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
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TL;DR: NotCH1 mutations are an independent predictor of CLL OS, tend to be mutually exclusive with TP53 abnormalities, and identify cases with a dismal prognosis, which is attributable to shorter treatment-free survival and higher risk of Richter transformation.
407 citations
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TL;DR: It is reported that the infertility of Ptx3–/– mice is associated with severe abnormalities of the cumulus oophorus and failure of in vivo, but not in vitro, oocyte fertilization.
Abstract: PTX3 is a prototypic long pentraxin that plays a non-redundant role in innate immunity against selected pathogens and in female fertility. Here, we report that the infertility of Ptx3 –/– mice is associated with severe abnormalities of the cumulus oophorus and failure of in vivo, but not in vitro, oocyte fertilization. PTX3 is produced by mouse cumulus cells during cumulus expansion and localizes in the matrix. PTX3 is expressed in the human cumulus oophorus as well. Cumuli from Ptx3 –/– mice synthesize normal amounts of hyaluronan (HA), but are unable to organize it in a stable matrix. Exogenous PTX3 restores a normal cumulus phenotype. Incorporation in the matrix of inter-α-trypsin inhibitor is normal in Ptx3 –/– cumuli. PTX3 does not interact directly with HA, but it binds the cumulus matrix hyaladherin tumor necrosis factor α-induced protein 6 (TNFAIP6, also known as TSG6) and thereby may form multimolecular complexes that can cross-link HA chains. Thus, PTX3 is a structural constituent of the cumulus oophorus extracellular matrix essential for female fertility.
406 citations
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TL;DR: These findings indicate that both the psychological (hidden injection) and pharmacological blockade of the placebo response reduce the effectiveness of, and the response variability to, analgesic drugs.
Abstract: Individual differences in pharmacokinetics and pharmacodynamics, the type of pain and the method of drug administration can account for the response variability to analgesics. By integrating a clinical and an experimental approach, we report here that another important source of variability is represented by individual differences in non-specific (placebo) activation of endogenous opioid systems. In the first part of this study, we analyzed the effectiveness of buprenorphine, tramadol, ketorolac and metamizol in the clinical setting, where the placebo effect was completely eliminated by means of hidden infusions. We found that the hidden injections were significantly less effective and less variable compared with open injections (in full view of the subject), suggesting that part of the response variability was due to non-specific factors (placebo). Since we could not administer the opioid antagonist, naloxone, to these patients, in the second part of this study, we induced experimental ischemic arm pain in healthy volunteers and found that, as occurred in clinical pain, the analgesic response to a hidden injection of the non-opioid ketorolac was less effective and less variable than an open injection. Most importantly, we obtained the same effects by adding naloxone to an open injection of ketorolac, thus blocking the opioid-mediated placebo component of analgesia. These findings indicate that both the psychological (hidden injection) and pharmacological (naloxone) blockade of the placebo response reduce the effectiveness of, and the response variability to, analgesic drugs. Therefore, an important source of response variability to analgesics appears to be due to differences in non-specific activation of endogenous opioid systems.
406 citations
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University of Warsaw1, Yerevan Physics Institute2, Argonne National Laboratory3, RWTH Aachen University4, Karlsruhe Institute of Technology5, City University of New York6, New York City College of Technology7, University of Turin8, University of Bern9, CERN10, University of Oxford11, Folkwang University of the Arts12, Florida State University13
TL;DR: An update of standard model predictions for the inclusive branching ratios of the B mesons is presented, incorporating all results for the O(α_{s}^{2}) and lower-order perturbative corrections that have been calculated after 2006.
Abstract: Weak radiative decays of the B mesons belong to the most important flavor changing processes that provide constraints on physics at the TeV scale. In the derivation of such constraints, accurate standard model predictions for the inclusive branching ratios play a crucial role. In the current Letter we present an update of these predictions, incorporating all our results for the O(α2s) and lower-order perturbative corrections that have been calculated after 2006. New estimates of nonperturbative effects are taken into account, too. For the CP- and isospin-averaged branching ratios, we find Bsγ=(3.36±0.23)×10−4 and Bdγ=(1.73+0.12−0.22)×10−5, for Eγ>1.6 GeV. Both results remain in agreement with the current experimental averages. Normalizing their sum to the inclusive semileptonic branching ratio, we obtain Rγ≡(Bsγ+Bdγ)/Bclν=(3.31±0.22)×10−3. A new bound from Bsγ on the charged Higgs boson mass in the two-Higgs-doublet-model II reads MH±>480 GeV at 95% C.L.
406 citations
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Radboud University Nijmegen Medical Centre1, deCODE genetics2, Radboud University Nijmegen3, University of Brescia4, National Institutes of Health5, Katholieke Universiteit Leuven6, University of Turin7, University of Zaragoza8, Karolinska Institutet9, St James's University Hospital10, Sahlgrenska University Hospital11, Maastricht University12, University of Birmingham13, University of London14, German Cancer Research Center15, Imperial College London16, University of Iceland17
TL;DR: No association was observed between UBC and the four 8q24 variants previously associated with prostate, colorectal and breast cancers, nor did rs9642880 associate with any of these three cancers.
Abstract: We conducted a genome-wide SNP association study on 1,803 urinary bladder cancer (UBC) cases and 34,336 controls from Iceland and The Netherlands and follow up studies in seven additional case-control groups (2,165 cases and 3,800 controls). The strongest association was observed with allele T of rs9642880 on chromosome 8q24, 30 kb upstream of MYC (allele-specific odds ratio (OR) = 1.22; P = 9.34 x 10(-12)). Approximately 20% of individuals of European ancestry are homozygous for rs9642880[T], and their estimated risk of developing UBC is 1.49 times that of noncarriers. No association was observed between UBC and the four 8q24 variants previously associated with prostate, colorectal and breast cancers, nor did rs9642880 associate with any of these three cancers. A weaker signal, but nonetheless of genome-wide significance, was captured by rs710521[A] located near TP63 on chromosome 3q28 (allele-specific OR = 1.19; P = 1. 15 x 10(-7)).
406 citations
Authors
Showing all 30045 results
Name | H-index | Papers | Citations |
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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 |