Giulia Di Benedetto

University of Catania

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Renato Bernardini

University of Catania

Giuseppina Cantarella

University of Catania

Chiara Burgaletto

University of Catania

Carlo Maria Bellanca

University of Catania

Antonio Munafò

University of Florence

Rosaria Di Mauro

University of Catania

Laurence Lempereur

University of Catania

Anna Cantone

University of Catania

Ysabel Conde

University of Szeged

Antonio Vitarelli

Sapienza University of Rome

Cooperative Institutions

University of Catania

Sapienza University of Rome

Istituti di Ricovero e Cura a Carattere Scientifico

University of Naples Federico II

University of Padua

National Research Council

University of Palermo

Azienda Ospedaliero-Universitaria Policlinico - Vittorio Emanuele

Policlinico Universitario di Catania

University of Milan

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Journal of Neurochemistry (2008)

Giuseppina Cantarella Giulia Di Benedetto Salvatore Pezzino Nunziata Risuglia Renato Bernardini

Abstract Tumor necrosis factor related apoptosis inducing ligand (TRAIL) is involved in amyloid beta dependent neurotoxicity via the extrinsic pathway. Recently, several genes modulating TRAIL cytotoxicity have been characterized, providing evidence for a role of wingless‐type mouse mammary tumor virus integration site family (Wnt), Jun‐N‐terminal kinase and other pathways in increased cell susceptibility to the cytokine. We investigated whether neurotoxic effects of TRAIL could be due to modulation of the Wnt signaling pathway. Western blot analysis of Wnt in SH‐SY5Y human neuroblastoma cells showed significantly decreased Wnt expression in cultures treated with TRAIL. Correspondingly, both phosphorylation of glycogen synthase kinase 3 beta and degradation of cytoplasmic β‐catenin were increased, as well as phosphorylation of the τ protein, bringing about the picture of neuronal damage. As a counterproof of the interaction of TRAIL with the Wnt pathway, the addition of the specific glycogen synthase kinase 3 beta inhibitor SB216763 resulted in rescue of a significant percent of cells from TRAIL‐induced apoptosis. The rescue was total when the caspase 8 inhibitor z‐IETD‐FMK was added in combination with SB216763. Results show that, probably, in addition to triggering caspase signaling, TRAIL also interferes with the Wnt pathway, additionally concurring to neuronal damage. These data suggest that the Wnt pathway substantially contributes to the TRAIL‐related neurotoxicity and indicate the TRAIL system as a candidate target for pharmacological treatment of Alzheimer’s disease and related disorders.

GSK3B

Neurotoxicity

10.1111/j.1471-4159.2008.05291.x

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Citations (17)

Incidence of Prostate Cancer in Sicily: Results of a Multicenter Case-Findings Protocol

European Urology (2004)

F Aragona Pietro Pepe Massimo Motta Alberto Saita Gregory Alexander Raciti

10.1016/j.eururo.2004.11.007

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The role of antioxidant supplement in immune system, neoplastic, and neurodegenerative disorders: a point of view for an assessment of the risk/benefit profile

Nutrition Journal (2008)

Daria Brambilla Cesare Mancuso Maria Grazia Scuderi Paolo Bosco Giuseppina Cantarella

Abstract This review will discuss some issues related to the risk/benefit profile of the use of dietary antioxidants. Thus, recent progress regarding the potential benefit of dietary antioxidants in the treatment of chronic diseases with a special focus on immune system and neurodegenerative disorders will be discussed here. It is well established that reactive oxygen species (ROS) play an important role in the etiology of numerous diseases, such as atherosclerosis, diabetes and cancer. Among the physiological defense system of the cell, the relevance of antioxidant molecules, such as glutathione and vitamins is quite well established. Recently, the interest of researchers has, for example, been conveyed on antioxidant enzyme systems, such as the heme oxygenase/biliverdin reductase system, which appears modulated by dietary antioxidant molecules, including polyphenols and beta-carotene. These systems possibly counteract oxidative damage very efficiently and finally modulate the activity of oxidative phenomena occurring, for instance, during pathophysiological processes. Although evidence shows that antioxidant treatment results in cytoprotection, the potential clinical benefit deriving from both nutritional and supplemental antioxidants is still under wide debate. In this line, the inappropriate assumption of some lipophylic vitamins has been associated with increased incidence of cancer rather than with beneficial effects.

Cancer Prevention

10.1186/1475-2891-7-29

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Prostate cancer detection after one or more negative extended needle biopsy: results of a multicenter case-findings protocol.

Pietro Pepe Giulia Di Benedetto Maurizio Gulletta F. Pietropaolo G. Minaldi

OBJECTIVES To evaluate PCa incidence in patients with one or more negative extended prostate biopsy who underwent repeat biopsy or TURP. MATERIAL AND METHODS From June 2003 to February 2008, 308 patients were submitted to repeat prostate biopsy (median 20.5 cores) and 120 patients underwent TURP after one or more 12 cores prostate biopsy. Indications for biopsy were: abnormal DRE; PSA > 10 ng/mL; PSA included between 4.1-10 or 2.6-4 ng/mL with free/total PSA < or = 25% and < or = 20%, respectively 262 and 46 underwent a second and a third biopsy: 218 because for high levels of PSA, 40 and 50 patients for a previous diagnosis of HGPIN and ASAP, 28 had an abnormal DRE. PSA in patients who underwent TURP was 11.6 ng/mL (median); in all cases DRE was negative and only 76 patients referred LUTS. RESULTS PCa incidence at repeat biopsy was 16.9%; 96.2% of cancers were diagnosed at a second biopsy and 3.8% at a third one. PCa incidence was higher in patients with previous ASAP (43.4% and 50%) vs patients with HGPIN (25% and 0%) or benign pathology (11.9% and 0%). PCa was diagnosed in 11.1% and 19% of patients who underwent TURP previously submitted to a first and a second biopsy, respectively. CONCLUSIONS In case of persistent suspicion of PCa after a repeated negative saturation biopsy, TURP should be proposed as part of the diagnostic procedure aside from LUTS, especially in patients with a life expectancy greater than 10 years.

Prostate biopsy

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Assessment of congenital coronary artery fistulas by transesophageal color Doppler echocardiography

The American Journal of Medicine (2002)

Antonio Vitarelli Guglielmo De Curtis Ysabel Conde Mario Colantonio Giulia Di Benedetto

Circumflex

Left coronary artery

10.1016/s0002-9343(02)01157-9

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Citations (115)

Dobutamine stress echo with tissue doppler imaging for assessing viability in patients with coronary artery disease and chronic left ventricular dysfunction

Journal of Cardiac Failure (1999)

Antonio Vitarelli Ysabel Conde Miguel Cortes Rossella Giubilei Giulia Di Benedetto

Dobutamine

Doppler imaging

Stress Echocardiography

Echo (communications protocol)

10.1016/s1071-9164(99)91356-8

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Calcium regulation of ciliary beat frequency in human respiratory epithelium in vitro.

The Journal of Physiology (1991)

Giulia Di Benedetto C. J. Magnus P. T. A. Gray Anil Mehta

1. The changes in ciliary beat frequency (CBF) of human nasal respiratory epithelial cells were measured in vitro with a photometric technique following exposure to either 4‐bromo‐calcium ionophore A23187 (4‐Br‐A23187) or trifluoperazine (TFP), an inhibitor of calmodulin‐sensitive calcium‐dependent protein kinases. Changes in intracellular free calcium concentrations in response to 4‐Br‐A23187 were studied using a fluorescent dye (Fura‐2). 2. Addition of 10(‐5) M‐4‐Br‐A23187 caused a time‐dependent (P less than 0.01) rise in CBF. The increment in CBF was statistically significant 10 min after challenge (+10%; P less than 0.01) and was sustained for at least 1 h, with maximal stimulation after 40 min (+ 18%; P less than 0.01). 3. Exposure to 10(‐5) M‐4‐Br‐A23187 caused an immediate increase in intracellular free calcium concentration, which preceded the rise in CBF. 4. TFP (10(‐4) M) caused a reduction of baseline CBF (‐10%; P less than 0.01) and prevented the expected rise when the cells were subsequently exposed to 10(‐5) M‐4‐Br‐A23187. 5. We conclude that: (1) calcium ionophore stimulates the CBF of human respiratory cells; (2) this effect is mediated through a calmodulin‐sensitive system, since it is abolished in the presence of TFP; (3) the same pathway appears to control the basal CBF of these cells, since TFP also decreases CBF.

Trifluoperazine

Fura-2

Calcium in biology

10.1113/jphysiol.1991.sp018659

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Citations (76)

Neutralization of Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand Reduces Spinal Cord Injury Damage in Mice

Neuropsychopharmacology (2010)

Giuseppina Cantarella Giulia Di Benedetto Mimmo Scollo Irene Paterniti Salvatore Cuzzocrea

10.1038/npp.2009.234

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Citations (36)

Rebalancing Immune Interactions within the Brain-Spleen Axis Mitigates Neuroinflammation in an Aging Mouse Model of Alzheimer’s Disease

Journal of Neuroimmune Pharmacology (2025)

Anna Cantone Chiara Burgaletto Giulia Di Benedetto Gabriella Gaudio Cesarina Giallongo

Alzheimer's disease (AD) is the most common cause of dementia worldwide, characterized by accumulation of amyloid-β protein and hyperphosphorylated tau protein in the brain. Neuroinflammation, resulting from chronic activation of brain-resident innate immune cells as well as enhanced peripheral leukocyte access across the blood-brain barrier, crucially affects AD progression. In this context, TNFSF10, a cytokine substantially expressed in the AD brain, has been shown to modulate both the innate and the adaptive branches of the immune response in AD-related neuroinflammation. In this study, we explored whether a TNFSF10-neutralizing treatment could represent a tool to re-balance the overall overshooting inflammatory response in a mouse model of AD. Specifically, 3xTg-AD mice were treated sub-chronically with an anti-TNFSF10 monoclonal antibody for three months, and were then sacrificed at 15 months. TNFSF10 neutralization reduced the expression of the inflammatory marker CD86, inversely related to levels of the anti-inflammatory marker CD206 in the brain of 3xTg-AD mice, suggesting a switch of microglia towards a neuroprotective phenotype. Similar results were observed in the splenic macrophage population. Moreover, flow cytometry revealed a significant decrease of CD4+CD25+FOXP3+ T regulatory cells as well as reduced number of CD11b+LY6Chigh proinflammatory monocytes in both the brain and the spleen of 3xTg-AD mice treated with anti-TNFSF10 monoclonal antibody. Finally, the treatment resulted in lower count of splenic CD4+ and CD8+ T cells expressing PD1. The data suggest that TNFSF10 system-targeted treatment effectively restrain overshooting central and peripheral inflammation by rebalancing the overall immune response, mitigating the progression of AD pathology.

10.1007/s11481-025-10177-7

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Dobutamine stress echocardiography with automated border detection and color kinesis identifies improved diastolic left ventricular function and viable myocardium in ischemic cardiomyopathy

Journal of Cardiac Failure (1999)

Antonio Vitarelli Miguel Cones Ysabel Conde Rossella Giubilei Giulia Di Benedetto

Dobutamine

Ventricular Function

Ischemic Cardiomyopathy

10.1016/s1071-9164(99)91367-2

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