Pontedera, Italy
Pontedera, Italy

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Aquaro G.D.,CNR Institute of Neuroscience | Gabutti A.,CNR Institute of Neuroscience | Meini M.,Azienda USL 5 | Prontera C.,CNR Institute of Neuroscience | And 4 more authors.
Heart | Year: 2011

Background: Cocaine addiction is associated with either ischaemic or non-ischaemic cardiac complications. The prevalence of myocardial damage in asymptomatic addicts has never been evaluated by cardiovascular magnetic resonance (CMR), which allows non-invasive detection of myocardial oedema and fibrosis. Objective: To prospectively evaluate the prevalence of myocardial damage in cocaine addicts with no history of cardiac disease by CMR. Methods: Thirty consecutive subjects (25 men, mean age 39±7 years), with no history of cardiac symptoms/disease were evaluated 48 h after the withdrawal of cocaine by a comprehensive humoral, clinical and instrumental assessment, including B-type natriuretic peptide and troponin I assay, echocardiography, exercise stress test and 24 h ECG recording, as well as CMR examination. The CMR study was performed using a 1.5 Tesla scanner. Myocardial oedema was evaluated by a T2-weighted STIR sequence and fibrosis using the late gadolinium enhancement technique. Results: Biohumoral markers of cardiac involvement were negative in all subjects except one. Fifteen subjects had subtle abnormalities at resting ECG, while exercise stress testing and Holter studies were negative for ischaemic or arrhythmic events. Echocardiography provided evidence of wall motion abnormalities in 12 subjects. At CMR evaluation, myocardial involvement was detected in 25 subjects (83%), oedema in 14 (47%) and fibrosis in 22 (73%). Eleven subjects (37%) showed both myocardial oedema and fibrosis with similar localisations in nine. Seven subjects had ischaemic patterns of fibrosis and 15 had non-ischaemic patterns of fibrosis. Conclusions: A high prevalence of cardiac damage in asymptomatic cocaine addicts can be found by CMR examination.


Lombardi S.,University of Pisa | Fuoco I.,University of Pisa | Di Fluri G.,Azienda Ospedaliera Universitaria Pisana | Costa F.,Azienda Ospedaliera Universitaria Pisana | And 4 more authors.
Oncotarget | Year: 2015

Inflammatory bowel disease (IBD) and polyps, are common colorectal pathologies in western society and are risk factors for development of colorectal cancer (CRC). Genomic instability is a cancer hallmark and is connected to changes in chromosomal structure, often caused by double strand break formation (DSB), and aneuploidy. Cellular stress, may contribute to genomic instability. In colorectal biopsies and peripheral blood lymphocytes of patients with IBD, polyps and CRC, we evaluated 1) genomic instability using the γH2AX assay as marker of DSB and micronuclei in mononuclear lymphocytes kept under cytodieresis inhibition, and 2) cellular stress through expression and cellular localization of glutathione-S-transferase omega 1 (GSTO1). Colon biopsies showed γH2AX increase starting from polyps, while lymphocytes already from IBD. Micronuclei frequency began to rise in lymphocytes of subjects with polyps, suggesting a systemic genomic instability condition. Colorectal tissues lost GSTO1 expression but increased nuclear localization with pathology progression. Lymphocytes did not change GSTO1 expression and localization until CRC formation, where enzyme expression was increased. We propose that the growing genomic instability found in our patients is connected with the alteration of cellular environment. Evaluation of genomic damage and cellular stress in colorectal pathologies may facilitate prevention and management of CRC.


PubMed | Azienda Ospedaliera Universitaria Pisana, University of Pisa and Azienda USL 5
Type: Journal Article | Journal: Oncotarget | Year: 2015

Inflammatory bowel disease (IBD) and polyps, are common colorectal pathologies in western society and are risk factors for development of colorectal cancer (CRC). Genomic instability is a cancer hallmark and is connected to changes in chromosomal structure, often caused by double strand break formation (DSB), and aneuploidy. Cellular stress, may contribute to genomic instability. In colorectal biopsies and peripheral blood lymphocytes of patients with IBD, polyps and CRC, we evaluated 1) genomic instability using the H2AX assay as marker of DSB and micronuclei in mononuclear lymphocytes kept under cytodieresis inhibition, and 2) cellular stress through expression and cellular localization of glutathione-S-transferase omega 1 (GSTO1). Colon biopsies showed H2AX increase starting from polyps, while lymphocytes already from IBD. Micronuclei frequency began to rise in lymphocytes of subjects with polyps, suggesting a systemic genomic instability condition. Colorectal tissues lost GSTO1 expression but increased nuclear localization with pathology progression. Lymphocytes did not change GSTO1 expression and localization until CRC formation, where enzyme expression was increased. We propose that the growing genomic instability found in our patients is connected with the alteration of cellular environment. Evaluation of genomic damage and cellular stress in colorectal pathologies may facilitate prevention and management of CRC.

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