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Sent on Friday, 2010 Sep 24Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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| PubMed Results |
| 1. | PLoS One. 2010 Sep 20;5(9). pii: e12879.Molecular characterization of leishmania species isolated from cutaneous leishmaniasis in yemen.Mahdy MA, Al-Mekhlafi HM, Al-Mekhlafi AM, Lim YA, Bin Shuaib NO, Azazy AA, Mahmud R.Department of Parasitology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. AbstractBACKGROUND: Cutaneous leishmaniasis (CL) is a neglected tropical disease endemic in the tropics and subtropics with a global yearly incidence of 1.5 million. Although CL is the most common form of leishmaniasis, which is responsible for 60% of DALYs lost due to tropical-cluster diseases prevalent in Yemen, available information is very limited. METHODOLOGY/PRINCIPAL FINDINGS: This study was conducted to determine the molecular characterization of Leishmania species isolated from human cutaneous lesions in Yemen. Dermal scrapes were collected and examined for Leishmania amastigotes using the Giemsa staining technique. Amplification of the ribosomal internal transcribed spacer 1(ITS-1) gene was carried out using nested PCR and subsequent sequencing. The sequences from Leishmania isolates were subjected to phylogenetic analysis using the neighbor-joining and maximum parsimony methods. The trees identified Leishmania tropica from 16 isolates which were represented by two sequence types. CONCLUSIONS/SIGNIFICANCE: The predominance of the anthroponotic species (i.e. L. tropica) indicates the probability of anthroponotic transmission of cutaneous leishmaniasis in Yemen. These findings will help public health authorities to build an effective control strategy taking into consideration person-to-person transmission as the main dynamic of transmission of CL. |
| PMID: 20862227 [PubMed - in process] | |
| 2. | Future Microbiol. 2010 Sep;5:1301-3.Treatment of visceral leishmaniasis in 2010: direction from Bihar State, India.M urray HW.Department of Medicine, Weill Cornell Medical College, 1300 York Avenue, NY 10065, USA. hwmurray@med.cornell.edu. |
| PMID: 20860475 [PubMed - in process] | |
| 3. | J Infect Dis. 2010 Oct 1;202(7):1104-13.Crucial role of the central leptin receptor in murine Trypanosoma cruzi (Brazil strain) infection.Nagajyothi F, Zhao D, Machado FS, Weiss LM, Schwartz GJ, Desruisseaux MS, Zhao Y, Factor SM, Huang H, Albanese C, Teixeira MM, Scherer PE, Chua SC Jr, Tanowitz HB.Department of Pathology, Albert Einstein College of Medicine, Bronx, New York, USA. AbstractMice carrying a defective leptin receptor gene (db/db mice) are metabolically challenged and upon infection with Trypanosoma cruzi (Brazil strain) suffer high mortality. In genetically modified db/db mice, (NSE-Rb db/db mice), central leptin signaling is reconstituted only in the brain, which is sufficient to correct the metabolic defects. NSE-Rb db/db mice were infected with T. cruzi to determine the impact of the lack of leptin signaling on infection in the absence of metabolic dysregulation. Parasitemia levels, mortality rates, and tissue parasitism were statistically significantly increased in infected db/db mice compared with those in infected NSE-Rb db/db and FVB wild-type mice. There was a reduction in fat mass and blood glucose level in infected db/db mice. Plasma levels of several cytokines and chemokines were statistically significantly increased in infected db/db mice compared with those in infected FVB and NSE-Rb db/db mice. These findings suggest that leptin resistance in individuals with obesity and diabetes mellitus may have adverse consequences in T. cruzi infection. |
| PMID: 20726767 [PubMed - indexed for MEDLINE] | |
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| 4. | J Am Soc Nephrol. 2010 Sep;21(9):1422-6. Epub 2010 Aug 5.The apolipoprotein L1 (APOL1) gene and nondiabetic nephropathy in African Americans.Freedman BI, Kopp JB, Langefeld CD, Genovese G, Friedman DJ, Nelson GW, Winkler CA, Bowden DW, Pollak MR.Section on Nephrology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1053, USA. bfreedma@wfubmc.edu AbstractMapping by admixture linkage disequilibrium (LD) detected strong association between nonmuscle myosin heavy chain 9 gene (MYH9) variants on chromosome 22 and nondiabetic nephropathy in African Americans. MYH9-related variants were posited to be the probable, but not necessarily the definitive, causal variants as a result of impressive statistical evidence of association, renal expression, and a role in autosomal dominant MYH9 disorders characterized by progressive glomerulosclerosis (Epstein and Fechtner syndromes). Dense mapping within MYH9 revealed striking LD patterns and racial variation in risk allele frequencies, suggesting population genetic factors such as selection may be operative in this region. Genovese and colleagues examined large chromosomal regions adjacent to MYH9 using genome-wide association methods and non-HapMap single nucleotide polymorphisms identified in Yoruba from the 1000 Genomes project. Statistically stronger associations were detected between two independent sequence variants in the Apolipoprotein L1 gene (APOL1) and nondiabetic nephropathy in African Americans, with odds ratios of 10.5 in idiopathic FSGS and 7.3 in hypertension-attributed ESRD. These kidney disease risk variants likely rose to high frequency in Africa because they confer resistance to trypanosomal infection and protect from African sleeping sickness. Risk variants in MYH9 and APOL1 are in strong LD, and the genetic risk that was previously attributed to MYH9 may reside, in part or in whole, in APOL1, although more complex models of risk cannot be excluded. This association likely explains racial disparities in nondiabetic nephropathy as a result of the high prevalence of risk alleles in individuals of African ancestry. |
| PMID: 20688934 [PubMed - indexed for MEDLINE] | |
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| 5. | Parasite Immunol. 2010 Jul;32(7):494-502.Frequency of specific CD8+ T cells for a promiscuous epi tope derived from Trypanosoma cruzi KMP-11 protein in chagasic patients.Lasso P, Mesa D, Cuéllar A, Guzmán F, Bolaños N, Rosas F, Velasco V, Thomas Mdel C, Lopez MC, Gonzalez JM, Puerta CJ.Laboratorio de Parasitología Molecular, Pontificia Universidad Javeriana, Bogotá, Colombia. AbstractThe K1 peptide is a CD8(+)T cell HLA-A*0201-restricted epitope derived from the Trypanosoma cruzi KMP-11 protein. We have previously shown that this peptide induces IFN-gamma secretion by CD8(+)T cells. The aim of this study was to characterize the frequency of K1-specific CD8(+)T cells in chagasic patients. Nineteen HLA-A2(+)individuals were selected from 50 T. cruzi infected patients using flow cytometry and SSP-PCR assays. Twelve HLA-A*0201(+)noninfected donors were included as controls. Peripheral blood mononuclear cells were stained with HLA-A2-K1 tetramer, showing that 15 of 19 infected patients have K1-specific CD8(+)T cells (0.09-0.34% frequency) without differences in disease stages or severity. Of note, five of these responders were A*0205, A*0222, A*0226, A*0259 and A*0287 after molecular typing. Thus, a phenotypic and functional comparison of K1-specific CD8(+)T cells from non-HLA-A*0201 and HLA-A*0201(+)infected patients was performed. The results showed that both non-HLA-A*0201 and HLA-A*0201(+)individuals have a predominant effector memory CD8(+)T cell phenotype (CCR7-, CD62L-). Moreover, CD8(+)T cells from non-HLA-A*0201 and HLA-A*0201(+)individuals expressed IL-2, IFN-gamma and perforin without any differences. These findings support that K1 peptide is a promiscuous epitope presented by HLA-A2 supertype molecules and is highly recognized by chagasic patients. |
| PMID: 20591120 [PubMed - indexed for MEDLINE] | |
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| 6. | Enferm Infecc Microbiol Clin. 2010 May;28(5):323-4. Epub 2009 Sep 20.[Traveler with multiple skin lesions of six months' evolution][Article in Spanish] Merino P, González F, Herreros B, Picazo J.Unidad de Medicina Tropical y del viajero, Servicio de Microbiología Clínica, Hospital Clínico San Carlos, Madrid, España. merinopaloma@yahoo.com |
| PMID: 19773093 [PubMed - indexed for MEDLINE] | |
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| 7. | Salud Publica Mex. 2009;51 Suppl 3:S410-23.[Genomic and proteomic contributions for Chagas disease control][A rticle in Spanish] López-Ordóñez T, Panzera F, Tun-Ku E, Ferrandis I, Ramsey JM.Centro Regional de Investigación en Salud Pública, Instituto Nacional de Salud Pública, Tapachula, Chiapas, México. AbstractChagas disease represents one of the more significant public health problems in the Americas. Information regarding the genome and proteome of vectors and parasite, as well as their interactions, will be essential to develop specific and effective diagnostic and preventive tools. Advances that have contributed to the design, implementation, and efficacy of disease surveillance and control activities are reviewed. Genomic and proteomic information has contributed to a better understanding of vector distributions and dispersion, diversity, population dynamics, and control targets (populations and species). In addition, genomic and proteomic studies have impacted parasite diagnostics, Trypanosoma cruzi population dynamics, pharmacological treatment and knowledge of parasite-host interactions. Discussion of these contributions includes expectations for future basic and applied research questions. |
| PMID: 20464215 [PubMed - indexed for MEDLINE] | |
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