Institution
Universidade Federal de Minas Gerais
Education•Belo Horizonte, Minas Gerais, Brazil•
About: Universidade Federal de Minas Gerais is a education organization based out in Belo Horizonte, Minas Gerais, Brazil. It is known for research contribution in the topics: Population & Immune system. The organization has 41631 authors who have published 75688 publications receiving 1249905 citations.
Papers published on a yearly basis
Papers
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Conservation International1, University of Washington2, University of Tasmania3, University of the Philippines Los Baños4, BirdLife International5, Universidade Federal de Minas Gerais6, Global Environment Facility7, International Union for Conservation of Nature and Natural Resources8, University of Virginia9
TL;DR: It is demonstrated that a substantial proportion and unexpected diversity of threatened species will be lost in the absence of urgent conservation interventions at the sea- or landscape scale.
Abstract: The spatial scale of conservation necessary to avoid species extinctions is one of the most vigorous debates in conservation biology. One approach holds that protecting sites should be the primary level for action on the ground, the other that conservation action targeting broader seascapes and landscapes is more important. We address this debate systematically by assessing the appropriate spatial scales of conservation for all 4,239 threatened mammals, birds, tortoises and turtles, and amphibians. We find that, in the short- to medium term, 20% of these species are dependent on conservation at single sites, 62% on multiple sites, 18% on both sites and sea- or landscape-scale efforts, and <1% on broad-scale actions alone (where sites are variably sized units that are actually or could potentially be managed for conservation, and “broad scale” refers to sea- or landscape-scale and is determined by the needs of the species in question). Calls for broad-scale conservation action have generally focused on terrestrial birds and mammals, and we confirm that a fifth and a tenth of these, respectively, require conservation action at the landscape scale. However, we also find that two-fifths of threatened freshwater turtles and one-fifth of threatened amphibians depend on broad-scale conservation action to address changes in freshwater processes. Furthermore, the overwhelming majority of threatened marine mammals, birds, and turtles require urgent conservation action at the seascape scale. Our key conclusion is that neither site-scale nor broad-scale approaches alone can prevent mass extinction. Although site protection should remain the cornerstone for almost all threatened species, we demonstrate that a substantial proportion and unexpected diversity of threatened species will be lost in the absence of urgent conservation interventions at the sea- or landscape scale.
155 citations
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University of São Paulo1, Imperial College London2, University of Oxford3, University of Edinburgh4, Federal University of Uberlandia5, Instituto Adolfo Lutz6, Universidade Federal de Minas Gerais7, State University of Campinas8, National Institute of Amazonian Research9, Harvard University10, University of California, Los Angeles11, Temple University12, University of Southampton13, University of Birmingham14, Katholieke Universiteit Leuven15, Royal Veterinary College16, University of Copenhagen17
TL;DR: In this paper, the emergence and circulation of a new SARS-CoV-2 variant of concern, lineage P.1, that acquired 17 mutations, including a trio in the spike protein (K417T, E484K and N501Y) associated with increased binding to the human ACE2 receptor.
Abstract: Cases of SARS-CoV-2 infection in Manaus, Brazil, resurged in late 2020, despite high levels of previous infection there. Through genome sequencing of viruses sampled in Manaus between November 2020 and January 2021, we identified the emergence and circulation of a novel SARS-CoV-2 variant of concern, lineage P.1, that acquired 17 mutations, including a trio in the spike protein (K417T, E484K and N501Y) associated with increased binding to the human ACE2 receptor. Molecular clock analysis shows that P.1 emergence occurred around early November 2020 and was preceded by a period of faster molecular evolution. Using a two-category dynamical model that integrates genomic and mortality data, we estimate that P.1 may be 1.4–2.2 times more transmissible and 25-61% more likely to evade protective immunity elicited by previous infection with non-P.1 lineages. Enhanced global genomic surveillance of variants of concern, which may exhibit increased transmissibility and/or immune evasion, is critical to accelerate pandemic responsiveness. One-Sentence Summary We report the evolution and emergence of a SARS-CoV-2 lineage of concern associated with rapid transmission in Manaus.
155 citations
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TL;DR: All aspects of how graphene is internalized after in vivo administration or in vitro cell exposure were brought about, and how blood-brain barrier can be overlapped by graphene nanomaterials are explained.
155 citations
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TL;DR: It is demonstrated that vertebrates and mosquitoes genomes are under very distinct lineage-specific constraints, and Flaviviridae viruses which specifically infect these lineages appear to be subject to the same evolutionary pressures that shaped their host coding regions, evidencing the lineage- specific coevolutionary processes between the viral and host groups.
Abstract: Virus-host biological interaction is a continuous coevolutionary process involving both host immune system and viral escape mechanisms. Flaviviridae family is composed of fast evolving RNA viruses that infects vertebrate (mammals and birds) and/or invertebrate (ticks and mosquitoes) organisms. These host groups are very distinct life forms separated by a long evolutionary time, so lineage-specific anti-viral mechanisms are likely to have evolved. Flaviviridae viruses which infect a single host lineage would be subjected to specific host-induced pressures and, therefore, selected by them. In this work we compare the genomic evolutionary patterns of Flaviviridae viruses and their hosts in an attempt to uncover coevolutionary processes inducing common features in such disparate groups. Especially, we have analyzed dinucleotide and codon usage patterns in the coding regions of vertebrate and invertebrate organisms as well as in Flaviviridae viruses which specifically infect one or both host types. The two host groups posses very distinctive dinucleotide and codon usage patterns. A pronounced CpG under-representation was found in the vertebrate group, possibly induced by the methylation-deamination process, as well as a prominent TpA decrease. The invertebrate group displayed only a TpA frequency reduction bias. Flaviviridae viruses mimicked host nucleotide motif usage in a host-specific manner. Vertebrate-infecting viruses possessed under-representation of CpG and TpA, and insect-only viruses displayed only a TpA under-representation bias. Single-host Flaviviridae members which persistently infect mammals or insect hosts (Hepacivirus and insect-only Flavivirus, respectively) were found to posses a codon usage profile more similar to that of their hosts than to related Flaviviridae. We demonstrated that vertebrates and mosquitoes genomes are under very distinct lineage-specific constraints, and Flaviviridae viruses which specifically infect these lineages appear to be subject to the same evolutionary pressures that shaped their host coding regions, evidencing the lineage-specific coevolutionary processes between the viral and host groups.
155 citations
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TL;DR: A key role for the Ang-(1-7)/Mas axis as a modulator of cardiomyocyte function is revealed and chronic Mas-deficiency leads to impaired Ca2+ handling inCardiomyocytes.
Abstract: Recently there has been growing evidence suggesting that beneficial effects of angiotensin-(1-7) [Ang-(1-7)] in the heart are mediated by its receptor Mas. However, the signaling pathways involved in these effects in cardiomyocytes are unknown. Here, we investigated the involvement of the Ang-(1-7)/Mas axis in NO generation and Ca(2+) handling in adult ventricular myocytes using a combination of molecular biology, intracellular Ca(2+) imaging, and confocal microscopy. Acute Ang-(1-7) treatment (10 nmol/L) leads to NO production and activates endothelial NO synthase and Akt in cardiomyocytes. Ang-(1-7)-dependent NO raise was abolished by pretreatment with A-779 (1 micromol/L). To confirm that Ang-(1-7) action is mediated by Mas, we used cardiomyocytes isolated from Mas-deficient mice. In Mas-deficient cardiomyocytes, Ang-(1-7) failed to increase NO levels. Moreover, Mas-ablation was accompanied by significant alterations in the proteins involved in the regulation of endothelial NO synthase activity, indicating that endothelial NO synthase and its binding partners are important effectors of the Mas-mediated pathway in cardiomyocytes. We then investigated the role of the Ang-(1-7)/Mas axis on Ca(2+) signaling. Cardiomyocytes treated with 10 nmol/L of Ang-(1-7) did not show changes in Ca(2+)-transient parameters such as peak Ca(2+) transients and kinetics of decay. Nevertheless, cardiomyocytes from Mas-deficient mice presented reduced peak and slower [Ca(2+)](i) transients when compared with wild-type cardiomyocytes. Lower Ca(2+) ATPase of the sarcoplasmic reticulum expression levels accompanied the reduced Ca(2+) transient in Mas-deficient cardiomyocytes. Therefore, chronic Mas-deficiency leads to impaired Ca(2+) handling in cardiomyocytes. Collectively, these observations reveal a key role for the Ang-(1-7)/Mas axis as a modulator of cardiomyocyte function.
155 citations
Authors
Showing all 42077 results
Name | H-index | Papers | Citations |
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Michael Marmot | 193 | 1147 | 170338 |
Pulickel M. Ajayan | 176 | 1223 | 136241 |
Alan D. Lopez | 172 | 863 | 259291 |
Jens Nielsen | 149 | 1752 | 104005 |
Mildred S. Dresselhaus | 136 | 762 | 112525 |
Jing Kong | 126 | 553 | 72354 |
Mauricio Terrones | 118 | 760 | 61202 |
Michael Brammer | 118 | 424 | 46763 |
Terence G. Langdon | 117 | 1158 | 61603 |
Caroline A. Sabin | 108 | 690 | 44233 |
Michael Brauer | 106 | 480 | 73664 |
Michael Bader | 103 | 735 | 37525 |
Michael S. Strano | 98 | 480 | 60141 |
Pablo Jarillo-Herrero | 91 | 245 | 39171 |
Riichiro Saito | 91 | 502 | 48869 |