Thursday, June 28, 2012

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 - 5 of 5

1. Iran Red Crescent Med J. 2011 May;13(5):348-51. Epub 2011 May 1.

Intestinal leishmaniasis in acquired immunodeficiency syndrome.

Molaei M, Minakari M, Pejhan Sh, Mashayekhi R, Modaress Fatthi AR, Zali MR.

Source

Department of Pathology, Research Center of Gastroenterology and Liver Disease, Shaheed Beheshti University of Medical Sciences, Tehran, Iran.

Abstract

In endemic regions, visceral leishmaniasis is one of the most common opportunistic infections in HIV positive patients. Simultaneous infection with Leishmania and HIV has been reported in some countries but this is the first report of such a case in Iran. Our patient was a 27 years old man with intermittent night fever, abdominal pain, loss of appetite, vomiting, watery diarrhea and severe weight loss for 6 months. He had low socio-economic status with an imprisonment history. The patient was quite cachectic and had low grade fever. Physical exam and upper GI endoscopy revealed oropharyngeal candidiasis. Microscopic evaluation of duodenal biopsy material showed Leishmania amastigotes in macrophages of lamina propria. Leishman bodies were also observed in bone marrow aspiration specimen. Serologic tests were positive for Leishmania infantum. HIV antibody was also positive with a CD4+cell count of 80/μl. The diagnosis was acquired immunodeficiency syndrome with simultaneous visceral leishmaniasis involving intestinal mucosa.

PMID: 22737493 [PubMed - in process]
2. Iran Red Crescent Med J. 2011 Dec;13(12):863-7. Epub 2011 Dec 1.

Detection of drug resistance gene in cutaneous leishmaniasis by PCR in some endemic areas of iran.

Alizadeh R, Hooshyar H, Bandehpor M, Arbabi M, Kazemi F, Talari A, Kazemi B.

Source

Department of Parasitology, School of Medicine, Kashan University of Medical Sciences, Kashan, Iran.

Abstract

BACKGROUND:

Cutaneous leishmaniasis is still a health problem in many rural and urban regions of Iran and drug resistance has emerged as a major impediment in the treatment of leishmaniasis. This study aims to determine the drug resistance gene in cutaneous leishmaniasis by PCR in some endemic areas of Iran.

METHODS:

Ninety seven samples were collected from ulcers of leishmaniasis patients from some endemic areas of Iran. The Giemsa stained samples were examined microscopically and cultured in NNN and RPMI 1640 mediums for parasite detection. After DNA extraction, PCR was done by a pair of specific primers. For detection of mutation in DNA, first PCR products were electrophoresed on CSGE gel. The suspected samples were compared by sequencing and RFLP results were demonstrated. Comparison of DNA derived from a wild type cell and mutant cell was undertaken by CSGE and sequencing methods.

RESULTS:

Among 90 isolates (92.8%) examined for detection of mutation in gene with CSGE and RFLP, 10 (11.1%) revealed a disorder in sequencing selection for unresponsive to drug.

CONCLUSION:

Drug resistance in cutaneous leishmaniasis to sodium stiboglocanat is probably due to a mutation in a genome. A field study is needed to determine the distribution of drug resistance and other gene mutations involved in unresponsiveness to drugs in leishmaniasis endemic areas of Iran.

PMID: 22737430 [PubMed - in process]
3. Exp Parasitol. 2012 Jun 23. [Epub ahead of print]

Mitochondrial damage contribute to Epigallocatechin-3-gallate induced death in Leishmania amazonensis.

F Inacio JD, Canto-Cavalheiro MM, S Menna-Barreto RF, Almeida-Amaral EE.

Source

Laboratório de Bioquímica de Tripanosomatideos, Instituto Oswaldo Cruz (IOC), Fundação Oswaldo Cruz (FIOCRUZ), Rio de Janeiro, Rio de Janeiro, Brazil.

Abstract

Epigallocatechin-3-gallate (EGCG), the most abundant flavonoid in green tea, has been reported to have antiproliferative effects on Trypanosoma cruzi however, the mechanism of protozoan action of EGCG has not been studied. In the present study, we demonstrate the mechanism for the antileishmanial activity of EGCG against Leishmania amazonensis promastigotes. Incubation with EGCG significantly inhibited L. amazonensis promastigote proliferation in a time- and dose-dependent manner. The IC(50) for EGCG at 120 hours was 0.063 mM. Ultrastructural alterations of the mitochondria were observed in promastigote treated with EGCG, being the organelle injury reinforced by the decrease in rhodamine 123 fluorescence. The effects of several drugs that interfere directly with mitochondrial physiology in parasites such as Leishmania have been described. The unique mitochondrial features of Leishmania make this organelle an ideal drug target while minimizing toxicity. These data suggest mitochondrial collapse as a part of the EGCG mechanism of action and demonstrate the leishmanicidal effect of EGCG.

Copyright © 2012. Published by Elsevier Inc.

PMID: 22735546 [PubMed - as supplied by publisher]
4. Curr Comput Aided Drug Des. 2012 Jun 25. [Epub ahead of print]

Structure- and Ligand-Based Structure-Activity Relationships for a Series of Inhibitors of Aldolase.

Ferreira LG, Andricopulo AD.

Source

Laboratório de Química Medicinal e Computacional, Instituto de Física de São Carlos, Universidade de São Paulo, Av. Trabalhador São-Carlense 400, 13560-970, São Carlos-SP, Brazil. aandrico@if.sc.usp.br.

Abstract

Aldolase has emerged as a promising molecular target for the treatment of human African trypanosomiasis. Over the last years, due to the increasing number of patients infected with Trypanosoma brucei, there is an urgent need for new drugs to treat this neglected disease. In the present study, two-dimensional fragment-based quantitative-structure activity relationship (QSAR) models were generated for a series of inhibitors of aldolase. Through the application of leave-one-out and leave-many-out cross-validation procedures, significant correlation coefficients were obtained (r2 = 0.98 and q2 = 0.77) as an indication of the statistical internal and external consistency of the models. The best model was employed to predict pKi values for a series of test set compounds, and the predicted values were in good agreement with the experimental results, showing the power of the model for untested compounds. Moreover, structure-based molecular modeling studies were performed to investigate the binding mode of the inhibitors in the active site of the parasitic target enzyme. The structural and QSAR results provided useful molecular information for the design of new aldolase inhibitors within this structural class.

PMID: 22734708 [PubMed - as supplied by publisher]
5. Clin Vaccine Immunol. 2012 Feb;19(2):167-73. Epub 2011 Dec 7.

Characterization of an immunodominant antigenic epitope from Trypanosoma cruzi as a biomarker of chronic Chagas' disease pathology.

Thomas MC, Fernández-Villegas A, Carrilero B, Marañón C, Saura D, Noya O, Segovia M, Alarcón de Noya B, Alonso C, López MC.

Source

Instituto de Parasitología y Biomedicina López Neyra, CSIC, Parque Tecnológico de Ciencias de la Salud, Granada, Spain.

Abstract

Nowadays, the techniques available for chronic Chagas' disease diagnosis are very sensitive; however, they do not allow discrimination of the patient's clinical stages of the disease. The present paper describes that three out of the five different repeats contained in the Trypanosoma cruzi TcCA-2 membrane protein (3972-FGQAAAGDKPPP, 6303-FGQAAAGDKPAP, and 3973-FGQAAAGDKPSL) are recognized with high sensitivity (>90%) by sera from chronic Chagas' disease patients and that they are not recognized by sera from patients in the acute phase of the disease. A total of 133 serum samples from chagasic patients and 50 serum samples from healthy donors were tested. In addition, sera from 15 patients with different autoimmune diseases, 43 serum samples from patients suffering an infectious disease other than Chagas' disease, and 38 serum samples from patients with nonchagasic cardiac disorders were also included in this study. The residue 3973 peptide shows a specificity of >98%, as it is not recognized by individuals with autoimmune and inflammatory processes or by patients with a nonchagasic cardiomyopathy. Remarkably, the levels of antibody against the 3973 epitope detected by the sera from Chagas' disease patients in the symptomatic chronic phase, involving cardiac or digestive alterations, are higher than those detected by the sera from Chagas' disease patients in the indeterminate phase of the disease. It is suggested that the diagnostic technique described could also be used to indicate the degree of pathology. The amino acids F, Q, and DKP located in the peptide at positions 1, 3, and 8 to 10, respectively, are essential to conform to the immunodominant antigenic epitope.

PMCID: PMC3272920 [Available on 2012/8/1]
PMID: 22155766 [PubMed - indexed for MEDLINE]
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