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Institution

University of Florence

EducationFlorence, Toscana, Italy
About: University of Florence is a education organization based out in Florence, Toscana, Italy. It is known for research contribution in the topics: Population & Carbonic anhydrase. The organization has 27292 authors who have published 79599 publications receiving 2341684 citations. The organization is also known as: Università degli studi di Firenze & Universita degli studi di Firenze.


Papers
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Journal ArticleDOI
TL;DR: It is reported that VacA also interferes with T cell activation by two different mechanisms, one of which involves activation of intracellular signaling through the mitogen-activated protein kinases MKK3/6 and p38 and the Rac-specific nucleotide exchange factor, Vav.
Abstract: Helicobacter pylori toxin, VacA, damages the gastric epithelium by erosion and loosening of tight junctions. Here we report that VacA also interferes with T cell activation by two different mechanisms. Formation of anion-specific channels by VacA prevents calcium influx from the extracellular milieu. The transcription factor NF-AT thus fails to translocate to the nucleus and activate key cytokine genes. A second, channel-independent mechanism involves activation of intracellular signaling through the mitogen-activated protein kinases MKK3/6 and p38 and the Rac-specific nucleotide exchange factor, Vav. As a consequence of aberrant Rac activation, disordered actin polymerization is stimulated. The resulting defects in T cell activation may help H. pylori to prevent an effective immune response leading to chronic colonization of its gastric niche.

313 citations

Journal ArticleDOI
TL;DR: In this paper, the authors investigated the role of different cell types in the deposition of fibrillar extracellular matrix during active hepatic fibrogenesis: hepatic stellate cells are mainly involved when hepatocellular damage is limited or concentrated within the liver lobule, whereas portal myofibroblasts and fibroblast provide a predominant contribution when the damage is located in the proximity of the portal tracts.

313 citations

Journal ArticleDOI
TL;DR: MeDuSa formalizes the scaffolding problem by means of a combinatorial optimization formulation on graphs and implements an efficient constant factor approximation algorithm to solve it, which does not require either prior knowledge on the microrganisms dataset under analysis or the availability of paired end read libraries.
Abstract: Completing the genome sequence of an organism is an important task in comparative, functional and structural genomics. However, this remains a challenging issue from both a computational and an experimental viewpoint. Genome scaffolding (i.e. the process of ordering and orientating contigs) of de novo assemblies usually represents the first step in most genome finishing pipelines. In this paper, we present MeDuSa (Multi-Draft based Scaffolder), an algorithm for genome scaffolding. MeDuSa exploits information obtained from a set of (draft or closed) genomes from related organisms to determine the correct order and orientation of the contigs. MeDuSa formalises the scaffolding problem by means of a combinatorial optimisation formulation on graphs and implements an efficient constant factor approximation algorithm to solve it. In contrast to currently used scaffolders, it does not require either prior knowledge on the microrganisms dataset under analysis (e.g. their phylogenetic relationships) or the availability of paired end read libraries. This makes usability and running time two additional important features of our method. Moreover, benchmarks and tests on real bacterial datasets showed that MeDuSa is highly accurate and, in most cases, outperforms traditional scaffolders. The possibility to use MeDuSa on eukaryotic datasets has also been evaluated, leading to interesting results. MeDuSa web server: http://combo.dbe.unifi.it/medusa A stand-alone version of the software can be downloaded from https://github.com/combogenomics/medusa/releases. All results presented in this work have been obtained with MeDuSa v. 1.3. marco.fondi@unifi.it.

313 citations

Journal ArticleDOI
29 Oct 1998-Nature
TL;DR: The steepness of the summation curves indicates that the mechanisms that analyse biological motion do not integrate linearly over space and time with constant efficiency, as may occur for other forms of complex motion, but instead adapt to the nature of the stimulus.
Abstract: One of the more stunning examples of the resourcefulness of human vision is the ability to see 'biological motion', which was first shown with an adaptation of earlier cinematic work: illumination of only the joints of a walking person is enough to convey a vivid, compelling impression of human animation, although the percept collapses to a jumble of meaningless lights when the walker stands still. The information is sufficient to discriminate the sex and other details of the walker, and can be interpreted by young infants. Here we measure the ability of the visual system to integrate this type of motion information over space and time, and compare this capacity with that for viewing simple translational motion. Sensitivity to biological motion increases rapidly with the number of illuminated joints, far more rapidly than for simple motion. Furthermore, this information is summed over extended temporal intervals of up to 3 seconds (eight times longer than for simple motion). The steepness of the summation curves indicates that the mechanisms that analyse biological motion do not integrate linearly over space and time with constant efficiency, as may occur for other forms of complex motion, but instead adapt to the nature of the stimulus.

313 citations

Journal ArticleDOI
TL;DR: Metformin significantly increases GLP-1 levels after an oral glucose load in obese nondiabetic subjects; this effect could be due to an inhibition of GLP(7-36)amide degradation.
Abstract: OBJECTIVE —To evaluate the effects of metformin on glucagon-like peptide 1 (GLP-1) and leptin levels. RESEARCH DESIGN AND METHODS —A total of 10 obese nondiabetic male patients were studied before and after a 14-day treatment with 2,550 mg/day metformin and were compared with 10 untreated obese control subjects. On days 0 and 15, leptin and GLP-1(7–36)amide/(7–37) levels were assessed before and after an oral glucose load during a euglycemic hyperinsulinemic clamp to avoid the interference of variations of insulinemia and glycemia on GLP-1 and leptin secretion. The effects of metformin on GLP-1(7–36)amide degradation in human plasma and in a buffer solution containing dipeptidyl peptidase IV (DPP-IV) were also studied. RESULTS —Leptin levels were not affected by the oral glucose load, and they were not modified after metformin treatment. Metformin induced a significant ( P CONCLUSIONS —Metformin significantly increases GLP-1 levels after an oral glucose load in obese nondiabetic subjects; this effect could be due to an inhibition of GLP-1 degradation.

312 citations


Authors

Showing all 27699 results

NameH-indexPapersCitations
Charles A. Dinarello1901058139668
D. M. Strom1763167194314
Gregory Y.H. Lip1693159171742
Christopher M. Dobson1501008105475
Dirk Inzé14964774468
Thomas Hebbeker1481984114004
Marco Zanetti1451439104610
Richard B. Devereux144962116403
Gunther Roland1411471100681
Markus Klute1391447104196
Tariq Aziz138164696586
Guido Tonelli138145897248
Giorgio Trinchieri13843378028
Christof Roland137130896632
Christoph Paus1371585100801
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023244
2022631
20215,298
20205,251
20194,652
20184,147