wiley & Sons A/S. |
| Related citations | |
| 6. | Anal Bioanal Chem. 2011 Jun 14. [Epub ahead of print]A piezoelectric immunosensor for Leishmania chagasi antibodies in canine serum.Ramos-Jesus J, Carvalho KA, Fonseca RA, Oliveira GG, Melo SM, Alcântara-Neves NM, Dutra RF.SourceLaboratório de Engenharia Biomédica, Universidade Federal de Pernambuco, Av. Prof. Moraes Rego, 1235-Cidade Universitária, Recife, Pernambuco, 50670-901, Brazil. AbstractThe American visceral leishmaniasis is an important cause of morbidity and mortality in Brazil for both humans and dogs. Attempts to make a diagnosis of this disease need to be improved, especially in endemic areas, and in the tracking and screening of asymptomatic dogs, which are their main host in urban areas. A quartz crystal microbalance immunosensor for the diagnosis of the canine visceral leishmaniasis using a recombinant antigen of Leishmania chagasi (rLci2B-NH6) was developed. The rLci2B-NH6 was tightly immobilized on a quartz crystal gold electrode by self-assembled monolayer based on short-chain length thiol. The strategy was the use of the antigen-histidine tail covalently linked to glutaraldehyde performing a Schift base which permits a major exposure of epitopes and a reduced steric hindrance. The immunosensor showed good results regarding sensitivity and reproducibility, being able to distinguish positive and negative canine serum for L. chagasi. Furthermore, the immunosensor can be reused through exposure to sodium dodecyl sulfate solution, which promotes the dissociation of antigen-antibody binding, restoring the sensor surface with immobilized biologically active antigens for further analysis. |
| Related citations | |
| 7. | PLoS Negl Trop Dis. 2011 Jun;5(6):e1196. Epub 2011 Jun 7.Population Genetics of Trypanosoma evansi from Camel in the Sudan.S alim B, de Meeûs T, Bakheit MA, Kamau J, Nakamura I, Sugimoto C.SourceDepartment of Collaboration and Education, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan. AbstractGenetic variation of microsatellite loci is a widely used method for the analysis of population genetic structure of microorganisms. We have investigated genetic variation at 15 microsatellite loci of T. evansi isolated from camels in Sudan and Kenya to evaluate the genetic information partitioned within and between individuals and between sites. We detected a strong signal of isolation by distance across the area sampled. The results also indicate that either, and as expected, T. evansi is purely clonal and structured in small units at very local scales and that there are numerous allelic dropouts in the data, or that this species often sexually recombines without the need of the "normal" definitive host, the tsetse fly or as the recurrent immigration from sexually recombined T. brucei brucei. Though the first hypothesis is the most likely, discriminating between these two incompatible hypotheses will require further studies at much localized scales. |
| Related citations | |
| 8. | PLoS Negl Trop Dis. 2011 Jun;5(6):e1173. Epub 2011 Jun 7.Genetic Control of Resistance to Trypanosoma brucei brucei Infection in Mice.Síma M, Havelková H, Quan L, Svobodová M, Jarošíková T, Vojtíšková J, Stassen AP, Demant P, Lipoldová M.SourceLaboratory of Molecular and Cellular Immunology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Prague, Czech Republic. AbstractBACKGROUND:Trypanosoma brucei brucei infects livestock, with severe effects in horses and dogs. Mouse strains differ greatly in susceptibility to this parasite. However, no genes controlling these differences were mapped. METHODS:We studied the genetic control of survival after T. b. brucei infection using recombinant congenic (RC) strains, which have a high mapping power. Each RC strain of BALB/c-c-STS/A (CcS/Dem) series contains a different random subset of 12.5% genes from the parental "donor" strain STS/A and 87.5% genes from the "background" strain BALB/c. Although BALB/c and STS/A mice are similarly susceptible to T. b. brucei, the RC strain CcS-11 is more susceptible than either of them. We analyzed genetics of survival in T. b. brucei-infected F(2) hybrids between BALB/c and CcS-11. CcS-11 strain carries STS-derived segments on eight chromosomes. They were genotyped in the F(2) hybrid mice and their linkage with survival was tested by analysis of variance. RESULTS:We mapped four Tbbr (Trypanosoma brucei brucei response) loci that influence survival after T. b. brucei infection. Tbbr1 (chromosome 3) and Tbbr2 (chromosome 12) have effects on survival independent of inter-genic interactions (main effects). Tbbr3 (chromosome 7) influences survival in interaction with Tbbr4 (chromosome 19). Tbbr2 is located on a segment 2.15 Mb short that contains only 26 genes. CONCLUSION:This study presents the first identification of chromosomal loci controlling susceptibility to T. b. brucei infection. While mapping in F(2) hybrids of inbred strains usually has a precision of 40-80 Mb, in RC strains we mapped Tbbr2 to a 2.15 Mb segment containing only 26 genes, which will enable an effective search for the candidate gene. Definition of susceptibility genes will improve the understanding of pathways and genetic diversity underlying the disease and may result in new strategies to overcome the active subversion of the immune system by T. b. brucei. |
| Related citations | |
| 9. | PLoS Negl Trop Dis. 2011 Jun;5(6):e1155. Epub 2011 Jun 7.Comparative Microsatellite Typing of New World Leishmania infantum Reveals Low Heterogeneity among Populations and Its Recent Old World Origin.Kuhls K, Alam MZ, Cupolillo E, Ferreira GE, Mauricio IL, Oddone R, Feliciangeli MD, Wirth T, Miles MA, Schönian G.SourceInstitut für Mikrobiologie und Hygiene, Charité Universitätsmedizin Berlin, Berlin, Germany. AbstractLeishmania infantum (syn. L. chagasi) is the causative agent of visceral leishmaniasis (VL) in the New World (NW) with endemic regions extending from southern USA to northern Argentina. The two hypotheses about the origin of VL in the NW suggest (1) recent importation of L. infantum from the Old World (OW), or (2) an indigenous origin and a distinct taxonomic rank for the NW parasite. Multilocus microsatellite typing was applied in a survey of 98 L. infantum isolates from different NW foci. The microsatellite profiles obtained were compared to those of 308 L. infantum and 20 L. donovani strains from OW countries previously assigned to well-defined populations. Two main populations were identified for both NW and OW L. infantum. Most of the NW strains belonged to population 1, which corresponded to the OW MON-1 population. However, the NW population was much more homogeneous. A second, more heterogeneous, population comprised most Caribbean strains and corresponded to the OW non-MON-1 population. All Brazilian L. infantum strains belonged to population 1, although they represented 61% of the sample and originated from 9 states. Population analysis including the OW L. infantum populations indicated that the NW strains were more similar to MON-1 and non-MON-1 sub-populations of L. infantum from southwest Europe, than to any other OW sub-population. Moreover, similarity between NW and Southwest European L. infantum was higher than between OW L. infantum from distinct parts of the Mediterranean region, Middle East and Central Asia. No correlation was found between NW L. infantum genotypes and clinical picture or host background. This study represents the first continent-wide analysis of NW L. infantum population structure. It confirmed that the agent of VL in the NW is L. infantum and that the parasite has been recently imported multiple times to the NW from southwest Europe. |
| Related citations | |
| 10. | PLoS Negl Trop Dis. 2011 Jun;5(6):e1153. Epub 2011 Jun 7.Predictors of Visceral Leishmaniasis Relapse in HIV-Infected Patients: A Systematic Review.Cota GF, de Sousa MR, Rabello A.SourcePost-Graduate Program in Health Sciences, René Rachou Institute, Fundação Oswaldo Cruz, Belo Horizonte, Minas Gerais, Brazil. AbstractBACKGROUND AND OBJECTIVES:Visceral leishmaniasis (VL) is a common complication in AIDS patients living in Leishmania-endemic areas. Although antiretroviral therapy has changed the clinical course of HIV infection and its associated illnesses, the prevention of VL relapses remains a challenge for the care of HIV and Leishmania co-infected patients. This work is a systematic review of previous studies that have described predictors of VL relapse in HIV-infected patients. REVIEW METHODS:We searched the electronic databases of MEDLINE, LILACS, and the Cochrane Central Register of Controlled Trials. Studies were selected if they included HIV-infected individuals with a VL diagnosis and patient follow-up after the leishmaniasis treatment with an analysis of the clearly defined outcome of prediction of relapse. RESULTS:Eighteen out 178 studies satisfied the specified inclusion criteria. Most patients were males between 30 and 40 years of age, and HIV transmission was primarily via intravenous drug use. Previous VL episodes were identified as risk factors for relapse in 3 studies. Two studies found that baseline CD4+ T cell count above 100 cells/mL was associated with a decreased relapse rate. The observation of an increase in CD4+ T cells at patient follow-up was associated with protection from relapse in 5 of 7 studies. Meta-analysis of all studies assessing secondary prophylaxis showed significant reduction of VL relapse rate following prophylaxis. None of the five observational studies evaluating the impact of highly active antiretroviral therapy use found a reduction in the risk of VL relapse upon patient follow-up. CONCLUSION:SOME PREDICTORS OF VL RELAPSE COULD BE IDENTIFIED: a) the absence of an increase in CD4+ cells at follow-up; b) lack of secondary prophylaxis; and c) previous history of VL relapse. CD4+ counts below 100 cells/mL at the time of primary VL diagnosis may also be a predictive factor for VL relapse. |
| Related citations | |
No comments:
Post a Comment