Institution
Oswaldo Cruz Foundation
Facility•Rio de Janeiro, Brazil•
About: Oswaldo Cruz Foundation is a facility organization based out in Rio de Janeiro, Brazil. It is known for research contribution in the topics: Population & Trypanosoma cruzi. The organization has 18673 authors who have published 36752 publications receiving 802378 citations. The organization is also known as: Fundação Oswaldo Cruz & FIOCRUZ.
Topics: Population, Trypanosoma cruzi, Immune system, Leishmania, Health care
Papers published on a yearly basis
Papers
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TL;DR: TheLeishmanicidal effects of a chloroform fraction and a purified indole alkaloid obtained from crude stem extract of Peschiera australis against Leishmania amazonensis, a causative agent of cutaneous leishmaniasis in the New World are shown.
Abstract: In this study, we show the leishmanicidal effects of a chloroform fraction (CLF) and a purified indole alkaloid obtained from crude stem extract of Peschiera australis against Leishmania amazonensis, a causative agent of cutaneous leishmaniasis in the New World. In a bioassay-guided chemical fractionation, the leishmanicidal activity in CLF completely and irreversibly inhibited promastigote growth. This fraction was also active against amastigotes in infected murine macrophages. Chemical analysis of CLF identified an iboga-type indole alkaloid coronaridine as one of its major compounds. Coronaridine showed potent antileishmanial activity, inhibiting promastigote and amastigote growth. Promastigotes and amastigotes treated with CLF or coronaridine showed pronounced alterations in their mitochondria as assessed by transmission electron microscopy.
200 citations
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TL;DR: Early after symptom onset, HCV-specific CD4+ T cell responses are primed and detectable in patients regardless of clinical outcome, but without early antiviral therapy these T cells become exhausted or deleted in chronically infected patients.
Abstract: Vigorous proliferative CD4+ T cell responses are the hallmark of spontaneous clearance of acute hepatitis C virus (HCV) infection, whereas comparable responses are absent in chronically evolving infection. Here, we comprehensively characterized the breadth, specificity, and quality of the HCV-specific CD4+ T cell response in 31 patients with acute HCV infection and varying clinical outcomes. We analyzed in vitro T cell expansion in the presence of interleukin-2, and ex vivo staining with HCV peptide-loaded MHC class II tetramers. Surprisingly, broadly directed HCV-specific CD4+ T cell responses were universally detectable at early stages of infection, regardless of the clinical outcome. However, persistent viremia was associated with early proliferative defects of the HCV-specific CD4+ T cells, followed by rapid deletion of the HCV-specific response. Only early initiation of antiviral therapy was able to preserve CD4+ T cell responses in acute, chronically evolving infection. Our results challenge the paradigm that HCV persistence is the result of a failure to prime HCV-specific CD4+ T cells. Instead, broadly directed HCV-specific CD4+ T cell responses are usually generated, but rapid exhaustion and deletion of these cells occurs in the majority of patients. The data further suggest a short window of opportunity to prevent the loss of CD4+ T cell responses through antiviral therapy.
200 citations
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VCU Medical Center1, National Autonomous University of Mexico2, University of Delhi3, Carlos III Health Institute4, University of Alberta5, Boston Children's Hospital6, Innsbruck Medical University7, Centers for Disease Control and Prevention8, Instituto Adolfo Lutz9, Radboud University Nijmegen10, University of Texas Health Science Center at Houston11, Complutense University of Madrid12, University of Iowa13, Duke University14, Oswaldo Cruz Foundation15, University of Adelaide16
TL;DR: In the absence of clinical breakpoints, the authors' ECVs may aid in the detection of isolates with acquired resistance mechanisms and should be listed in the revised CLSI M27-A3 and CLSIM27-S3 documents.
Abstract: Epidemiological cutoff values (ECVs) for the Cryptococcus neoformans-Cryptococcus gattii species complex versus fluconazole, itraconazole, posaconazole, and voriconazole are not available. We established ECVs for these species and agents based on wild-type (WT) MIC distributions. A total of 2,985 to 5,733 CLSI MICs for C. neoformans (including isolates of molecular type VNI [MICs for 759 to 1,137 isolates] and VNII, VNIII, and VNIV [MICs for 24 to 57 isolates]) and 705 to 975 MICs for C. gattii (including 42 to 260 for VGI, VGII, VGIII, and VGIV isolates) were gathered in 15 to 24 laboratories (Europe, United States, Argentina, Australia, Brazil, Canada, Cuba, India, Mexico, and South Africa) and were aggregated for analysis. Additionally, 220 to 359 MICs measured using CLSI yeast nitrogen base (YNB) medium instead of CLSI RPMI medium for C. neoformans were evaluated. CLSI RPMI medium ECVs for distributions originating from at least three laboratories, which included ≥95% of the modeled WT population, were as follows: fluconazole, 8 μg/ml (VNI, C. gattii nontyped, VGI, VGIIa, and VGIII), 16 μg/ml (C. neoformans nontyped, VNIII, and VGIV), and 32 μg/ml (VGII); itraconazole, 0.25 μg/ml (VNI), 0.5 μg/ml (C. neoformans and C. gattii nontyped and VGI to VGIII), and 1 μg/ml (VGIV); posaconazole, 0.25 μg/ml (C. neoformans nontyped and VNI) and 0.5 μg/ml (C. gattii nontyped and VGI); and voriconazole, 0.12 μg/ml (VNIV), 0.25 μg/ml (C. neoformans and C. gattii nontyped, VNI, VNIII, VGII, and VGIIa,), and 0.5 μg/ml (VGI). The number of laboratories contributing data for other molecular types was too low to ascertain that the differences were due to factors other than assay variation. In the absence of clinical breakpoints, our ECVs may aid in the detection of isolates with acquired resistance mechanisms and should be listed in the revised CLSI M27-A3 and CLSI M27-S3 documents.
200 citations
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TL;DR: Sequence analysis of all 41 known ZIKV RNA open reading frames to date indicates that ZikV has undergone significant changes in both protein and nucleotide sequences during the past half century.
200 citations
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TL;DR: The current challenge remains in the development of potent selective inhibitors that would specifically target HDAC8 with fewer adverse effects compared with pan-HDAC inhibitors.
200 citations
Authors
Showing all 18833 results
Name | H-index | Papers | Citations |
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Douglas T. Golenbock | 123 | 317 | 61267 |
Guy A. Zimmerman | 109 | 328 | 39740 |
David Brown | 105 | 1257 | 46827 |
Liam Smeeth | 104 | 753 | 53433 |
Ann M. Dvorak | 99 | 437 | 41073 |
David C. Spray | 95 | 400 | 28732 |
Theodore A. Slotkin | 89 | 575 | 30070 |
Fernando Q. Cunha | 88 | 682 | 31501 |
Mauro M. Teixeira | 86 | 713 | 31301 |
Ricardo T. Gazzinelli | 86 | 340 | 28233 |
Peter F. Weller | 85 | 331 | 22005 |
João B. Calixto | 81 | 460 | 23029 |
Frederic J. Seidler | 80 | 372 | 19564 |
João Santana da Silva | 80 | 399 | 19060 |
Deborah Carvalho Malta | 77 | 706 | 61000 |