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Sent on Wednesday, 2010 Jan 27Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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| PubMed Results |
| 1. | Turkiye Parazitol Derg. 2009;33(4):259-62.Visceral leishmaniasis in 13 pediatric patients in Turkey: treatment experience.Yilmaz EA, Tanir G, Tuygun N, Ozkan AT.Dr Sami Ulus Maternity and Children Training and Research Hospital, Department of Pediatric Infection Diseases, Ankara, Turkey. Visceral leishmaniasis (VL) is a life-threatening systemic infection caused by protozoa of the genus Leishmania and transmitted by phlebotomine sandflies. Leishmaniases are widespread in most countries in the Mediterranean basin, including Turkey. Leishmania infantum is responsible for VL in Turkey. We previously reported 19 children with VL who were diagnosed during the period of January 2000 to December 2003. In this study, 13 consecutive cases of VL admitted to our hospital between December 2003 and January 2008 were analysed retrospectively. Fever, splenomegaly and hepatomegaly were most common findings in physical examination while anemia, elevated erythrocyte sedimentation rate and C-reactive protein were the most common laboratory findings. Bone marrow aspirate was obtained in all cases and Leishmania amastigotes were detected in 9 of them (69.2%). Leishmania antibodies by the immunofluorescent antibody test were positive in all cases. All of the patients were treated initally with meglumine antimonate. Treatment failure occurred in two children, who were subsequently cured with liposomal amphotericin B. One additional child was treated with liposomal amphotericin B because of the side effects of meglumine antimonate. All the children were finally cured. Meglumine antimonate still seems to be the first choice in the treatment of pediatric VL in Turkey. |
| PMID: 20101572 [PubMed - in process] | |
| 2. | Glycobiology. 2010 Jan 24. [Epub ahead of print]Application of electrospray mass spectrometry to the structural determination of glycosylphosphatidylinositol membrane anchors.Nett IR, Mehlert A, Lamont D, Ferguson MA.Division of Biological Chemistry and Drug Discovery, College of Life Sciences, University of Dundee, Dundee DD1 5EH, Scotland, UK. The addition of glycosylphosphatidylinositol (GPI) anchors to proteins is an important posttranslational modification in eukaryotic cells. The complete structural elucidation of GPI-anchors is a complex process that requires relatively large amounts of starting material. In this paper, we assess the degree of structural information that can be obtained by applying electrospray mass spectrometry and tandem mass spectrometry (ES-MS and ES-MS/MS) to permethylated GPI glycans prepared from a well-characterized GPI-anchored glycoprotein, the variant surface glycoprotein from Trypanosoma brucei. All GPI glycans contain a non-N-acetylated glucosamine reside and permethylation leads to the formation of a fixed positive charge on the glycans, in the form of a quaternary amine. The permethylated glycans were detected as [M+//0]2 ions and tandem mass spectrometry of these ions produced substantial, albeit incomplete, structural information on the branching patterns and linkage types for various GPI glycoforms of the variant surface glycoprotein. |
| PMID: 20100693 [PubMed - as supplied by publisher] | |
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| 3. | Clin Infect Dis. 2009 Dec 1;49(11):1685-7.New advances in the management of a long-neglected disease.Urbina JA.Comment on: |
| PMID: 19877968 [PubMed - indexed for MEDLINE] | |
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| 4. | Clin Infect Dis. 2009 Dec 1;49(11):1675-84.Changes in Trypanosoma cruzi-specific immune responses after treatment: surrogate markers of treatment efficacy.Laucella SA, Mazliah DP, Bertocchi G, Alvarez MG, Cooley G, Viotti R, Albareda MC, Lococo B, Postan M, Armenti A, Tarleton RL.Instituto Nacional de Parasitología Dr Mario Fatala Chabén, Buenos Aires, San Martín, Provincia de Buenos Aires, Argentina. Comment in: BACKGROUND: As many as 20 million people are living with Trypanosoma cruzi infection in Latin American, yet few receive any treatment. The major limitation in developing and evaluating potential new drugs for their efficacy is the lack of reliable tests to assess parasite burden and elimination. METHODS: Adults volunteers with chronic T. cruzi infection were evaluated clinically and stratified according to the Kuschnir classification. Individuals with group 0 and group 1 clinical status were treated with benznidazole (5 mg/kg per day for 30 days). The changes in T. cruzi-specific T cell and antibody responses, as well as in clinical status, were measured periodically over the 3-5-year follow-up period and were compared with pretreatment conditions and with values in an untreated control group. RESULTS: The frequency of peripheral interferon (IFN)-gamma-producing T cells specific for T. cruzi declined as early as 12 months after benznidazole treatment and subsequently became undetectable in a substantial proportion of treated subjects. In addition, decreases in antibody responses to a pool of recombinant T. cruzi proteins also decreased in many of these same subjects. The shift to negative IFN-gamma T cell responses was highly associated with an early increase in IFN-gamma-producing T cells with phenotypic features of effector/effector memory cells in a subset of subjects. Benznidazole treatment also resulted in an increase in naive and early differentiated memory-like CD8(+) T cells in a majority of subjects. CONCLUSIONS: Benznidazole treatment during chronic Chagas disease has a substantial impact on parasite-specific immune response that is likely indicative of treatment efficacy and cure. PMCID: PMC2805187 [Available on 2010/12/1] |
| PMID: 19877967 [PubMed - indexed for MEDLINE] | |
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| 5. | Clin Infect Dis. 2009 Dec 1;49(11):1667-74.Congenital Trypanosoma cruzi transmission in Santa Cruz, Bolivia.Bern C, Verastegui M, Gilman RH, Lafuente C, Galdos-Cardenas G, Calderon M, Pacori J, Del Carmen Abastoflor M, Aparicio H, Brady MF, Ferrufino L, Angulo N, Marcus S, Sterling C, Maguire JH.Division of Parasitic Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, USA. Comment in: BACKGROUND: We conducted a study of congenital Trypanosoma cruzi infection in Santa Cruz, Bolivia. Our objective was to apply new tools to identify weak points in current screening algorithms, and find ways to improve them. METHODS: Women presenting for delivery were screened by rapid and conventional serological tests. For infants of infected mothers, blood specimens obtained on days 0, 7, 21, 30, 90, 180, and 270 were concentrated and examined microscopically; serological tests were performed for the day 90, 180, and 270 specimens. Maternal and infant specimens, including umbilical tissue, were tested by polymerase chain reaction (PCR) targeting the kinetoplast minicircle and by quantitative PCR. RESULTS: Of 530 women, 154 (29%) were seropositive. Ten infants had congenital T. cruzi infection. Only 4 infants had positive results of microscopy evaluation in the first month, and none had positive cord blood microscopy results. PCR results were positive for 6 (67%) of 9 cord blood and 7 (87.5%) of 8 umbilical tissue specimens. PCR-positive women were more likely to transmit T. cruzi than were seropositive women with negative PCR results (P < .05). Parasite loads determined by quantitative PCR were higher for mothers of infected infants than for seropositive mothers of uninfected infants P < .01). Despite intensive efforts, only 58% of at-risk infants had a month 9 specimen collected. CONCLUSIONS: On the basis of the low sensitivity of microscopy in cord blood and high rate of loss to follow-up, we estimate that current screening programs miss one-half of all infected infants. Molecular techniques may improve early detection. |
| PMID: 19877966 [PubMed - indexed for MEDLINE] | |
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