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Institution

Oswaldo Cruz Foundation

FacilityRio 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.


Papers
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Journal ArticleDOI
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

Journal ArticleDOI
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

Journal ArticleDOI
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

Journal ArticleDOI
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

Journal ArticleDOI
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

NameH-indexPapersCitations
Douglas T. Golenbock12331761267
Guy A. Zimmerman10932839740
David Brown105125746827
Liam Smeeth10475353433
Ann M. Dvorak9943741073
David C. Spray9540028732
Theodore A. Slotkin8957530070
Fernando Q. Cunha8868231501
Mauro M. Teixeira8671331301
Ricardo T. Gazzinelli8634028233
Peter F. Weller8533122005
João B. Calixto8146023029
Frederic J. Seidler8037219564
João Santana da Silva8039919060
Deborah Carvalho Malta7770661000
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202334
2022250
20212,842
20202,942
20192,404
20182,302