Institution
University of Turin
Education•Turin, Piemonte, Italy•
About: University of Turin is a education organization based out in Turin, Piemonte, Italy. It is known for research contribution in the topics: Population & Cancer. The organization has 29607 authors who have published 77952 publications receiving 2480900 citations. The organization is also known as: Universita degli Studi di Torino & Università degli Studi di Torino.
Topics: Population, Cancer, Medicine, Transplantation, Context (language use)
Papers published on a yearly basis
Papers
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Cornell University1, University of Turin2, Columbia University3, Polytechnic University of Turin4, Katholieke Universiteit Leuven5, University of Würzburg6, Medical University of Graz7, University Hospital of Basel8, University of Pavia9, City of Hope National Medical Center10, University of Nebraska Medical Center11, University of Verona12, University of Eastern Piedmont13, European Institute of Oncology14, University of Bologna15, University of Perugia16, Janssen-Cilag17, Janssen Pharmaceutica18, New York University19
TL;DR: By integrating massive sequencing strategies, this work provides a comprehensive characterization of driver genetic alterations (somatic point mutations, copy number alterations, and gene fusions) in ALK(-) ALCLs and identifies activating mutations of JAK1 and/or STAT3 genes that led to constitutive activation of the JAK/STAT3 pathway.
367 citations
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TL;DR: In this article, a finite-size Lyapunov exponent was introduced to measure the growth rate of finite size perturbations, which coincides with the size of the perturbation.
Abstract: We investigate the predictability problem in dynamical systems with many degrees of freedom and a wide spectrum of temporal scales. In particular, we study the case of three-dimensional turbulence at high Reynolds numbers by introducing a finite-size Lyapunov exponent which measures the growth rate of finite-size perturbations. For sufficiently small perturbations this quantity coincides with the usual Lyapunov exponent. When the perturbation is still small compared to large-scale fluctuations, but large compared to fluctuations at the smallest dynamically active scales, the finite-size Lyapunov exponent is inversely proportional to the square of the perturbation size. Our results are supported by numerical experiments on shell models. We find that intermittency corrections do not change the scaling law of predictability. We also discuss the relation between the finite-size Lyapunov exponent and information entropy.
367 citations
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TL;DR: B-neuT mice protected against mammary carcinogenesis fail to efficiently reject a TUBO cell challenge, suggesting that the mechanisms required for the rejection of transplantable tumors may not coincide with those that inhibit the slow progression of carcinogenesis.
Abstract: The ability of vaccination with plasmids coding for the extracellular and the transmembrane domain of the product of transforming rat Her-2/neu oncogene (r-p185) to protect against r-p185(+) transplantable carcinoma (TUBO) cells and mammary carcinogenesis was evaluated. In normal BALB/c mice, DNA vaccination elicits anti-r-p185 Ab, but only a marginal CTL reactivity, and protects against a TUBO cell challenge. Massive reactive infiltration is associated with TUBO cell rejection. In BALB/c mice transgenic for the rat Her-2/neu gene (BALB-neuT), DNA vaccination elicits a lower anti-r-p185 Ab response, no CTL activity and only incompletely protects against TUBO cells, but markedly hampers the progression of carcinogenesis. At 33 wk of age, when control BALB-neuT mice display palpable tumors in all mammary glands, about 60% of immunized mice are tumor free, and tumor multiplicity is markedly reduced. Tumor-free mammary glands still display the atypical hyperplasia of the early stages of carcinogenesis, and a marked down-modulation of r-p185, along with a massive reactive infiltrate. However, BALB-neuT mice protected against mammary carcinogenesis fail to efficiently reject a TUBO cell challenge. This suggests that the mechanisms required for the rejection of transplantable tumors may not coincide with those that inhibit the slow progression of carcinogenesis.
367 citations
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TL;DR: Through induction of the hydrolase and the resulting up-regulation of the ubiquitin pathway, learning recruits a regulated form of proteolysis that removes inhibitory constraints on long-term memory storage.
367 citations
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TL;DR: The finding that human heart can produce PAF, expresses PAF receptor, and is sensitive to the negative inotropic action of PAF suggests that this mediator may have a role also in human cardiovascular pathophysiology.
Abstract: Platelet-activating factor (PAF) is a phospholipid mediator that belongs to a family of biologically active, structurally related alkyl phosphoglycerides. PAF acts via a specific receptor that is coupled with a G protein, which activates a phosphatidylinositol-specific phospholipase C. In this review we focus on the aspects that are more relevant for the cell biology of the cardiovascular system. The in vitro studies provided evidence for a role of PAF both as intercellular and intracellular messenger involved in cell-to-cell communication. In the cardiovascular system, PAF may have a role in embryogenesis because it stimulates endothelial cell migration and angiogenesis and may affect cardiac function because it exhibits mechanical and electrophysiological actions on cardiomyocytes. Moreover, PAF may contribute to modulation of blood pressure mainly by affecting the renal vascular circulation. In pathological conditions, PAF has been involved in the hypotension and cardiac dysfunctions occurring in various cardiovascular stress situations such as cardiac anaphylaxis and hemorrhagic, traumatic, and septic shock syndromes. In addition, experimental studies indicate that PAF has a critical role in the development of myocardial ischemia-reperfusion injury. Indeed, PAF cooperates in the recruitment of leukocytes in inflamed tissue by promoting adhesion to the endothelium and extravascular transmigration of leukocytes. The finding that human heart can produce PAF, expresses PAF receptor, and is sensitive to the negative inotropic action of PAF suggests that this mediator may have a role also in human cardiovascular pathophysiology.
366 citations
Authors
Showing all 30045 results
Name | H-index | Papers | Citations |
---|---|---|---|
Michael Grätzel | 248 | 1423 | 303599 |
Lewis C. Cantley | 196 | 748 | 169037 |
Kenneth C. Anderson | 178 | 1138 | 126072 |
Elio Riboli | 158 | 1136 | 110499 |
Giacomo Bruno | 158 | 1687 | 124368 |
Silvia Franceschi | 155 | 1340 | 112504 |
Thomas E. Starzl | 150 | 1625 | 91704 |
Paolo Boffetta | 148 | 1455 | 93876 |
Marco Costa | 146 | 1458 | 105096 |
Pier Paolo Pandolfi | 146 | 529 | 88334 |
Andrew Ivanov | 142 | 1812 | 97390 |
Chiara Mariotti | 141 | 1426 | 98157 |
Tomas Ganz | 141 | 480 | 73316 |
Jean-Pierre Changeux | 138 | 672 | 76462 |
Dong-Chul Son | 138 | 1370 | 98686 |