Institution
University of Costa Rica
Education•San José, Costa Rica•
About: University of Costa Rica is a education organization based out in San José, Costa Rica. It is known for research contribution in the topics: Population & Venom. The organization has 9817 authors who have published 16781 publications receiving 238208 citations. The organization is also known as: UCR & Universidad de Costa Rica.
Topics: Population, Venom, Antivenom, Snake venom, Context (language use)
Papers published on a yearly basis
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TL;DR: Since only scanty hemorrhagic and necrotic areas were observed in heart muscle, the drastic and rapid increase in CPK levels mainly reflected skeletal muscle necrosis.
111 citations
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TL;DR: This study confirms for the first time that AMBN mutations cause non-syndromic human AI and that mouse models with disrupted Ambn function are valid.
Abstract: Amelogenesis imperfecta (AI) describes a heterogeneous group of inherited dental enamel defects reflecting failure of normal amelogenesis. Ameloblastin (AMBN) is the second most abundant enamel matrix protein expressed during amelogenesis. The pivotal role of AMBN in amelogenesis has been confirmed experimentally using mouse models. However, no AMBN mutations have been associated with human AI. Using autozygosity mapping and exome sequencing, we identified genomic deletion of AMBN exon 6 in a second cousin consanguineous family with three of the six children having hypoplastic AI. The genomic deletion corresponds to an in-frame deletion of 79 amino acids, shortening the protein from 447 to 368 residues. Exfoliated primary teeth (unmatched to genotype) were available from family members. The most severely affected had thin, aprismatic enamel (similar to that reported in mice homozygous for Ambn lacking exons 5 and 6). Other teeth exhibited thicker but largely aprismatic enamel. One tooth had apparently normal enamel. It has been suggested that AMBN may function in bone development. No clinically obvious bone or other co-segregating health problems were identified in the family investigated. This study confirms for the first time that AMBN mutations cause non-syndromic human AI and that mouse models with disrupted Ambn function are valid.
111 citations
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TL;DR: It is shown that Brucella escapes recognition in early stages of infection by expressing a shield against recognition by innate immunity in its LPS core and a novel virulence mechanism in intracellular pathogenic gram-negative bacteria is identified.
Abstract: Innate immunity recognizes bacterial molecules bearing pathogen-associated molecular patterns to launch inflammatory responses leading to the activation of adaptive immunity. However, the lipopolysaccharide (LPS) of the gram-negative bacterium Brucella lacks a marked pathogen-associated molecular pattern, and it has been postulated that this delays the development of immunity, creating a gap that is critical for the bacterium to reach the intracellular replicative niche. We found that a B. abortus mutant in the wadC gene displayed a disrupted LPS core while keeping both the LPS O-polysaccharide and lipid A. In mice, the wadC mutant induced proinflammatory responses and was attenuated. In addition, it was sensitive to killing by non-immune serum and bactericidal peptides and did not multiply in dendritic cells being targeted to lysosomal compartments. In contrast to wild type B. abortus, the wadC mutant induced dendritic cell maturation and secretion of pro-inflammatory cytokines. All these properties were reproduced by the wadC mutant purified LPS in a TLR4-dependent manner. Moreover, the core-mutated LPS displayed an increased binding to MD-2, the TLR4 co-receptor leading to subsequent increase in intracellular signaling. Here we show that Brucella escapes recognition in early stages of infection by expressing a shield against recognition by innate immunity in its LPS core and identify a novel virulence mechanism in intracellular pathogenic gram-negative bacteria. These results also encourage for an improvement in the generation of novel bacterial vaccines.
111 citations
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TL;DR: Since the first case of brucellosis detected in a dolphin aborted fetus, an increasing number of Brucella ceti isolates has been reported in members of the two suborders of cetaceans: Mysticeti and Odontoceti, and three different groups have been recognized according to their preferred host, bacteriological properties, and distinct genetic traits.
Abstract: Since the first case of brucellosis detected in a dolphin aborted fetus, an increasing number of Brucella ceti isolates has been reported in members of the two suborders of cetaceans: Mysticeti and Odontoceti. Serological surveys have shown that cetacean brucellosis may be distributed worldwide in the oceans. Although all B. ceti isolates have been included within the same species, three different groups have been recognized according to their preferred host, bacteriological properties, and distinct genetic traits: B. ceti dolphin type, B. ceti porpoise type, and B. ceti human type. It seems that B. ceti porpoise type is more closely related to B. ceti human isolates and B. pinnipedialis group, while B. ceti dolphin type seems ancestral to them. Based on comparative phylogenetic analysis, it is feasible that the B. ceti ancestor radiated in a terrestrial artiodactyl host close to the Raoellidae family about 58 million years ago. The more likely mode of transmission of B. ceti seems to be through sexual intercourse, maternal feeding, aborted fetuses, placental tissues, vertical transmission from mother to the fetus or through fish or helminth reservoirs. The B. ceti dolphin and porpoise types seem to display variable virulence in land animal models and low infectivity for humans. However, brucellosis in some dolphins and porpoises has been demonstrated to be a severe chronic disease, displaying significant clinical and pathological signs related to abortions, male infertility, neurobrucellosis, cardiopathies, bone and skin lesions, strandings, and death.
111 citations
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TL;DR: In this paper, the authors present a general algebraic-combinatorial proof of the cancellation-free formula for antipodes, in its original diagrammatic form, for Hopf algebras.
Abstract: This manuscript stands at the interface between combinatorial Hopf algebra theory and renormalization theory. Its plan is as follows: Section 1 is the introduction, and contains as well an elementary invitation to the subject. The rest of part I, comprising Sections 2-6, is devoted to the basics of Hopf algebra theory and examples, in ascending level of complexity. Part II turns around the all-important Faa di Bruno Hopf algebra. Section 7 contains a first, direct approach to it. Section 8 gives applications of the Faa di Bruno algebra to quantum field theory and Lagrange reversion. Section 9 rederives the related Connes-Moscovici algebras. In Part III we turn to the Connes-Kreimer Hopf algebras of Feynman graphs and, more generally, to incidence bialgebras. In Section10 we describe the first. Then in Section11 we give a simple derivation of (the properly combinatorial part of) Zimmermann's cancellation-free method, in its original diagrammatic form. In Section 12 general incidence algebras are introduced, and the Faa di Bruno bialgebras are described as incidence bialgebras. In Section 13, deeper lore on Rota's incidence algebras allows us to reinterpret Connes-Kreimer algebras in terms of distributive lattices. Next, the general algebraic-combinatorial proof of the cancellation-free formula for antipodes is ascertained; this is the heart of the paper. The structure results for commutative Hopf algebras are found in Sections 14 and 15. An outlook section very briefly reviews the coalgebraic aspects of quantization and the Rota-Baxter map in renormalization.
111 citations
Authors
Showing all 9922 results
Name | H-index | Papers | Citations |
---|---|---|---|
Alberto Ascherio | 136 | 462 | 69578 |
Gervasio Gomez | 133 | 1844 | 99695 |
Myron M. Levine | 123 | 789 | 60865 |
Hong-Cai Zhou | 114 | 489 | 66320 |
Edward O. Wilson | 101 | 406 | 89994 |
Mary Claire King | 100 | 336 | 47454 |
Olga Martín-Belloso | 86 | 384 | 23428 |
José María Gutiérrez | 84 | 607 | 26779 |
Cesare Montecucco | 84 | 382 | 27738 |
Rodolphe Clérac | 78 | 506 | 22604 |
Kim R. Dunbar | 74 | 470 | 20262 |
Paul J. Hanson | 70 | 251 | 19504 |
Hannia Campos | 69 | 210 | 15164 |
Jean-Pierre Gorvel | 67 | 231 | 15005 |
F. Albert Cotton | 66 | 1023 | 27647 |