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: 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
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Rush University Medical Center1, Columbia University2, Duke University3, George Washington University4, University of Pennsylvania5, Georgetown University6, Yale University7, Jefferson Community and Technical College8, Anschutz Medical Campus9, United States Department of Veterans Affairs10, Johns Hopkins University11, Wake Forest University12, University of California, Los Angeles13
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
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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
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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
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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
Name | H-index | Papers | Citations |
---|---|---|---|
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 |