Institution
University of Palermo
Education•Palermo, Italy•
About: University of Palermo is a education organization based out in Palermo, Italy. It is known for research contribution in the topics: Population & Medicine. The organization has 15621 authors who have published 40250 publications receiving 964384 citations. The organization is also known as: Università degli Studi di Palermo & Universita degli Studi di Palermo.
Topics: Population, Medicine, Cancer, Context (language use), Catalysis
Papers published on a yearly basis
Papers
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TL;DR: In this article, 1 3 C NMR chemical shift calculations at Hartree-Fock level, using the 6-31G(d) basis set, are proposed as a tool to be applied in the structural characterization of new organic compounds, thus providing useful support in the interpretation of experimental NMR data.
Abstract: Geometry optimization and GIAO (gauge including atomic orbitals) 1 3 C NMR chemical shift calculations at Hartree-Fock level, using the 6-31G(d) basis set, are proposed as a tool to be applied in the structural characterization of new organic compounds, thus providing useful support in the interpretation of experimental NMR data. Parameters related to linear correlation plots of computed versus experimental 1 3 C NMR chemical shifts for fourteen low-polar natural products, containing 10-20 carbon atoms, were employed to assess the reliability of the proposed structures. A comparison with the hybrid B3LYP method was carried out to evaluate electron correlation contributions to the calculation of 1 3 C NMR chemical shifts and, eventually, to extend the applicability of such computational methods to the interpretation of NMR spectra in apolar solutions. The method was tested by studying three examples of revised structure assignments, analyzing how the theoretical 1 3 C chemical shifts of both correct and incorrect structures matched the experimental data.
206 citations
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TL;DR: In this article, the authors studied the asymptotic behavior of the sequence of codimensions of a PI-algebra over a field and showed that if A is finitely generated over F thenInv(A)=limn→∞ c n (A) always exists and is an integer.
206 citations
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TL;DR: It is shown that both mice and humans with autoimmune arthritis can have dysbiosis and barrier leakiness prior to major signs of inflammatory arthritis, and treatment of mice with a zonulin antagonist can limit collagen-induced arthritis.
Abstract: Gut microbial dysbiosis is associated with the development of autoimmune disease, but the mechanisms by which microbial dysbiosis affects the transition from asymptomatic autoimmunity to inflammatory disease are incompletely characterized. Here, we identify intestinal barrier integrity as an important checkpoint in translating autoimmunity to inflammation. Zonulin family peptide (zonulin), a potent regulator for intestinal tight junctions, is highly expressed in autoimmune mice and humans and can be used to predict transition from autoimmunity to inflammatory arthritis. Increased serum zonulin levels are accompanied by a leaky intestinal barrier, dysbiosis and inflammation. Restoration of the intestinal barrier in the pre-phase of arthritis using butyrate or a cannabinoid type 1 receptor agonist inhibits the development of arthritis. Moreover, treatment with the zonulin antagonist larazotide acetate, which specifically increases intestinal barrier integrity, effectively reduces arthritis onset. These data identify a preventive approach for the onset of autoimmune disease by specifically targeting impaired intestinal barrier function. Intestinal dysbiosis is associated with an ever-growing list of autoimmune diseases. Here the authors show that both mice and humans with autoimmune arthritis can have dysbiosis and barrier leakiness prior to major signs of inflammatory arthritis, and treatment of mice with a zonulin antagonist can limit collagen-induced arthritis.
205 citations
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TL;DR: Flow cytometric and cytogenetic analyses demonstrated that the polyploidy resulted from genome-wide rereplication without an intervening mitosis, indicating that p53 and pRb help maintain normal cell ploidy by preventing DNA rereplications prior to mitotic division.
Abstract: Cell cycle checkpoints are biochemical signal transduction pathways that prevent downstream events from being initiated until upstream processes are completed. We analyzed whether the p53 or pRb tumor suppressors are involved in a checkpoint(s) that prevents DNA rereplication in the presence of drugs that interfere with spindle assembly. Normal mouse and human fibroblasts arrested with a 4N DNA content when treated with nocodazole and Colcemid, whereas isogeneic p53-deficient or pRb-deficient derivatives became polyploid. Flow cytometric and cytogenetic analyses demonstrated that the polyploidy resulted from genome-wide rereplication without an intervening mitosis. Thus, p53 and pRb help maintain normal cell ploidy by preventing DNA rereplication prior to mitotic division.
205 citations
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TL;DR: This analysis did not detect any significant benefit of interferon alfa on morbidity in patients with compensated cirrhosis type C, although it suggests a reduction in complications of Cirrhosis for those with a sustained response to therapy, and it indicates the need for better therapies.
205 citations
Authors
Showing all 15895 results
Name | H-index | Papers | Citations |
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Robin M. Murray | 171 | 1539 | 116362 |
Frede Blaabjerg | 147 | 2161 | 112017 |
Jean Bousquet | 145 | 1288 | 96769 |
Zhanhu Guo | 128 | 886 | 53378 |
Jean Ballet | 115 | 263 | 46301 |
Antonio Facchetti | 111 | 602 | 51885 |
Michele Pagano | 97 | 306 | 42211 |
Frank Z. Stanczyk | 93 | 620 | 30244 |
Eleonora Troja | 91 | 271 | 30873 |
Francesco Sciortino | 90 | 536 | 28956 |
Zev Rosenwaks | 89 | 772 | 32039 |
Antonio Russo | 88 | 934 | 34563 |
Carlo Salvarani | 88 | 730 | 31699 |
Giuseppe Basso | 87 | 643 | 33320 |
Antonio Craxì | 86 | 659 | 39463 |