Institution
University of Utah
Education•Salt Lake City, Utah, United States•
About: University of Utah is a education organization based out in Salt Lake City, Utah, United States. It is known for research contribution in the topics: Population & Medicine. The organization has 52894 authors who have published 124076 publications receiving 5265834 citations. The organization is also known as: The U & The University of Utah.
Topics: Population, Medicine, Poison control, Health care, Cancer
Papers published on a yearly basis
Papers
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TL;DR: The potential for 3D printing to revolutionise manufacturing in the same way as the printing press revolutionised conventional printing is discussed; the production process is demonstrated by producing a set of eyeglass frames from 3D blueprints.
Abstract: 3D printing is a method of manufacturing in which materials, such as plastic or metal, are deposited onto one another in layers to produce a three dimensional object, such as a pair of eye glasses or other 3D objects. This process contrasts with traditional ink-based printers which produce a two dimensional object (ink on paper). To date, 3D printing has primarily been used in engineering to create engineering prototypes. However, recent advances in printing materials have now enabled 3D printers to make objects that are comparable with traditionally manufactured items. In contrast with conventional printers, 3D printing has the potential to enable mass customisation of goods on a large scale and has relevance in medicine including ophthalmology. 3D printing has already been proved viable in several medical applications including the manufacture of eyeglasses, custom prosthetic devices and dental implants. In this review, we discuss the potential for 3D printing to revolutionise manufacturing in the same way as the printing press revolutionised conventional printing. The applications and limitations of 3D printing are discussed; the production process is demonstrated by producing a set of eyeglass frames from 3D blueprints.
590 citations
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TL;DR: Frequent VMS lasted more than 7 years during the menopausal transition for more than half of the women and persisted for 4.5 years after the FMP, and they may last longer for African American women.
Abstract: Importance The expected duration of menopausal vasomotor symptoms (VMS) is important to women making decisions about possible treatments. Objectives To determine total duration of frequent VMS (≥6 days in the previous 2 weeks) (hereafter total VMS duration) during the menopausal transition, to quantify how long frequent VMS persist after the final menstrual period (FMP) (hereafter post-FMP persistence), and to identify risk factors for longer total VMS duration and longer post-FMP persistence. Design, Setting, and Participants The Study of Women’s Health Across the Nation (SWAN) is a multiracial/multiethnic observational study of the menopausal transition among 3302 women enrolled at 7 US sites. From February 1996 through April 2013, women completed a median of 13 visits. Analyses included 1449 women with frequent VMS. Main Outcomes and Measures Total VMS duration (in years) (hot flashes or night sweats) and post-FMP persistence (in years) into postmenopause. Results The median total VMS duration was 7.4 years. Among 881 women who experienced an observable FMP, the median post-FMP persistence was 4.5 years. Women who were premenopausal or early perimenopausal when they first reported frequent VMS had the longest total VMS duration (median, >11.8 years) and post-FMP persistence (median, 9.4 years). Women who were postmenopausal at the onset of VMS had the shortest total VMS duration (median, 3.4 years). Compared with women of other racial/ethnic groups, African American women reported the longest total VMS duration (median, 10.1 years). Additional factors related to longer duration of VMS (total VMS duration or post-FMP persistence) were younger age, lower educational level, greater perceived stress and symptom sensitivity, and higher depressive symptoms and anxiety at first report of VMS. Conclusions and Relevance Frequent VMS lasted more than 7 years during the menopausal transition for more than half of the women and persisted for 4.5 years after the FMP. Individual characteristics (eg, being premenopausal and having greater negative affective factors when first experiencing VMS) were related to longer-lasting VMS. Health care professionals should counsel women to expect that frequent VMS could last more than 7 years, and they may last longer for African American women.
590 citations
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Northwestern University1, University of California, San Francisco2, University of Michigan3, City of Hope National Medical Center4, Vanderbilt University5, Seattle Cancer Care Alliance6, Fox Chase Cancer Center7, University of Wisconsin-Madison8, University of Texas Southwestern Medical Center9, University of Utah10, University of Nebraska Medical Center11, University of Alabama at Birmingham12, University of California, Los Angeles13, University of South Florida14, Mayo Clinic15, Washington University in St. Louis16, Yale Cancer Center17, Stanford University18, Case Western Reserve University19, University of Colorado Boulder20, Brigham and Women's Hospital21, Ohio State University22, Roswell Park Cancer Institute23, University of Texas MD Anderson Cancer Center24, Harvard University25, University of California, San Diego26, Memorial Sloan Kettering Cancer Center27, University of Pennsylvania28, University of Tennessee29, Johns Hopkins University30, Duke University31, National Comprehensive Cancer Network32
TL;DR: The NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for Colon Cancer focuses on systemic therapy options for the treatment of metastatic colorectal cancer (mCRC), because important updates have recently been made to this section as discussed by the authors.
Abstract: This selection from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for Colon Cancer focuses on systemic therapy options for the treatment of metastatic colorectal cancer (mCRC), because important updates have recently been made to this section. These updates include recommendations for first-line use of checkpoint inhibitors for mCRC, that is deficient mismatch repair/microsatellite instability-high, recommendations related to the use of biosimilars, and expanded recommendations for biomarker testing. The systemic therapy recommendations now include targeted therapy options for patients with mCRC that is HER2-amplified, or BRAF V600E mutation-positive. Treatment and management of nonmetastatic or resectable/ablatable metastatic disease are discussed in the complete version of the NCCN Guidelines for Colon Cancer available at NCCN.org. Additional topics covered in the complete version include risk assessment, staging, pathology, posttreatment surveillance, and survivorship.
589 citations
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TL;DR: A potential therapeutic use for this novel immunomodulatory approach in an array of T cell-mediated diseases is suggested.
Abstract: Engagement of the B7 family of molecules on antigen-presenting cells with their T cell-associated ligands, CD28 and CD152 (cytotoxic T lymphocyte-associated antigen-4 [CTLA-4]), provides a pivotal costimulatory signal in T-cell activation. We investigated the role of the CD28/CD152 pathway in psoriasis in a 26-week, phase I, open-label dose-escalation study. The importance of this pathway in the generation of humoral immune responses to T cell-dependent neoantigens, bacteriophage phiX174 and keyhole limpet hemocyanin, was also evaluated. Forty-three patients with stable psoriasis vulgaris received 4 infusions of the soluble chimeric protein CTLA4Ig (BMS-188667). Forty-six percent of all study patients achieved a 50% or greater sustained improvement in clinical disease activity, with progressively greater effects observed in the highest-dosing cohorts. Improvement in these patients was associated with quantitative reduction in epidermal hyperplasia, which correlated with quantitative reduction in skin-infiltrating T cells. No markedly increased rate of intralesional T-cell apoptosis was identified, suggesting that the decreased number of lesional T cells was probably likely attributable to an inhibition of T-cell proliferation, T-cell recruitment, and/or apoptosis of antigen-specific T cells at extralesional sites. Altered antibody responses to T cell-dependent neoantigens were observed, but immunologic tolerance to these antigens was not demonstrated. This study illustrates the importance of the CD28/CD152 pathway in the pathogenesis of psoriasis and suggests a potential therapeutic use for this novel immunomodulatory approach in an array of T cell-mediated diseases.
589 citations
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TL;DR: To endow enhanced tumor specificity and endosome disruption property on the carrier, a multifunctional polymeric micelle was investigated, causing the enhanced release of doxorubicin from the carrier in early endosomal pH.
Abstract: To endow enhanced tumor specificity and endosome disruption property on the carrier, a multifunctional polymeric micelle was investigated. The micelle exposes the cell interacting ligand (biotin) on the surface under slightly acidic environmental conditions of various solid tumors and is internalized by biotin receptor-mediated endocytosis in a short time period. The micelle also showed pH-dependent dissociation, causing the enhanced release of doxorubicin from the carrier in early endosomal pH. The dissociated micellar components subsequently disrupt endosomal membrane.
589 citations
Authors
Showing all 53431 results
Name | H-index | Papers | Citations |
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Bert Vogelstein | 247 | 757 | 332094 |
George M. Whitesides | 240 | 1739 | 269833 |
Hongjie Dai | 197 | 570 | 182579 |
Robert M. Califf | 196 | 1561 | 167961 |
Frank E. Speizer | 193 | 636 | 135891 |
Yusuke Nakamura | 179 | 2076 | 160313 |
David L. Kaplan | 177 | 1944 | 146082 |
Marc G. Caron | 173 | 674 | 99802 |
George M. Church | 172 | 900 | 120514 |
Steven P. Gygi | 172 | 704 | 129173 |
Lily Yeh Jan | 162 | 467 | 73655 |
Tobin J. Marks | 159 | 1621 | 111604 |
David W. Bates | 159 | 1239 | 116698 |
Alfred L. Goldberg | 156 | 474 | 88296 |
Charles M. Perou | 156 | 573 | 202951 |