Institution
University of Palermo
Education•Palermo, Italy•
About: University of Palermo is a education organization based out in Palermo, Italy. It is known for research contribution in the topics: Population & Medicine. The organization has 15621 authors who have published 40250 publications receiving 964384 citations. The organization is also known as: Università degli Studi di Palermo & Universita degli Studi di Palermo.
Topics: Population, Medicine, Cancer, Context (language use), Catalysis
Papers published on a yearly basis
Papers
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TL;DR: This letter presents a new approach to evaluate the throughput/delay performance of the 802.11 distributed coordination function (DCF) that relies on elementary conditional probability arguments rather than bidimensional Markov chains and can be easily extended to account for backoff operation more general than DCF's one.
Abstract: This letter presents a new approach to evaluate the throughput/delay performance of the 802.11 distributed coordination function (DCF). Our approach relies on elementary conditional probability arguments rather than bidimensional Markov chains (as proposed in previous models) and can be easily extended to account for backoff operation more general than DCF's one.
296 citations
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TL;DR: Statin use was associated with protection towards the full spectrum of liver damage in individuals at risk of non-alcoholic steatohepatitis, however, the I148M PNPLA3 risk variant limited this beneficial effect.
295 citations
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10 Aug 2007
TL;DR: In this paper, a detailed analysis of Swift multiwavelength observations of GRB 070110 and its remarkable afterglow is presented, showing that the early X-ray light curve, interpreted as the tail of the prompt emission, displays a spectral evolution already seen in other gamma-ray bursts.
Abstract: We present a detailed analysis of Swift multiwavelength observations of GRB 070110 and its remarkable afterglow. The early X-ray light curve, interpreted as the tail of the prompt emission, displays a spectral evolution already seen in other gamma-ray bursts. The optical afterglow shows a shallow decay up to similar to 2 days after the burst, which is not consistent with standard afterglow models. The most intriguing feature is a very steep decay in the X-ray flux at similar to 2 x 10(4) s after the burst, ending an apparent plateau. The abrupt drop of the X-ray light curve rules out an external shock as the origin of the plateau in this burst and implies long-lasting activity of the central engine. The temporal and spectral properties of the plateau phase point toward a continuous central engine emission rather than the episodic emission of X-ray flares. We suggest that the observed X-ray plateau is powered by a spinning-down central engine, possibly a millisecond pulsar, which dissipates energy at an internal radius before depositing energy into the external shock.
294 citations
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TL;DR: Spectroscopic measurements performed during both quiescent degassing and explosions on Stromboli volcano are used to demonstrate that gas slugs originate from as deep as the volcano-crust interface (∼3 kilometers), where both structural discontinuities and differential bubble-rise speed can promote slug coalescence.
Abstract: Strombolian-type eruptive activity, common at many volcanoes, consists of regular explosions driven by the bursting of gas slugs that rise faster than surrounding magma. Explosion quakes associated with this activity are usually localized at shallow depth; however, where and how slugs actually form remain poorly constrained. We used spectroscopic measurements performed during both quiescent degassing and explosions on Stromboli volcano (Italy) to demonstrate that gas slugs originate from as deep as the volcano-crust interface (∼3 kilometers), where both structural discontinuities and differential bubble-rise speed can promote slug coalescence. The observed decoupling between deep slug genesis and shallow (∼250-meter) explosion quakes may be a common feature of strombolian activity, determined by the geometry of plumbing systems.
294 citations
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TL;DR: How cancers can become insensitive to various inhibitors and potential strategies to overcome this resistance are discussed.
Abstract: // James A. McCubrey 1 , Linda S. Steelman 1 , William H. Chappell 1 , Stephen L. Abrams 1 , Richard A. Franklin 1 , Giuseppe Montalto 2 , Melchiorre Cervello 3 , Massimo Libra 4 , Saverio Candido 4 , Grazia Malaponte 4 , Maria C. Mazzarino 4 , Paolo Fagone 4 , Ferdinando Nicoletti 4 , Jorg Basecke 5 , Sanja Mijatovic 6 , Danijela Maksimovic-Ivanic 6 , Michele Milella 7 , Agostino Tafuri 8 , Francesca Chiarini 9 , Camilla Evangelisti 9 , Lucio Cocco 10 , Alberto M. Martelli 9,10 1 Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC, USA 2 Department of Internal Medicine and Specialties, University of Palermo, Palermo, Italy 3 Consiglio Nazionale delle Ricerche, Istituto di Biomedicina e Immunologia Molecolare “Alberto Monroy”, Palermo, Italy 4 Department of Bio-Medical Sciences, University of Catania, Catania, Italy 5 Department of Medicine, University of Gottingen, Gottingen, Germany 6 Department of Immunology, Instititue for Biological Research “Sinisa Stankovic”, University of Belgrade, Belgrade, Serbia 7 Regina Elena National Cancer Institute, Rome, Italy 8 Sapienza, University of Rome, Department of Cellular Biotechnology and Hematology, Rome, Italy 9 Institute of Molecular Genetics, National Research Council-Rizzoli Orthopedic Institute, Bologna, Italy 10 Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy Correspondence: James A. McCubrey, email: // Keywords : Targeted Therapy, Therapy Resistance, Cancer Stem Cells, Raf, Akt, PI3K, mTOR Received : September 12, 2012, Accepted : October 18, 2012, Published : October 20, 2012 Abstract The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Targeting these pathways is often complex and can result in pathway activation depending on the presence of upstream mutations (e.g., Raf inhibitors induce Raf activation in cells with wild type (WT) RAF in the presence of mutant, activated RAS ) and rapamycin can induce Akt activation. Targeting with inhibitors directed at two constituents of the same pathway or two different signaling pathways may be a more effective approach. This review will first evaluate potential uses of Raf, MEK, PI3K, Akt and mTOR inhibitors that have been investigated in pre-clinical and clinical investigations and then discuss how cancers can become insensitive to various inhibitors and potential strategies to overcome this resistance.
294 citations
Authors
Showing all 15895 results
Name | H-index | Papers | Citations |
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Robin M. Murray | 171 | 1539 | 116362 |
Frede Blaabjerg | 147 | 2161 | 112017 |
Jean Bousquet | 145 | 1288 | 96769 |
Zhanhu Guo | 128 | 886 | 53378 |
Jean Ballet | 115 | 263 | 46301 |
Antonio Facchetti | 111 | 602 | 51885 |
Michele Pagano | 97 | 306 | 42211 |
Frank Z. Stanczyk | 93 | 620 | 30244 |
Eleonora Troja | 91 | 271 | 30873 |
Francesco Sciortino | 90 | 536 | 28956 |
Zev Rosenwaks | 89 | 772 | 32039 |
Antonio Russo | 88 | 934 | 34563 |
Carlo Salvarani | 88 | 730 | 31699 |
Giuseppe Basso | 87 | 643 | 33320 |
Antonio Craxì | 86 | 659 | 39463 |