Institution
Eli Lilly and Company
Company•Indianapolis, Indiana, United States•
About: Eli Lilly and Company is a company organization based out in Indianapolis, Indiana, United States. It is known for research contribution in the topics: Population & Receptor. The organization has 17826 authors who have published 22835 publications receiving 946714 citations. The organization is also known as: Eli Lily.
Topics: Population, Receptor, Placebo, Insulin, Agonist
Papers published on a yearly basis
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10 Jun 1981TL;DR: In this paper, a drug carrier formulation consisting of magnetically-localizable, biodegradable lipid microspheres containing a magneticallyresponsive substance, one or more diodegradably lipids and a nontoxic surfactant is described.
Abstract: A drug carrier formulation consisting of magnetically-localizable, biodegradable lipid microspheres containing a magnetically-responsive substance, one or more diodegradable lipids and one or more nontoxic surfactants is described herein. There is also described a process for preparing such microspheres wherein the magnetically-responsive substance is wetted with surfactant and part of the lipids, then this material is added to the remaining lipids and heated to 90-100°C., water is added, the mixture is sonicated to obtain a microemulsion, which is then cooled and lyophilized to obtain the product.
258 citations
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Bosch1, University of New South Wales2, University of Pittsburgh3, Indiana University – Purdue University Indianapolis4, Tufts University5, University of Maryland, Baltimore6, Geneva College7, University of Montpellier8, Washington University in St. Louis9, French Institute of Health and Medical Research10, Paris Descartes University11, Eli Lilly and Company12
TL;DR: The humanised monoclonal antibody LY2495655 (LY) as discussed by the authors was used to test whether LY increases appendicular lean body mass and improves physical performance in older individuals who have had recent falls and low muscle strength and power.
258 citations
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TL;DR: The treatment of the human pancreatic cancer cell line L3.6pl with the VEGFR-1 ligands VEGF-A and V EGF-B led to morphologic changes characteristic of EMT, including loss of polarity, increased intercellular separation, and the presence of pseudopodia.
Abstract: Our laboratory has shown that vascular endothelial growth factor receptor-1 (VEGFR-1) expression on human pancreatic cancer cell lines mediates cell migration and invasion. Because epithelial to mesenchymal transition (EMT) also plays a role in cell motility by altering the cell phenotype and morphology, we hypothesized that VEGFR-1 activation induces molecular alterations that mediate EMT. Our treatment of the human pancreatic cancer cell line L3.6pl with the VEGFR-1 ligands VEGF-A and VEGF-B led to morphologic changes characteristic of EMT, including loss of polarity, increased intercellular separation, and the presence of pseudopodia. Immunofluorescent staining with antibodies to E-cadherin and beta-catenin showed that VEGFR-1 activation led to translocation of E-cadherin and beta-catenin from their usual cell membrane-bound location to the cytoplasm and nucleus, respectively. Western blotting showed that VEGFR-1 activation led to decreased expression of the epithelial markers E-cadherin and plakoglobin, increased expression of the mesenchymal markers vimentin and N-cadherin, and increased nuclear expression of beta-catenin. Pretreatment of tumor cells with a VEGFR-1 blocking antibody inhibited the VEGFR-1-induced immunohistochemical and molecular changes in E-cadherin. VEGFR-1 activation led to an increase in expression of the EMT-associated transcription factors Snail, Twist, and Slug. The changes mediated by VEGFR-1 in this pancreatic carcinoma cell line are highly consistent with the changes characteristic of EMT. Given our previous finding of VEGFR-1-mediated tumor cell invasion and migration in pancreatic carcinoma cells, we hypothesize that VEGFR-1 plays a role in tumor progression in pancreatic cancer through the induction of EMT.
257 citations
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TL;DR: Although the incidence of serious heart failure was increased with pioglitazone versus placebo in the total PROactive population of patients with type 2 diabetes and macrovascular disease, subsequent mortality or morbidity was not increased in patients withserious heart failure.
Abstract: active) enrolled patients with type 2 diabetes and preexisting cardiovascular disease These patients were at high risk for heart failure, so any therapeutic benefit could potentially be offset by risk of associated heart failure mortality We analyzed the heart failure cases to assess the effects of treatment on morbidity and mortality after reports of serious heart failure RESEARCH DESIGN AND METHODS — PROactive was an outcome study in 5,238 patients randomized to pioglitazone or placebo Patients with New York Heart Association Class II–IV heart failure at screening were excluded A serious adverse event of heart failure was defined as heart failure that required hospitalization or prolonged a hospitalization stay, was fatal or life threatening, or resulted in persistent significant disability or incapacity Heart failure risk was evaluated by multivariate regression RESULTS — More pioglitazone (57%) than placebo patients (41%) had a serious heart failure event during the study (P 0007) However, mortality due to heart failure was similar (25 of 2,605 [096%] for pioglitazone vs 22 of 2,633 [084%] for placebo; P 0639) Among patients with a serious heart failure event, subsequent all-cause mortality was proportionately lower with pioglitazone (40 of 149 [268%] vs 37 of 108 [343%] with placebo; P 01338) Proportionately fewer pioglitazone patients with serious heart failure went on to have an event in the primary (477% with pioglitazone vs 574% with placebo; P 00593) or main secondary end point (349% with pioglitazone vs 472% with placebo; P 0025) CONCLUSIONS — Although the incidence of serious heart failure was increased with pioglitazone versus placebo in the total PROactive population of patients with type 2 diabetes and macrovascular disease, subsequent mortality or morbidity was not increased in patients with serious heart failure Diabetes Care 30:2773–2778, 2007
257 citations
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TL;DR: An examination of the retention and separation of several pyrimidines, purines, and amides on silica and amino columns from three manufacturers revealed that mobile phases should contain a buffer or acid for pH control to achieve similar and reproducible results among columns from different sources.
256 citations
Authors
Showing all 17866 results
Name | H-index | Papers | Citations |
---|---|---|---|
Mark J. Daly | 204 | 763 | 304452 |
Irving L. Weissman | 201 | 1141 | 172504 |
Eric J. Topol | 193 | 1373 | 151025 |
Tony Hunter | 175 | 593 | 124726 |
Xiang Zhang | 154 | 1733 | 117576 |
Jerrold M. Olefsky | 143 | 595 | 77356 |
Stephen F. Badylak | 133 | 530 | 57083 |
George A. Bray | 131 | 896 | 100975 |
Lloyd Paul Aiello | 131 | 506 | 85550 |
Levi A. Garraway | 129 | 366 | 99989 |
Mark Sullivan | 126 | 802 | 63916 |
James A. Russell | 124 | 1024 | 87929 |
Tony L. Yaksh | 123 | 806 | 60898 |
Elisabetta Dejana | 122 | 430 | 48254 |
Hagop S. Akiskal | 118 | 565 | 50869 |