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Nigro E.,CEINGE Biotecnologie Avanzate Scarl | Sangiorgio D.,University Telematica Pegaso | Scudiero O.,CEINGE Biotecnologie Avanzate Scarl | Scudiero O.,University of Naples Federico II | And 5 more authors.
Cytokine | Year: 2016

Metabolic Syndrome prevalence has reaching epidemic proportions worldwide. Adiponectin (Acrp30), and in particular its High Molecular Weight (HMW) oligomers, contributes to enhance insulin sensitivity and to reduce inflammation levels. Physical exercise improves body's biochemical balance and metabolism resulting effective in prevention of metabolic diseases. Whether improvement of metabolic features mediated by physical exercise is associated with changes in Acrp30 serum composition is not yet clarified. In the present study, we investigated total Acrp30 expression, its oligomeric status and genetic variants in adiponectin gene (ACDC) in twenty-two professional Water Polo (WP) Players and 40 age- and sex-matched controls. Anthropometric, metabolic parameters and total Acrp30 were assessed; Acrp30 oligomeric profile was characterized by Western blot as well as by FPLC analysis. ACDC gene was analyzed by direct-sequencing analysis. Significant elevated body mass index, aspartate aminotransferase and lactate dehydrogenase levels and, conversely, significantly lower concentrations of total and cholesterol low density lipoprotein were present in WP players. No significant difference was found in total Acrp30 and/or HMW oligomers. Interestingly, in WP players, a direct relationship between total Acrp30 and monocytes as well as an inverse relationship between total Acrp30 and AST levels were found. ACDC screening revealed previously described SNPs. In conclusion, our study confirms the long-term beneficial effects of high physical training on metabolism and suggests that they are not associated with Acrp30 and/or HMW oligomers changes. Moreover, the correlation of Acrp30 with monocytes in WP athletes could represent a mechanism by which Acrp30 participates in exercise-induced anti-inflammatory functions and/or cardiovascular health. © 2016. Source

Scorza M.,CEINGE Biotecnologie Avanzate | Scorza M.,University of Naples Federico II | Elce A.,CEINGE Biotecnologie Avanzate | Elce A.,University of Naples Federico II | And 11 more authors.
Biochimica Clinica | Year: 2013

Mutation epidemiology is crucial for cystic fibrosis (CF) diagnosis and counselling. ∼6%-7% of alleles from CF patients do not bear mutations in the coding regions of the Cystic Fibrosis Transmembrane Regulator (CFTR) disease gene. In these patients, mutations may be present in non-coding, regulatory regions of the gene as i) intronic regions (particularly in high conserved sequences), ii) the promoter region or iii) the area at the 3' of the gene, which is the target of microRNA regulation. We studied these regions by gene sequencing in a group of CF patients with one or both unidentified mutations after the analysis of CFTR coding regions, and in a group of CF patients with a different clinical expression of disease to evaluate if mutations in such regions may have a role in modulating CF clinical expression. Our analysis revealed: i) a dozen of mutations (most novel) in the large promoter area of 6000 bp at the 5' of the gene; expression studies in four cell lines demonstrated that a half of such mutations may have a pathogenic effect; ii) a series of mutations in 52 conserved sequence tags (CSTs), i.e. intronic regions with a high homology between humans and mouse; expression studies revealed the pathogenic effect of one of these mutations; iii) finally, three mutations in the 1500 bp region at the 3' of the gene; one of this has a pathogenic role, enhancing the interaction of CFTR with two inhibitory microRNAs. To the best of our knowledge, this is the first example of such pathogenic mechanism in a monogenic disorder. On the contrary, no mutations were identified in patients with different clinical expression in any of the three non-coding regions. To conclude, the sequencing of non coding regions may improve the detection rate of molecular analysis in CF, but functional studies are required to define the pathogenic effect of novel mutations. Source

Persia F.,University of Naples Federico II | D'Auria D.,University of Naples Federico II | Sperli G.,University of Naples Federico II | Tufano A.,University Telematica Pegaso
Communications in Computer and Information Science | Year: 2015

Security has been raised at major public buildings in the most famous and crowded cities all over the world following the terrorist attacks of the last years, the latest one at the Bardo museum in the centre of Tunis. For that reason, video surveillance systems have become more and more essential for detecting and hopefully even prevent dangerous events in public areas. In this paper, we present a prototype for anomaly detection in video surveillance context. The whole process is described, starting from the video frames captured by sensors/cameras till at the end some well-known reasoning algorithms for finding potentially dangerous activities are applied. The conducted experiments confirm the efficiency and the effectiveness achieved by our prototype. © Springer International Publishing Switzerland 2015. Source

Borbone N.,University of Naples Federico II | Elce A.,University Telematica Pegaso | Amato J.,University of Naples Federico II | D'Errico S.,University of Naples Federico II | And 4 more authors.
MedChemComm | Year: 2014

Recently, microRNAs (miRNAs) were identified as being able to inhibit the expression of the Cystic Fibrosis Transmembrane Regulator (CFTR) disease-gene of Cystic Fibrosis (CF) and CFTR-Related Disorders (CFTR-RD). This study shows the use of peptide nucleic acids (PNAs) as inhibitors of miR-509-3p, one of the CFTR regulating miRNAs, by reverting the expression of the luciferase gene containing the 3′UTR of CFTR gene. © 2014 The Royal Society of Chemistry. Source

Zarrilli F.,University of Molise | Elce A.,CEINGE Biotecnologie Avanzate Scarl | Elce A.,University Telematica Pegaso | Scorza M.,CEINGE Biotecnologie Avanzate Scarl | And 7 more authors.
BioMed Research International | Year: 2013

Liver inherited diseases are a group of genetically determined clinical entities that appear with an early chronic liver involvement. They include Wilson's disease (hepatolenticular degeneration), hereditary hemochromatosis, and alpha-1-antitrypsin deficiency. In addition, cystic fibrosis, although it is not specifically a liver disease, may cause a severe liver involvement in a significant percentage of cases. For all these pathologies, the disease gene is known, and molecular analysis may contribute to the unequivocal diagnosis. This approach could avoid the patient invasive procedures and limit complications associated with a delay in diagnosis. We review liver inherited diseases on the basis of the genetic defect, focusing on the contribution of molecular analysis in the multistep diagnostic workup. © 2013 Federica Zarrilli et al. Source

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