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Your search keyword '"Nicocia, Giacomo"' showing total 13 results
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13 results on '"Nicocia, Giacomo"'

10. Role of oxidative stress in Retinitis pigmentosa: new involved pathways by an RNA-Seq analysis.

Author

Donato, Luigi, Scimone, Concetta, Nicocia, Giacomo, D'Angelo, Rosalia, and Sidoti, Antonina

Abstract

Retinitis pigmentosa (RP) is a very heterogeneous inherited ocular disorder group characterized by progressive retinal disruption. Retinal pigment epithelium (RPE) degeneration, due to oxidative stress which arrests the metabolic support to photoreceptors, represents one of the principal causes of RP. Here, the role of oxidative stress in RP onset and progression was analyzed by a comparative whole transcriptome analysis of human RPE cells, treated with 100 µg/ml of oxLDL and untreated, at different time points. Experiment was thrice repeated and performed on Ion ProtonTM sequencing system. Data analysis, including low quality reads trimming and gene expression quantification, was realized by CLC Genomics Workbench software. The whole analysis highlighted 14 clustered "macro-pathways" and many sub-pathways, classified by selection of 5271 genes showing the highest alteration of expression. Among them, 23 genes were already known to be RP causative ones (15 over-expressed and 8 down-expressed), and their enrichment and intersection analyses highlighted new 77 candidate related genes (49 over-expressed and 28 down-expressed). A final filtering analysis then highlighted 29 proposed candidate genes. This data suggests that many new genes, not yet associated with RP, could influence its etiopathogenesis. [ABSTRACT FROM AUTHOR]

Published
2019
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11. RETRACTED ARTICLE: Role of oxidative stress in Retinitis pigmentosa: new involved pathways by an RNA-Seq analysis

Author

Donato, Luigi, Scimone, Concetta, Nicocia, Giacomo, D’Angelo, Rosalia, and Sidoti, Antonina

Abstract

Statement of RetractionWe, the Editor[s] and Publisher of Cell Cycle, have retracted the following article:Role of oxidative stress in Retinitis pigmentosa: new involved pathways by an RNA-Seq analysisLuigi Donato, Concetta Scimone, Giacomo Nicocia, Rosalia D’Angelo & Antonina SidotiPages 84-104 | https://doi.org/10.1080/15384101.2018.1558873The above article has been retracted as a result of concerns regarding the use of raw data by one of the authors upon which the presented research has been based. After examination and approval from the author concerned, the consensus is that the data was used without consent, and that therefore the article must be retracted.We note that we received, peer-reviewed, accepted, and published the article in good faith based on the purported veracity of these representations and warranties. We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines on retractions.The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted”.

Published
2019
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13. The future of phosphate binders: a perspective on novel therapeutics.

Author

Cernaro V, Santoro D, Lucisano S, Nicocia G, Lacquaniti A, and Buemi M

Subjects
Animals, Biomarkers blood, Bone Diseases, Metabolic etiology, Drug Design, Fibroblast Growth Factor-23, Fibroblast Growth Factors blood, Humans, Phosphates blood, Renal Insufficiency, Chronic complications, Bone Diseases, Metabolic drug therapy, Chelating Agents therapeutic use, Renal Insufficiency, Chronic drug therapy
Abstract

Chronic kidney disease-mineral bone disorder (CKD-MBD) is a common complication of CKD. The therapeutic strategies for the treatment of CKD-MBD include phosphate binders, active vitamin D analogs and calcimimetics. The first class of drugs provided nephrologists with a range of phosphate binders that are able to decrease circulating phosphate and parathyroid hormone but involve some tolerability and safety issues. In the past 2 years, new phosphate binders have been launched and others are still under development. Serum phosphate increases only in the late stages of CKD but clinical abnormalities begin to occur earlier when multiple mechanisms try to compensate for the progressive reduced ability of the kidney to eliminate phosphorus with urine. Accordingly, starting phosphate binders when phosphatemia reaches values higher than normal may represent a late therapeutic approach. Serum phosphorus is not the ideal biomarker for the diagnosis and treatment of phosphate imbalance. This role could be better played by fibroblast growth factor 23, whose serum concentrations rise earlier in CKD. A more detailed knowledge of the mechanisms underlying CKD-MBD development will provide new therapeutic targets and then new perspectives for the treatment of phosphate imbalance in the future.

Published
2014
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