Institution
Mayo Clinic
Healthcare•Rochester, Minnesota, United States•
About: Mayo Clinic is a healthcare organization based out in Rochester, Minnesota, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 63387 authors who have published 169578 publications receiving 8114006 citations.
Topics: Population, Cancer, Medicine, Transplantation, Breast cancer
Papers published on a yearly basis
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University of Glasgow1, Boehringer Ingelheim2, Dresden University of Technology3, Mayo Clinic4, Sapienza University of Rome5, University of Texas at Austin6, Stanford University7, Helsinki University Central Hospital8, Food and Drug Administration9, University of Melbourne10, Heidelberg University11
TL;DR: Patients with ischaemic stroke selected by clinical symptoms and CT benefit from intravenous alteplase when treated up to 4.5 h should be taken to shorten delay in initiation of treatment to increase benefit to a maximum.
1,951 citations
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University of Texas MD Anderson Cancer Center1, Case Western Reserve University2, Cleveland Clinic3, University of Colorado Denver4, University of Texas Health Science Center at San Antonio5, National Institutes of Health6, University of California, San Diego7, University of Western Ontario8, Duke University9, Mayo Clinic10, University of Washington11, University of California, Los Angeles12, Columbia University13, University of British Columbia14, University of California, Irvine15, University of Michigan16
TL;DR: Selenium or vitamin E, alone or in combination at the doses and formulations used, did not prevent prostate cancer in this population of relatively healthy men.
Abstract: Context Secondary analyses of 2 randomized controlled trials and supportive epidemiologic and preclinical data indicated the potential of selenium and vitamin E for preventing prostate cancer. Objective To determine whether selenium, vitamin E, or both could prevent prostate cancer and other diseases with little or no toxicity in relatively healthy men. Design, Setting, and Participants A randomized, placebo-controlled trial (Selenium and Vitamin E Cancer Prevention Trial [SELECT]) of 35 533 men from 427 participating sites in the United States, Canada, and Puerto Rico randomly assigned to 4 groups (selenium, vitamin E, selenium + vitamin E, and placebo) in a double-blind fashion between August 22, 2001, and June 24, 2004. Baseline eligibility included age 50 years or older (African American men) or 55 years or older (all other men), a serum prostate-specific antigen level of 4 ng/mL or less, and a digital rectal examination not suspicious for prostate cancer. Interventions Oral selenium (200 μg/d from L-selenomethionine) and matched vitamin E placebo, vitamin E (400 IU/d of all rac-α-tocopheryl acetate) and matched selenium placebo, selenium + vitamin E, or placebo + placebo for a planned follow-up of minimum of 7 years and a maximum of 12 years. Main Outcome Measures Prostate cancer and prespecified secondary outcomes, including lung, colorectal, and overall primary cancer. Results As of October 23, 2008, median overall follow-up was 5.46 years (range, 4.17-7.33 years). Hazard ratios (99% confidence intervals [CIs]) for prostate cancer were 1.13 (99% CI, 0.95-1.35; n = 473) for vitamin E, 1.04 (99% CI, 0.87-1.24; n = 432) for selenium, and 1.05 (99% CI, 0.88-1.25; n = 437) for selenium + vitamin E vs 1.00 (n = 416) for placebo. There were no significant differences (all P>.15) in any other prespecified cancer end points. There were statistically nonsignificant increased risks of prostate cancer in the vitamin E group (P = .06) and type 2 diabetes mellitus in the selenium group (relative risk, 1.07; 99% CI, 0.94-1.22; P = .16) but not in the selenium + vitamin E group. Conclusion Selenium or vitamin E, alone or in combination at the doses and formulations used, did not prevent prostate cancer in this population of relatively healthy men. Trial Registration clinicaltrials.gov identifier: NCT00006392Published online December 9, 2008 (doi:10.1001/jama.2008.864).
1,942 citations
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TL;DR: Data suggest that autoantibodies to aquaporin 4 derived from peripheral B cells cause the activation of complement, inflammatory demyelination, and necrosis that is seen in neuromyelitis optica.
Abstract: Summary Neuromyelitis optica (also known as Devic's disease) is an idiopathic, severe, demyelinating disease of the central nervous system that preferentially affects the optic nerve and spinal cord. Neuromyelitis optica has a worldwide distribution, poor prognosis, and has long been thought of as a variant of multiple sclerosis; however, clinical, laboratory, immunological, and pathological characteristics that distinguish it from multiple sclerosis are now recognised. The presence of a highly specific serum autoantibody marker (NMO-IgG) further differentiates neuromyelitis optica from multiple sclerosis and has helped to define a neuromyelitis optica spectrum of disorders. NMO-IgG reacts with the water channel aquaporin 4. Data suggest that autoantibodies to aquaporin 4 derived from peripheral B cells cause the activation of complement, inflammatory demyelination, and necrosis that is seen in neuromyelitis optica. The knowledge gained from further assessment of the exact role of NMO-IgG in the pathogenesis of neuromyelitis optica will provide a foundation for rational therapeutic trials for this rapidly disabling disease.
1,928 citations
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TL;DR: A joint meeting of the 19th annual Diabetic Neuropathy Study Group of the European Association for the Study of Diabetes (NEURODIAB) and the 8th International Symposium on Diabetes in Toronto, Canada, 13-18 October 2009, expert panels were convened to provide updates on classification, definitions, diagnostic criteria, and treatments of diabetic peripheral neuropathies as mentioned in this paper.
Abstract: Preceding the joint meeting of the 19th annual Diabetic Neuropathy Study Group of the European Association for the Study of Diabetes (NEURODIAB) and the 8th International Symposium on Diabetic Neuropathy in Toronto, Canada, 13-18 October 2009, expert panels were convened to provide updates on classification, definitions, diagnostic criteria, and treatments of diabetic peripheral neuropathies (DPNs), autonomic neuropathy, painful DPNs, and structural alterations in DPNs.
1,922 citations
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TL;DR: Ovarian-type stroma has been proposed as a requisite to distinguish MCN from IPMN, and some other distinct features to characterize IPMN and MCN have been identified, but there remain ambiguities between the two diseases.
1,912 citations
Authors
Showing all 64325 results
Name | H-index | Papers | Citations |
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Eugene Braunwald | 230 | 1711 | 264576 |
Peter Libby | 211 | 932 | 182724 |
Cyrus Cooper | 204 | 1869 | 206782 |
Rob Knight | 201 | 1061 | 253207 |
Robert M. Califf | 196 | 1561 | 167961 |
Eric J. Topol | 193 | 1373 | 151025 |
Dennis W. Dickson | 191 | 1243 | 148488 |
Gordon B. Mills | 187 | 1273 | 186451 |
Julie E. Buring | 186 | 950 | 132967 |
Patrick W. Serruys | 186 | 2427 | 173210 |
Cornelia M. van Duijn | 183 | 1030 | 146009 |
Paul G. Richardson | 183 | 1533 | 155912 |
John C. Morris | 183 | 1441 | 168413 |
Valentin Fuster | 179 | 1462 | 185164 |
Ronald C. Petersen | 178 | 1091 | 153067 |