Tuesday, December 14, 2010

What's new for 'Trypanosomatids' in PubMed

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 Tuesday, 2010 Dec 14
Search 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
Items 1 - 10 of 63

1. MMW Fortschr Med. 2010 Oct 7;152(40):4.

[Attention tropical medicine specialist. An unpleasant travel souvenir].

[Article in German]

Palm HG, Speck U, Weisel G.

Sanitätskompanie PRT Kunduz, ISAF, Afghanistan.

PMID: 21049629 [PubMed - indexed for MEDLINE]
2. Nat Med. 2010 Nov;16(11):1305-12. Epub 2010 Oct 31.

CX3CR1 is required for airway inflammation by promoting T helper cell survival and maintenance in inflamed lung.

Mionnet C, Buatois V, Kanda A, Milcent V, Fleury S, Lair D, Langelot M, Lacoeuille Y, Hessel E, Coffman R, Magnan A, Dombrowicz D, Glaichenhaus N, Julia V.

University of Nice-Sophia Antipolis, U924, Valbonne, France.

Comment in:

  • Nat Rev Immunol. 2010 Dec;10(12):810.

Abstract

Allergic asthma is a T helper type 2 (T(H)2)-dominated disease of the lung. In people with asthma, a fraction of CD4(+) T cells express the CX3CL1 receptor, CX3CR1, and CX3CL1 expression is increased in airway smooth muscle, lung endothelium and epithelium upon allergen challenge. Here we found that untreated CX3CR1-deficient mice or wild-type (WT) mice treated with CX3CR1-blocking reagents show reduced lung disease upon allergen sensitization and challenge. Transfer of WT CD4(+) T cells into CX3CR1-deficient mice restored the cardinal features of asthma, and CX3CR1-blocking reagents prevented airway inflammation in CX3CR1-deficient recipients injected with WT T(H)2 cells. We found that CX3CR1 signaling promoted T(H)2 survival in the inflamed lungs, and injection of B cell leukemia/lymphoma-2 protein (BCl-2)-transduced CX3CR1-deficient T(H)2 cells into CX3CR1-deficient mice restored asthma. CX3CR1-induced survival was also observed for T(H)1 cells upon airway inflammation but not under homeostatic conditions or upon peripheral inflammation. Therefore, CX3CR1 and CX3CL1 may represent attractive therapeutic targets in asthma.

PMID: 21037587 [PubMed - indexed for MEDLINE]
Related citations
Click here to read

3. Am J Trop Med Hyg. 2010 Nov;83(5):1040-3.

Improving outcome of treatment of kala-azar by supplementation of amphotericin B with physiologic saline and potassium chloride.

Thakur CP, Kumar A, Mitra DK, Roy A, Sinha AK, Ranjan A.

Balaji Utthan Sansthan, Patna, India. cpthakur1@rediffmail.com

Abstract

Complications of amphotericin B limit its wide application in the treatment of patients with kala-azar. This study was undertaken with an aim to minimize anti-renal complications and severe rigor in course of treatment with this drug. Parasitologically confirmed kala-azar cases (n = 230) were randomized equally into two groups: a control group received amphotericin B only at a dose of 1 mg/kg of body weight/day for 20 days and a patient (test) group received 500 mL of physiologic saline and 30 mL (60 meq/L) of KC1 with amphotericin B. We observed a significantly lower increase in serum creatinine levels (P = 0.0001) and a lower incidence of severe rigor and fever (P = 0.0165) in the test group than in the control group. However, the ultimate cure rate was not significantly different (P = 0.5637) between two groups after 12 months of follow-up. Relapses occurred after even after six months in both groups. Persons with relapses were treated with 25 infusions of amphotericin B and cured. Supplementation of amphotericin B with 500 mL of physiologic saline and 30 mL (60 meq/L) of KCl during treatment could help prevent an increase in serum creatinine levels and severe rigor and would make the treatment of kala-azar with amphotericin B easier.

PMCID: PMC2963966 [Available on 2011/11/5]
PMID: 21036834 [PubMed - indexed for MEDLINE]
Related citations
Click here to read

4. Am J Trop Med Hyg. 2010 Nov;83(5):1020-2.

Infection rates of Triatoma protracta (Uhler) with Trypanosoma cruz i in Southern California and molecular identification of trypanosomes.

Hwang WS, Zhang G, Maslov D, Weirauch C.

Department of Entomology, and Department of Biology, University of California, Riverside, California 92521, USA.

Abstract

We report Trypanosoma cruzi infection rates of the native kissing bug Triatoma protracta in southern California. The rates are within the historically reported range, but differ significantly between the two sites (19% in Escondido and 36% in Glendora). Identification of T. cruzi in T. protracta was conducted for the first time by using partial 18S ribosomal RNA and 24Sα ribosomal RNA sequences. Incongruence of 24Sα ribosomal RNA phylogeny with current T. cruzi genotype classification supports non-clonality of some T. cruzi genotypes.

PMCID: PMC2963962 [Available on 2011/11/5]
PMID: 21036830 [PubMed - indexed for MEDLINE]
Related citations
Click here to read

5. Gac Med Mex. 2010 Jul-Aug;146(4):298-9.

[The unexpected: chronic renal insufficiency, parasitism, and selective advantage].

[Article in Spanish]

Salamanca-Gómez F.

Coordinación de Investigación en Salud, Instituto Mexicano del Seguro Social, México DF, México.

PMID: 20964076 [PubMed - indexed for MEDLINE]
Related citations
6. RNA. 2010 Dec;16(12):2435-41. Epub 2010 Oct 12.

Identification of specific inhibitors for a trypanosomatid RNA editing reaction.

Liang S, Connell GJ.

Department of Pharmacology, Medical School, University of Minnesota, Minneapolis, Minnesota 55455, USA.

Abstract

Several mitochondrial mRNAs of the trypanosomatid protozoa are edited through the post-transcriptional insertion and deletion of uridylates. The reaction has provided insights into basic cellular biology and is also important as a potential therapeutic target for the diseases caused by trypanosomatid pathogens. Despite this importance, the field has been hindered by the lack of specific inhibitors that could be used as probes of the reaction mechanism or developed into novel therapeutics. In this study, an electrochemiluminescent aptamer-switch was utilized in a high-throughput screen for inhibitors of a trypanosomatid RNA editing reaction. The screen identified GW5074, mitoxantrone, NF 023, protoporphyrin IX, and D-sphingosine as inhibitors of insertion editing, with IC(50) values ranging from 1 to 3 μM. GW5074 and protoporphyrin IX are demonstrated to inhibit at or before the endonuclease cleavage that initiates editing and will be valuable biochemical probes for the early events of the in vitro reaction. Since protoporphyrin IX and sphingosine are both naturally present within the trypanosomatids, their effectiveness as in vitro inhibitors is also suggestive of the potential for in vivo modulatory roles.

PMID: 20940340 [PubMed - indexed for MEDLINE]
Related citations
Click here to read

7. Rev Med Inst Mex Seguro Soc. 2010 Mar-Apr;48(2):139-44.

[Detection of Trypanosoma cruzi in blood donors].

[Article in Spanish]

Novelo-Garza BA, Benítez-Arvizu G, Peña-Benítez A, Galván-Cervantes J, Morales-Rojas A.

Coordinación de Planeación de Infraestructura Médica, Dirección de Prestaciones Médicas, Instituto Mexicano del Seguro Social, Distrito Federal, Mexico. barbara.novello@imss.gob.mx

Comment in:

Abstract

BACKGROUND: The American trypanosomiasis is the second parasitic disease in importance after paludism and one of the main mechanism of transmission is a blood transfusion. Our objective was to measure the effect the Tripanosoma Cruzi screening test in blood banks in the Mexican Institute of Social Security.

METHODS: Information was obtained from each unit of blood collected. The Tripanosoma cruzi prevalence was calculated only in samples with double reactivity in the blood banks.

RESULTS: Of 71 blood banks, only 26 had been doing T. Cruzi screen; after implementation of integrated services 55 are doing the screening. There were 935 donors with double reactivity to the T. Cruzi test from 230,074 samples. The national prevalence was 0.406%. The seroprevalence was 0.013% to 3.118%.

CONCLUSIONS: The screening of the T. cruzi improved the detection and increased the safety and the prevention of its transmission by blood transfusion.

PMID: 20929616 [PubMed - indexed for MEDLINE]
Related citations
8. J Leukoc Biol. 2010 Nov;88(5):965-71. Epub 2010 Aug 31.

T-bet-independent effects of IL-12 family cytokines on regulation of Th17 responses to experimental T. cruzi infection.

Cobb D, Hambright D, Smeltz RB.

Virginia Commonwealth University, Medical College of Virginia, Richmond, VA 23298, USA.

Abstract

Tbx21 (i.e., T-bet) is an IFN-γ-inducible transcription factor that promotes Th1 differentiation. Previously, we reported that Tbx21(-/-) mice develop a robust Th17 response to the parasite Trypanosoma cruzi, including CD4(+) T cell subsets producing IL-17 and IFN-γ. Because of the known inhibitory effects of IFN-γ on Th17 cells, the purpose of this study was to determine the contribution of IFN-γ to regulation of Th17 differentiation during the course of T. cruzi infection. We observed that infection of IFN-γ(-/-) or Stat-1(-/-) mice generated increased numbers of IL-17-producing cells. In sharp contrast to infected Stat-1(-/-) or Tbx21(-/-) mice, however, IFN-γ(-/-) mice developed a lower overall Th17 response, suggesting that IFN-γ was not required for T-bet-dependent activity, including T-bet-dependent expression of CXCR3. To determine if IFN-γ could influence Th17 responses indirectly by acting on APCs, we neutralized IFN-γ in cultures containing APC and T. cruzi antigens. Although anti-IFN-γ increased IL-17 production modestly, anti-IFN-γ and anti-IL-12 led to a significant enhancement of T. cruzi-specific IL-17 (P<0.01). In contrast to the inhibitory effects of IL-12, IL-23 was able to stimulate Tbx21(-/-) T cells and cause a striking increase in T. cruzi-specific IL-17. These data show that the IL-12 family of cytokines can influence Th17 responses in a T-bet-independent manner and that the effects of IFN-γ are not necessarily related to its ability to induce T-bet expression in T cells.

PMID: 20807701 [PubMed - indexed for MEDLINE]
Related citations
Click here to read

9. Chem Pharm Bull (Tokyo). 2010;58(8):1047-50.

In vitro leishmanicidal activity of benzophenanthridine alkaloi ds from Bocconia pearcei and related compounds.

Fuchino H, Kawano M, Mori-Yasumoto K, Sekita S, Satake M, Ishikawa T, Kiuchi F, Kawahara N.

Research Center for Medicinal Plant Resources, National Institute of Biomedical Innovation, 1-2 Hachimandai, Tsukuba, Ibaraki, Japan. fuchino@nibio.go.jp

Abstract

Leishmanicidal activities of benzophenanthridine alkaloids isolated from fruits of Bocconia pearcei and their derivatives were examined. Seven benzophenanthridine compounds were isolated from the methanolic extracts of B. pearcei. Among them, dihydrosanguinarine showed the most potent leishmanicidal activities (IC(50) value: 0.014 microg/ml, respectively). To examine the structure-activity relationship of the benzophenanthridine skeleton, the leishmanicidal activities for 32 synthetic samples were examined. The existence of bulky groups at the C(7)-C(8) position was found to enhance the activity. On the other hand, the bulkiness at the C(2)-C(3) position on the D-ring, a carbonyl group at C-6, substitution at C-6 and cleavage or saturation of the C(5)-C(6) bond reduced activity. A methyl group on nitrogen of the C-ring was thought to be necessary for significant activity.

Free Article
PMID: 20686258 [PubMed - indexed for MEDLINE]
Related citations


10. Bioorg Chem. 2010 Oct;38(5):190-5. Epub 2010 Jul 1.

3-Hydroxy-2-methylene-3-(4-nitrophenylpropanenitrile): A new highly active compound against epimastigote and tr ypomastigote form of Trypanosoma cruzi.

Sandes JM, Borges AR, Junior CG, Silva FP, Carvalho GA, Rocha GB, Vasconcellos ML, Figueiredo RC.

Departamento de Microbiologia, Centro de Pesquisas Aggeu Magalhães, FIOCRUZ, Recife, PE, Brazil.

Abstract

We have synthesized the Morita-Baylis-Hillman adduct (MBHA) 3-hydroxy-2-methylene-3-(4-nitrophenyl)-propanenitrile (3) in quantitative yield and evaluated on Trypanosoma cruzi epimastigote and bloodstream trypomastigote forms. Compound 3 strongly inhibited epimastigote growth, with IC(50)/72hof 28.5 microM and also caused intense trypomastigotes lysis, with an IC(50)/24h of 25.5 microM. Ultrastructural analysis showed significant morphological changes on both parasite forms treated with 3, including increase of cell volume and rounding of cell body as well as intense intracellular disorganization. Morphological changes indicative of apoptosis, autophagy or necrosis were observed in most affected cells. Docking calculations of 1, 2 and 3 pointed out the possibility of T. cruzi Farnesyl Pyrophosphate Synthase (TcFPPS) enzyme inhibition in 3 mechanism of action.

2010 Elsevier Inc. All rights reserved.
PMID: 20638707 [PubMed - indexed for MEDLINE]
Related citations
Click here to read

No comments:

Post a Comment