Tuesday, March 17, 2009

What's new for 'Trypanosomatids' in PubMed

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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 -7 of 7

1: Rev Soc Bras Med Trop. 2009 Jan-Feb;42(1):77-8.Click here to read

[Canine visceral leishmaniasis in Maricá, State of Rio de Janeiro: first report of an autochthonous case.]

[Article in Portuguese]

Laboratório de Vigilância em Leishmanioses, Instituto de Pesquisa Clínica Evandro Chagas, Fundação Oswaldo Cruz, Rio de Janeiro, RJ.

Visceral leishmaniasis is a zoonosis of public health importance, and dogs represent one of the main problems. This paper describes the first autochthonous case of canine visceral leishmaniasis in the municipality of Maricá. It provides new facts regarding the geographical distribution of Leishmania (Leishmania) chagasi in the State of Rio de Janeiro.

PMID: 19287941 [PubMed - in process]

2: Trop Biomed. 2008 Dec;25(3):178-83.

American cutaneous leishmaniasis in children and adolescents from Northcentral Venezuela.

Immunoparasitology Section, Tropical Medicine Institute, Universidad Central de Venezuela, Caracas, Venezuela.

American Cutaneous Leishmaniasis (ACL) comprises a broad range of cutaneous manifestations caused by different Leishmania species which may produce severe and chronic sequelae in adults. However, it has been suggested that ACL may show different clinical and epidemiological features in children and adolescents that need to be further elucidated. We evaluated the epidemiological features of ACL in a cohort of pediatric patients from Northcentral Venezuela between years 1997 and 2005. Mean age of patients was 9 years old, with a mean clinical evolution of 3 months. Lesions were located mostly in extremities. Forty patients (93%) were positive by MST, 97.7% by IFAT and 48.8% by smear. MST values tended to be related to patients' age, higher values being recorded in older patients (p=0.153).

PMID: 19287354 [PubMed - in process]

3: Eur J Dermatol. 2009 Mar 10. [Epub ahead of print]Click here to read

Leishmaniasis due to L. infantum presenting as macrocheilitis and responding to liposomal amphotericin B.

PMID: 19286487 [PubMed - as supplied by publisher]

4: Int J Parasitol. 2009 Mar 12. [Epub ahead of print]Click here to read

Identification of total and differentially expressed excreted-secreted proteins from Trypanosoma congolense strains exhibiting different virulence and pathogenicity.

CIRAD UMR 17 Trypanosomes [UMR 177 IRD-CIRAD "Interactions Hôtes-Vecteurs-Parasites dans les Trypanosomoses"], TA A-17/G, Campus International de Baillarguet, 34398 Montpellier cedex 5, France.

Animal trypanosomosis is a major constraint to livestock productivity in the tropics and has a significant impact on the life of millions of people globally (mainly in Africa, South America and south-east Asia). In Africa, the disease in livestock is caused mainly by Trypanosoma congolense, Trypanosoma vivax, Trypanosoma evansi and Trypanosoma brucei brucei. The extracellular position of trypanosomes in the bloodstream of their host requires consideration of both the parasite and its naturally excreted-secreted factors (secretome) in the course of pathophysiological processes. We therefore developed and standardised a method to produce purified proteomes and secretomes of African trypanosomes. In this study, two strains of T. congolense exhibiting opposite properties of both virulence and pathogenicity were further investigated through their secretome expression and its involvement in host-parasite interactions. We used a combined proteomic approach (one-dimensional SDS-PAGE and two-dimensional differential in-gel electrophoresis coupled to mass spectrometry) to characterise the whole and differentially expressed protein contents of secretomes. The molecular identification of differentially expressed trypanosome molecules and their correlation with either the virulence process or pathogenicity are discussed with regard to their potential as new diagnostic or therapeutic tools against animal trypanosomosis.

PMID: 19285981 [PubMed - as supplied by publisher]

5: Eur J Med Chem. 2009 Feb 20. [Epub ahead of print]Click here to read

Synthesis of a series of N(6)-substituted adenosines with activity against trypanosomatid parasites.

Institute of Pharmacy, Ernst-Moritz-Arndt-University, Friedrich-Ludwig-Jahn-Strasse 17, 17487 Greifswald, Germany.

The involvement of purine salvage in the accumulation of current trypanocidal drugs is important for the treatment of African sleeping sickness. The substrate specificity of essential nucleoside transporters is therefore of physiological and pharmacological interest. With the intention to contribute to the knowledge in the field, a series of 16 adenosine derivatives with substituents in N(6)-position were prepared in order to evaluate their potential to inhibit Trypanosoma brucei spp. in vitro. An unmodified ribose moiety was selected to conserve key molecular recognition motifs of the arsenal of integral membrane proteins expressed in large numbers on the protozoan plasma membrane. Two of the new compounds prepared using a polymer-assisted acylation protocol showed antitrypanosomal activities in the single digit micromolar concentration range.

PMID: 19285758 [PubMed - as supplied by publisher]

6: Rev Med Interne. 2009 Mar 11. [Epub ahead of print]Click here to read

[Cutaneous leishmaniasis in rheumatoid arthritis.]

[Article in French]

Service de rhumatologie, CHU Hédi Chaker, 3029 Sfax, Tunisie.

INTRODUCTION: Cutaneous leishmaniasis is a protozoal infection. Its prevalence is increasing, especially in immunocompromized subjects. CASE REPORTS: We report four patients with rheumatoid arthritis, treated with methotrexate and prednisone who developed cutaneous leishmaniasis. Clinical outcome was favorable after institution of antimony therapy in three cases despite the continuation of methotrexate and prednisone. One patient failed to respond to therapy. DISCUSSION: The frequency of cutaneous leishmaniasis is increasing especially in immunocompromized subjects. In our patients, rheumatoid arthritis, corticosteroid therapy and methotrexate were predisposing factors of cutaneous leishmaniasis.

PMID: 19285366 [PubMed - as supplied by publisher]

7: Biochem J. 2009 Mar 15;418(3):595-604.Click here to read LinkOut

Mitochondrial calcium overload triggers complement-dependent superoxide-mediated programmed cell death in Trypanosoma cruzi.

Departamento de Histología y Embriología, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay.

The epimastigote stage of Trypanosoma cruzi undergoes PCD (programmed cell death) when exposed to FHS (fresh human serum). Although it has been known for over 30 years that complement is responsible for FHS-induced death, the link between complement activation and triggering of PCD has not been established. We have previously shown that the mitochondrion participates in the orchestration of PCD in this model. Several changes in mitochondrial function were described, and in particular it was shown that mitochondrion-derived O(2)(*-) (superoxide radical) is necessary for PCD. In the present study, we establish mitochondrial Ca(2+) overload as the link between complement deposition and the observed changes in mitochondrial physiology and the triggering of PCD. We show that complement activation ends with the assembly of the MAC (membrane attack complex), which allows influx of Ca(2+) and release of respiratory substrates to the medium. Direct consequences of these events are accumulation of Ca(2+) in the mitochondrion and decrease in cell respiration. Mitochondrial Ca(2+) causes partial dissipation of the inner membrane potential and consequent mitochondrial uncoupling. Moreover, we provide evidence that mitochondrial Ca(2+) overload is responsible for the increased O(2)(*-) production, and that if cytosolic Ca(2+) rise is not accompanied by the accumulation of the cation in the mitochondrion and consequent production of O(2)(*-), epimastigotes die by necrosis instead of PCD. Thus our results suggest a model in which MAC assembly on the parasite surface allows Ca(2+) entry and its accumulation in the mitochondrion, leading to O(2)(*-) production, which in turn constitutes a PCD signal.

PMID: 19053945 [PubMed - indexed for MEDLINE]

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