Scientific Institute of Telese Terme

Telese Terme, Italy

Scientific Institute of Telese Terme

Telese Terme, Italy
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Sagliano L.,The Second University of Naples | D'Olimpio F.,The Second University of Naples | Conson M.,The Second University of Naples | Cappuccio A.,The Second University of Naples | And 3 more authors.
Experimental Brain Research | Year: 2013

Closing-in (CI) is the tendency to act very close to the model in tasks such as drawing, 3D construction, gesture imitation, or writing. Closing-in is observed in degenerative and focal brain diseases, but also in normally developing children. In the present paper, three experiments were conducted to evaluate whether CI can be triggered during a copying task in normal young adults by increasing stimulus complexity and attentional load. Participants were required to copy complex lines in one of three conditions: without interfering activities (baseline), during counting, or during execution of a 2-back short-term memory task. In Experiment 1, participants were required to reproduce horizontally aligned stimuli, starting from a dot placed below each stimulus and proceeding from left to right; in Experiment 2, stimuli were again horizontally aligned, but the starting dot was placed above each stimulus, and writing proceeded from right to left; in Experiment 3, stimuli were aligned vertically and copying proceeded in upward direction. Results from all experiments showed that when normal young adults are engaged in an attentional-demanding concurrent activity, they tend to approach to the model, whereas the effect of stimulus complexity disappeared with unusual writing direction (Experiments 2 and 3). These findings demonstrate that even in normal young adults, a reduction in available attentional resources can release an attraction toward the model. © 2013 Springer-Verlag Berlin Heidelberg.


Femminella G.D.,University of Naples Federico II | Leosco D.,University of Naples Federico II | Ferrara N.,University of Naples Federico II | Ferrara N.,Scientific Institute of Telese Terme | And 2 more authors.
CNS and Neurological Disorders - Drug Targets | Year: 2016

The adrenergic system has an important role in normal central nervous system function as well as in brain disease. The locus coeruleus, the main source of norepinephrine in brain, is involved in the regulation of learning and memory, reinforcement of sleep-wake cycle and synaptic plasticity. In Alzheimer’s disease, locus coeruleus degeneration is observed early in the course of the disease, years before the onset of clinical cognitive signs, with neurofibrillary detected at the stage of mild cognitive impairment, preceding amyloid deposition. Thus, in the last years, a great interest has grown in evaluating the possibility of central adrenergic system modulation as a therapeutic tool in Alzheimer’s disease. However, evidences do not show univocal results, with some studies suggesting that adrenergic stimulation might be beneficial in Alzheimer’s Disease and some others favoring adrenergic blockade. In this review, we summarize data from both hypothesis and describe the pathophysiological role of the adrenergic system in neurodegeneration. © 2016 Bentham Science Publishers.


Conson M.,The Second University of Naples | Mazzarella E.,The Second University of Naples | Trojano L.,The Second University of Naples | Trojano L.,Scientific Institute of Telese Terme
Experimental Brain Research | Year: 2011

Several studies showed that mental rotation of body parts is interfered with by manipulation of the subjects' posture. However, the experimental manipulations in such studies, e.g., to hold one arm flexed on one's own chest, activated not only proprioceptive but also self-tactile information. Here, we tested the hypothesis that the combination of self-touch and proprioception is more effective than proprioception alone in interfering with motor imagery. In Experiment 1 right- and left-handers were required to perform the hand laterality task, while holding one arm (right or left) flexed with the hand in direct contact with their chest (self-touch condition, STC) or with the hand placed on a wooden smooth surface in correspondence with their chest (no self-touch condition, NoSTC); in a third neutral condition, subjects kept both arms extended (neutral posture condition, NPC). Right-handers were slower when judging hand laterality in STC with respect to NoSTC and NPC, particularly when the sensory manipulation involved their dominant arm. No posture-related effect was observed in left-handers. In Experiment 2, by applying the same sensory manipulations as above to both arms, we verified that previous results were not due to a conflict between perceived position of the two hands. These data highlighted a complex interaction between body schema and motor imagery, and underlined the role of hand dominance in shaping such interaction. © 2011 Springer-Verlag.


Conti V.,University of Salerno | Russomanno G.,University of Salerno | Corbi G.,University of Molise | Guerra G.,University of Molise | And 6 more authors.
Medicine and Science in Sports and Exercise | Year: 2013

Purpose: Moderate aerobic exercise reduces oxidative stress, whereas intense physical activity may produce the opposite result. At present, the effects of different exercise loads on oxidative stress markers and the response of human cells to different exercise volumes have not been fully elucidated. Methods: Human (Eahy-926) endothelial cells (EC), exposed or not exposed to oxidative stress, were conditioned with sera from two groups of triathletes practicing at different workloads. Results: Although no differences in functional and hemodynamic variables were observed between the two groups of triathletes, significant changes in some markers for oxidative stress were found in their sera. Thiobarbituric acid reactive substances and superoxide dismutase activity were similar, but triathletes practicing the sport at lower volume (T1) had higher serum nitric oxide and lower catalase activity than triathletes performing the training at greater load (T2). The EC conditioned with serum from T1 (T1-EC) showed higher survival and proliferation rates and lower senescence levels than the EC supplemented with T2 (T2-EC) serum both before and after oxidative stress induction. These effects depended on catalase as demonstrated via enzyme activity inhibition using 3-amino-1,2,4-triazole. After oxidative stress induction, Sirt1 activity, a regulator of the oxidative stress response, was significantly increased in the T1-EC but not in the T2-EC. Moreover, the T1-EC required less catalase activity than the T2-EC to counteract an equal amount of oxidative stress after H2O2 administration. Conclusion: This study demonstrates that the beneficial effects of aerobic exercise are eliminated when the training is performed at a greater workload. Moreover, we suggest an oxidative stress marker, serum catalase activity, as a valid tool to use in the supervision of changes to exercise volume. Copyright © 2013 by the American College of Sports Medicine.


Lymperopoulos A.,Nova Southeastern University | Lymperopoulos A.,Thomas Jefferson University | Rengo G.,Thomas Jefferson University | Rengo G.,Scientific Institute of Telese Terme | And 4 more authors.
Journal of Biological Chemistry | Year: 2010

Chronic heart failure (HF) is characterized by sympathetic overactivity and enhanced circulating catecholamines (CAs), which significantly increase HF morbidity and mortality. We recently reported that adrenal G protein-coupled receptor kinase 2 (GRK2) is up-regulated in chronic HF, leading to enhanced CA release via desensitization/down-regulation of the chromaffin cell α2-adrenergic receptors that normally inhibit CA secretion. We also showed that adrenal GRK2 inhibition decreases circulating CAs and improves cardiac inotropic reserve and function. Herein, we hypothesized that adrenal-targeted GRK2 gene deletion before the onset of HF might be beneficial by reducing sympathetic activation. To specifically delete GRK2 in the chromaffin cells of the adrenal gland, we crossed PNMTCre mice, expressing Cre recombinase under the chromaffin cell-specific phenylethanolamine N-methyltransferase (PNMT) gene promoter, with floxedGRK2 mice. After confirming a significant (∼50%) reduction of adrenal GRK2 mRNA and protein levels, the PNMT-driven GRK2 knockout (KO) offspring underwent myocardial infarction (MI) to induce HF. At 4 weeks post-MI, plasma levels of both norepinephrine and epinephrine were reduced in PNMT-driven GRK2 KO, compared with control mice, suggesting markedly reduced post-MI sympathetic activation. This translated in PNMT-driven GRK2 KO mice into improved cardiac function and dimensions as well as amelioration of abnormal cardiac β-adrenergic receptor signaling at 4 weeks post-MI. Thus, adrenal-targeted GRK2 gene KO decreases circulating CAs, leading to improved cardiac function and β-adrenergic reserve in post-MI HF. GRK2 inhibition in the adrenal gland might represent a novel sympatholytic strategy that can aid in blocking HF progression. © 2010 by The American Society for Biochemistry and Molecular Biology, Inc.


Lymperopoulos A.,Nova Southeastern University | Lymperopoulos A.,Thomas Jefferson University | Rengo G.,Thomas Jefferson University | Rengo G.,Scientific Institute of Telese Terme | And 3 more authors.
Journal of the American College of Cardiology | Year: 2011

Objectives We investigated whether adrenal beta-arrestin 1 (βarr1)-mediated aldosterone production plays any role in post-myocardial infarction (MI) heart failure (HF) progression. Background Heart failure represents 1 of the most significant health problems worldwide, and new and innovative treatments are needed. Aldosterone contributes significantly to HF progression after MI by accelerating adverse cardiac remodeling and ventricular dysfunction. It is produced by the adrenal cortex after angiotensin II activation of angiotensin II type 1 receptors (AT1Rs), G protein-coupled receptors that also signal independently of G proteins. The G protein-independent signaling is mediated by βarr1 and βarr2. We recently reported that adrenal βarr1 promotes AT1R-dependent aldosterone production leading to elevated circulating aldosterone levels in vivo. Methods Adrenal-targeted, adenoviral-mediated gene delivery in vivo in 2-week post-MI rats, a time point around which circulating aldosterone significantly increases to accelerate HF progression, was performed to either increase the expression of adrenal βarr1 or inhibit its function via expression of a βarr1 C-terminal-derived peptide fragment. Results We found that adrenal βarr1 overexpression promotes aldosterone elevation after MI, resulting in accelerated cardiac adverse remodeling and deterioration of ventricular function. Importantly, these detrimental effects of aldosterone are prevented when adrenal βarr1 is inhibited in vivo, which markedly decreases circulating aldosterone after MI. Finally, the prototypic AT1R antagonist losartan seems unable to lower this adrenal βarr1-driven aldosterone elevation. Conclusions Adrenal βarr1 inhibition, either directly or with AT1R "biased" antagonists that prevent receptor-βarr1 coupling, might be of therapeutic value for curbing HF-exacerbating hyperaldosteronism. © 2011 American College of Cardiology Foundation.


Femminella G.D.,University of Naples Federico II | Rengo G.,Scientific Institute of Telese Terme | Komici K.,University of Naples Federico II | Iacotucci P.,University of Naples Federico II | And 8 more authors.
Journal of Alzheimer's Disease | Year: 2014

Autonomic dysfunction is very common in patients with dementia, and its presence might also help in differential diagnosis among dementia subtypes. Various central nervous system structures affected in Alzheimer's disease are also implicated in autonomic nervous system regulation, and it has been hypothesized that the deficit in central cholinergic function observed in Alzheimer's disease could likely lead to autonomic dysfunction. Several feasible tests can be used in clinical practice for the assessment of parasympathetic and sympathetic functions, especially in terms of cardiovascular autonomic modulation. In this review, we describe the different tests available and the evidence from the literature which indicate a definite presence of autonomic dysfunction in dementia at various degrees. Importantly, the recognition of dysautonomia, besides possibly being an early marker of dementia, would help prevent the disabling complications which increase the risk of morbidity, institutionalization, and mortality in these individuals. © 2014 - IOS Press and the authors. All rights reserved.


Estraneo A.,Scientific Institute of Telese Terme | Moretta P.,Scientific Institute of Telese Terme | Loreto V.,Scientific Institute of Telese Terme | Santoro L.,University of Naples Federico II | Trojano L.,The Second University of Naples
Archives of Physical Medicine and Rehabilitation | Year: 2014

Objective To report clinical conditions and neuropsychological functioning of patients with late recovery of responsiveness at least 5 years after injury. Design Patient series. Setting Patients discharged from an inpatient rehabilitation unit. Participants Patients (N=13) who recovered from a vegetative state 1 year after severe traumatic brain injury or 6 months after nontraumatic brain injury. Interventions Not applicable. Main Outcome Measures Coma Recovery Scale-Revised, Disability Rating Scale, and FIM. For patients who recovered full consciousness, neuropsychological tests specifically adapted for patients with very severe disabilities were used. Results After regaining responsiveness, 2 patients died because of severe clinical complications. Among the remaining 11 patients, 5 were still in a minimally conscious state at their last assessment, but 4 of them had recovered some complex behavioral responses to the environment (eg, they could follow simple commands, albeit inconsistently). Six patients had emerged from a minimally conscious state at the last evaluation. Severe functional disability was present in both patients who were conscious and patients who were minimally conscious. No patient was autonomous in common daily life activities or in transfers. All patients who were conscious showed variable cognitive impairments, and some of them also developed behavioral and psychological symptoms. However, such disturbances did not impede the patients' interaction with relatives and caregivers. Conclusions This study provides systematic data about the course of the disease in a cohort of patients that was previously considered as exceptional. Patients with late recovery show a variable degree of functional recovery, although they experience marked residual motor and cognitive disabilities. The present findings contribute to enhance the understanding of the course of the disease in patients with late recovery and might help clinicians optimize the levels of care and provide the patients' families with correct information. © 2014 by the American Congress of Rehabilitation Medicine.


Cannavo A.,University of Naples Federico II | Cannavo A.,Temple University | Rengo G.,University of Naples Federico II | Rengo G.,Scientific Institute of Telese Terme | And 16 more authors.
Circulation | Year: 2013

BACKGROUND - The sphingosine-1-phosphate receptor 1 (S1PR1) and β1-adrenergic receptor (β1AR) are G-protein-coupled receptors expressed in the heart. These 2 receptors have opposing actions on adenylyl cyclase because of differential G-protein coupling. Importantly, both of these receptors can be regulated by the actions of G-protein-coupled receptor kinase-2, which triggers desensitization and downregulation processes. Although classic signaling paradigms suggest that simultaneous activation of β1ARs and S1PR1s in a myocyte would simply result in opposing action on cAMP production, in this report we have uncovered a direct interaction between these 2 receptors, with regulatory involvement of G-protein-coupled receptor kinase-2. METHODS AND RESULTS - In HEK (human embryonic kidney) 293 cells overexpressing both β1AR and S1PR1, we demonstrated that β1AR downregulation can occur after stimulation with sphingosine-1-phosphate (an S1PR1 agonist), whereas S1PR1 downregulation can be triggered by isoproterenol (a β-adrenergic receptor agonist) treatment. This cross talk between these 2 distinct G-protein-coupled receptors appears to have physiological significance, because they interact and show reciprocal regulation in mouse hearts undergoing chronic β-adrenergic receptor stimulation and in a rat model of postischemic heart failure. CONCLUSIONS - We demonstrate that restoration of cardiac plasma membrane levels of S1PR1 produces beneficial effects that counterbalance the deleterious β1AR overstimulation in heart failure. © 2013 American Heart Association, Inc.


Conti V.,The Second University of Naples | Corbi G.,University of Molise | Russomanno G.,The Second University of Naples | Simeon V.,The Second University of Naples | And 9 more authors.
Medicine and Science in Sports and Exercise | Year: 2012

PURPOSE: Exercise training is a nonpharmacological intervention that improves cardiovascular function and enhances endothelial homeostasis in patients with cardiovascular diseases. However, the amount of benefit achieved varies widely depending on the type and duration of exercise. Moreover, data about the long-term effects of physical activity are scarce. METHODS: In this study, endothelial cells, exposed or not to oxidative stress, were conditioned with sera from athletes regularly participating in sports classified as "aerobic" (triathlon), "mixed aerobic-anaerobic" (soccer), and "anaerobic" (sprint running). RESULTS: Functional and hemodynamic variables did not differ between groups of athletes, whereas there were dramatic changes in serum markers for oxidative stress. Lipid peroxidation assessed by the thiobarbituric acid reactive substances assay and catalase activity were the lowest and nitric oxide availability was the highest in sera of triathletes. Endothelial cells cultured in serum from triathletes (T-endothelial cells) had the highest survival, evaluated by viability assay, BrdU incorporation, and senescence-associated β galactosidase assays, and preserved the endothelial appearance before and after stress in contrast to the cells grown in sera from the other athletes. T-endothelial cells also had the highest catalase messenger RNA expression and, after stress, the highest catalase activity of all the endothelial cells. Moreover, poststress activity of Sirt1, a NAD-dependent deacetylase involved in cellular stress resistance and a key regulator of longevity, was significantly increased in T-endothelial cells. CONCLUSIONS: Different types of exercise training induced different molecular effects in terms of survival, morphology, and antioxidant system efficiency. The in vitro technique used herein may help to shed light on the molecular basis of effects of long-term physical activity in humans.

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