Institution
University of Rochester
Education•Rochester, New York, United States•
About: University of Rochester is a education organization based out in Rochester, New York, United States. It is known for research contribution in the topics: Population & Laser. The organization has 63915 authors who have published 112762 publications receiving 5484122 citations. The organization is also known as: Rochester University.
Topics: Population, Laser, Poison control, Health care, Large Hadron Collider
Papers published on a yearly basis
Papers
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State University of New York System1, McGill University2, University of Connecticut3, Cornell University4, Umeå University5, Wayne State University6, University of Iowa7, University of Miami8, University of Pennsylvania9, Mayo Clinic10, University of Sydney11, University of Buenos Aires12, University of Chicago13, Shanghai Jiao Tong University14, North-West University15, University of Rochester16, University of Glasgow17, Virginia Commonwealth University18, University of Melbourne19
TL;DR: Clinical practice guidelines for the management of hypertension in the community a statement by the American Society of Hypertension and the International Society of hypertension as mentioned in this paper, which is based on guidelines from the National Institute of Neurological Disorders and Strochastic Hemorrhage.
Abstract: Clinical practice guidelines for the management of hypertension in the community a statement by the American society of hypertension and the International society of hypertension
665 citations
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TL;DR: It is demonstrated that OPN modifies primitive hematopoietic cell number and function in a stem cell–nonautonomous manner and may provide a mechanism for restricting excess stem cell expansion under conditions of niche stimulation.
Abstract: Stem cells reside in a specialized niche that regulates their abundance and fate. Components of the niche have generally been defined in terms of cells and signaling pathways. We define a role for a matrix glycoprotein, osteopontin (OPN), as a constraining factor on hematopoietic stem cells within the bone marrow microenvironment. Osteoblasts that participate in the niche produce varying amounts of OPN in response to stimulation. Using studies that combine OPN-deficient mice and exogenous OPN, we demonstrate that OPN modifies primitive hematopoietic cell number and function in a stem cell-nonautonomous manner. The OPN-null microenvironment was sufficient to increase the number of stem cells associated with increased stromal Jagged1 and Angiopoietin-1 expression and reduced primitive hematopoietic cell apoptosis. The activation of the stem cell microenvironment with parathyroid hormone induced a superphysiologic increase in stem cells in the absence of OPN. Therefore, OPN is a negative regulatory element of the stem cell niche that limits the size of the stem cell pool and may provide a mechanism for restricting excess stem cell expansion under conditions of niche stimulation.
665 citations
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TL;DR: The nature of the debate, the parameters by which CSCs can or cannot be defined, and the identification of new potential therapeutic targets elucidated by considering cancer as a problem in stem cell biology are discussed.
Abstract: The investigation and study of cancer stem cells (CSCs) have received enormous attention over the past 5 to 10 years but remain topics of considerable controversy. Opinions about the validity of the CSC hypothesis, the biological properties of CSCs, and the relevance of CSCs to cancer therapy differ widely. In the following commentary, we discuss the nature of the debate, the parameters by which CSCs can or cannot be defined, and the identification of new potential therapeutic targets elucidated by considering cancer as a problem in stem cell biology.
664 citations
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Northwestern University1, University of British Columbia2, Harvard University3, City of Hope National Medical Center4, Memorial Sloan Kettering Cancer Center5, University of Texas MD Anderson Cancer Center6, University of Michigan7, Roswell Park Cancer Institute8, Fox Chase Cancer Center9, University of Rochester10
TL;DR: The NCCN-IPI is easy to apply and more powerful than the IPI for predicting survival in the rituximab era and demonstrated enhanced discrimination for both low- and high-risk patients.
664 citations
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TL;DR: It is demonstrated that NPAT activates histone gene transcription and that this activation is dependent on the promoter elements (SSCSs) previously proposed to mediate cell cycle-dependent transcription.
Abstract: In eukaryotic cells, histone gene expression is one of the major events that mark entry into S phase. While this process is tightly linked to cell cycle position, how it is regulated by the cell cycle machinery is not known. Here we show that NPAT, a substrate of the cyclin E–Cdk2 complex, is associated with human replication-dependent histone gene clusters on both chromosomes 1 and 6 in S phase. We demonstrate that NPAT activates histone gene transcription and that this activation is dependent on the promoter elements (SSCSs) previously proposed to mediate cell cycle–dependent transcription. Cyclin E is also associated with the histone gene loci, and cyclin E–Cdk2 stimulates the NPAT-mediated activation of histone gene transcription. Thus, our results both show that NPAT is involved in a key S phase event and provide a link between the cell cycle machinery and activation of histone gene transcription.
664 citations
Authors
Showing all 64186 results
Name | H-index | Papers | Citations |
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Eugene Braunwald | 230 | 1711 | 264576 |
Cyrus Cooper | 204 | 1869 | 206782 |
Eric J. Topol | 193 | 1373 | 151025 |
Dennis W. Dickson | 191 | 1243 | 148488 |
Scott M. Grundy | 187 | 841 | 231821 |
John C. Morris | 183 | 1441 | 168413 |
Ronald C. Petersen | 178 | 1091 | 153067 |
David R. Williams | 178 | 2034 | 138789 |
John Hardy | 177 | 1178 | 171694 |
Russel J. Reiter | 169 | 1646 | 121010 |
Michael Snyder | 169 | 840 | 130225 |
Jiawei Han | 168 | 1233 | 143427 |
Gang Chen | 167 | 3372 | 149819 |
Marc A. Pfeffer | 166 | 765 | 133043 |
Salvador Moncada | 164 | 495 | 138030 |