What's new for 'Trypanosomatids' in PubMed

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Sent on Friday, 2011 Aug 05
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 - 6 of 6

1.	PLoS Negl Trop Dis. 2011 Jul;5(7):e1219. Epub 2011 Jul 26. Leishmaniasis: middle East and north Africa research and development priorities. McDowell MA, Rafati S, Ramalho-Ortigao M, Ben Salah A. Source Eck Institute for Global Health, Department of Biological Sciences, University of Notre Dame, Notre Dame, Indiana, United States of America.
	PMID: 21814585 [PubMed - in process]

2.	Kidney Int. 2011 Aug 3. doi: 10.1038/ki.2011.251. [Epub ahead of print] Renal tubular dysfunction in patients with American cutaneous leishmaniasis. Oliveira RA, Diniz LF, Teotônio LO, Lima CG, Mota RM, Martins A, Sanches TR, Seguro AC, Andrade L, Silva GB Jr, Libório AB, Daher EF. Source Department of Internal Medicine, School of Medicine, Federal University of Ceará, Cariri Campus, Barbalha, Brazil. Abstract Renal dysfunction seen in patients with American cutaneous leishmaniasis (ACL) has been attributed to the use of antimonials for treatment. To determine whether ACL itself causes tubular dysfunction, we measured renal function in 37 patients with ACL prior to their treatment and compared results to that in 10 healthy volunteers of similar mean age. None of the patients presented with glomerular dysfunction; however, 27 had a urinary concentrating defect. There was no statistical difference between groups in the pre- and post-desmopressin test of urine osmolality, but the post-test urine osmolality of the controls was significantly higher. Urinary AQP2 levels, determined by western blot of isolated exosomes, were found to be significantly lower in patients than in controls, whereas that of the cotransporter (NKCC2) was significantly higher. A urinary acidification defect (post-test pH greater than 5.50 following calcium chloride) was found in 15 patients. Pretest plasma bicarbonate was below normal in 12 patients as was the pretest plasma pH in 14. Expression of the Na/H exchanger (NHE3), H(+)-ATPase, and pendrin were all significantly higher in patients with ACL than in controls. A combined urinary concentration and acidification defect was found in 12 patients. Thus, the urinary concentrating defect of ACL may be caused by decreased AQP2, with increased NKCC2 compensatory. Pendrin upregulation may be related to the urinary acidification defect with increased NHE3 and H(+)-ATPase also compensatory. Hence, ACL can cause asymptomatic renal tubular dysfunction.Kidney International, 3 August 2011; doi:10.1038/ki.2011.251.
	PMID: 21814169 [PubMed - as supplied by publisher]

3.	Am J Trop Med Hyg. 2011 Aug;85(2):193-4. Post-kala-azar dermal leishmaniasis in mymensingh, bangladesh. Islam S, Ashraful Alam Bhuiyan M, Bern C. Source Children's Hospital and Research Center Oakland, Oakland, California; ICDDR,B, Dhaka, Bangladesh; Division of Parasitic Diseases and Malaria, Center for Global Health, Centers for Disease Control and Prevention, Atlanta, Georgia.
	PMID: 21813832 [PubMed - in process]

4.	J Biol Chem. 2011 Aug 3. [Epub ahead of print] Glycerol-3-phosphate alters trypanosoma brucei hexokinase activity in response to environmental change. Dodson HC, Morris MT, Morris JC. Source Clemson University, United States. Abstract The African trypanosome, Trypanosoma brucei, compartmentalizes some metabolic enzymes within peroxisome-like organelles, glycosomes. The amounts, activities, and types of glycosomal enzymes are modulated coincident with developmental and environmental changes. Pexophagy, fusion of glycosomes with acidic lysosomes, has been proposed to facilitate this glycosome remodeling. Here, we report that while the glycosome-resident enzyme T. brucei hexokinase 1 (TbHK1) protein levels are maintained during pexophagy, acidification inactivates the activity. Glycerol-3-phosphate (Gly3P), which is produced in vivo by a glycosome-resident glycerol kinase, mitigated acid inactivation of lysate-derived TbHK activity. Using recombinant TbHK1, we found that Gly3P influences enzyme activity at pH 6.5 by preventing substrate and product inhibition by ATP and ADP, respectively. Additionally, TbHK1 inhibition by the flavonol quercetin is partially reversed by Gly3P at pH 7.4, while at pH 6.5, enzyme activity in the presence of quercetin is completely maintained by Gly3P. However, Gly3P does not alter the interaction of quercetin with TbHK1, as the lone Trp (Trp177) was quenched under all conditions tested. These findings suggest potential novel mechanisms for the regulation of TbHK1, particularly given the acidification of glycosomes that can be induced under a variety of parasite growth conditions.
	PMID: 21813651 [PubMed - as supplied by publisher]

5.	Parasitology. 2011 Aug;138(9):1082-92. Leishmania donovani: proteasome-mediated down-regulation of methionine adenosyltransferase. Pérez-Pertejo Y, Alvarez-Velilla R, Estrada CG, Balaña-Fouce R, Reguera RM. Source Departamento de Farmacología y Toxicología (INTOXCAL), Universidad de León, Campus de Vegazana s/n; 24071 León, Spain. Abstract SUMMARYMethionine adenosyltransferase (MAT) is an important enzyme for metabolic processes, to the extent that its product, S-adenosylmethionine (AdoMet), plays a key role in trans-methylation, trans-sulphuration and polyamine synthesis. Previous studies have shown that a MAT-overexpressing strain of Leishmania donovani controls AdoMet production, keeping the intracellular AdoMet concentration at levels that are compatible with cell survival. This unexpected result, together with the fact that MAT activity and abundance changed with time in culture, suggests that different regulatory mechanisms acting beyond the post-transcriptional level are controlling this protein. In order to gain an insight into these mechanisms, several experiments were carried out to explain the MAT abundance during promastigote cell growth. Determination of MAT turnover in cycloheximide (CHX)-treated cultures resulted in a surprising 5-fold increase in MAT turnover compared to CHX-untreated cultures. This increase agrees with a stabilization of the MAT protein, whose integrity was maintained during culture. The presence of proteasome inhibitors, namely MG-132, MG-115, epoxomycin and lactacystin in the culture medium prevented MAT degradation in both MAT-overexpressing and 'mock-transfected' leishmanial strains. The role of the ubiquitin (Ub) pathway in MAT down-regulation was supported using immunoprecipitation experiments. Immunoprecipitated MAT cross-reacted with anti-Ub antibodies, which provides evidence of a proteasome-mediated down-regulation of the leishmanial MAT abundance.
	PMID: 21813028 [PubMed - in process]

6.	Z Naturforsch C. 2011 May-Jun;66(5-6):225-34. Indole alkaloids from Aspidosperma rigidum and A. schultesii and their antiparasitic effects. Reina M, Ruiz-Mesia W, Ruiz-Mesia L, Martínez-Díaz R, González-Coloma A. Source Instituto de Productos Naturales y Agrobiología (IPNA), CSIC, Avda. Astrofísico F, Sánchez 3, P. O. Box 195, 38206 - La Laguna, Tenerife, Canary Islands, Spain. mreina@ipna.csic.es Abstract Five oxindole alkaloids, three plumerane-type alkaloids, subtype haplophitine, and one aspidospermatane-type alkaloid, subtype tubotaiwine, were isolated from the medicinal plants Aspidosperma rigidum and A. schultesii. One compound was identified as the transoid conformer of 18-oxo-O-methylaspidoalbine which was not previously described. The antiparasitic activity of all compounds against Trypanosoma cruzi and Leishmania infantum and their non-specific cytotoxicity against mammalian cells were also determined.
	PMID: 21812339 [PubMed - in process]