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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: It is reported that Aedes aegypti harboring Wolbachia are highly resistant to infection with two currently circulating Zika virus isolates from the recent Brazilian epidemic and should be included as part of Zika control strategies.

441 citations

Journal ArticleDOI
30 Mar 2021-Cell
TL;DR: In this paper, structural analysis of the ACE2 binding sites of the SARS-CoV-2 pandemic strain has been carried out and the authors show that the 222 light chain is able to largely restore neutralization potency to a major class of public antibodies.

439 citations

Journal ArticleDOI
TL;DR: These minimal standards are recommended as guidelines to assist authors in the preparation of descriptions for novel taxa to encourage broad polyphasic characterization and the construction of descriptions that are practically useful in routine diagnostic laboratories.
Abstract: Minimal standards for describing new taxa within the aerobic endospore-forming bacteria are proposed, following Recommendation 30b of the Bacteriological Code (1990 Revision). These minimal standards are recommended as guidelines to assist authors in the preparation of descriptions for novel taxa. They encourage broad polyphasic characterization and the construction of descriptions that are practically useful in routine diagnostic laboratories. The proposals have been endorsed by the Subcommittee on the Taxonomy of the Genus Bacillus and Related Organisms of the International Committee on Systematics of Prokaryotes.

438 citations

Journal ArticleDOI
TL;DR: FNDC5/irisin is placed as a novel agent capable of opposing synapse failure and memory impairment in AD, and restoration of its expression can ameliorate these phenotypes in rodent models.
Abstract: Defective brain hormonal signaling has been associated with Alzheimer's disease (AD), a disorder characterized by synapse and memory failure. Irisin is an exercise-induced myokine released on cleavage of the membrane-bound precursor protein fibronectin type III domain-containing protein 5 (FNDC5), also expressed in the hippocampus. Here we show that FNDC5/irisin levels are reduced in AD hippocampi and cerebrospinal fluid, and in experimental AD models. Knockdown of brain FNDC5/irisin impairs long-term potentiation and novel object recognition memory in mice. Conversely, boosting brain levels of FNDC5/irisin rescues synaptic plasticity and memory in AD mouse models. Peripheral overexpression of FNDC5/irisin rescues memory impairment, whereas blockade of either peripheral or brain FNDC5/irisin attenuates the neuroprotective actions of physical exercise on synaptic plasticity and memory in AD mice. By showing that FNDC5/irisin is an important mediator of the beneficial effects of exercise in AD models, our findings place FNDC5/irisin as a novel agent capable of opposing synapse failure and memory impairment in AD.

433 citations

Journal ArticleDOI
13 Jan 2000-Nature
TL;DR: The results suggest that continual lymphocyte apoptosis and phagocytosis of apoptotic cells by macrophages have a role in parasite persistence in the host, and that cyclooxygenase inhibitors have potential therapeutic application in the control of parasite replication and spread in Chagas' disease.
Abstract: After apoptosis, phagocytes prevent inflammation and tissue damage by the uptake and removal of dead cells. In addition, apoptotic cells evoke an anti-inflammatory response through macrophages. We have previously shown that there is intense lymphocyte apoptosis in an experimental model of Chagas' disease, a debilitating cardiac illness caused by the protozoan Trypanosoma cruzi. Here we show that the interaction of apoptotic, but not necrotic T lymphocytes with macrophages infected with T. cruzi fuels parasite growth in a manner dependent on prostaglandins, transforming growth factor-beta (TGF-beta) and polyamine biosynthesis. We show that the vitronectin receptor is critical, in both apoptotic-cell cytoadherence and the induction of prostaglandin E2/TGF-beta release and ornithine decarboxylase activity in macrophages. A single injection of apoptotic cells in infected mice increases parasitaemia, whereas treatment with cyclooxygenase inhibitors almost completely ablates it in vivo. These results suggest that continual lymphocyte apoptosis and phagocytosis of apoptotic cells by macrophages have a role in parasite persistence in the host, and that cyclooxygenase inhibitors have potential therapeutic application in the control of parasite replication and spread in Chagas' disease.

433 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