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Institution

University of Colorado Denver

EducationDenver, Colorado, United States
About: University of Colorado Denver is a education organization based out in Denver, Colorado, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 27444 authors who have published 57213 publications receiving 2539937 citations. The organization is also known as: CU Denver & UCD.


Papers
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Journal ArticleDOI
TL;DR: The National Library of Medicine's Visible Human Male data set consists of digital magnetic resonance (MR), computed tomography (CT), and anatomic images derived from a single male cadaver.

623 citations

Journal ArticleDOI
TL;DR: Induction of labor at 39 weeks in low‐risk nulliparous women did not result in a significantly lower frequency of a composite adverse perinatal outcome, but it did result in less frequency of cesarean delivery.
Abstract: Background The perinatal and maternal consequences of induction of labor at 39 weeks among low-risk nulliparous women are uncertain. Methods In this multicenter trial, we randomly assigned...

623 citations

Journal ArticleDOI
TL;DR: In patients with NAFLD, daily fructose ingestion is associated with reduced hepatic steatosis but increased fibrosis, a readily modifiable environmental risk factor that may ameliorate disease progression in patients withNAFLD.

622 citations

Journal ArticleDOI
TL;DR: An updated diagnostic algorithm for EoE was developed, with removal of the PPI trial requirement, and the evidence suggests that PPIs are better classified as a treatment for esophageal eosinophilia that may be due to EOE than as a diagnostic criterion.

621 citations

Journal ArticleDOI
01 Jul 2002-Diabetes
TL;DR: In this article, the longitudinal changes in insulin sensitivity during pregnancy were correlated with changes in placental hormones, cortisol, leptin, and tumor necrosis factor (TNF)-alpha.
Abstract: Historically, insulin resistance during pregnancy has been ascribed to increased production of placental hormones and cortisol. The purpose of this study was to test this hypothesis by correlating the longitudinal changes in insulin sensitivity during pregnancy with changes in placental hormones, cortisol, leptin, and tumor necrosis factor (TNF)-alpha. Insulin resistance was assessed in 15 women (5 with gestational diabetes mellitus [GDM] and 10 with normal glucose tolerance) using the euglycemic-hyperinsulinemic clamp procedure, before pregnancy (pregravid) and during early (12-14 weeks) and late (34-36 weeks) gestation. Body composition, plasma TNF-alpha, leptin, cortisol, and reproductive hormones (human chorionic gonadotropin, estradiol, progesterone, human placental lactogen, and prolactin) were measured in conjunction with the clamps. Placental TNF-alpha was measured in vitro using dually perfused human placental cotyledon from five additional subjects. Compared with pregravid, insulin resistance was evident during late pregnancy in all women (12.4 +/- 1.2 vs. 8.1 +/- 0.8 10(-2) mg. kg(-1) fat-free mass. min(-1). microU(-1). ml(-1)). TNF-alpha, leptin, cortisol, all reproductive hormones, and fat mass were increased in late pregnancy (P < 0.001). In vitro, most of the placental TNF-alpha (94%) was released into the maternal circulation; 6% was released to the fetal side. During late pregnancy, TNF-alpha was inversely correlated with insulin sensitivity (r = -0.69, P < 0.006). Furthermore, among all of the hormonal changes measured in this study, the change in TNF-alpha from pregravid to late pregnancy was the only significant predictor of the change in insulin sensitivity (r = -0.60, P < 0.02). The placental reproductive hormones and cortisol did not correlate with insulin sensitivity in late pregnancy. Multivariate stepwise regression analysis revealed that TNF-alpha was the most significant independent predictor of insulin sensitivity (r = -0.67, P < 0.0001), even after adjustment for fat mass by covariance (r = 0.46, P < 0.01). These observations challenge the view that the classical reproductive hormones are the primary mediators of change in insulin sensitivity during gestation and provide the basis for including TNF-alpha in a new paradigm to explain insulin resistance in pregnancy.

621 citations


Authors

Showing all 27683 results

NameH-indexPapersCitations
Matthew Meyerson194553243726
Charles A. Dinarello1901058139668
Gad Getz189520247560
Gordon B. Mills1871273186451
Jasvinder A. Singh1762382223370
David Haussler172488224960
Donald G. Truhlar1651518157965
Charles M. Perou156573202951
David Cella1561258106402
Bruce D. Walker15577986020
Marco A. Marra153620184684
Thomas E. Starzl150162591704
Marc Humbert1491184100577
Rajesh Kumar1494439140830
Martin J. Blaser147820104104
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20241
202383
2022358
20213,830
20203,913
20193,632