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Institution

University of Turin

EducationTurin, 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.


Papers
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Journal ArticleDOI
24 Jul 2003-Nature
TL;DR: During angiogenesis endothelial SEMA3 proteins endow the vascular system with the plasticity required for its reshaping by controlling integrin function.
Abstract: The motility and morphogenesis of endothelial cells is controlled by spatio-temporally regulated activation of integrin adhesion receptors, and integrin activation is stimulated by major determinants of vascular remodelling. In order for endothelial cells to be responsive to changes in activator gradients, the adhesiveness of these cells to the extracellular matrix must be dynamic, and negative regulators of integrins could be required. Here we show that during vascular development and experimental angiogenesis, endothelial cells generate autocrine chemorepulsive signals of class 3 semaphorins (SEMA3 proteins) that localize at nascent adhesive sites in spreading endothelial cells. Disrupting endogenous SEMA3 function in endothelial cells stimulates integrin-mediated adhesion and migration to extracellular matrices, whereas exogenous SEMA3 proteins antagonize integrin activation. Misexpression of dominant negative SEMA3 receptors in chick embryo endothelial cells locks integrins in an active conformation, and severely impairs vascular remodelling. Sema3a null mice show vascular defects as well. Thus during angiogenesis endothelial SEMA3 proteins endow the vascular system with the plasticity required for its reshaping by controlling integrin function.

552 citations

Journal ArticleDOI
TL;DR: It is argued that an economic solution to the problem of invasive species has two components: one is to use incentives to change human behavior so as to enhance protection against the introduction, establishment, and spread of invasive behavior, and the other is to develop institutions that support the weakest members of global society.
Abstract: We postulate that the causes of the problem of invasive alien species are primarily economic and, as such, require economic solutions. Invasive alien species are of increasing concern for four reasons. First, introductions are increasing sharply, while mechanisms for excluding or eradicating alien species have been either withdrawn or progressively weakened. Both trends are due to the liberalization of and increase in international travel and trade, an economic phenomenon. Second, the costs of invasions are rising rapidly due partly to increasing human population density, and partly to increasing intensity of production in genetically impoverished agricultural systems. Third, biological invasions are associated with a high degree of uncertainty both because they involve novel interactions, and because invasion risks are endogenous. Actual risks depend on how people react to the possibility of invasions. Fourth, the exclusion and control of invasive species is a "weakest-link" public good. This places the well-being of society in the hands of the least effective provider. We argue that an economic solution to the problem of invasive species has two components. One is to use incentives to change human behavior so as to enhance protection against the introduction, establishment, and spread of invasive behavior. The other is to develop institutions that support the weakest members of global society, converting a "weakest-link" to a "best-shot" public good.

551 citations

Journal ArticleDOI
01 Feb 1991-Brain
TL;DR: It is proposed that many of these perceptual disorders might be the combined result of a selective loss of the cortical elaboration of the magnocellular visual processing stream, and a selective output disconnection from a central processor of visual boundaries and shape primitives in the occipital cortex.
Abstract: A single case study of a patient with 'visual form agnosia' is presented. A severe visual recognition deficit was accompanied by impairments in discriminating shape, reflectance, and orientation, although visual acuity and colour vision, along with tactile recognition and intelligence, were largely preserved. Neuropsychological and behavioural investigations have indicated that the patient is able to utilize visual pattern information surprisingly well for the control of hand movements during reaching, and can even read many whole words, despite being unable to make simple discriminative judgements of shape or orientation. She seems to have no awareness of shape primitives through Gestalt grouping by similarity, continuity or symmetry. It is proposed that many of these perceptual disorders might be the combined result of (1) a selective loss of the cortical elaboration of the magnocellular visual processing stream, and (2) a selective output disconnection from a central processor of visual boundaries and shape primitives in the occipital cortex.

551 citations

Journal ArticleDOI
TL;DR: Blocking CCL2 nitration in tumors promoted CD8+ influx and reduced tumor growth and prolonged survival in mice when combined with adoptive cell therapy.
Abstract: Tumor-promoted constraints negatively affect cytotoxic T lymphocyte (CTL) trafficking to the tumor core and, as a result, inhibit tumor killing. The production of reactive nitrogen species (RNS) within the tumor microenvironment has been reported in mouse and human cancers. We describe a novel RNS-dependent posttranslational modification of chemokines that has a profound impact on leukocyte recruitment to mouse and human tumors. Intratumoral RNS production induces CCL2 chemokine nitration and hinders T cell infiltration, resulting in the trapping of tumor-specific T cells in the stroma that surrounds cancer cells. Preconditioning of the tumor microenvironment with novel drugs that inhibit CCL2 modification facilitates CTL invasion of the tumor, suggesting that these drugs may be effective in cancer immunotherapy. Our results unveil an unexpected mechanism of tumor evasion and introduce new avenues for cancer immunotherapy.

549 citations

Journal ArticleDOI
14 Mar 2012-PLOS ONE
TL;DR: MVs released from MSCs were found to exert a pro-survival effect on renal cells in vitro and in vivo, suggesting that MVs may contribute to renal protection conferred by M SCs.
Abstract: Several studies demonstrated that treatment with mesenchymal stem cells (MSCs) reduces cisplatin mortality in mice. Microvesicles (MVs) released from MSCs were previously shown to favor renal repair in non lethal toxic and ischemic acute renal injury (AKI). In the present study we investigated the effects of MSC-derived MVs in SCID mice survival in lethal cisplatin-induced AKI. Moreover, we evaluated in vitro the effect of MVs on cisplatin-induced apoptosis of human renal tubular epithelial cells and the molecular mechanisms involved. Two different regimens of MV injection were used. The single administration of MVs ameliorated renal function and morphology, and improved survival but did not prevent chronic tubular injury and persistent increase in BUN and creatinine. Multiple injections of MVs further decreased mortality and at day 21 surviving mice showed normal histology and renal function. The mechanism of protection was mainly ascribed to an anti-apoptotic effect of MVs. In vitro studies demonstrated that MVs up-regulated in cisplatin-treated human tubular epithelial cells anti-apoptotic genes, such as Bcl-xL, Bcl2 and BIRC8 and down-regulated genes that have a central role in the execution-phase of cell apoptosis such as Casp1, Casp8 and LTA. In conclusion, MVs released from MSCs were found to exert a pro-survival effect on renal cells in vitro and in vivo, suggesting that MVs may contribute to renal protection conferred by MSCs.

547 citations


Authors

Showing all 30045 results

NameH-indexPapersCitations
Michael Grätzel2481423303599
Lewis C. Cantley196748169037
Kenneth C. Anderson1781138126072
Elio Riboli1581136110499
Giacomo Bruno1581687124368
Silvia Franceschi1551340112504
Thomas E. Starzl150162591704
Paolo Boffetta148145593876
Marco Costa1461458105096
Pier Paolo Pandolfi14652988334
Andrew Ivanov142181297390
Chiara Mariotti141142698157
Tomas Ganz14148073316
Jean-Pierre Changeux13867276462
Dong-Chul Son138137098686
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023202
2022623
20215,734
20205,428
20194,544
20184,233