Institution
Rush University Medical Center
Healthcare•Chicago, Illinois, United States•
About: Rush University Medical Center is a healthcare organization based out in Chicago, Illinois, United States. It is known for research contribution in the topics: Population & Medicine. The organization has 13915 authors who have published 29027 publications receiving 1379216 citations. The organization is also known as: Rush Presbyterian St. Luke's Medical Center.
Topics: Population, Medicine, Dementia, Transplantation, Health care
Papers published on a yearly basis
Papers
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TL;DR: The results suggest that ethnic differences in pain, pain-related sequelae, and affective factors may be small when ethnic groups are closely matched on confounding variables.
Abstract: Objective Ethnic differences in the perception, experience, and impact of pain have received growing attention in recent years Although studies comparing pain among African Americans, Hispanics, and whites have yielded mixed findings, increasing evidence suggests an enhancement of the pain experience for African American and Hispanic patients Mechanisms proposed to account for this effect include systematic differences in psychological distress and in pain-coping strategies, or differential relationships between these factors and pain However, few studies have evaluated all of these variables, or matched ethnic groups precisely on potential confounds
Design The present study compares African American, Hispanic, and white chronic pain patients across multiple dimensions of pain, emotional distress, pain-related disability, and pain coping after matching patients on a variety of potentially confounding variables
Results Results indicated no significant ethnic differences on measures of pain, depression, psychopathology, or pain-related disability While most coping variables did not differ by ethnicity, substantive group differences were evident on the praying and hoping subscale of the Coping Strategies Questionnaire, with African Americans and Hispanics reporting higher scores relative to whites on items relating to prayer Inter-relationships among pain, coping, and distress were generally quite similar across ethnic groups, although active coping showed some variation in its relationship with pain-related outcomes Catastrophizing was generally associated with greater pain and distress, and use of prayer/hope as a coping strategy was associated with greater disability across ethnic groups
Conclusions These results suggest that ethnic differences in pain, pain-related sequelae, and affective factors may be small when ethnic groups are closely matched on confounding variables Moreover, interventions designed to facilitate adaptive coping are likely to be effective across ethnic groups
260 citations
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TL;DR: This study of the transcriptome of the aging brain provides evidence that dysregulation of mRNA splicing is a feature of Alzheimer’s disease and is, in some cases, genetically driven.
Abstract: Here we use deep sequencing to identify sources of variation in mRNA splicing in the dorsolateral prefrontal cortex (DLPFC) of 450 subjects from two aging cohorts. Hundreds of aberrant pre-mRNA splicing events are reproducibly associated with Alzheimer’s disease. We also generate a catalog of splicing quantitative trait loci (sQTL) effects: splicing of 3,006 genes is influenced by genetic variation. We report that altered splicing is the mechanism for the effects of the PICALM, CLU and PTK2B susceptibility alleles. Furthermore, we performed a transcriptome-wide association study and identified 21 genes with significant associations with Alzheimer’s disease, many of which are found in known loci, whereas 8 are in novel loci. These results highlight the convergence of old and new genes associated with Alzheimer’s disease in autophagy–lysosomal-related pathways. Overall, this study of the transcriptome of the aging brain provides evidence that dysregulation of mRNA splicing is a feature of Alzheimer’s disease and is, in some cases, genetically driven.
260 citations
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TL;DR: A relation between Diabetes and cerebral infarction but not between diabetes and Alzheimer disease pathology in older persons is found.
Abstract: Objective: To examine the potential relation of diabetes to common neuropathologic causes of dementia, cerebral infarction and Alzheimer disease (AD) neuropathology. Methods: Subjects were 233 older Catholic clergy in the Religious Orders Study, who underwent detailed annual evaluations, including neuropsychological testing, and brain autopsy at time of death (mean age 86 years, 45% men). Diabetes was identified by annual direct medication inspection and history. Cognitive function proximate to death was summarized into five cognitive domains, based on 19 neuropsychological tests. Macroscopic cerebral infarctions were recorded from 1 cm coronal slabs. Neuritic plaques, diffuse plaques, and neurofibrillary tangles were counted in Bielschowsky silver-stained sections and summarized to yield composite measures of neuritic plaques, diffuse plaques, tangles, and overall AD pathology. We also used immunohistochemistry with antibodies to amyloid-β and PHF-tau to obtain quantitative measures of amyloid burden and neurofibrillary tangle density. Multiple logistic and linear regression analyses were used to examine the relation of diabetes to cerebral infarctions and AD pathology, controlling for age, sex, and education. Results: AD pathology was related to all five cognitive domains (p Conclusion: We found a relation between diabetes and cerebral infarction but not between diabetes and Alzheimer disease pathology in older persons.
260 citations
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TL;DR: TiAlV particles appeared to be the most competent to elicit the synthesis and release of inflammatory mediators in human monocytes, albeit at a lower level, whereas the particles of polyethylene retrieved from interfacial membranes were less stimulatory in these short‐term in vitro experiments.
260 citations
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TL;DR: Oral tramadol is an effective, if expensive, alternative to other analgesics in some clinical situations and is less likely to cause neonatal respiratory depression.
Abstract: The pharmacology, pharmacokinetics, efficacy, adverse effects, and dosage and administration of tramadol are reviewed. Tramadol is a synthetic analogue of codeine that binds to mu opiate receptors and inhibits norepinephrine and serotonin reuptake. It is rapidly and extensively absorbed after oral doses and is metabolized in the liver. Analgesia begins within one hour and starts to peak in two hours. In patients with moderate postoperative pain, i.v. or i.m. tramadol is roughly equal in efficacy to meperidine or morphine; for severe acute pain, tramadol is less effective than morphine. Oral tramadol can also be effective after certain types of surgery. Tramadol and meperidine are equally effective in postoperative patient-controlled analgesia. In epidural administration for pain after abdominal surgery, tramadol is more effective than bupivacaine but less effective than morphine. In patients with ureteral calculi, both dipyrone and butylscopolamine are more effective than tramadol. For labor pain, i.m. tramadol works as well as meperidine and is less likely to cause neonatal respiratory depression. Oral tramadol is as effective as codeine for acute dental pain. In several types of severe or refractory cancer pain, tramadol is effective, but less so than morphine; for other types of chronic pain, such as low-back pain, oral tramadol works as well as acetaminophen-codeine. Common adverse effects of tramadol include dizziness, nausea, dry mouth, and sedation. The abuse potential seems low. The recommended oral dosage is 50-100 mg every four to six hours. Tramadol is an effective, if expensive, alternative to other analgesics in some clinical situations.
260 citations
Authors
Showing all 14032 results
Name | H-index | Papers | Citations |
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John Q. Trojanowski | 226 | 1467 | 213948 |
Virginia M.-Y. Lee | 194 | 993 | 148820 |
Luigi Ferrucci | 193 | 1601 | 181199 |
David A. Bennett | 167 | 1142 | 109844 |
Todd R. Golub | 164 | 422 | 201457 |
David Cella | 156 | 1258 | 106402 |
M.-Marsel Mesulam | 150 | 558 | 90772 |
John D. E. Gabrieli | 142 | 480 | 68254 |
David J. Kupfer | 141 | 862 | 102498 |
Clifford B. Saper | 136 | 406 | 72203 |
Pasi A. Jänne | 136 | 685 | 89488 |
Nikhil C. Munshi | 134 | 906 | 67349 |
Martin B. Keller | 131 | 541 | 65069 |
Michael E. Thase | 131 | 923 | 75995 |
Steven R. Simon | 129 | 1090 | 80331 |