30 research outputs found

    Using citizen science data for predicting the timing of ecological phenomena across regions

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    The scarcity of long-term observational data has limited the use of statistical or machine-learning techniques for predicting intraannual ecological variation. However, time-stamped citizen-science observation records, supported by media data such as photographs, are increasingly available. In the present article, we present a novel framework based on the concept of relative phenological niche, using machine-learning algorithms to model observation records as a temporal sample of environmental conditions in which the represented ecological phenomenon occurs. Our approach accurately predicts the temporal dynamics of ecological events across large geographical scales and is robust to temporal bias in recording effort. These results highlight the vast potential of citizen-science observation data to predict ecological phenomena across space, including in near real time. The framework is also easily applicable for ecologists and practitioners already using machine-learning and statistics-based predictive approaches

    Hepcidin is regulated by promoter-associated histone acetylation and HDAC3.

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    Hepcidin regulates systemic iron homeostasis. Suppression of hepcidin expression occurs physiologically in iron deficiency and increased erythropoiesis but is pathologic in thalassemia and hemochromatosis. Here we show that epigenetic events govern hepcidin expression. Erythropoiesis and iron deficiency suppress hepcidin via erythroferrone-dependent and -independent mechanisms, respectively, in vivo, but both involve reversible loss of H3K9ac and H3K4me3 at the hepcidin locus. In vitro, pan-histone deacetylase inhibition elevates hepcidin expression, and in vivo maintains H3K9ac at hepcidin-associated chromatin and abrogates hepcidin suppression by erythropoietin, iron deficiency, thalassemia, and hemochromatosis. Histone deacetylase 3 and its cofactor NCOR1 regulate hepcidin; histone deacetylase 3 binds chromatin at the hepcidin locus, and histone deacetylase 3 knockdown counteracts hepcidin suppression induced either by erythroferrone or by inhibiting bone morphogenetic protein signaling. In iron deficient mice, the histone deacetylase 3 inhibitor RGFP966 increases hepcidin, and RNA sequencing confirms hepcidin is one of the genes most differentially regulated by this drug in vivo. We conclude that suppression of hepcidin expression involves epigenetic regulation by histone deacetylase 3.Hepcidin controls systemic iron levels by inhibiting intestinal iron absorption and iron recycling. Here, Pasricha et al. demonstrate that the hepcidin-chromatin locus displays HDAC3-mediated reversible epigenetic modifications during both erythropoiesis and iron deficiency

    Hepcidin is regulated by promoter-associated histone acetylation and HDAC3

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    Hepcidin regulates systemic iron homeostasis. Suppression of hepcidin expression occurs physiologically in iron deficiency and increased erythropoiesis but is pathologic in thalassemia and hemochromatosis. Here we show that epigenetic events govern hepcidin expression. Erythropoiesis and iron deficiency suppress hepcidin via erythroferrone-dependent and -independent mechanisms, respectively, in vivo, but both involve reversible loss of H3K9ac and H3K4me3 at the hepcidin locus. In vitro, pan-histone deacetylase inhibition elevates hepcidin expression, and in vivo maintains H3K9ac at hepcidin-associated chromatin and abrogates hepcidin suppression by erythropoietin, iron deficiency, thalassemia, and hemochromatosis. Histone deacetylase 3 and its cofactor NCOR1 regulate hepcidin; histone deacetylase 3 binds chromatin at the hepcidin locus, and histone deacetylase 3 knockdown counteracts hepcidin suppression induced either by erythroferrone or by inhibiting bone morphogenetic protein signaling. In iron deficient mice, the histone deacetylase 3 inhibitor RGFP966 increases hepcidin, and RNA sequencing confirms hepcidin is one of the genes most differentially regulated by this drug in vivo. We conclude that suppression of hepcidin expression involves epigenetic regulation by histone deacetylase 3.Hepcidin controls systemic iron levels by inhibiting intestinal iron absorption and iron recycling. Here, Pasricha et al. demonstrate that the hepcidin-chromatin locus displays HDAC3-mediated reversible epigenetic modifications during both erythropoiesis and iron deficiency

    Catálogo Taxonômico da Fauna do Brasil: setting the baseline knowledge on the animal diversity in Brazil

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    The limited temporal completeness and taxonomic accuracy of species lists, made available in a traditional manner in scientific publications, has always represented a problem. These lists are invariably limited to a few taxonomic groups and do not represent up-to-date knowledge of all species and classifications. In this context, the Brazilian megadiverse fauna is no exception, and the Catálogo Taxonômico da Fauna do Brasil (CTFB) (http://fauna.jbrj.gov.br/), made public in 2015, represents a database on biodiversity anchored on a list of valid and expertly recognized scientific names of animals in Brazil. The CTFB is updated in near real time by a team of more than 800 specialists. By January 1, 2024, the CTFB compiled 133,691 nominal species, with 125,138 that were considered valid. Most of the valid species were arthropods (82.3%, with more than 102,000 species) and chordates (7.69%, with over 11,000 species). These taxa were followed by a cluster composed of Mollusca (3,567 species), Platyhelminthes (2,292 species), Annelida (1,833 species), and Nematoda (1,447 species). All remaining groups had less than 1,000 species reported in Brazil, with Cnidaria (831 species), Porifera (628 species), Rotifera (606 species), and Bryozoa (520 species) representing those with more than 500 species. Analysis of the CTFB database can facilitate and direct efforts towards the discovery of new species in Brazil, but it is also fundamental in providing the best available list of valid nominal species to users, including those in science, health, conservation efforts, and any initiative involving animals. The importance of the CTFB is evidenced by the elevated number of citations in the scientific literature in diverse areas of biology, law, anthropology, education, forensic science, and veterinary science, among others

    Consumo e dinâmica ruminal da fibra em detergente neutro em bovinos em pastejo no período das águas recebendo suplementação com nitrogênio não-proteico e/ou proteína verdadeira Intake and rumen dynamics of neutral detergent fiber in grazing cattle supplemented with non-protein nitrogen and, or true protein during the rainy season

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    Objetivou-se avaliar o efeito de diferentes relações entre proteína verdadeira e nitrogênio não-proteico sobre o consumo e a dinâmica de trânsito e degradação ruminal da fibra em detergente neutro (FDN) da forragem em bovinos em pastejo durante o período das águas. Foram utilizados cinco novilhos mestiços Holandês × Zebu, castrados, com peso corporal inicial de 335±35 kg fistulados no rúmen e no abomaso. Os tratamentos foram: controle (somente pasto); e suplementos com ureia; com 2/3 de compostos nitrogenados oriundos da ureia e 1/3 de compostos nitrogenados oriundos da albumina; com 1/3 de compostos nitrogenados oriundos da ureia e 2/3 de compostos nitrogenados oriundos da albumina; e com albumina. Foram fornecidos 200 g/dia de proteína bruta (PB) a partir dos suplementos. O experimento foi conduzido segundo delineamento em quadrado latino 5 × 5, com cinco períodos experimentais de 15 dias. Não foram observados efeitos da suplementação sobre o consumo voluntário, com exceção do consumo de PB, que aumentou com a suplementação. A substituição da ureia por albumina nos suplementos teve efeito linear sobre o consumo de PB. Os consumos dos demais componentes da dieta não foram afetados pela composição dos suplementos. Nenhum efeito foi observado sobre a taxa de passagem ruminal de compostos fibrosos. O fornecimento de suplementos ampliou, em média, a estimativa da taxa comum de latência e degradação da FDN. Contudo, não houve efeito da alteração na composição dos suplementos sobre este parâmetro. A suplementação de bovinos com fontes de compostos nitrogenados degradáveis no rúmen proteicos ou não-proteicos durante o período das águas não afeta o consumo voluntário de pasto.<br>The objective of this study was to evaluate the effect of different true protein:non-protein nitrogen ratios in supplements on intake and ruminal transit and degradation dynamics of neutral detergent fiber (NDF) in grazing cattle during rainy season. Five crossbred Holstein × Zebu steers, averaging 335±35 kg of body weight and fitted with rumen and abomasum canullaes were used. The treatments were: control (only pasture), and supplements based on urea, 2/3 of nitrogenous compounds from urea and 1/3 of nitrogenous compounds from albumin, 1/3 of nitrogenous compounds from urea and 2/3 of nitrogenous compounds from albumin, and albumin. Two hundred grams/d of crude protein (CP) were supplied from supplements. The experiment was carried out according to a 5 × 5 Latin square design, with five 15-day experimental periods. There were no effects of supplementation on voluntary intake, except for CP intake, which was increased by supplementation. The replacement of urea by albumin in the supplements caused linear effect on the CP intake. The intakes of the other diet components were not affected by the supplement composition. There was no effect on ruminal rate of passage of fibrous compounds. Supplementation increased the estimates of common rate of lag and degradation of NDF. However, no effect of supplement composition alteration was observed on this parameter. Supplementation of cattle with rumen degradable (protein or non-protein) nitrogenous compounds for grazing cattle during rainy season does not affect voluntary intake of pasture

    Indirect effects of habitat loss via habitat fragmentation: A cross-taxa analysis of forest-dependent species

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    Recent studies suggest that habitat amount is the main determinant of species richness, whereas habitat fragmentation has weak and mostly positive effects. Here, we challenge these ideas using a multi-taxa database including 2230 estimates of forest-dependent species richness from 1097 sampling sites across the Brazilian Atlantic Forest biodiversity hotspot. We used a structural equation modeling approach, accounting not only for direct effects of habitat loss, but also for its indirect effects (via habitat fragmentation), on the richness of forest-dependent species. We reveal that in addition to the effects of habitat loss, habitat fragmentation has negative impacts on animal species richness at intermediate (30–60%) levels of habitat amount, and on richness of plants at high (>60%) levels of habitat amount, both of which are mediated by edge effects. Based on these results, we argue that dismissing habitat fragmentation as a powerful force driving species extinction in tropical forest landscapes is premature and unsafe

    Many Labs 5: Testing Pre-Data-Collection Peer Review as an Intervention to Increase Replicability

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    Replication studies in psychological science sometimes fail to reproduce prior findings. If these studies use methods that are unfaithful to the original study or ineffective in eliciting the phenomenon of interest, then a failure to replicate may be a failure of the protocol rather than a challenge to the original finding. Formal pre-data-collection peer review by experts may address shortcomings and increase replicability rates. We selected 10 replication studies from the Reproducibility Project: Psychology (RP:P; Open Science Collaboration, 2015) for which the original authors had expressed concerns about the replication designs before data collection; only one of these studies had yielded a statistically significant effect (p &lt; .05). Commenters suggested that lack of adherence to expert review and low-powered tests were the reasons that most of these RP:P studies failed to replicate the original effects. We revised the replication protocols and received formal peer review prior to conducting new replication studies. We administered the RP:P and revised protocols in multiple laboratories (median number of laboratories per original study = 6.5, range = 3–9; median total sample = 1,279.5, range = 276–3,512) for high-powered tests of each original finding with both protocols. Overall, following the preregistered analysis plan, we found that the revised protocols produced effect sizes similar to those of the RP:P protocols (Δr = .002 or .014, depending on analytic approach). The median effect size for the revised protocols (r = .05) was similar to that of the RP:P protocols (r = .04) and the original RP:P replications (r = .11), and smaller than that of the original studies (r = .37). Analysis of the cumulative evidence across the original studies and the corresponding three replication attempts provided very precise estimates of the 10 tested effects and indicated that their effect sizes (median r = .07, range = .00–.15) were 78% smaller, on average, than the original effect sizes (median r = .37, range = .19–.50)
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