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Institution

Rush University Medical Center

HealthcareChicago, 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 & Dementia. 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.


Papers
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Journal ArticleDOI
TL;DR: High intake of folate may be associated with cognitive decline in older persons, and these unexpected findings call for further study of the cognitive implications of high levels of dietary folate in older populations.
Abstract: Results: High folate intake was associated with a faster rate of cognitive decline in mixed models adjusted for multiple risk factors. The rate of cognitive decline among persons in the top fifth of total folate intake (median, 742 µg/d) was more than twice that of those in the lowest fifth of intake (median, 186 µg/d), a statistically significant difference of 0.02 standardized unit per year (P=.002). A faster rate of cognitive decline was also associated with high folate intake from food (P for trend=.04) and with folate vitamin supplementation of more than 400 µg/d compared with nonusers (=�.03, P.001). High total B12 intake was associated with slower cognitive decline only among the oldest participants. Conclusions: High intake of folate may be associated with cognitive decline in older persons. These unexpected findings call for further study of the cognitive implications of high levels of dietary folate in older populations.

243 citations

Journal ArticleDOI
TL;DR: The effects of subcortical infarcts with Alzheimer's disease (AD) pathology on dementia, episodic memory, and other cognitive abilities in older persons are studied.
Abstract: Objective Examine the effects of subcortical infarcts with Alzheimer's disease (AD) pathology on dementia, episodic memory, and other cognitive abilities in older persons. Methods Participants included 148 autopsied subjects of the Rush Memory and Aging Project (mean age, 88.0 years), a longitudinal clinicopathological study. Cognition was assessed yearly with 21 neuropsychological tests. Infarcts were visualized on coronal slabs, and plaques and neurofibrillary tangles were counted and standardized to form a composite measure of AD pathology. Multiple regression analyses were used controlling for age, sex, and education. Results Fifty-three (35.8%) subjects had cerebral infarcts. After accounting for AD pathology, infarcts increased the odds of dementia by 5.1-fold (95% confidence interval, 1.98–12.92) and lowered cognitive function by 0.50 standard unit (p = 0.001). After controlling for cortical infarcts and AD pathology, subcortical infarcts, present in 39 of 53 (73.6%) subjects with infarcts, increased the odds of dementia by almost 4-fold and reduced cognitive function by more than a third of a unit (parameter estimate = −0.37; p = 0.03). In analyses with cognitive abilities, subcortical infarcts were associated with lower episodic, semantic, and working memory (p ≤ 0.05), and had an interaction with AD pathology to further worsen working memory (p = 0.02). Interpretation Subcortical infarcts add to deleterious effects of AD pathology by increasing the odds of dementia and lowering memory function. Ann Neurol 2007

243 citations

Journal Article
TL;DR: It is concluded that synaptophysin is a significant as well as novel NE marker, and the use of antibody SY 38 as a broad range marker for the study and diagnosis of NE neoplasms is proposed.
Abstract: Synaptophysin is an integral membrane glycoprotein originally isolated from presynaptic vesicles of bovine neurons. The authors have studied a wide spectrum of neuroendocrine (NE) neoplasms by immunofluorescence microscopy on cryostat sections of freshly frozen tissues using a monoclonal antibody to this protein (SY 38). Without exception, they found the identical--or a very similar--protein expressed in all neuroblastomas, ganglioneuroblastomas, ganglioneuromas, pheochromocytomas, and paragangliomas studied. In these "neural" type NE neoplasms, synaptophysin was coexpressed with neurofilament proteins. Synaptophysin was also demonstrated in NE neoplasms of "epithelial" type in which it was predominantly coexpressed with cytokeratins and desmoplakin. It was invariably found in all variants of islet cell neoplasms and in all medullary thyroid carcinomas. Synaptophysin was also demonstrated in several adenomas of the hypophysis and parathyroids, in the majority of carcinoids of the bronchopulmonary and gastrointestinal tracts, and in many, though not all, NE carcinomas of the same sites, and of the skin. Conversely, SY 38 did not immunostain any of a large number of benign and malignant non-NE epithelial neoplasms; nor was any immunostaining obtained in a group of mesenchymal tumors. It is remarkable that SY 38 did not immunostain a number of malignant melanomas, including several that were immunostained for neuron-specific enolase (NSE) and several neuropeptides. Parallel studies conducted on conventionally fixed, paraffin-embedded tissue sections immunostained by the use of the avidin-biotin complex technique yielded very similar results. The findings indicate that synaptophysin is expressed in the whole range of NE neoplasms without detectable relation to the expression of other NE markers such as NSE, serotonin, and neuropeptides. Nor could the expression of synaptophysin by these tumors be correlated with their epithelial and/or neural cytoskeletal characteristics, their clinical aggressiveness, or the presence or absence of endocrinologic abnormalities. While the consistent expression of synaptophysin by the "neural" type of NE neoplasms would seem predictable its presence in diverse benign and malignant NE tumors of "epithelial" type is remarkable. It is concluded that synaptophysin is a significant as well as novel NE marker, and the use of antibody SY 38 as a broad range marker for the study and diagnosis of NE neoplasms is proposed.

243 citations

Journal ArticleDOI
TL;DR: This open-label, dose-escalation phase 1-2a study gave monthly intrathecal HPβCD to participants with NPC1 with neurological manifestation at the National Institutes of Health and evaluated Serum and CSF 24(S)-hydroxycholesterol (24[S]-HC), which serves as a biomarker of target engagement, andCSF protein biomarkers were evaluated.

243 citations

Journal ArticleDOI
TL;DR: In this paper, the Bone and Joint Decade 2000-2010 for prevention of musculo-skeletal disorders: Lund, Sweden, April 17-18, 1998, pp. 28-31.
Abstract: (1998). Epidemiology of low back pain. Acta Orthopaedica Scandinavica: Vol. 69, The Bone and Joint Decade 2000–2010 for prevention of musculo-skeletal disorders: Lund, Sweden, April 17–18, 1998, pp. 28-31.

243 citations


Authors

Showing all 14032 results

NameH-indexPapersCitations
John Q. Trojanowski2261467213948
Virginia M.-Y. Lee194993148820
Luigi Ferrucci1931601181199
David A. Bennett1671142109844
Todd R. Golub164422201457
David Cella1561258106402
M.-Marsel Mesulam15055890772
John D. E. Gabrieli14248068254
David J. Kupfer141862102498
Clifford B. Saper13640672203
Pasi A. Jänne13668589488
Nikhil C. Munshi13490667349
Martin B. Keller13154165069
Michael E. Thase13192375995
Steven R. Simon129109080331
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202336
2022166
20212,147
20201,939
20191,708
20181,410