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Institution

University of California, Davis

EducationDavis, 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
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Journal ArticleDOI
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

Journal ArticleDOI
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

Book
01 Jan 2004
TL;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

Journal ArticleDOI
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

Journal ArticleDOI
28 Oct 2004-Nature
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

NameH-indexPapersCitations
Eric S. Lander301826525976
Ronald C. Kessler2741332328983
George M. Whitesides2401739269833
Ronald M. Evans199708166722
Virginia M.-Y. Lee194993148820
Scott M. Grundy187841231821
Julie E. Buring186950132967
Patrick O. Brown183755200985
Anil K. Jain1831016192151
John C. Morris1831441168413
Douglas R. Green182661145944
John R. Yates1771036129029
Barry Halliwell173662159518
Roderick T. Bronson169679107702
Hongfang Liu1662356156290
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023262
20221,122
20218,398
20208,661
20198,165
20187,556