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Institution

University of Iowa

EducationIowa 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.


Papers
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Journal ArticleDOI
TL;DR: The regulation of glucose transport as the rate-limiting step in glucose utilization and storage is focused on.
Abstract: Insulin is the most potent anabolic hormone known and is essential for appropriate tissue development, growth, and maintenance of whole-body glucose homeostasis. This hormone is secreted by the β cells of the pancreatic islets of Langerhans in response to increased circulating levels of glucose and amino acids after a meal. Insulin regulates glucose homeostasis at many sites, reducing hepatic glucose output (via decreased gluconeogenesis and glycogenolysis) and increasing the rate of glucose uptake, primarily into striated muscle and adipose tissue. In muscle and fat cells, the clearance of circulating glucose depends on the insulin-stimulated translocation of the glucose transporter GLUT4 isoform to the cell surface (see Shulman, this Perspective series, ref. 1). Insulin also profoundly affects lipid metabolism, increasing lipid synthesis in liver and fat cells, and attenuating fatty acid release from triglycerides in fat and muscle. Insulin resistance occurs when normal circulating concentrations of the hormone are insufficient to regulate these processes appropriately. Thus, by definition, insulin resistance is a defect in signal transduction. The signaling mechanisms involved in the various biologic responses to insulin remain somewhat elusive, but recent progress has shed light on a few pathways that are critical for its regulation of glucose and lipid metabolism. Although insulin affects such diverse processes as cellular growth, differentiation, apoptosis, and lipid, protein, and glucose synthesis and breakdown, we focus here on the regulation of glucose transport as the rate-limiting step in glucose utilization and storage.

928 citations

Journal ArticleDOI
TL;DR: The research evidence is presented that GMA predicts both occupational level attained and performance within one's chosen occupation and does so better than any other ability, trait, or disposition and better than job experience.
Abstract: The psychological construct of general mental ability (GMA), introduced by C. Spearman (1904) nearly 100 years ago, has enjoyed a resurgence of interest and attention in recent decades. This article presents the research evidence that GMA predicts both occupational level attained and performance within one's chosen occupation and does so better than any other ability, trait, or disposition and better than job experience. The sizes of these relationships with GMA are also larger than most found in psychological research. Evidence is presented that weighted combinations of specific aptitudes tailored to individual jobs do not predict job performance better than GMA alone, disconfirming specific aptitude theory. A theory of job performance is described that explicates the central role of GMA in the world of work. These findings support Spearman's proposition that GMA is of critical importance in human affairs.

928 citations

Journal ArticleDOI
TL;DR: The utility of needle EMG and nerve conduction studies was affirmed and electrophysiological evidence for chronic neurogenic change should be taken as equivalent to clinical information in the recognition of involvement of individual muscles in a limb.

928 citations

Journal ArticleDOI
TL;DR: The weighted sum of gray gases model as discussed by the authors is a generalization of the weighted sum-of-gray-gas model, which assumes that total emissivity and absorptivity may be represented by the sum of the gray gas emissivities weighted with a temperature dependent factor.
Abstract: The weighted sum of gray gases model postulates that total emissivity and absorptivity may be represented by the sum of a gray gas emissivity weighted with a temperature dependent factor. The gray gas emissivity is expressed in terms of a temperature-independent absorption coefficient, absorbing gas partial pressure, and path length. The weighting factors are given by polynomials in gas temperature with associated polynomial coefficients. For absorptivity, a second polynomial for the irradiation temperature is introduced. A regression scheme is employed to fit the model to total emissivity and absorptivity values obtained from the exponential wide-band model. Absorption and polynomial coefficients are reported for carbon dioxide, water vapor, and mixtures of these gases. The model with these coefficients more accurately represents the total properties over a wider range of temperatures and partial pressure-path length products than previously available coefficients.

928 citations

Journal ArticleDOI
08 May 2003-Nature
TL;DR: It is shown that disruption of the muscle membrane repair machinery is responsible for dysferlin-deficient muscle degeneration, and the importance of this basic cellular mechanism of membrane resealing in human disease is highlighted.
Abstract: Muscular dystrophy includes a diverse group of inherited muscle diseases characterized by wasting and weakness of skeletal muscle. Mutations in dysferlin are linked to two clinically distinct muscle diseases, limb-girdle muscular dystrophy type 2B and Miyoshi myopathy, but the mechanism that leads to muscle degeneration is unknown. Dysferlin is a homologue of the Caenorhabditis elegans fer-1 gene, which mediates vesicle fusion to the plasma membrane in spermatids. Here we show that dysferlin-null mice maintain a functional dystrophin-glycoprotein complex but nevertheless develop a progressive muscular dystrophy. In normal muscle, membrane patches enriched in dysferlin can be detected in response to sarcolemma injuries. In contrast, there are sub-sarcolemmal accumulations of vesicles in dysferlin-null muscle. Membrane repair assays with a two-photon laser-scanning microscope demonstrated that wild-type muscle fibres efficiently reseal their sarcolemma in the presence of Ca2+. Interestingly, dysferlin-deficient muscle fibres are defective in Ca2+-dependent sarcolemma resealing. Membrane repair is therefore an active process in skeletal muscle fibres, and dysferlin has an essential role in this process. Our findings show that disruption of the muscle membrane repair machinery is responsible for dysferlin-deficient muscle degeneration, and highlight the importance of this basic cellular mechanism of membrane resealing in human disease.

927 citations


Authors

Showing all 49661 results

NameH-indexPapersCitations
Stephen V. Faraone1881427140298
Jie Zhang1784857221720
D. M. Strom1763167194314
Bradley T. Hyman169765136098
John H. Seinfeld165921114911
David Jonathan Hofman1591407140442
Stephen J. O'Brien153106293025
John T. Cacioppo147477110223
Mark Raymond Adams1471187135038
E. L. Barberio1431605115709
Andrew Ivanov142181297390
Stephen J. Lippard141120189269
Russell Richard Betts140132395678
Barry Blumenfeld1401909105694
Marcus Hohlmann140135694739
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023154
2022727
20214,128
20203,902
20193,763
20183,659