Institution
University of Iowa
Education•Iowa City, Iowa, United States•
About: University of Iowa is a education organization based out in Iowa City, Iowa, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 49229 authors who have published 109171 publications receiving 5021465 citations. The organization is also known as: UI & The University of Iowa.
Topics: Population, Poison control, Large Hadron Collider, Health care, Gene
Papers published on a yearly basis
Papers
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TL;DR: It is shown that common CF pathogens were killed when added to the apical surface of normal airway epithelia, showing how the loss of CFTR Cl- channels may lead to lung disease and suggest new approaches to therapy.
953 citations
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TL;DR: The available evidence indicates that normal matrix turnover depends on the ability of chondrocytes to detect alterations in the macromolecular composition and organization of the matrix, including the presence of degraded molecules, and to respond by synthesizing appropriate types and amounts of new molecules.
Abstract: The unique biologic and mechanical properties of articular cartilage depend on the design of the tissue and the interactions between the chondrocytes and the matrix that maintain the tissue. Chondrocytes form the macromolecular framework of the tissue matrix from three classes of molecules: collagens, proteoglycans, and noncollagenous proteins. Type II, IX, and XI collagens form a fibrillar meshwork that gives the tissue as form and tensile stiffness and strength. Type VI collagen forms part of the matrix immediately surrounding the chondrocytes and may help the chondrocytes to attach to the macromolecular framework of the matrix. Large aggregating proteoglycans (aggrecans) give the tissue its stiffness to compression and its resilience and contribute to its durability. Small proteoglycans, including decorin, biglycan, and fibromodulin, bind to other matrix macromolecules and thereby help to stabilize the matrix. They may also influence the function of the chondrocytes and bind growth factors. Anchorin CII, a noncollagenous protein, appears to help to anchor chondrocytes to the matrix. Cartilage oligomeric protein may have value as a marker of turnover and degeneration of cartilage, and other noncollagenous proteins, including tenascin and fibronectin, can influence interactions between the chondrocytes and the matrix. The matrix protects the cells from injury due to normal use of the joint, determines the types and concentrations of molecules that reach the tells and helps to maintain the chondrocyte phenotype. Throughout life, the tissue undergoes continual internal remodeling as the cells replace matrix macromolecules lost through degradation. The available evidence indicates that normal matrix turnover depends on the ability of chondrocytes to detect alterations in the macromolecular composition and organization of the matrix, including the presence of degraded molecules, and to respond by synthesizing appropriate types and amounts of new molecules. In addition, the matrix acts as a signal transducer for the cells. Loading of the tissue due to use of the joint creates mechanical, electrical, and physicochemical signals that help to direct the synthetic and degradative activity of chondrocytes. A prolonged severe decrease in the use of the joint leads to alterations in the composition of the matrix and eventually to loss of tissue structure and mechanical properties, whereas use of the joint stimulates the synthetic activity of chondrocytes and possibly the internal tissue remodeling Aging leads to alterations in the composition of the matrix and the activity of the chondrocytes, including the ability of the cells to respond to a variety of stimuli such as growth factors. These alterations may increase the probability of degeneration of the cartilage.
952 citations
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TL;DR: It is shown that class II HDACs are substrates for a stress-responsive kinase specific for conserved serines that regulate MEF2-HDAC interactions, and act as signal-responsive suppressors of the transcriptional program governing cardiac hypertrophy and heart failure.
952 citations
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TL;DR: The results of this study are consistent with the hypothesis that the visual N1 component reflects the operation of a discrimination process within the focus of attention.
Abstract: Many previous studies have demonstrated that the visual N1 component is larger for attended-location stimuli than for unattended-location stimuli. This difference is observed typically only for tasks involving a discrimination of the attended-location stimuli, suggesting that the N1 wave reflects a discrimination process that is applied to the attended location. The present study tested this hypothesis by examining the N1 component elicited by attended stimuli under conditions that either required or did not require the subject to perform a discrimination. Specifically, the N1 elicited by foveal stimuli during choice-reaction time (RT) tasks was compared with the N1 elicited by identical stimuli during simple-RT tasks. In three experiments, a larger posterior N1 was observed in choice-RT tasks than in simple-RT tasks, even when several potential confounds were eliminated (e.g., arousal and motor preparation). This N1 discrimination effect was observed even when no motor response was required and was present for both color- and form-based discriminations. Moreover, this discrimination effect was equally large for easy and difficult discriminations, arguing against a simple resource-based explanation of the present results. Instead, the results of this study are consistent with the hypothesis that the visual N1 component reflects the operation of a discrimination process within the focus of attention.
948 citations
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San Francisco General Hospital1, University of Michigan2, National Jewish Health3, Cornell University4, University of California, San Francisco5, Tulane University6, Vanderbilt University7, University of Chicago8, University of Alabama at Birmingham9, University of Washington10, Emory University11, Mayo Clinic12, University of California, Los Angeles13, University of Iowa14, University College Dublin15, Osaka University16, University of Pittsburgh17, University of Ulsan18, University of Freiburg19
TL;DR: An international effort to summarize the current state of knowledge regarding acute exacerbations of IPF is presented, and proposed diagnostic criteria include subjective worsening over 30 days or less, new bilateral radiographic opacities, and the absence of infection or another identifiable etiology.
Abstract: The natural history of idiopathic pulmonary fibrosis (IPF) has been characterized as a steady, predictable decline in lung function over time. Recent evidence suggests that some patients may experience a more precipitous course, with periods of relative stability followed by acute deteriorations in respiratory status. Many of these acute deteriorations are of unknown etiology and have been termed acute exacerbations of IPF. This perspective is the result of an international effort to summarize the current state of knowledge regarding acute exacerbations of IPF. Acute exacerbations of IPF are defined as acute, clinically significant deteriorations of unidentifiable cause in patients with underlying IPF. Proposed diagnostic criteria include subjective worsening over 30 days or less, new bilateral radiographic opacities, and the absence of infection or another identifiable etiology. The potential pathobiological roles of infection, disordered cell biology, coagulation, and genetics are discussed, and future research directions are proposed.
947 citations
Authors
Showing all 49661 results
Name | H-index | Papers | Citations |
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Stephen V. Faraone | 188 | 1427 | 140298 |
Jie Zhang | 178 | 4857 | 221720 |
D. M. Strom | 176 | 3167 | 194314 |
Bradley T. Hyman | 169 | 765 | 136098 |
John H. Seinfeld | 165 | 921 | 114911 |
David Jonathan Hofman | 159 | 1407 | 140442 |
Stephen J. O'Brien | 153 | 1062 | 93025 |
John T. Cacioppo | 147 | 477 | 110223 |
Mark Raymond Adams | 147 | 1187 | 135038 |
E. L. Barberio | 143 | 1605 | 115709 |
Andrew Ivanov | 142 | 1812 | 97390 |
Stephen J. Lippard | 141 | 1201 | 89269 |
Russell Richard Betts | 140 | 1323 | 95678 |
Barry Blumenfeld | 140 | 1909 | 105694 |
Marcus Hohlmann | 140 | 1356 | 94739 |