Institution
University of Perugia
Education•Perugia, Umbria, Italy•
About: University of Perugia is a education organization based out in Perugia, Umbria, Italy. It is known for research contribution in the topics: Population & Large Hadron Collider. The organization has 13365 authors who have published 39516 publications receiving 1265601 citations. The organization is also known as: Universitá degli Studi di Perugia & Universita degli Studi di Perugia.
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TL;DR: These mucoadhesive formulations offer many advantages in comparison to traditional treatments and can be proposed as a new therapeutic tool against dental and buccal diseases and disturbs.
264 citations
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TL;DR: In this article, a study on the reinforcement of existing wood elements under bending loads through the use of FRP materials is presented, in which an experimental program based on a four-point bending test configuration is proposed to characterize the stiffness, ductility and strength response of this article-reinforced wood beams.
Abstract: This paper presents a study on the reinforcement of existing wood elements under bending loads through the use of FRP materials. An analytical investigation was first conducted on the behavior of a generic FRP-reinforced wood section. This study, in turn, led to a numerical procedure based on non-linear wood properties, suitable for application in the design of FRP reinforcement of old, pre-existing wood beams under varying configurations of intervention layouts and materials. An experimental programme based on a four-point bending test configuration is proposed to characterize the stiffness, ductility and strength response of FRP-wood beams. Mechanical tests on the reinforced wood showed that external bonding of FRP materials may produce increases in flexural stiffness and capacity. The FRP composite material was made of High Tensile Carbon monodirectional reinforcing fabrics embedded in an epoxy resin matrix. This reinforcing method can be applied without necessitating the removal of the overhanging part of the pre-existing wood structure, thus maintaining the original historical structure. In addition, a beam non-linear model was proposed to predict ultimate load. At the end of this paper results of the experimental programme are presented and used for comparison with the numerical procedure.
264 citations
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TL;DR: Data show that H2S inhibits nociception induced by CRD in both healthy and postcolitic rats, and this effect is mediated by KATP channels and NO.
Abstract: Hydrogen sulfide (H(2)S) functions as a neuromodulator, but whether it modulates visceral perception and pain is unknown. Cystathionine beta-synthase (CBS) and cystathionine-gamma-lyase (CSE) mediate enzymatic generation of H(2)S in mammalian cells. Here we have investigated the role of H(2)S in modulating nociception to colorectal distension, a model that mimics some features of the irritable bowel syndrome. Four graded (0.4-1.6 ml of water) colorectal distensions (CRDs) were produced in conscious rats (healthy and postcolitic), and rectal nociception was assessed by measuring the behavioral response during CRD. Healthy rats were administered with sodium hydrogen sulfide (NaHS) (as a source of H(2)S), L-cysteine, or vehicle. In a second model, we investigated nociception to CRD in rats recovering from a chemically induced acute colitis. We found that CBS and CSE are expressed in the colon and spinal cord. Treating rats with NaHS resulted in a dose-dependent attenuation of CRD-induced nociception with the maximal effect at 60 micromol/kg (p < 0.05). Administration of L-cysteine, a CSE/CBS substrate, reduced rectal sensitivity to CRD (p < 0.05). NaHS-induced antinociception was reversed by glibenclamide, a ATP-sensitive K(+) (K(ATP)) channel inhibitor, and N(omega)-nitro-L-arginine methyl ester hydrochloride (L-NAME), a nitric-oxide (NO) synthase inhibitor. The antinociceptive effect of NaHS was maintained during the resolution of colon inflammation induced by intrarectal administration of a chemical irritant. In summary, these data show that H(2)S inhibits nociception induced by CRD in both healthy and postcolitic rats. This effect is mediated by K(ATP) channels and NO. H(2)S-releasing drugs might be beneficial in treating painful intestinal disorders.
263 citations
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TL;DR: An improvement on the oxygen barrier and stretchability was achieved in PLA-PHB-CNCs-ATBC which also displayed somewhat UV light blocking effect suggesting their possible applications as biodegradable packaging materials.
263 citations
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Casa Sollievo della Sofferenza1, Istituto Superiore di Sanità2, University of Perugia3, Catholic University of the Sacred Heart4, Sapienza University of Rome5, Erasmus University Rotterdam6, University of Bologna7, Policlinico Umberto I8, University of Turin9, University of Genoa10, Icahn School of Medicine at Mount Sinai11
TL;DR: To investigate the phenotypic spectrum and molecular diversity of germline mutations affecting BRAF, subjects with a diagnosis of NS, LS, and CFCS were screened for the entire coding sequence of the gene.
Abstract: Noonan, LEOPARD, and cardiofaciocutaneous syndromes (NS, LS, and CFCS) are developmental disorders with overlapping features including distinctive facial dysmorphia, reduced growth, cardiac defects, skeletal and ectodermal anomalies, and variable cognitive deficits. Dysregulated RAS–mitogen-activated protein kinase (MAPK) signal traffic has been established to represent the molecular pathogenic cause underlying these conditions. To investigate the phenotypic spectrum and molecular diversity of germline mutations affecting BRAF, which encodes a serine/threonine kinase functioning as a RAS effector frequently mutated in CFCS, subjects with a diagnosis of NS (N=270), LS (N=6), and CFCS (N=33), and no mutation in PTPN11, SOS1, KRAS, RAF1, MEK1, or MEK2, were screened for the entire coding sequence of the gene. Besides the expected high prevalence of mutations observed among CFCS patients (52%), a de novo heterozygous missense change was identified in one subject with LS (17%) and five individuals with NS (1.9%). Mutations mapped to multiple protein domains and largely did not overlap with cancer-associated defects. NS-causing mutations had not been documented in CFCS, suggesting that the phenotypes arising from germline BRAF defects might be allele specific. Selected mutant BRAF proteins promoted variable gain of function of the kinase, but appeared less activating compared to the recurrent cancer-associated p.Val600Glu mutant. Our findings provide evidence for a wide phenotypic diversity associated with mutations affecting BRAF, and occurrence of a clinical continuum associated with these molecular lesions. Hum Mutat 0:1–8, 2009. © 2009 Wiley-Liss, Inc.
263 citations
Authors
Showing all 13488 results
Name | H-index | Papers | Citations |
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Michael Grätzel | 248 | 1423 | 303599 |
Luigi Ferrucci | 193 | 1601 | 181199 |
Tobin J. Marks | 159 | 1621 | 111604 |
Johan Auwerx | 158 | 653 | 95779 |
Tony Pawson | 150 | 425 | 85196 |
Jack Hirsh | 146 | 734 | 86332 |
Alexander Belyaev | 142 | 1895 | 100796 |
R. L. McCarthy | 141 | 1238 | 115696 |
Harvey B Newman | 139 | 1594 | 88308 |
Guido Tonelli | 138 | 1458 | 97248 |
Elias Campo | 135 | 761 | 85160 |
Alberto Messineo | 134 | 1511 | 96492 |
Franco Ligabue | 134 | 1404 | 95389 |
Roberto Tenchini | 133 | 1390 | 94541 |
R. Bartoldus | 132 | 1624 | 97405 |