Institution
University of Rhode Island
Education•Kingston, Rhode Island, United States•
About: University of Rhode Island is a education organization based out in Kingston, Rhode Island, United States. It is known for research contribution in the topics: Population & Bay. The organization has 11464 authors who have published 22770 publications receiving 841066 citations. The organization is also known as: URI & Rhode Island College of Agriculture and the Mechanic Arts.
Topics: Population, Bay, Poison control, Transtheoretical model, Behavior change
Papers published on a yearly basis
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TL;DR: The WET Labs ac-9 is a recently developed in situ absorption and attenuation meter with a precision better than ± 0.001 m−1 in the raw signal, which is sufficient to make these measurements in pristine samples as mentioned in this paper.
Abstract: Measuring coastal and oceanic absorption coefficients of dissolved and particulate matter in the visible domain usually requires a methodology for amplifying the natural signal because conventional spectrophotometers lack the necessary sensitivity. The WET Labs ac-9 is a recently developed in situ absorption and attenuation meter with a precision better than ±0.001 m−1 in the raw signal, which is sufficient to make these measurements in pristine samples. Whereas the superior sensitivity of the ac-9 has been well documented, the accuracy of in situ measurements for bio-optical applications has not been rigorously evaluated. Obtaining accurate results with an ac-9 requires careful attention to calibration procedures because baselines drift as a result of the changing optical properties of several ac-9 components. To correct in situ measurements for instrument drift, a pressurized flow procedure was developed for calibrating an ac-9 with optically clean water. In situ, micro- (cm) to fine- (m) scale...
161 citations
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TL;DR: In this article, a parallel tempering Monte Carlo algorithm was proposed for the 38-atom Lennard-Jones cluster with microcanonical and molecular dynamics ensembles to overcome quasi-ergodicity and to extract both equilibrium and dynamical properties.
Abstract: We study the 38-atom Lennard-Jones cluster with parallel tempering Monte Carlo methods in the microcanonical and molecular dynamics ensembles. A new Monte Carlo algorithm is presented that samples rigorously the molecular dynamics ensemble for a system at constant total energy, linear and angular momenta. By combining the parallel tempering technique with molecular dynamics methods, we develop a hybrid method to overcome quasi-ergodicity and to extract both equilibrium and dynamical properties from Monte Carlo and molecular dynamics simulations. Several thermodynamic, structural and dynamical properties are investigated for LJ$_{38}$, including the caloric curve, the diffusion constant and the largest Lyapunov exponent. The importance of insuring ergodicity in molecular dynamics simulations is illustrated by comparing the results of ergodic simulations with earlier molecular dynamics simulations.
161 citations
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TL;DR: The pathophysiological significance of Fas activation in nonpulmonary/shock-induced ALI and the feasibility of intrapulmonary administration of anti-apoptotic siRNA in vivo are indicated.
Abstract: Apoptosis and inflammation play an important role in the pathogenesis of direct/pulmonary acute lung injury (ALI). However, the role of the Fas receptor-driven apoptotic pathway in indirect/nonpulmonary ALI is virtually unstudied. We hypothesized that if Fas or caspase-8 plays a role in the induction of indirect ALI, their local silencing using small interfering RNA (siRNA) should be protective in hemorrhage-induced septic ALI. Initially, as a proof of principle, green fluorescent protein-siRNA was administered intratracheally into transgenic mice overexpressing green fluorescent protein. Twenty-four hours after siRNA delivery, lung sections revealed a significant decrease in green fluorescence. Intratracheally administered Cy-5-labeled Fas-siRNA localized primarily in pulmonary epithelial cells. Intratracheal instillation of siRNA did not induce lung inflammation via toll-like receptor or protein kinase PKR pathways as assessed by lung tissue interferon-α, tumor necrosis factor-α, and interleukin (IL)-6 levels. Mice subjected to hemorrhagic shock and sepsis received either Fas-, caspase-8-, or control-siRNA intratracheally 4 hours after hemorrhage. Fas- or caspase-8-siRNA significantly reduced lung tissue Fas or caspase-8 mRNA, respectively. Only Fas-siRNA markedly diminished lung tissue tumor necrosis factor-α, IL-6, IL-10, interferon-γ, IL-12, and caspase-3 activity. Fas-siRNA also preserved alveolar architecture and reduced lung neutrophil infiltration and pulmonary epithelial apoptosis. These data indicate the pathophysiological significance of Fas activation in nonpulmonary/shock-induced ALI and the feasibility of intrapulmonary administration of anti-apoptotic siRNA in vivo.
161 citations
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TL;DR: Drug-polymer hydrogen bonding in indoprofen-PVP dispersions favors solid solubility and phase separation rate of drug from the solid dispersions depends on the initial drug content and the nature of drug- polymer interactions.
Abstract: Purpose.
To determine the factors influencing “solid solubility” and phase separation kinetics of drugs from amorphous solid dispersions.
161 citations
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Griffith University1, Texas Biomedical Research Institute2, European Bioinformatics Institute3, Medical College of Wisconsin4, Chiba Institute of Science5, Kumamoto University6, Jichi Medical University7, University of Alberta8, Tokai University9, Eli Lilly and Company10, University of North Carolina at Chapel Hill11, Chiba University12, Iwate University13, University of Rhode Island14, Kanazawa University15, University of Graz16
TL;DR: A new nomenclature system is described that identifies homolog gene families and allocates a unique name for each gene in human, mouse, and rat carboxylesterase genes and serves as a model for naming CES genes from other mammalian species.
Abstract: Mammalian carboxylesterase (CES or Ces) genes encode enzymes that participate in xenobiotic, drug, and lipid metabolism in the body and are members of at least five gene families. Tandem duplications have added more genes for some families, particularly for mouse and rat genomes, which has caused confusion in naming rodent Ces genes. This article describes a new nomenclature system for human, mouse, and rat carboxylesterase genes that identifies homolog gene families and allocates a unique name for each gene. The guidelines of human, mouse, and rat gene nomenclature committees were followed and “CES” (human) and “Ces” (mouse and rat) root symbols were used followed by the family number (e.g., human CES1). Where multiple genes were identified for a family or where a clash occurred with an existing gene name, a letter was added (e.g., human CES4A; mouse and rat Ces1a) that reflected gene relatedness among rodent species (e.g., mouse and rat Ces1a). Pseudogenes were named by adding “P” and a number to the human gene name (e.g., human CES1P1) or by using a new letter followed by ps for mouse and rat Ces pseudogenes (e.g., Ces2d-ps). Gene transcript isoforms were named by adding the GenBank accession ID to the gene symbol (e.g., human CES1_AB119995 or mouse Ces1e_BC019208). This nomenclature improves our understanding of human, mouse, and rat CES/Ces gene families and facilitates research into the structure, function, and evolution of these gene families. It also serves as a model for naming CES genes from other mammalian species.
161 citations
Authors
Showing all 11569 results
Name | H-index | Papers | Citations |
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James M. Tiedje | 150 | 688 | 102287 |
Roberto Kolter | 120 | 315 | 52942 |
Robert S. Stern | 120 | 761 | 62834 |
Michael S. Feld | 119 | 552 | 51968 |
William C. Sessa | 117 | 383 | 52208 |
Kenneth H. Mayer | 115 | 1351 | 64698 |
Staffan Kjelleberg | 114 | 425 | 44414 |
Kevin C. Jones | 114 | 744 | 50207 |
David R. Nelson | 110 | 615 | 66627 |
Peter K. Smith | 107 | 855 | 49174 |
Peter M. Groffman | 106 | 457 | 40165 |
Ming Li | 103 | 1669 | 62672 |
Victor Nizet | 102 | 564 | 44193 |
Anil Kumar | 99 | 2124 | 64825 |
James O. Prochaska | 97 | 320 | 73265 |