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 & 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.
Topics: Population, Dementia, Transplantation, Cognitive decline, Health care
Papers published on a yearly basis
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TL;DR: Shift work is common in many occupations that directly affect the health and safety of others (e.g., protective services, transportation, healthcare), whereas quality of life, health, and safety during shift work and commute home can affect workers in any field as mentioned in this paper.
294 citations
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University of California, Davis1, Queen Mary University of London2, University of Pittsburgh3, State University of Campinas4, Rush University Medical Center5, University of the Witwatersrand6, Puget Sound Blood Center7, Cambridge University Hospitals NHS Foundation Trust8, University of Colorado Denver9, Murdoch University10, University of Hong Kong11, University of Cape Town12, The Chinese University of Hong Kong13, Biogen Idec14
TL;DR: Prophylactic rFIXFc, administered every 1 to 2 weeks, resulted in low annualized bleeding rates in patients with hemophilia B, mostly consistent with those expected in the general population of patients withhemophilia.
Abstract: Background Prophylactic factor replacement in patients with hemophilia B improves outcomes but requires frequent injections. A recombinant factor IX Fc fusion protein (rFIXFc) with a prolonged half-life was developed to reduce the frequency of injections required. Methods We conducted a phase 3, nonrandomized, open-label study of the safety, efficacy, and pharmacokinetics of rFIXFc for prophylaxis, treatment of bleeding, and perioperative hemostasis in 123 previously treated male patients. All participants were 12 years of age or older and had severe hemophilia B (endogenous factor IX level of ≤2 IU per deciliter, or ≤2% of normal levels). The study included four treatment groups: group 1 received weekly dose-adjusted prophylaxis (50 IU of rFIXFc per kilogram of body weight to start), group 2 received interval-adjusted prophylaxis (100 IU per kilogram every 10 days to start), group 3 received treatment as needed for bleeding episodes (20 to 100 IU per kilogram), and group 4 received treatment in the perio...
293 citations
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Duke University1, Emory University2, Ohio State University3, University of Miami4, University of Kansas5, University of Pennsylvania6, Marshfield Clinic7, Baylor College of Medicine8, Rush University Medical Center9, University of California, Los Angeles10, University of Western Australia11, GlaxoSmithKline12, Veterans Health Administration13
TL;DR: The data suggest that the parkin gene is important in early-onset PD and that multiple genetic factors may be important in the development of idiopathic late-ONSet PD.
Abstract: ContextThe relative contribution of
genes
vs environment in idiopathic Parkinson
disease (PD) is controversial. Although genetic studies have identified 2
genes in which
mutations cause rare single-gene variants of PD and observational
studies have suggested a genetic component, twin studies have suggested that
little genetic contribution exists in the common forms of PD.ObjectiveTo identify genetic risk factors for idiopathic PD.Design, Setting, and ParticipantsGenetic
linkage study conducted 1995-2000 in which a complete
genomic screen (n = 344 markers) was performed in 174 families with multiple individuals
diagnosed as having idiopathic PD, identified through probands in 13 clinic
populations in the continental United States and Australia. A total of 870
family members were studied: 378 diagnosed as having PD, 379 unaffected by
PD, and 113 with unclear status.Main Outcome MeasuresLogarithm of odds (lod) scores generated from
parametric and nonparametric genetic linkage analysis.ResultsTwo-point parametric maximum parametric lod score (MLOD) and multipoint
nonparametric lod score (LOD) linkage analysis detected significant evidence
for linkage to 5 distinct chromosomal regions:
chromosome 6 in the parkin
gene (MLOD = 5.07; LOD = 5.47) in families with at least 1 individual with
PD onset at younger than 40 years, chromosomes 17q (MLOD = 2.28; LOD = 2.62),
8p (MLOD = 2.01; LOD = 2.22), and 5q (MLOD = 2.39; LOD = 1.50) overall and
in families with late-onset PD, and chromosome 9q (MLOD = 1.52; LOD = 2.59)
in families with both levodopa-responsive and levodopa-nonresponsive patients.ConclusionsOur data suggest that the parkin gene is important in early-onset PD
and that multiple genetic factors may be important in the development of idiopathic
late-onset PD.
293 citations
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TL;DR: While significant improvements were seen at 6 months, 1 year, and 2.5 years of follow-up regardless of the closure technique, patients who underwent CR of the hip capsule demonstrated superior sport-specific outcomes compared with those undergoing PR.
Abstract: Background:Hip capsular management after hip arthroscopic surgery for femoroacetabular impingement (FAI) is controversial.Purpose/Hypothesis:To compare the clinical outcomes of patients undergoing hip arthroscopic surgery for FAI with T-capsulotomy with partial capsular repair (PR; closed vertical incision, open interportal incision) versus complete capsular repair (CR; full closure of both incisions). The hypothesis was that there would be improved clinical outcomes in patients undergoing CR compared with those undergoing PR.Study Design:Cohort study; Level of evidence, 3.Methods:Consecutive patients undergoing hip arthroscopic surgery for FAI by a single fellowship-trained surgeon from January 2011 to January 2012 were prospectively collected and analyzed. Inclusion criteria included all patients between ages 16 and 65 years with physical examination and radiographic findings consistent with symptomatic FAI, with a minimum 2-year follow-up. For analysis, patients were matched according to sex and age ±2...
293 citations
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University of Pennsylvania1, University of Southern California2, Columbia University3, Stanford University4, Duke University5, Harvard University6, NorthShore University HealthSystem7, Rush University Medical Center8, Texas Oncology9, University of Texas MD Anderson Cancer Center10, University of Washington11, University of Utah12, Yale University13, Case Western Reserve University14
TL;DR: Rindopepimut as discussed by the authors is designed to generate a specific immune response against EGFRvIII+ tumor cells, an approach which may be particularly relevant for glioblastoma, where diffuse infiltration of tumor into healthy white matter presents a treatment challenge.
Abstract: The epidermal growth factor receptor variant III deletion mutation, EGFRvIII, results in a constitutively activated receptor with a novel, highly immunogenic extracelluar epitope. EGFRvIII is present in 25%–30% of glioblastomas1 but is not significantly expressed in healthy tissue. Expression of EGFRvIII correlates with increased tumorigenicity in mouse models.2 In glioblastoma, EGFRvIII has been associated with poor long-term survival, independent of other known significant prognostic factors, such as gross total resection (GTR).3–6 EGFRvIII expression is often heterogeneous in glioblastoma specimens, but EGFRvIII+ cells may influence neighboring EGFRvIII–tumor cells through cytokines and microvesicles, providing a proliferative signal even to nonexpressing cells.7–9 EGFRvIII is also frequently expressed in glioblastoma tumor stem cells.10,11 EGFRvIII and isocitrate dehydrogenase (IDH) 1/2 mutations, the latter associated with long-term survival, rarely coexist in the same patient.12,13
Rindopepimut vaccine consists of the unique 13 amino acid sequence created by the in-frame deletion of EGFRvIII, chemically conjugated to keyhole limpet hemocyanin (KLH) as described by Heimberger and colleagues.14 Rindopepimut is designed to generate a specific immune response against EGFRvIII+ tumor cells, an approach which may be particularly relevant for glioblastoma, where diffuse infiltration of tumor into healthy white matter presents a treatment challenge. Preclinical models have demonstrated that induction of humoral and cellular anti-EGFRvIII immune responses can be effective against EGFRvIII+ intracranial tumors.14 In 2 small single-arm phase II trials conducted at MD Anderson and Duke University (“ACTIVATE” and “ACT II”),6,15 rindopepimut was well tolerated in patients with resected, EGFRvIII+ glioblastoma with promising progression-free survival (PFS) and overall survival (OS) compared with a contemporary cohort of patients matched for major study eligibility. In addition, the vaccine elicited robust anti-EGFRvIII immune responses despite concurrent temozolomide chemotherapy, and EGFRvIII was routinely eliminated in posttreatment tumor samples obtained at recurrence. The current study (“ACT III”) was performed to confirm these results in a larger, multicenter trial.
293 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 |