Institution
University of California, Davis
Education•Davis, California, United States•
About: University of California, Davis is a education organization based out in Davis, California, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 78770 authors who have published 180033 publications receiving 8064158 citations. The organization is also known as: UC Davis & UCD.
Topics: Population, Poison control, Gene, Galaxy, Genome
Papers published on a yearly basis
Papers
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TL;DR: Consumption of a high-fat diet induces changes in the gut microbiota, but it is the development of inflammation that is associated with the appearance of hyperphagia and an obese phenotype.
Abstract: Consumption of diets high in fat and calories leads to hyperphagia and obesity, which is associated with chronic "low-grade" systemic inflammation. Ingestion of a high-fat diet alters the gut microbiota, pointing to a possible role in the development of obesity. The present study used Sprague-Dawley rats that, when fed a high-fat diet, exhibit either an obesity-prone (DIO-P) or obesity-resistant (DIO-R) phenotype, to determine whether changes in gut epithelial function and microbiota are diet or obese associated. Food intake and body weight were monitored daily in rats maintained on either low- or high-fat diets. After 8 or 12 wk, tissue was removed to determine adiposity and gut epithelial function and to analyze the gut microbiota using PCR. DIO-P but not DIO-R rats exhibit an increase in toll-like receptor (TLR4) activation associated with ileal inflammation and a decrease in intestinal alkaline phosphatase, a luminal enzyme that detoxifies lipopolysaccharide (LPS). Intestinal permeability and plasma LPS were increased together with phosphorylation of myosin light chain and localization of occludin in the cytoplasm of epithelial cells. Measurement of bacterial 16S rRNA showed a decrease in total bacterial density and an increase in the relative proportion of Bacteroidales and Clostridiales orders in high-fat-fed rats regardless of phenotype; an increase in Enterobacteriales was seen in the microbiota of DIO-P rats only. Consumption of a high-fat diet induces changes in the gut microbiota, but it is the development of inflammation that is associated with the appearance of hyperphagia and an obese phenotype.
805 citations
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TL;DR: An infinite-site neutral allele model with crossing-over possible at any of an infinite number of sites is studied and the effect of intragenic recombination on the homozygosity test of Watterson and on the number of unique alleles in a sample is determined.
805 citations
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01 Jan 2004TL;DR: A minimal theory of social transfers and a guide to the tests for accounting for social spending, jobs and growth in the OECD Appendices is given in this paper, along with an explanation of the rise of mass public schooling.
Abstract: Part V. The Underlying Framework: 13. A minimal theory of social transfers 14. A guide to the tests Part VI. Accounting for Social Spending, Jobs and Growth: 15. Explaining the rise of mass public schooling 16. Explaining the rise of social transfers 17. What drove postwar social spending? 18. Social transfers hardly affected growth 19. Reconciling unemployment and growth in the OECD Appendices.
804 citations
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TL;DR: In this article, a new calibration and validation of the PROSPECT optical model is presented, which separates plant pigment contributions to the visible spectrum using several comprehensive datasets containing hundreds of leaves collected in a wide range of ecosystem types.
803 citations
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TL;DR: It is reported that inactivation of the MYC oncogene is sufficient to induce sustained regression of invasive liver cancers and how oncogenic inactivation may reverse tumorigenesis in the most clinically difficult cancers is shown.
Abstract: Hepatocellular carcinoma is generally refractory to clinical treatment. Here, we report that inactivation of the MYC oncogene is sufficient to induce sustained regression of invasive liver cancers. MYC inactivation resulted en masse in tumour cells differentiating into hepatocytes and biliary cells forming bile duct structures, and this was associated with rapid loss of expression of the tumour marker alpha-fetoprotein, the increase in expression of liver cell markers cytokeratin 8 and carcinoembryonic antigen, and in some cells the liver stem cell marker cytokeratin 19. Using in vivo bioluminescence imaging we found that many of these tumour cells remained dormant as long as MYC remain inactivated; however, MYC reactivation immediately restored their neoplastic features. Using array comparative genomic hybridization we confirmed that these dormant liver cells and the restored tumour retained the identical molecular signature and hence were clonally derived from the tumour cells. Our results show how oncogene inactivation may reverse tumorigenesis in the most clinically difficult cancers. Oncogene inactivation uncovers the pluripotent capacity of tumours to differentiate into normal cellular lineages and tissue structures, while retaining their latent potential to become cancerous, and hence existing in a state of tumour dormancy.
801 citations
Authors
Showing all 79538 results
Name | H-index | Papers | Citations |
---|---|---|---|
Eric S. Lander | 301 | 826 | 525976 |
Ronald C. Kessler | 274 | 1332 | 328983 |
George M. Whitesides | 240 | 1739 | 269833 |
Ronald M. Evans | 199 | 708 | 166722 |
Virginia M.-Y. Lee | 194 | 993 | 148820 |
Scott M. Grundy | 187 | 841 | 231821 |
Julie E. Buring | 186 | 950 | 132967 |
Patrick O. Brown | 183 | 755 | 200985 |
Anil K. Jain | 183 | 1016 | 192151 |
John C. Morris | 183 | 1441 | 168413 |
Douglas R. Green | 182 | 661 | 145944 |
John R. Yates | 177 | 1036 | 129029 |
Barry Halliwell | 173 | 662 | 159518 |
Roderick T. Bronson | 169 | 679 | 107702 |
Hongfang Liu | 166 | 2356 | 156290 |