What's new for 'Trypanosomatids' in PubMed

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Sent on Tuesday, 2011 Apr 26
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 - 3 of 3

1.	Infect Genet Evol. 2011 Apr 14. [Epub ahead of print] Population genetic structure of Guinea Trypanosoma brucei gambiense isolates according to host factors. Kaboré J, Macleod A, Jamonneau V, Ilboudo H, Duffy C, Camara M, Camara O, Belem AM, Bucheton B, De Meeûs T. Source Centre International de Recherche-Développement sur l'Élevage en zones Subhumides (CIRDES), Unité de recherches sur les bases biologiques de la lutte intégrée, 01 BP 454 Bobo-Dioulasso 01, Burkina Faso. Abstract Human African trypanosomiasis (HAT) or sleeping sickness is a major public health problem in sub-Saharan Africa and is due to the kinetoplastid parasite Trypanosoma brucei gambiense in West and Central Africa. The exact role of multiple infections, the basis of clinical diversity observed in patients and the determinism that leads trypanosomes into different body fluids of the host remain opened questions to date. In this paper we investigate, in three Guinean foci, whether strains found in blood, lymph or cerebrospinal fluid (CSF) or in patients at different phase of HAT (phase 1, early phase 2 and late phase 2) are representative of the focus they belong to. Amplifications of parasites directly from body fluids led to substantial amounts of allelic drop outs, especially so for blood and CSF samples, which required data recoding of all homozygous sites into missing data. While controlling for geography, date of sampling and patient's phase of the disease, we found no effect of body fluids in the genetic structure of T. b. gambiense despite the presence of mixed infections. On the contrary, we found that the strains found in patients in different phase of the disease differed genetically, with early phase patients being more likely to be infected with more recent strains than patients at a more advanced phase of the disease. Thus, the combination of date of sampling and patient's status represents a parameter to be controlled for in population genetic structure analyses. Additional studies will also be required to explore further the phenomenon of mixed infections and its consequences. Copyright © 2011. Published by Elsevier B.V.
	PMID: 21515408 [PubMed - as supplied by publisher]
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2.	Int J Parasitol. 2011 Apr 7. [Epub ahead of print] A novel sucrose/H(+) symport system and an intracellular sucrase in Leishmania donovani. Singh A, Mandal D. Source Division of Infectious Diseases and Immunology, Indian Institute of Chemical Biology, West Bengal, India. Abstract The flagellated form of pathogenic parasitic protozoa Leishmania, resides in the alimentary tract of its sandfly vector, where sucrose serves as a major nutrient source. In this study we report the presence of a sucrose transport system in Leishmania donovani promastigotes. The kinetics of sucrose uptake in promastigotes are biphasic in nature with both high affinity K(m) (K(m) of ∼75μM) and low affinity K(m) (K(m)∼1.38mM) components. By contrast the virulent amastigotes take up sucrose via a low affinity process with a K(m) of 2.5mM. The transport of sucrose into promastigotes leads to rapid intracellular acidification, as indicated by changes in the fluorescence of the pH indicator 2',7'-bis-(2-carboxyethyl)-5-(6) Carboxyfluorescein (BCECF). In experiments with right side-out plasma membrane vesicles derived from L. donovani promastigotes, an artificial pH gradient was able to drive the active accumulation of sucrose. These data are consistent with the operation of a H(+)-sucrose symporter. The symporter was shown to be independent of Na(+) and to be insensitive to cytochalasin B, to the flavonoid phloretin and to the Na(+)/K(+) ATPase inhibitor ouabain. However, the protonophore carbonylcyanide P- (trifluromethoxy) phenylhydrazone (FCCP) and a number of thiol reagents caused significant inhibition of sucrose uptake. Evidence was also obtained for the presence of a stable intracellular pool of the sucrose splitting enzyme, sucrase, in promastigote stage parasites. The results are consistent with the hypothesis that L. donovani promastigotes take up sucrose via a novel H(+)-sucrose symport system and that, on entering the cell, the sucrose is hydrolysed to its component monosaccharides by an intracellular sucrase, thereby providing an energy source for the parasites. Copyright © 2011. Published by Elsevier Ltd.
	PMID: 21515279 [PubMed - as supplied by publisher]
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3.	Histol Histopathol. 2011 Mar;26(3):307-13. Matrix metalloproteinases and their role in the renal epithelial mesenchymal transition. Aresu L, Benali S, Garbisa S, Gallo E, Castagnaro M. Source Department of Public Health, Comparative Pathology and Veterinary Hygiene, University of Padova, Agripolis Legnaro, Padova, Italy. luca.aresu@unipd.it Abstract Tubular cell epithelial-mesenchymal transition (EMT) is a fundamental contributor to renal fibrosis. The aim of this study was to investigate the activity of different matrix metalloproteinases by immunohistochemistry and gel-zymography in a model of chronic canine kidney disease. Immunohistochemistry for antibodies against MMP-9, MMP-2, MMP-13, MMP-14 and TIMP-2 was performed on 28 renal biopsy specimens. Selected cases were chosen for gelatin zymography. In moderate and severe tubulo-interstitial damage, increased expression of MMP-2 was noted. A peculiar staining pattern for MMP-2 in variable-sized vesicles, corresponding to the area of basement membrane splitting, was observed. The immunoexpression of MMP-9 and TIMP-2 was reduced in the same cases, compared to control dogs. The splitting of the membrane suggests an active role of this gelatinase in the disruption of type-IV collagen, the main basement membrane component, confirmed by MMP2 gelatinolytic activity by gel-zymography. These data could provide the basis for clinical trials examining the potential benefits of selective MMP-2 inhibitors in dogs with chronic kidney disease.
	PMID: 21210343 [PubMed - indexed for MEDLINE]
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