The Mediterranean diet (MD) is a dietary pattern described by Ancel B. Keys in the 1950s as a typical dietary habit of some populations bordering the Mediterranean sea in the south of Europe characterized by frugal living style. Findings of the Seven Country Study showed that people faced in the Mediterranean area had a reduced incidence of cardiovascular and metabolic disease, cancer and age-related diseases. The mechanisms through which the MD exerts its health benefit and prevents the onset of several diseases are not completely clarified because of various and complex aspects. Several studies suggest that the claimed benefits of the MD dietary pattern is mainly linked to decreased inflammation and oxidative stress, strongly related to each other and involved in many chronic diseases. The high content of compounds with antioxidant and anti-inflammatory activity present in most foods of the MD pattern has been considered effective for the improvement of many functions and parameters, therefore useful for the maintenance of the health status and the prevention of many chronic diseases. However, the extensive metabolism to which antioxidant compounds are subjected, once ingested with foods, reduces their antioxidant activity within the systemic circulation and tissues and their concentrations are very low in comparison with endogenous antioxidants. Foods produced for human nutrition have significant consequences for both the environment and the health of a specific population, and, in turn, the environment may address food choices and affect eating habit. The MD is a sustainable diet model that presents a very low environmental footprint, promotes the bio-diversity and protects human health and well-being. However, we must not ignore the planet changes and global environmental aspects that might convert the MD into a theoretical eating model far away from that described by Keys.

The prognostic role of increased mean platelet volume (MPV), as an indicator of platelet activation and large, more reactive platelets, in clinical and functional outcome of ischemic stroke is still conflicting. Studies are not currently available on the association between MPV and stroke recovery after neurorehabilitation. The relationship between MPV and clinical and functional outcome measures was assessed in twenty-four patients in the acute phase of first-ever ischemic stroke, and before and after 8-week intensive multifunctional neurorehabilitation. Neurorehabilitation was associated with improved scores of the National Institutes of Health Stroke Scale (NIHSS), the modified Rankin Scale (mRS), and the modified PULSES profile (mPULSES). When compared with apparently healthy subjects, higher MPV values were observed in stroke patients 24 hours after stroke and before neurorehabilitative treatment started not later than 14 days after stroke. Decreased MPV values were found after neurorehabilitation, even if the absolute values were still higher than those detected in control subjects. No correlation was observed between MPV values and scores of the NIHSS and mRS scales evaluated in stroke acute phase. No correlation was also observed before and after neurorehabilitative treatment between MPV and NIHSS, mRS and mPULSES scores. Our data provide evidence of the effectiveness of neurorehabilitation on modulating MPV values and support the hypothesis that high MPV could represent an expression of proinflammatory condition of the stroke patients, realistically pre-existent to acute ischemic event, than a marker of neurologic deficit and disability or of stroke recovery including motor performance and functional independence.

Objective To assess the effectiveness of appropriate dietary changes on body composition and fatigue in patients with RRMS.BackgroundThe most common symptoms associated with the reduced quality of life of patients suffering from relapsing remitting multiple sclerosis (RRMS) may be exacerbated by an altered nutritional status and consequent modifications of body composition. Fatigue is one of the most disabling symptoms among patients and might be induced, at least in part, both by weakness and deconditioning of the muscle mass and by chronic inflammatory process sustained by adipose tissue. Design/Methods Seventeen patients (mean age 37.4±2.3 years; mean duration of the disease: 9.7±1.7 years, mean EDSS score 1.3±0.2) underwent detailed evaluation of body composition by means of direct segmental multi-frequency bioelectrical impedance analysis and evaluation of fatigue symptoms by the modified fatigue impact scale (MFIS) before and after the 6-week specific diet treatment consisting in low saturated fatty acids of animal origin, high antioxidant foods, and adequacy to caloric expenditure of each patient. Results Adherence to diet treatment led to a decrease ( P vs . 32.5 ±2.0]; in body fat mass [Kg: 22.7± 2.3 vs . 20.7±1.9] and in visceral fat mass [cm 2 : 88.9±8.7 vs . 96.02±10.4]. No significant modifications were observed in skeletal muscle mass [Kg: 24.6±0.8 vs. 24.5±0.9]. Significant improvement ( P vs . 43.3±5.6]. A significant improvement of all subscale scores for physical, cognitive, and psychosocial functioning was also observed (P Conclusions Compliance to appropriate dietary modifications, even for a short time, is sufficient to promote a significant improvement of those body regions were adipose tissue shows active pro-inflammatory properties. Moreover, it reduces the burden of fatigue on the activities of daily living and in the self-care management of RRMS patients. Disclosure: Dr. Totaro has received personal compensation for activities with Bayer Shering Pharma, Biogen Idec, Merck Serono, Sanofi-Aventis Pharmaceuticals, Inc., Teva Neuroscience, and Novartis as a speaker and/or consultant. Dr. Di Massimo has nothing to disclose. Dr. De Amicis has nothing to disclose. Dr. Di Scanno has nothing to disclose. Dr. Di Carmine has nothing to disclose. Dr. Raparelli has nothing to disclose. Dr. Marini has nothing to disclose. Dr. Tozzi Ciancarelli has nothing to disclose.

The influence of intensive multifunctional neurorehabilitation on serum levels of Cu/Zn-superoxide dismutase (Cu/Zn-SOD), neuron-specific enolase (NSE), and 8-hydroxy-2-deoxyguanosine (8-OHdG), as markers of oxidative damage, was evaluated in symptomatic patients with Huntington's disease (HD). Improved clinical outcome measures were observed after neurorehabilitation. Baseline levels of Cu/Zn-SOD, NSE and 8-OHdG were higher than those observed in controls. Cu/Zn-SOD and NSE values decreased after neurorehabilitation, but were still higher than those measured in controls. Cu/Zn-SOD and NSE correlated positively before (r=0.659; p=0.003) and after rehabilitation (r=0.553, p=0.017). 8-OHdG values decreased after neurorehabilitation without reaching significance when compared with baseline values (p=0.145). No correlation was observed between the measured oxidative markers and the assessed clinical outcome measures, either before or after neurorehabilitation. The findings reported in the present paper provide evidence of the effectiveness of neurorehabilitation in reducing oxidative damage in HD patients and underline the limit of serum oxidative markers for the evaluation of clinical features of HD.

No evidence is currently provided on the involvement of uric acid (UA) and Cu/Zn Superoxide Dismutase (Cu/Zn SOD) in functional recovery of stroke patients after neurorehabilitation. For this purpose, the relationship between UA and Cu/Zn SOD plasma levels and clinical and functional outcome measures were analysed in twenty-five post-acute stroke patients undergoing intensive neurorehabilitation. UA and Cu/Zn SOD plasma levels were evaluated in fifteen healthy subjects as control values. Neurorehabilitation was associated with improved scores (P< 0.05) of the National Institutes of Health Stroke Scale (NIHSS), the modified Rankin Scale (mRS), and the mPULSES profile. UA plasma levels were higher before neurorehabilitation, decreased after, but were still higher than control values. Conversely, Cu/Zn SOD plasma levels were lower than control values before neurorehabilitation and increased after, even though the absolute values were still lower than controls. An inverse correlation was found between variations of UA plasma levels observed before and after neurorehabilitation (Delta UA) and those of Cu/Zn SOD (Delta Cu/Zn SOD) (r= -0.386; P< 0.001). No significant correlations were observed between Delta UA and the variations of the scores observed in all clinical outcome measures before and after neurorehabilitation (Delta scores of clinical outcome measures). Delta Cu/Zn SOD correlated positively with Delta NIHSS, Delta mRS and Delta mPULSES scores. Our data provide evidence of neurorehabilitation effectiveness on modulating UA and Cu/Zn SOD plasma levels and suggest that Cu/Zn SOD could assume the significance of biomarker of functional recovery, rather than UA that could be a marker of the magnitude of oxidative injury.

CONTEXT:Peripheral oxidative biomarkers could be useful for monitoring clinical features of Huntington's disease (HD).MATERIALS AND METHODS:Cu/Zn-superoxide dismutase (Cu/Zn-SOD), neuron-specific enolase (NSE) and 8-hydroxy-2'-deoxyguanosine (8-oxoGua) serum levels were analysed in 18 HD patients and 10 controls. Clinical measures were recorded from each HD patients.RESULTS:Cu/Zn-SOD, NSE and 8-oxoGua values were higher in HD patients than in controls. Cu/Zn-SOD and NSE correlated positively. No correlation was observed between the biomarkers analysed and the clinical measures assessed.DISCUSSION AND CONCLUSION:Serum oxidative biomarkers could express the neuronal oxidative processes going on in HD patients but are inadequate to evaluate clinical features of the disease.

We investigated in post-acute ischemic stroke patients the influence of intensive neurorehabilitation on oxidative stress balance during recovery of neurological deficits. For this purpose, fourteen patients were included in the study within 30 days of stroke onset. Outcome measures were the National Institutes of Health Stroke Scale (NIHSS), the modified Rankin Scale (mRS), the Barthel Index, and the Katz Index. Redox balance was assessed by measuring plasma peroxidative by-products, nitrite/nitrate metabolites (NOx), as an index of nitric oxide (NO), Cu/Zn Superoxide Dismutase (Cu/Zn SOD) activity, serum urate concentration, autoantibodies against ox-LDL (OLAB) serum level and plasma antioxidant capacity. Assessments were made before and after neurorehabilitation. Fifteen apparently healthy controls were investigated to compare redox markers. Intensive neurorehabilitation was associated with an improvement of all the outcome measures (P < 0.05). Decreased values of peroxidative by-products and of NOx (P < 0.05) were observed after neurorehabilitation in stroke patients even though their values were higher than in controls (P < 0.05). Changes observed before and after neurorehabilitation in NIHSS scores (Δ NIHSS scores) and in plasma NOx amount (Δ NOx) correlated positively (r=0.79; P < 0.005). No differences in EC-SOD activity, OLAB and serum urate concentrations were found between stroke patients and controls, before and after neurorehabilitation. Total plasma antioxidant capacity, lower in stroke patients than in controls before neurorehabilitation, was unchanged thereafter. Our data provide evidence of the effectiveness of neurorehabilitation on reducing redox unbalance in stroke patients and hints the role of NO as a messenger involved in post-ischemic neuronal plasticity influencing recovery of neurological deficits.

Measurements of the redox balance after the ischemic stroke occurrence might be useful to monitor the outcome of patients who suffered an ischemic stroke in terms of stroke recurrence and other vascular events. For this purpose, fifteen patients (mean age 71.40±2.50 years) with a first-ever ischemic stroke were included in the study within 30 days of stroke onset. Stroke severity was evaluated according to the National Institutes of Health Stroke Scale (NIHSS). Redox balance was assessed by measuring plasma amount of total peroxidative by-products, nitrite/nitrate metabolites (NOx), as expression of nitric oxide (NO) plasma bioavailability, total plasma antioxidant capacity (TEAC), Cu/Zn Superoxide Dismutase (Cu/Zn SOD) activity, serum urate concentration and autoantibodies against ox-LDL (OLAB) serum level. Total cholesterol, triglycerides, high density lipoprotein-cholesterol (HDL-C) and low density lipoprotein-cholesterol (LDL-C) were also measured. Fifteen apparently healthy controls (mean age 70.28±2.03 years) were investigated to compare redox markers. Stroke patients had higher plasma values of total peroxidative by-products, NOx stable metabolites and of total cholesterol, triglycerides, and LDL-C than controls (P < 0.05). No differences in OLAB levels, Cu/Zn-SOD activity, serum urate concentration, and plasma HDL-C amount were found in stroke patients when compared to controls. Total plasma antioxidant capacity was lower in stroke patients than in controls. NOx values correlated positively with the NIHSS score in stroke patients (r=0.668; P=0.0065). The observed presence of redox unbalance in stroke patients could represent an early indicator of diffuse endothelial activation during which patients may be at increased risk of stroke recurrence and other vascular events.

Available studies showed an inverse association between red wine consumption and prevalence of vascular risk factors in coronary hearth disease and stroke. Effects were mainly associated to wine antioxidant and antiaggregant properties. Actually, in vitro studies indicate a favourable effect of wine and/or of its non-alcoholic components in decreasing platelet sensitivity and aggregability. In a 4-week supplementation in 15 healthy male volunteers, we evaluated whether moderate red wine consumption might improve antioxidant defence mechanisms and promote positive modulation of inflammatory cytokines and cell adhesion molecules in relation to platelet responsiveness. We did not find any change of ADP- and collagen-induced platelet aggregation ex vivo, any change of biomarkers of oxidative stress, and any change of plasma lipid profile and haemostatic parameters, with the only exception of decreased fibrinogen levels (P<0.05). We also found an increase of mean platelet volume (P<0.05) without any significant modification of CD40 Ligand and P-selectin levels. Increased expressions of intercellular adhesion molecule-1, soluble E-selectin and interleukin-6 (P<0.05) were also observed. According to our findings increased circulating levels of inflammatory and endothelial cell activation markers may indicate a low-grade systemic inflammation and vascular activation that could be responsible for the lack of inhibition or of decreased platelet responsiveness, possibly because the plasmatic increase of wine antioxidant compounds is insufficient to improve endothelial function and to counteract the influence of ethanol on endothelial activation.

PURPOSE Emerging insights underline a link among chronic inflammation and endothelial activation with benign prostatic hyperplasia (BPH) and prostate cancer (PCa). We aim to investigate whether specific plasma markers of inflammation and endothelial activation allow to discriminate BPH and PCa. MATERIALS AND METHODS Fifteen patients affected by BPH, 15 by PCa and 15 controls, were enrolled. Interleukin-6 (IL-6), CD40 ligand (CD40L), endothelial-selectin (E-selectin), platelet-selectin (P-selectin), vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) were measured. RESULTS In systemic blood samples, IL-6 has been found increased in patients affected by BPH (4.25 ± 0. pg/mL) and PCa (5.08 ± 0.24) respect to controls (2.62 ± 0.34; p < 0.05). CD40L was higher in BPH (4.25 ± 0.65 ng/mL; p < 0.05) than in control (2.31 ± 0.20) and PCa group (2.60 ± 0.56). E-selectin, P-selectin and VCAM-1 did not show any significant difference. Higher levels of ICAM-1 were detected in patients with PCa (573.04 ± 52.23) and BPH (564.40 ± 74.67) than in the controls (215.30 ± 11.53 ng/mL; p < 0.05). In local blood samples, IL-6 has been found significantly increased in PCa in comparison with patients with BPH; there was no difference in CD40L, E-selectin, P-selectin, VCAM-1 ed ICAM-1. CONCLUSIONS Changes in inflammation and endothelial activation markers may be not considered to be of value in discriminating BPH and PCa.

OBJECTIVE:The aim was to verify whether oxidative stress could represent a common key factor of benign prostatic hyperplasia (BPH) and prostate cancer (PCa).SUBJECTS AND METHODS:15 patients affected by BPH, 15 with PCa and 15 controls were enrolled. Blood samples were withdrawn systemically and locally during radical retropubic prostatectomy in patients with PCa and during transvesical retropubic adenomectomy in patients diagnosed with BPH. Plasma oxidized low-density lipoprotein, peroxides, and total equivalent antioxidant capacity (TEAC) including plasma superoxide dismutase (SOD) determination were analyzed as oxidative markers.RESULTS:With respect to the control group, high plasma peroxides and decreased TEAC levels were measured in patients affected by both PCa and BPH. Plasma peroxides were significantly higher in patients with PCa with respect to BPH. A positive correlation was found between peroxides and TEAC values in samples withdrawn locally in patients affected by PCa. An inverse correlation between peroxides and TEAC was observed in patients with BPH. No statistically significant modifications were observed as concerns SOD activity and LDL oxidability.CONCLUSIONS:Our findings confirm a significant unbalance of redox status in patients affected by BPH and PCa, and suggest a potential involvement of oxidative stress as a determinant in the pathogenesis of these diseases.