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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Duke University1, Johns Hopkins University2, University of Florence3, Leiden University4, Stanford University5, University of Vienna6, University of California, San Francisco7, University of Texas Health Science Center at Houston8, University of Barcelona9, University of Wisconsin-Madison10, University of Zurich11, University of Helsinki12, Yale University13, Mayo Clinic14, University of Turin15, Humboldt University of Berlin16, University of Paris17, St Thomas' Hospital18
TL;DR: These revisions are made to incorporate advances related to tumor cell biology and diagnostic techniques as pertains to mycosis fungoides and Sézary syndrome to clarify certain variables that currently impede effective interinstitution and interinvestigator communication and/or the development of standardized clinical trials in MF and SS.
1,167 citations
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TL;DR: Pupillary light response, corneal reflexes, motor responses to pain, myoclonus status epilepticus, serum neuron-specific enolase, and somatosensory evoked potential studies can reliably assist in accurately predicting poor outcome in comatose patients after cardiopulmonary resuscitation for cardiac arrest.
Abstract: Objective: To systematically review outcomes in comatose survivors after cardiac arrest and cardiopulmonary resuscitation (CPR). Methods: The authors analyzed studies (1966 to 2006) that explored predictors of death or unconsciousness after 1 month or unconsciousness or severe disability after 6 months. Results: The authors identified four class I studies, three class II studies, and five class III studies on clinical findings and circumstances. The indicators of poor outcome after CPR are absent pupillary light response or corneal reflexes, and extensor or no motor response to pain after 3 days of observation (level A), and myoclonus status epilepticus (level B). Prognosis cannot be based on circumstances of CPR (level B) or elevated body temperature (level C). The authors identified one class I, one class II, and nine class III studies on electrophysiology. Bilateral absent cortical responses on somatosensory evoked potential studies recorded 3 days after CPR predicted poor outcome (level B). Burst suppression or generalized epileptiform discharges on EEG predicted poor outcomes but with insufficient prognostic accuracy (level C). The authors identified one class I, 11 class III, and three class IV studies on biochemical markers. Serum neuron-specific enolase higher than 33 μg/L predicted poor outcome (level B). Ten class IV studies on brain monitoring and neuroimaging did not provide data to support or refute usefulness in prognostication (level U). Conclusion: Pupillary light response, corneal reflexes, motor responses to pain, myoclonus status epilepticus, serum neuron-specific enolase, and somatosensory evoked potential studies can reliably assist in accurately predicting poor outcome in comatose patients after cardiopulmonary resuscitation for cardiac arrest.
1,165 citations
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TL;DR: Based on a meta-analysis of studies of paired liver biopsy studies, liver fibrosis progresses in patients with NAFL and NASH.
1,165 citations
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TL;DR: The segregation of RBC TPMT activity among 215 first-degree relatives in 50 randomly selected families and among 35 members of two kindreds and one family selected because they included probands with undetectable RBC enzyme activity were also compatible with the autosomal codominant inheritance of RBNT.
Abstract: Thiopurine methyltransferase (TPMT) catalyzes thiopurine S-methylation, an important metabolic pathway for drugs such as 6-mercaptopurine. Erythrocyte (RBC) TPMT activity was measured in blood samples from 298 randomly selected subjects. Of the subjects, 88.6% were included in a subgroup with high enzyme activity (13.50 ± 1.86 U, mean ± SD), 11.1% were included in a subgroup with intermediate activity (7.20 ± 1.08 U), and 0.3% had undetectable activity. This distribution conforms to Hardy-Weinberg predictions for the autosomal codominant inheritance of a pair of alleles for low and high TPMT activity, TPMTL and TPMTH, with gene frequencies of .059 and .941, respectively. If RBC TPMT activity is inherited in an autosomal codominant fashion, then subjects homozygous for TPMTH would have high enzyme activity, subjects heterozygous for the two alleles would have intermediate activity, and subjects homozygous for TPMTL would have undetectable activity. The segregation of RBC TPMT activity among 215 first-degree relatives in 50 randomly selected families and among 35 members of two kindreds and one family selected because they included probands with undetectable RBC enzyme activity were also compatible with the autosomal codominant inheritance of RBC TPMT. For example, in eight matings between subjects with intermediate activity (presumed genotype TPMTL TPMTH) and subjects with high activity (presumed genotype TPMTH TPMTH), 47% (8/17) of the offspring had intermediate activity. This value is very similar to the 50% figure expected on the basis of autosomal codominant inheritance (χ2[1] = .059). Further experiments are required to determine whether this genetic polymorphism for an important drug metabolizing enzyme may represent one factor in individual variations in sensitivity to thiopurines.
1,164 citations
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TL;DR: The recently proposed consensus definitions of PJI and approaches to accurate diagnosis are reviewed in detail and an overview of the treatment and prevention of this challenging condition is provided.
Abstract: Prosthetic joint infection (PJI) is a tremendous burden for individual patients as well as the global health care industry. While a small minority of joint arthroplasties will become infected, appropriate recognition and management are critical to preserve or restore adequate function and prevent excess morbidity. In this review, we describe the reported risk factors for and clinical manifestations of PJI. We discuss the pathogenesis of PJI and the numerous microorganisms that can cause this devastating infection. The recently proposed consensus definitions of PJI and approaches to accurate diagnosis are reviewed in detail. An overview of the treatment and prevention of this challenging condition is provided.
1,164 citations
Authors
Showing all 64325 results
Name | H-index | Papers | Citations |
---|---|---|---|
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 |