Institution
University of Pittsburgh
Education•Pittsburgh, Pennsylvania, United States•
About: University of Pittsburgh is a education organization based out in Pittsburgh, Pennsylvania, United States. It is known for research contribution in the topics: Population & Transplantation. The organization has 87042 authors who have published 201012 publications receiving 9656783 citations. The organization is also known as: Pitt & Western University of Pennsylvania.
Topics: Population, Transplantation, Poison control, Cancer, Health care
Papers published on a yearly basis
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TL;DR: Data is indicated that these oncoproteins actually serve quite different roles in vivo, indicating that the deregulated expression of each MYC gene is reproducibly associated with only certain naturally occurring malignancies in humans and that these genes are not interchangeable with respect to their aberrant functional consequences.
Abstract: c-myc, N-myc and L-myc are the three members of the myc oncoprotein family whose role in the pathogenesis of many human neoplastic diseases has received wide empirical support. In this review, we first summarize data, derived mainly from non-clinical studies, indicating that these oncoproteins actually serve quite different roles in vivo. This concept necessarily lies at the heart of the basis for the observation that the deregulated expression of each MYC gene is reproducibly associated with only certain naturally occurring malignancies in humans and that these genes are not interchangeable with respect to their aberrant functional consequences. We also review evidence implicating each of the above MYC genes in specific neoplastic diseases and have attempted to identify unresolved questions which deserve further basic or clinical investigation. We have made every attempt to review those diseases for which significant and confirmatory evidence, based on studies with primary tumor material, exists to implicate MYC members in their causation and/or progression.
1,164 citations
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TL;DR: The authors presented a comprehensive account of their Motivational Theory of Life-Span Development, which integrated the model of optimization in primary and secondary control and the action-phase model of developmental regulation with their original life-span theory of control to present a comprehensive theory of development.
Abstract: This article had four goals. First, the authors identified a set of general challenges and questions that a life-span theory of development should address. Second, they presented a comprehensive account of their Motivational Theory of Life-Span Development. They integrated the model of optimization in primary and secondary control and the action-phase model of developmental regulation with their original life-span theory of control to present a comprehensive theory of development. Third, they reviewed the relevant empirical literature testing key propositions of the Motivational Theory of Life-Span Development. Finally, because the conceptual reach of their theory goes far beyond the current empirical base, they pointed out areas that deserve further and more focused empirical inquiry.
1,163 citations
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Medical College of Wisconsin1, Harvard University2, University of Cincinnati3, Dresden University of Technology4, University of California, Los Angeles5, Stanford University6, Northwestern University7, Mayo Clinic8, Vanderbilt University9, University of Edinburgh10, Oregon State University11, University of Pittsburgh12, Cardiovascular Institute of the South13, University at Buffalo14, University of Virginia15, Stony Brook University16, University of Toronto17, Heidelberg University18, Washington University in St. Louis19, Case Western Reserve University20, Emory University21, University of Miami22, University of Calgary23
TL;DR: A multidisciplinary panel of neurointerventionalists, neuroradiologists, and stroke neurologists with extensive experience in neuroimaging and IAT, convened at the “Consensus Meeting on Revascularization Grading Following Endovascular Therapy” with the goal of addressing heterogeneity in cerebral angiographic revascularization grading.
Abstract: See related article, p 2509
Intra-arterial therapy (IAT) for acute ischemic stroke (AIS) has dramatically evolved during the past decade to include aspiration and stent-retriever devices. Recent randomized controlled trials have demonstrated the superior revascularization efficacy of stent-retrievers compared with the first-generation Merci device.1,2 Additionally, the Diffusion and Perfusion Imaging Evaluation for Understanding Stroke Evolution (DEFUSE) 2, the Mechanical Retrieval and Recanalization of Stroke Clots Using Embolectomy (MR RESCUE), and the Interventional Management of Stroke (IMS) III trials have confirmed the importance of early revascularization for achieving better clinical outcome.3–5 Despite these data, the current heterogeneity in cerebral angiographic revascularization grading (CARG) poses a major obstacle to further advances in stroke therapy. To date, several CARG scales have been used to measure the success of IAT.6–14 Even when the same scale is used in different studies, it is applied using varying operational criteria, which further confounds the interpretation of this key metric.10 The lack of a uniform grading approach limits comparison of revascularization rates across clinical trials and hinders the translation of promising, early phase angiographic results into proven, clinically effective treatments.6–14 For these reasons, it is critical that CARG scales be standardized and end points for successful revascularization be refined.6 This will lead to a greater understanding of the aspects of revascularization that are strongly predictive of clinical response.
The optimal grading scale must demonstrate (1) a strong correlation with clinical outcome, (2) simplicity and feasibility of scale interpretation while ensuring characterization of relevant angiographic findings, and (3) high inter-rater reproducibility.
To address these issues, a multidisciplinary panel of neurointerventionalists, neuroradiologists, and stroke neurologists with extensive experience in neuroimaging and IAT, convened at the “Consensus Meeting on Revascularization Grading Following Endovascular Therapy” with the goal …
1,162 citations
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TL;DR: Post-transplant lymphomas or other lymphoproliferative lesions developed in 8, 4, 3, and 2 recipients, respectively, of cadaveric kidney, liver, heart, and heart-lung homografts, often without subsequent rejection of the grafts.
1,161 citations
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TL;DR: Amyloid‐β42 (Aβ42) appears central to Alzheimer's disease pathogenesis and is a major component of amyloid plaques, and its decrease may reflect plaques acting as an Aβ42 “sink,” hindering transport of soluble A β42 between brain and CSF.
Abstract: Objectives Amyloid-beta(42) (Abeta(42)) appears central to Alzheimer's disease (AD) pathogenesis and is a major component of amyloid plaques. Mean cerebrospinal fluid (CSF) Abeta(42) is decreased in dementia of the Alzheimer's type. This decrease may reflect plaques acting as an Abeta(42) "sink," hindering transport of soluble Abeta(42) between brain and CSF. We investigated this hypothesis. Methods We compared the in vivo brain amyloid load (via positron emission tomography imaging of the amyloid-binding agent, Pittsburgh Compound-B [PIB]) with CSF Abeta(42) and other measures (via enzyme-linked immunosorbent assay) in clinically characterized research subjects. Results Subjects fell into two nonoverlapping groups: those with positive PIB binding had the lowest CSF Abeta(42) level, and those with negative PIB binding had the highest CSF Abeta(42) level. No relation was observed between PIB binding and CSF Abeta(40), tau, phospho-tau(181), plasma Abeta(40), or plasma Abeta(42). Importantly, PIB binding and CSF Abeta(42) did not consistently correspond with clinical diagnosis; three cognitively normal subjects were PIB-positive with low CSF Abeta(42), suggesting the presence of amyloid in the absence of cognitive impairment (ie, preclinical AD). Interpretation These observations suggest that brain amyloid deposition results in low CSF Abeta(42), and that amyloid imaging and CSF Abeta(42) may potentially serve as antecedent biomarkers of (preclinical) AD.
1,161 citations
Authors
Showing all 87737 results
Name | H-index | Papers | Citations |
---|---|---|---|
JoAnn E. Manson | 270 | 1819 | 258509 |
Graham A. Colditz | 261 | 1542 | 256034 |
Yi Chen | 217 | 4342 | 293080 |
David J. Hunter | 213 | 1836 | 207050 |
David Miller | 203 | 2573 | 204840 |
Rakesh K. Jain | 200 | 1467 | 177727 |
Lewis C. Cantley | 196 | 748 | 169037 |
Dennis W. Dickson | 191 | 1243 | 148488 |
Terrie E. Moffitt | 182 | 594 | 150609 |
Dennis S. Charney | 179 | 802 | 122408 |
Ronald C. Petersen | 178 | 1091 | 153067 |
David L. Kaplan | 177 | 1944 | 146082 |
Jasvinder A. Singh | 176 | 2382 | 223370 |
Richard K. Wilson | 173 | 463 | 260000 |
Deborah J. Cook | 173 | 907 | 148928 |