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: Diagnostic aspects, pathogenesis, and implications of NTIS as well as its distinction from severe, primary thyroid disorders in patients in the ICU are discussed.
255 citations
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TL;DR: The data suggest that α-synuclein aggregation is a key feature associated with reductions of axonal transport motor proteins in Parkinson's disease and support the hypothesis that dopaminergic neurodegeneration following a 'dying-back' pattern involving axonal travel disruption is supported.
Abstract: The progressive loss of the nigrostriatal pathway is a distinguishing feature of Parkinson’s disease. As terminal field loss seems to precede cell body loss, we tested whether alterations of axonal transport motor proteins would be early features in Parkinson’s disease. There was a decline in axonal transport motor proteins in sporadic Parkinson’s disease that preceded other well-known nigral cell-related pathology such as phenotypic downregulation of dopamine. Reductions in conventional kinesin levels precede the alterations in dopaminergic phenotypic markers (tyrosine hydroxylase) in the early stages of Parkinson’s disease. This reduction was significantly greater in nigral neurons containing α-synuclein inclusions. Unlike conventional kinesin, reductions in the levels of the cytoplasmic dynein light chain Tctex type 3 subunit were only observed at late Parkinson’s disease stages. Reductions in levels of conventional kinesin and cytoplasmic dynein subunits were recapitulated in a rat genetic Parkinson’s disease model based on over-expression of human mutant α-synuclein (A30P). Together, our data suggest that α-synuclein aggregation is a key feature associated with reductions of axonal transport motor proteins in Parkinson’s disease and support the hypothesis that dopaminergic neurodegeneration following a ‘dying-back’ pattern involving axonal transport disruption.
254 citations
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TL;DR: The hypothesis that distress proneness is associated with increased risk of dementia and suggest that neurobiologic mechanisms other than AD pathology may underlie the association are supported.
Abstract: Clinical and pathological data from the Rush Memory and Aging Project were used to test the hypothesis that distress proneness is associated with increased risk of Alzheimer's disease (AD). More than 600 older persons without dementia completed a 6-item measure of neuroticism, a stable indicator of proneness to psychological distress. At annual intervals thereafter, they underwent uniform evaluations that included clinical classification of AD and administration of 18 cognitive tests. Those who died underwent brain autopsy from which composite measures of AD pathology were derived. During a mean of about 3 years of follow-up, 55 people were clinically diagnosed with AD. In analyses that controlled for age, sex, and education, persons with a high level of distress proneness (score = 24, 90th percentile) were 2.7 times more likely to develop AD than those not prone to distress (score = 6, 10th percentile). Adjustment for depressive symptomatology or frequency of cognitive, social, and physical activity did not substantially change this effect. Distress proneness was also associated with more rapid cognitive decline. Among 45 participants who died and underwent brain autopsy, distress proneness was unrelated to diverse measures of AD pathology and was inversely related to cognition after controlling for AD pathology. The results support the hypothesis that distress proneness is associated with increased risk of dementia and suggest that neurobiologic mechanisms other than AD pathology may underlie the association.
254 citations
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TL;DR: Although existing research supports the use of nurse practitioners and physician assistants in acute and critical care settings, a low level of evidence was found with only two randomized control trials assessing the impact of nurse practitioner care.
Abstract: Background:Advanced practitioners including nurse practitioners and physician assistants are contributing to care for critically ill patients in the intensive care unit through their participation on the multidisciplinary team and in collaborative physician practice roles. However, the impact of nur
254 citations
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TL;DR: It is suggested that TLR4-mediated inflammation plays an important role in intestinal and/or brain inflammation, which may be one of the key factors leading to neurodegeneration in PD.
Abstract: Objective Recent evidence suggesting an important role of gut-derived inflammation in brain disorders has opened up new directions to explore the possible role of the gut-brain axis in neurodegenerative diseases. Given the prominence of dysbiosis and colonic dysfunction in patients with Parkinson’s disease (PD), we propose that toll-like receptor 4 (TLR4)-mediated intestinal dysfunction could contribute to intestinal and central inflammation in PD-related neurodegeneration. Design To test this hypothesis we performed studies in both human tissue and a murine model of PD. Inflammation, immune activation and microbiota composition were measured in colonic samples from subjects with PD and healthy controls subjects and rotenone or vehicle-treated mice. To further assess the role of the TLR4 signalling in PD-induced neuroinflammation, we used TLR4-knockout (KO) mice in conjunction with oral rotenone administration to model PD. Results Patients with PD have intestinal barrier disruption, enhanced markers of microbial translocation and higher pro-inflammatory gene profiles in the colonic biopsy samples compared with controls. In this regard, we found increased expression of the bacterial endotoxin-specific ligand TLR4, CD3+ T cells, cytokine expression in colonic biopsies, dysbiosis characterised by a decrease abundance of SCFA-producing colonic bacteria in subjects with PD. Rotenone treatment in TLR4-KO mice revealed less intestinal inflammation, intestinal and motor dysfunction, neuroinflammation and neurodegeneration, relative to rotenone-treated wild-type animals despite the presence of dysbiotic microbiota in TLR4-KO mice. Conclusion Taken together, these studies suggest that TLR4-mediated inflammation plays an important role in intestinal and/or brain inflammation, which may be one of the key factors leading to neurodegeneration in PD.
254 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 |