Institution
University of Missouri
Education•Columbia, Missouri, United States•
About: University of Missouri is a education organization based out in Columbia, Missouri, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 41427 authors who have published 83598 publications receiving 2911437 citations. The organization is also known as: Mizzou & Missouri-Columbia.
Topics: Population, Poison control, Gene, Context (language use), Health care
Papers published on a yearly basis
Papers
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TL;DR: A coarse-grained model for gold nanoparticles (AuNPs) is developed to simulate their interactions with model lipid membranes and suggests a way of controlling the AuNP-cell interactions by manipulating surface charge densities of AuNPs to achieve designated goals in their biomedical applications.
Abstract: Nanoparticle penetration into cell membranes is an interesting phenomenon that may have crucial implications on the nanoparticles’ biomedical applications. In this paper, a coarse-grained model for gold nanoparticles (AuNPs) is developed (verified against experimental data available) to simulate their interactions with model lipid membranes. Simulations reveal that AuNPs with different signs and densities of surface charges spontaneously adhere to the bilayer surface or penetrate into the bilayer interior. The potential of mean force calculations show that the energy gains upon adhesion or penetration is significant. In the case of penetration, it is found that defective areas are induced across the entire surface of the upper leaflet of the bilayer and a hydrophilic pore that transports water molecules was formed with its surrounding lipids highly disordered. Penetration and its concomitant membrane disruptions can be a possible mechanism of the two observed phenomena in experiments: AuNPs bypass endocyt...
568 citations
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TL;DR: Conservation for declining avian species may need to be customized according to the nest-predator species primarily responsible for local nest mortality and the nature of the landscape mosaic, which is complex, taxon-specific, and context-dependent.
Abstract: Population declines of many avian species are often attributed to increased rates of nest predation in fragmented landscapes, yet mechanisms underlying these effects have rarely been examined. We reviewed the literature to determine the extent to which hypotheses about nest predators and fragmentation have been invoked and compared this to the number of direct tests of predators with respect to habitat edge, patch size, or landscape type. We also conducted a meta-analysis of tested predator effects to evaluate whether predator responses—numerical, functional, or species richness—to fragmentation depend on spatial scale (edge, patch, or landscape), landscape type, geographic region, or predator taxa. We found 120 papers containing hypoth- eses about nest predators and fragmentation, but only 31 with hypothesis tests. Most tests were of a single predator species or guild, whereas most cited hypotheses generalized across broader taxonomic groups. Re- sults of predator tests were variable, but some general patterns were evident. Predator effects, including in- creased abundance, activity, or species richness in edges, small patches, or certain landscapes, were more prevalent (1) in tests conducted at the landscape scale than at the local scale, (2) in agricultural landscapes than in predominantly forested landscapes, (3) in certain biogeographic regions, and (4) for avian predators than for mammalian predators. Local-scale (edge and patch) effects were most common when the land sur- rounding patches was agricultural and when tests were conducted within agricultural landscapes. The re- sponse of nest predators to fragmentation is complex, taxon-specific, and context-dependent. Conservation ef- forts for declining avian species may therefore need to be customized according to the nest-predator species primarily responsible for local nest mortality and the nature of the landscape mosaic.
568 citations
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National Institutes of Health1, Wellcome Trust Sanger Institute2, Rockefeller University3, University of California, Davis4, European Bioinformatics Institute5, Seoul National University6, Max Planck Society7, Durham University8, University of Massachusetts Amherst9, University of Adelaide10, University of Missouri11, East Carolina University12, University of Queensland13, Queen Mary University of London14, Wellington Management Company15, University of Arizona16, Natural History Museum17, Bangor University18, University of Konstanz19, Northeastern University20, Naturalis21, University of Graz22, Florida Museum of Natural History23, University of California, Santa Cruz24, Pacific Biosciences25, University of Maryland, College Park26, Harbin Institute of Technology27, University of Chicago28, Oregon Health & Science University29, Monash University Malaysia Campus30, University of Milan31, University of Copenhagen32, Pennsylvania State University33, University of Los Andes34, Agency for Science, Technology and Research35, Royal Ontario Museum36, Smithsonian Conservation Biology Institute37, University of East Anglia38, Pompeu Fabra University39, University College Dublin40, University of Illinois at Urbana–Champaign41, La Trobe University42, University of California, San Diego43, UPRRP College of Natural Sciences44, Dresden University of Technology45
TL;DR: The Vertebrate Genomes Project is embarked on, an effort to generate high-quality, complete reference genomes for all ~70,000 extant vertebrate species and help enable a new era of discovery across the life sciences.
Abstract: High-quality and complete reference genome assemblies are fundamental for the application of genomics to biology, disease, and biodiversity conservation. However, such assemblies are only available for a few non-microbial species. To address this issue, the international Genome 10K (G10K) consortium has worked over a five-year period to evaluate and develop cost-effective methods for assembling the most accurate and complete reference genomes to date. Here we summarize these developments, introduce a set of quality standards, and present lessons learned from sequencing and assembling 16 species representing major vertebrate lineages (mammals, birds, reptiles, amphibians, teleost fishes and cartilaginous fishes). We confirm that long-read sequencing technologies are essential for maximizing genome quality and that unresolved complex repeats and haplotype heterozygosity are major sources of error in assemblies. Our new assemblies identify and correct substantial errors in some of the best historical reference genomes. Adopting these lessons, we have embarked on the Vertebrate Genomes Project (VGP), an effort to generate high-quality, complete reference genomes for all ~70,000 extant vertebrate species and help enable a new era of discovery across the life sciences.
567 citations
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TL;DR: Cell wall damage followed by cytoplasmic membrane damage leading to a direct intracellular attack has been proposed as the sequence of events when microorganisms undergo TiO 2 photocatalytic attack.
Abstract: When exposed to near-UV light, titanium dioxide (TiO 2 ) exhibits a strong bactericidal activity. However, the killing mechanism(s) underlying the TiO 2 photocatalytic reaction is not yet well understood. The aim of the present study is to investigate the cellular damage sites and their contribution to cell death. A sensitive approach using o -nitrophenol β- d– galactopyranosideside (ONPG) as the probe and Escherichia coli as model cells has been developed. This approach is used to illustrate damages to both the cell envelope and intracellular components caused by TiO 2 photocatalytic reaction. Treatment of E. coli with TiO 2 and near-UV light resulted in an immediate increase in permeability to small molecules such as ONPG, and the leakage of large molecules such as β- d– galactosidase after 20 min. Kinetic data showed that cell wall damage took place in less than 20 min, followed by a progressive damage of cytoplasmic membrane and intracellular components. The results from the ONPG assay correlated well with the loss of cell viability. Cell wall damage followed by cytoplasmic membrane damage leading to a direct intracellular attack has therefore been proposed as the sequence of events when microorganisms undergo TiO 2 photocatalytic attack. It has been found that smaller TiO 2 particles cause quicker intracellular damage. Evidence has been obtained that indicated that the TiO 2 photocatalytic reaction results in continued bactericidal activity after the UV illumination terminates.
567 citations
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TL;DR: In the mid-Proterozoic oceans between 1.8 and 1.0 billion years ago, oxygenation of the oceans may have lagged that of the atmosphere by over a billion years as discussed by the authors.
Abstract: How much dissolved oxygen was present in the mid-Proterozoic oceans between 1.8 and 1.0 billion years ago is debated vigorously. One model argues for oxygenation of the oceans soon after the initial rise of atmospheric oxygen 2.3 billion years ago. Recent evidence for H 2 S in some mid-Proterozoic marine basins suggests, however, that the deep ocean remained anoxic until much later. New molybdenum isotope data from modern and ancient sediments indicate expanded anoxia during the mid-Proterozoic compared to the present-day ocean. Consequently, oxygenation of the deep oceans may have lagged that of the atmosphere by over a billion years.
566 citations
Authors
Showing all 41750 results
Name | H-index | Papers | Citations |
---|---|---|---|
Walter C. Willett | 334 | 2399 | 413322 |
Meir J. Stampfer | 277 | 1414 | 283776 |
Russel J. Reiter | 169 | 1646 | 121010 |
Chad A. Mirkin | 164 | 1078 | 134254 |
Robert Stone | 160 | 1756 | 167901 |
Howard I. Scher | 151 | 944 | 101737 |
Rajesh Kumar | 149 | 4439 | 140830 |
Joseph T. Hupp | 141 | 731 | 82647 |
Lihong V. Wang | 136 | 1118 | 72482 |
Stephen R. Carpenter | 131 | 464 | 109624 |
Jan A. Staessen | 130 | 1137 | 90057 |
Robert S. Brown | 130 | 1243 | 65822 |
Mauro Giavalisco | 128 | 412 | 69967 |
Kenneth J. Pienta | 127 | 671 | 64531 |
Matthew W. Gillman | 126 | 529 | 55835 |