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Institution

University of Naples Federico II

EducationNaples, Campania, Italy
About: University of Naples Federico II is a education organization based out in Naples, Campania, Italy. It is known for research contribution in the topics: Population & Cancer. The organization has 29291 authors who have published 68803 publications receiving 1920149 citations. The organization is also known as: Università degli Studi di Napoli Federico II & Naples University.


Papers
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Journal ArticleDOI
Leor Barack1, Vitor Cardoso2, Vitor Cardoso3, Samaya Nissanke4  +228 moreInstitutions (101)
TL;DR: A comprehensive overview of the state of the art in the relevant fields of research, summarize important open problems, and lay out a roadmap for future progress can be found in this article, which is an initiative taken within the framework of the European Action on 'Black holes, Gravitational waves and Fundamental Physics'.
Abstract: The grand challenges of contemporary fundamental physics-dark matter, dark energy, vacuum energy, inflation and early universe cosmology, singularities and the hierarchy problem-all involve gravity as a key component. And of all gravitational phenomena, black holes stand out in their elegant simplicity, while harbouring some of the most remarkable predictions of General Relativity: event horizons, singularities and ergoregions. The hitherto invisible landscape of the gravitational Universe is being unveiled before our eyes: the historical direct detection of gravitational waves by the LIGO-Virgo collaboration marks the dawn of a new era of scientific exploration. Gravitational-wave astronomy will allow us to test models of black hole formation, growth and evolution, as well as models of gravitational-wave generation and propagation. It will provide evidence for event horizons and ergoregions, test the theory of General Relativity itself, and may reveal the existence of new fundamental fields. The synthesis of these results has the potential to radically reshape our understanding of the cosmos and of the laws of Nature. The purpose of this work is to present a concise, yet comprehensive overview of the state of the art in the relevant fields of research, summarize important open problems, and lay out a roadmap for future progress. This write-up is an initiative taken within the framework of the European Action on 'Black holes, Gravitational waves and Fundamental Physics'. © 2019 IOP Publishing Ltd.

314 citations

Journal ArticleDOI
TL;DR: This work addresses several genetic events and critical factors that define the metastatic phenotype acquired during tumorigenesis that provide the basis for the development of new aspects in the treatment of metastatic cancers, which involves inhibition of these proteins and their molecular networks.

314 citations

Journal ArticleDOI
TL;DR: In this article, it was shown that inactivation of p53 by deletion, depletion or inhibition can trigger autophagy in enucleated cells, indicating that the cytoplasmic, non-nuclear pool of P53 can regulate autophagia.
Abstract: Genotoxic stress can induce autophagy in a p53-dependent fashion and p53 can transactivate autophagy-inducing genes. We have observed recently that inactivation of p53 by deletion, depletion or inhibition can trigger autophagy. Thus, human and mouse cells subjected to knockout, knockdown or pharmacological inhibition of p53 manifest signs of autophagy such as depletion of p62/SQSTM1, LC3 lipidation, redistribution of GFP-LC3 in cytoplasmic puncta, and accumulation of autophagosomes and autolysosomes, both in vitro and in vivo. Inhibition of p53 causes autophagy in enucleated cells, indicating that the cytoplasmic, non-nuclear pool of p53 can regulate autophagy. Accordingly, retransfection of p53(-/-) cells with wild-type p53 as well as a p53 mutant that is excluded from the nucleus (due to the deletion of the nuclear localization sequence) can inhibit autophagy, whereas retransfection with a nucleus-restricted p53 mutant (in which the nuclear localization sequence has been deleted) does not inhibit autophagy. Several distinct autophagy inducers (e.g., starvation, rapamycin, lithium, tunicamycin and thapsigargin) stimulate the rapid degradation of p53. In these conditions, inhibition of the p53-specific E3 ubiquitin ligase HDM2 can avoid p53 depletion and simultaneously prevent the activation of autophagy. Moreover, a p53 mutant that lacks the HDM2 ubiquitinylation site and hence is more stable than wild-type p53 is particularly efficient in suppressing autophagy. In conclusion, p53 plays a dual role in the control of autophagy. On the one hand, nuclear p53 can induce autophagy through transcriptional effects. On the other hand, cytoplasmic p53 may act as a master repressor of autophagy.

313 citations

Journal ArticleDOI
01 Aug 1993
TL;DR: The parallel approach to force/position control of robotic manipulators is presented, which shows a complete use of the available sensor measurements by operating the control action in a full-dimensional space without using selection matrices.
Abstract: Force/position control strategies provide an effective framework to deal with tasks involving interaction with the environment. In this paper the parallel approach to force/position control of robotic manipulators is presented. It shows a complete use of the available sensor measurements by operating the control action in a full-dimensional space without using selection matrices. Conflicting situations between the position and force tasks are managed using a priority strategy: the force control loop is designed to prevail over the position control loop. This choice ensures limited deviations from the prescribed force trajectory in every situation, guaranteeing automatic recovery from unplanned collisions. A dynamic force/position parallel control law is presented and its performance in presence of an elastic environment is analyzed; simplification of the dynamic control law is also discussed leading to a PID-type parallel controller. Two case studies are worked out that show the effectiveness of the approach in application to an industrial robot. >

313 citations

Journal ArticleDOI
16 Aug 2007-BMJ
TL;DR: Not all commercially available probiotic preparations are effective in children with acute diarrhoea, and Paediatricians should choose bacterial preparations based on effectiveness data.
Abstract: Objective To compare the efficacy of five probiotic preparations recommended to parents in the treatment of acute diarrhoea in children. Design Randomised controlled clinical trial in collaboration with family paediatricians over 12 months. Setting Primary care. Participants Children aged 3-36 months visiting a family paediatrician for acute diarrhoea. Intervention Children's parents were randomly assigned to receive written instructions to purchase a specific probiotic product: oral rehydration solution (control group); Lactobacillus rhamnosus strain GG; Saccharomyces boulardii; Bacillus clausii; mix of L delbrueckii var bulgaricus, Streptococcus thermophilus, L acidophilus, and Bifidobacterium bifidum; or Enterococcus faecium SF68. Main outcome measures Primary outcomes were duration of diarrhoea and daily number and consistency of stools. Secondary outcomes were duration of vomiting and fever and rate of admission to hospital. Safety and tolerance were also recorded. Results 571 children were allocated to intervention. Median duration of diarrhoea was significantly shorter (P<0.001) in children who received L rhamnosus strain GG (78.5 hours) and the mix of four bacterial strains (70.0 hours) than in children who received oral rehydration solution alone (115.0 hours). One day after the first probiotic administration, the daily number of stools was significantly lower (P<0.001) in children who received L rhamnosus strain GG and in those who received the probiotic mix than in the other groups. The remaining preparations did not affect primary outcomes. Secondary outcomes were similar in all groups. Conclusions Not all commercially available probiotic preparations are effective in children with acute diarrhoea. Paediatricians should choose bacterial preparations based on effectiveness data. Trial registration number Current Controlled Trials ISRCTN56067537.

312 citations


Authors

Showing all 29740 results

NameH-indexPapersCitations
D. M. Strom1763167194314
Yang Gao1682047146301
Robert Stone1601756167901
Elio Riboli1581136110499
Barry J. Maron15579291595
H. Eugene Stanley1541190122321
Paul Elliott153773103839
Robert O. Bonow149808114836
Kai Simons14742693178
Peter Buchholz143118192101
Martino Margoni1412059107829
H. A. Neal1411903115480
Luca Lista1402044110645
Pierluigi Paolucci1381965105050
Ari Helenius13729864789
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023234
2022660
20216,021
20205,957
20194,881
20184,267