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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 & 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.


Papers
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Journal ArticleDOI
TL;DR: AA with chronic hepatitis C genotype 1 have lower rates of virologic response to peginterferon and ribavirin than CA, and these differences are not explained by disease characteristics, baseline viral levels, or amount of medication taken.

482 citations

Journal ArticleDOI
24 Mar 1999-JAMA
TL;DR: A literature review was carried out by the Department of Healthcare Services Research, Cedars-Sinai Health System, Los Angeles, California, using the MEDLINE database search for 1990 through April 1998 and updated in November 1998 as discussed by the authors.
Abstract: ObjectiveTo establish, in a single resource, up-to-date recommendations for primary care physicians regarding prevention strategies for a first strokeParticipantsMembers of the National Stroke Association's (NSA's) Stroke Prevention Advisory Board and Cedars-Sinai Health System Department of Health Services Research convened on April 9, 1998, in an open meeting The conference attendees, selected to participate by the NSA, were recognized experts in neurology (9), cardiology (2), family practice (1), nursing (1), physician assistant practices (1), and health services research (2)EvidenceA literature review was carried out by the Department of Health Services Research, Cedars-Sinai Health System, Los Angeles, Calif, using the MEDLINE database search for 1990 through April 1998 and updated in November 1998 English-language guidelines, statements, meta-analyses, and overviews on prevention of a first stroke were reviewedConsensus ProcessAt the meeting, members of the advisory board identified 6 important stroke risk factors (hypertension, myocardial infarction [MI], atrial fibrillation, diabetes mellitus, blood lipids, asymptomatic carotid artery stenosis), and 4 lifestyle factors (cigarette smoking, alcohol use, physical activity, diet)ConclusionsSeveral interventions that modify well-documented and treatable cardiovascular and cerebrovascular risk factors can reduce the risk of a first stroke Good evidence for direct stroke reduction exists for hypertension treatment; using warfarin for patients after MI who have atrial fibrillation, decreased left ventricular ejection fraction, or left ventricular thrombus; using 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors for patients after MI; using warfarin for patients with atrial fibrillation and specific risk factors; and performing carotid endarterectomy for patients with stenosis of at least 60% Observational studies support the role of modifying lifestyle-related risk factors (eg, smoking, alcohol use, physical activity, diet) in stroke prevention Measures to help patients improve adherence are an important component of a stroke prevention plan

479 citations

Journal ArticleDOI
Vivianna M. Van Deerlin1, Patrick M. A. Sleiman1, Maria Martinez-Lage2, Maria Martinez-Lage1, Alice Chen-Plotkin1, Li-San Wang1, Neill R. Graff-Radford3, Dennis W. Dickson3, Rosa Rademakers3, Bradley F. Boeve3, Murray Grossman1, Steven E. Arnold1, David M. A. Mann4, Stuart Pickering-Brown4, Harro Seelaar5, Peter Heutink6, John C. van Swieten5, Jill R. Murrell7, Bernardino Ghetti7, Salvatore Spina7, Salvatore Spina8, Jordan Grafman9, John R. Hodges10, Maria Grazia Spillantini11, Sid Gilman12, Andrew P. Lieberman12, Jeffrey Kaye13, Randall L. Woltjer13, Eileen H. Bigio14, M.-Marsel Mesulam14, Safa Al-Sarraj15, Claire Troakes15, Roger N. Rosenberg16, Charles L. White17, Isidro Ferrer18, Albert Lladó18, Manuela Neumann19, Hans A. Kretzschmar20, Christine M. Hulette21, Kathleen A. Welsh-Bohmer21, Bruce L. Miller22, Ainhoa Alzualde, Adolfo López de Munain, Ann C. McKee23, Ann C. McKee24, Marla Gearing25, Allan I. Levey25, James J. Lah25, John Hardy26, Jonathan D. Rohrer26, Tammaryn Lashley26, Ian R. A. Mackenzie27, Howard Feldman27, Ronald L. Hamilton28, Steven T. DeKosky29, Julie van der Zee30, Julie van der Zee31, Samir Kumar-Singh31, Samir Kumar-Singh30, Christine Van Broeckhoven30, Christine Van Broeckhoven31, Richard Mayeux32, Jean Paul G. Vonsattel32, Juan C. Troncoso33, Jillian J. Kril34, John B.J. Kwok35, Glenda M. Halliday35, Thomas D. Bird36, Paul G. Ince37, Pamela J. Shaw37, Nigel J. Cairns38, John C. Morris38, Catriona McLean39, Charles DeCarli, William G. Ellis40, Stefanie H. Freeman41, Matthew P. Frosch41, John H. Growdon41, Daniel P. Perl, Mary Sano42, Mary Sano23, David A. Bennett43, Julie A. Schneider43, Thomas G. Beach, Eric M. Reiman44, Bryan K. Woodruff3, Jeffrey L. Cummings45, Harry V. Vinters45, Carol A. Miller46, Helena C. Chui46, Irina Alafuzoff47, Irina Alafuzoff48, Päivi Hartikainen48, Danielle Seilhean49, Douglas Galasko50, Eliezer Masliah50, Carl W. Cotman51, M. Teresa Tũón, M. Cristina Caballero Martínez, David G. Munoz52, Steven L. Carroll53, Daniel C. Marson53, Peter Riederer54, Nenad Bogdanovic55, Gerard D. Schellenberg1, Hakon Hakonarson1, John Q. Trojanowski1, Virginia M.-Y. Lee1 
University of Pennsylvania1, Autonomous University of Barcelona2, Mayo Clinic3, University of Manchester4, Erasmus University Rotterdam5, VU University Amsterdam6, Indiana University – Purdue University Indianapolis7, University of Siena8, National Institutes of Health9, Neuroscience Research Australia10, University of Cambridge11, University of Michigan12, Oregon Health & Science University13, Northwestern University14, King's College London15, University of Texas at Dallas16, University of Texas Southwestern Medical Center17, University of Barcelona18, University of Zurich19, Ludwig Maximilian University of Munich20, Duke University21, University of California, San Francisco22, Veterans Health Administration23, Boston University24, Emory University25, University College London26, University of British Columbia27, University of Pittsburgh28, University of Virginia29, University of Antwerp30, Flanders Institute for Biotechnology31, Columbia University32, Johns Hopkins University33, University of Sydney34, University of New South Wales35, University of Washington36, University of Sheffield37, Washington University in St. Louis38, Alfred Hospital39, University of California, Davis40, Harvard University41, Icahn School of Medicine at Mount Sinai42, Rush University Medical Center43, University of Arizona44, University of California, Los Angeles45, University of Southern California46, Uppsala University47, University of Eastern Finland48, Pierre-and-Marie-Curie University49, University of California, San Diego50, University of California, Irvine51, University of Toronto52, University of Alabama at Birmingham53, University of Würzburg54, Karolinska Institutet55
TL;DR: It is found that FTLD-TDP associates with multiple SNPs mapping to a single linkage disequilibrium block on 7p21 that contains TMEM 106B, which implicate variants in TMEM106B as a strong risk factor for FTLD, suggesting an underlying pathogenic mechanism.
Abstract: Frontotemporal lobar degeneration (FTLD) is the second most common cause of presenile dementia. The predominant neuropathology is FTLD with TAR DNA-binding protein (TDP-43) inclusions (FTLD-TDP). FTLD-TDP is frequently familial, resulting from mutations in GRN (which encodes progranulin). We assembled an international collaboration to identify susceptibility loci for FTLD-TDP through a genome-wide association study of 515 individuals with FTLD-TDP. We found that FTLD-TDP associates with multiple SNPs mapping to a single linkage disequilibrium block on 7p21 that contains TMEM106B. Three SNPs retained genome-wide significance following Bonferroni correction (top SNP rs1990622, P = 1.08 x 10(-11); odds ratio, minor allele (C) 0.61, 95% CI 0.53-0.71). The association replicated in 89 FTLD-TDP cases (rs1990622; P = 2 x 10(-4)). TMEM106B variants may confer risk of FTLD-TDP by increasing TMEM106B expression. TMEM106B variants also contribute to genetic risk for FTLD-TDP in individuals with mutations in GRN. Our data implicate variants in TMEM106B as a strong risk factor for FTLD-TDP, suggesting an underlying pathogenic mechanism.

479 citations

Journal ArticleDOI
TL;DR: In the authors' functional dissection of the CD33 Alzheimer's disease susceptibility locus, it was found that the rs3865444C risk allele was associated with greater cell surface expression of CD33 in the monocytes of young and older individuals.
Abstract: In our functional dissection of the CD33 Alzheimer's disease susceptibility locus, we found that the rs3865444(C) risk allele was associated with greater cell surface expression of CD33 in the monocytes (t50 = 10.06, P(joint) = 1.3 × 10(-13)) of young and older individuals. It was also associated with diminished internalization of amyloid-β 42 peptide, accumulation of neuritic amyloid pathology and fibrillar amyloid on in vivo imaging, and increased numbers of activated human microglia.

479 citations

Journal Article
TL;DR: Although severe angiographic allograft coronary artery disease occurs in only 7% of the patients at 5 years, its presence is highly predictive of subsequent coronary artery Disease-related events or retransplantation.
Abstract: Background: Controversy exists regarding donor and recipient factors that promote the development and progression of coronary artery disease after heart transplantation and the likelihood of coronary artery disease causing death or retransplantation Methods: To investigate this issue in a large cohort of patients, we analyzed 5963 postoperative angiograms performed in 2609 of the 3837 patients undergoing heart transplantation at 39 institutions between January 1990 and December 1994 Coronary artery disease was classified as mild, moderate, or severe on the basis of left main involvement, primary vessel stenoses, and branch stenoses Coronary artery disease was considered severe if left main stenosis was > 70% or 2 or more primary vessels stenoses were > 70% or branch stenoses were > 70% in all 3 systems Results: By the end of 5 years after heart transplantation, coronary artery disease was present in 42% of the patients, mild in 27%, moderate in 8%, and severe in 7% Coronary artery disease-related events (death or retransplantation) had an actuarial incidence of 7% at 5 years and occurred in 2 of 3 of the patients with development of angiographically severe coronary artery disease By multivariable logistic analysis, risk factors for donor coronary artery disease included older donor age (P <0001) and donor hypertension (P =0002) By multivariable analysis in the hazard function domain, risk factors identified for the earlier onset of allograft coronary artery disease included older donor age (P <0001), donor male sex (P =0006), donor hypertension (P =07), recipient male sex (P =02), and recipient black race (P =01 ) The actuarial incidence of severe coronary artery disease was 9% at 5 years Conclusions: Angiographic coronary artery disease is very common after heart transplantation, occurring in approximately 42% of the patients by 5 years Older donor age, donor hypertension, and male donor or recipient predict earlier onset of angiographic allograft coronary artery disease Although severe angiographic allograft coronary artery disease occurs in only 7% of the patients at 5 years, its presence is highly predictive of subsequent coronary artery disease-related events or retransplantation J Heart Lung Transplant 1998;17:744-53

478 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