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The recovery of neurological deficits after ischemic stroke largely depends on the brain's ability to reorganize its undamaged neuronal circuits and neuronal plasticity phenomena. The consolidated evidence highlights the involvement of the patient's impaired nutritional conditions in post-stroke recovery and unsatisfying rehabilitative outcomes. Standardized nutritional protocols usually applied in hospitalized patients in a rehabilitation setting aim mainly to improve the general health conditions of patients, do not consider the high inter-individual variability in neurorehabilitation outcomes, and are not sufficiently modifiable to provide neuroprotective and restorative dietary patterns that could promote neuronal plasticity and functional recovery during neurorehabilitation. Neuronutrition, an emergent scientific field of neuroscience, represents a valid model of a personalized nutritional approach, assuring, for each patient, nutrients having antioxidant and anti-inflammatory properties, ensuring a balanced microbiota composition, and providing adequate neurotrophic support, essential for improving neuronal plasticity, brain functional recovery, and rehabilitative outcomes. In the present narrative review, we provide an overview of the current knowledge on neuronutrition as an adjuvant strategy of a personalized nutritional approach potentially effective in improving post-stroke neuroplasticity and neurorehabilitation by counteracting or at least limiting post-stroke oxidative/nitrosative stress, neuroinflammation, and gut–brain axis disturbance. [ABSTRACT FROM AUTHOR]

Beyond brain deficits caused by strokes, the effectiveness of neurorehabilitation is strongly influenced by the baseline clinical features of stroke patients, including a patient's current nutritional status. Malnutrition, either as a pre-stroke existing condition or occurring because of ischemic injury, predisposes patients to poor rehabilitation outcomes. On the other hand, a proper nutritional status compliant with the specific needs required by the process of brain recovery plays a key role in post-stroke rehabilitative outcome favoring neuroplasticity mechanisms. Oxidative stress and inflammation play a role in stroke-associated malnutrition, as well as in the cascade of ischemic events in the brain area, where ischemic damage leads to neuronal death and brain infarction, and, via cell-to-cell signaling, the alteration of neuroplasticity processes underlying functional recovery induced by multidisciplinary rehabilitative treatment. Nutrition strategies based on food components with oxidative and anti-inflammatory properties may help to reverse or stop malnutrition and may be a prerequisite for supporting the ability of neuronal plasticity to result in satisfactory rehabilitative outcome in stroke patients. To expand nutritional recommendations for functional rehabilitation recovery, studies considering the evolution of nutritional status changes in post-stroke patients over time are required. The assessment of nutritional status must be included as a routine tool in rehabilitation settings for the integrated care of stroke-patients. [ABSTRACT FROM AUTHOR]

Oxidative stress has probably a role in coronary heart disease (CHD), but studies focused on the behaviour of oxidative status in patients with stable CHD have obtained controversial results. On the other hand, an increased release of leukocyte elastase is considered a marker of CHD. Exercise can induce oxidative stress and leukocyte activation, so the aim of this study was to evaluate oxidative status and plasma elastase level in a group of subjects with stable coronary heart disease (CHD), at baseline and during an exercise test. We enrolled 15 patients with previous acute myocardial infarction, all treated with statins and platelet antiaggregating agents. As parameters of oxidative status we determined the thiobarbituric acid reactive substances and total antioxidant status (TAS). The exercise test was performed according to the Bruce protocol. At baseline, elastase level was higher in CHD subjects than in normal controls and during the exercise test it increased in both groups in comparison with basal values. Regarding oxidative status, only TAS was slightly lower in CHD subjects than in normal controls. In both groups, during exercise test, no parameter of oxidative status was significantly different compared to basal values. In conclusion, CHD patients showed, at rest, an abnormal neutrophil activation and a lower antioxidant status. The exercise test further activated neutrophils but did not influence oxidative status. The absence of a marked oxidative stress in our patients may be partly due to the pharmacological treatment, which apparently did not influence the abnormal leukocyte activation. [ABSTRACT FROM AUTHOR]

Objectives: A catabolic state and a progressive body weight loss are a well-documented hallmark of Huntington Disease (HD). No study is still available on the effectiveness of intensive in-hospital rehabilitation in HD patients with low body mass index (BMI)., Methods: Twenty HD patients with low BMI value were enrolled in this study. Disease severity was assessed before and after rehabilitation by the Barthel Index, the Total Functional Capacity Scale, and the Physical Performance Test., Results: BMI-scores correlated with clinical measures before and after rehabilitation. All patients showed an improvement in outcome measures (p<0.001), and an increase in BMI values (p<0.001) after rehabilitation. Effectiveness of rehabilitation correlated with the values of BMI assessed before reheducational programs (p=0.024) and with BMI values observed in each patient in the three months before admission to hospital (p=0.002)., Conclusions: Findings of the current study show that the effectiveness of the rehabilitation is positively correlated with the BMI values and confirm the efficacy of in-hospital intensive rehabilitation as a valid strategy finalized to improve neuromotor performances and global functional recovery even in HD patients with low BMI and at risk of malnutrition., Competing Interests: The authors have no conflict of interest.

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 (Δ UA) and those of Cu/Zn SOD (Δ Cu/Zn SOD) (r= -0.386; P<0.001). No significant correlations were observed between ΔUA and the variations of the scores observed in all clinical outcome measures before and after neurorehabilitation (Δ scores of clinical outcome measures). Δ Cu/Zn SOD correlated positively with Δ NIHSS, Δ mRS and Δ 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.

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.

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.

The aim of this study is to investigate the effects in vitro induced by androgenic anabolic steroids (AAS) (testosterone, nandrolone, androstenedione, norandrostenedione, and norandrostenediol) used illicitly in sport competitions, on the proliferation ability, apoptosis and the intracellular calcium concentration ([Ca2+]i) in human umbilical vein endothelial cells (HUVECs), selected as a prototype of a biological target system whose structure and function can be affected by steroids. For this purpose, we evaluated the proliferation inhibition by cytotoxic assay expressed as the concentration of drug inducing a 50% decrease in growth (IC50). The IC50 was reached for testosterone at 100 microM, androstenedione at 375 microM, nandrolone at 9 microM, norandrostenedione at 500 microM. The IC50 value for norandrostenediol was not reached until a concentration of 6000 microM. The apoptotic effect was evaluated by flow cytometry at IC50 for each drug. We observed that testosterone induced 31% of apoptotic cells, norandrostenedione 25%, androstenedione 15% and nandrolone 18%. We have analyzed the effects of these drugs on [Ca2+]i both in the immediate and long-term continuous presence of each compound. Our data show a statistically significant increase of [Ca2+]i in the acute condition and in long-term treated cultures, suggesting that androgen steroids modulate intracellular levels of calcium independent of incubation time or compound identity. As a whole, this study demonstrates that AAS might alter endothelial homeostasis, predisposing to the early endothelial cell activation that is responsible for vascular complications observed frequently in AAS users.

An abnormal activation state of polymorphonuclear leukocytes (PMN) plays a key role in organ injury induced by vascular atherosclerotic disease (VAD) and diabetes mellitus (DM). PMN membrane fluidity and cytosolic Ca2+ content can be considered markers of PMN activation. In this research we evaluated the PMN membrane fluidity and cytosolic Ca2+ content in VAD subjects with and without type 2 DM and examined the association between these parameters and the mono- or polyvascular localization. We enrolled 155 VAD subjects, including 92 non-diabetic (group A: mean age 63.6 +/- 9.2 years) and 63 diabetic patients (group B: mean age 65.4 +/- 7.8 years). Among group A 63 patients had monovascular and 29 polyvascular disease; among group B 30 patients had monovascular and 22 polyvascular disease. In each patient we evaluated the PMN membrane fluidity labelling the cells with the fluorescent probe 1,4-(trimethylamino)-phenyl-4-phenylhexatriene (TMA-DPH) and the PMN cytosolic Ca2+ content marking the cells with the fluorescent probe Fura 2-AM. PMN membrane fluidity did not discriminate normal subjects from diabetic and non-diabetic VAD subjects, while cytosolic Ca2+ content was increased in both groups. PMN membrane fluidity did not distinguish normal subjects from mono- or polyvascular VAD patients with and without type 2 DM. PMN cytosolic Ca2+ content was increased especially in monovascular VAD patients; both mono- and polyvascular VAD subjects with DM had a PMN cytosolic Ca2+ content higher than normals. Our results show the presence of an increased PMN cytosolic Ca2+ content in diabetic and non-diabetic VAD subjects but no association was observed between this increase and the mono- or polyvascular localization.

Acute myocardial infarction (AMI) is associated with an elevated polymorphonuclear leukocyte (PMN) count and a PMN rheological impairment. In this study we evaluated two major rheological aspects (membrane fluidity and cytosolic Ca2+ concentration) in a group of young adults with AMI. We enrolled 41 AMI patients (39 men and 2 women; mean age 41.0 +/- 4.0 years), who were examined 5-10 days after AMI (T1) and 12 months later (T2). The membrane fluidity was obtained labelling granulocytes with the fluorescent probe 1-[4-(trimethylamino)phenyl]-6-phenyl-1,3,5-hexatriene (TMA-DPH) and considering the degree of fluorescence polarization, inversely correlated to the membrane lipid fluidity. The cytosolic Ca2+ content was obtained marking PMN cells with the fluorescent probe Fura-2AM and considering the ratio between the Fura 2-Ca2+ complex and the unchelated Fura 2 fluorescence intensity. Both parameters were evaluated at baseline and after in vitro activation with 4-phorbol 12-myristate 13-acetate (PMA) at the concentration of 4.5 muM, prolonged for 5 and 15 minutes. At T1 the PMN membrane fluidity and cytosolic Ca2+ content in AMI patients were respectively decreased and increased in comparison with control group. At T2 the membrane fluidity was not any more different from control subjects, but there was also a further increase in cytosolic Ca2+ content. In vitro, PMN activation caused no significant variation of these parameters in the control group, while in AMI patients membrane fluidity significantly decreased and cytosolic Ca2+ content increased not only during the initial stage, but also after 12 months. The long-term functional alteration of PMN cells observed in young adults with AMI confirms the role of these cells in the inflammatory response following AMI. In the light of these data, the use of molecules able to modulate granulocyte activity, such as calcium channel blockers or pentoxifylline, should be reconsidered in myocardial infarction, together with the usual pharmacological treatment.