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: Genome follow-up of SARS-CoV-2 spread is urgently needed in order to identify mutations that could significantly modify virus pathogenicity.
212 citations
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TL;DR: The clinical-epidemiological parameters evaluated for indigenous women point to the accentuated occurrence of nutrition transition in all regions of Brazil.
Abstract: Background
Although case studies indicate that indigenous peoples in Brazil often suffer from higher morbidity and mortality rates than the national population, they were not included systematically in any previous national health survey. Reported here for the first time, the First National Survey of Indigenous People’s Health and Nutrition in Brazil was conducted in 2008–2009 to obtain baseline information based on a nationwide representative sample. This paper presents the study’s rationale, design and methods, and selected results.
212 citations
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TL;DR: A2, but not LACK, fits the requirements for a safe vaccine against American leishmaniasis, and the association between rA2 and rLACK antigens in the same vaccine completely inhibited the rA 2-specific IFN-γ and humoral responses and, consequently, the protective effect of the r a2 antigen against L. amazonensis infection.
Abstract: Leishmania amazonensis is one of the major etiologic agents of a broad spectrum of clinical forms of leishmaniasis and has a wide geographical distribution in the Americas, which overlaps with the areas of transmission of many other Leishmania species. The LACK and A2 antigens are shared by various Leishmania species. A2 was previously shown to induce a potent Th1 immune response and protection against L. donovani infection in BALB/c mice. LACK is effective against L. major infection, but no significant protection against L. donovani infection was observed, in spite of the induction of a potent Th1 immune response. In an attempt to select candidate antigens for an American leishmaniasis vaccine, we investigated the protective effect of these recombinant antigens (rLACK and rA2) and recombinant interleukin-12 (rIL-12) against L. amazonensis infection in BALB/c mice. As expected, immunization with either rA2-rIL-12 or rLACK-rIL-12 induced a robust Th1 response prior to infection. However, only the BALB/c mice immunized with rA2-rIL-12 were protected against infection. Sustained gamma interferon (IFN-γ) production, high levels of anti-A2 antibodies, and low levels of parasite-specific antibodies were detected in these mice after infection. In contrast, mice immunized with rLACK-rIL-12 displayed decreased levels of IFN-γ and high levels of both anti-LACK and parasite-specific antibodies. Curiously, the association between rA2 and rLACK antigens in the same vaccine completely inhibited the rA2-specific IFN-γ and humoral responses and, consequently, the protective effect of the rA2 antigen against L. amazonensis infection. We concluded that A2, but not LACK, fits the requirements for a safe vaccine against American leishmaniasis.
212 citations
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TL;DR: It is shown that the gut microbe Akkermansia muciniphila can mediate negative effects of IFNγ on glucose tolerance in mice and humans, and Irgm1 is identified as anIFNγ-regulated gene in the mouse ileum that controls gut A. muc iniphila levels.
Abstract: Cross-talk between the gut microbiota and the host immune system regulates host metabolism, and its dysregulation can cause metabolic disease. Here, we show that the gut microbe Akkermansia muciniphila can mediate negative effects of IFNγ on glucose tolerance. In IFNγ-deficient mice, A. muciniphila is significantly increased and restoration of IFNγ levels reduces A. muciniphila abundance. We further show that IFNγ-knockout mice whose microbiota does not contain A. muciniphila do not show improvement in glucose tolerance and adding back A. muciniphila promoted enhanced glucose tolerance. We go on to identify Irgm1 as an IFNγ-regulated gene in the mouse ileum that controls gut A. muciniphila levels. A. muciniphila is also linked to IFNγ-regulated gene expression in the intestine and glucose parameters in humans, suggesting that this trialogue between IFNγ, A. muciniphila and glucose tolerance might be an evolutionally conserved mechanism regulating metabolic health in mice and humans.
211 citations
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TL;DR: Rotavirus serotype G5 in fecal specimens of 38 Brazilian children with diarrhea was identified by PCR and enzyme immunoassays and exhibited long RNA electropherotypes and either subgroup II or nonsubgroup I-nonsubgroup II specificities.
Abstract: Rotavirus serotype G5 in fecal specimens of 38 Brazilian children with diarrhea was identified by PCR and enzyme immunoassays The strains exhibited long RNA electropherotypes and either subgroup II or nonsubgroup I-nonsubgroup II specificities Serotype G5 has been found in piglets and horses but not yet in humans Images
210 citations
Authors
Showing all 18833 results
Name | H-index | Papers | Citations |
---|---|---|---|
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 |