The epidemiological studies confirm an increased risk of cardiovascular disease in multiple sclerosis, especially prothrombotic events directly associated with abnormal platelet activity. The aim of our study was to investigate the level of blood platelet activation in the circulation of patients with chronic phase of multiple sclerosis (SP MS) and their reactivity in response to typical platelets’ physiological agonists. We examined 85 SP MS patients diagnosed according to the revised McDonald’s criteria and 50 healthy volunteers as a control group. The platelet activation and reactivity were assessed using flow cytometry analysis of the following: P-selectin expression (CD62P), activation of GP IIb/IIIa complex (PAC-1 binding), and formation of platelet microparticles (PMPs) and platelet aggregates (PA) in agonist-stimulated (ADP, collagen) and unstimulated whole blood samples. Furthermore, we measured the level of soluble P-selectin (sP-selectin) in plasma using ELISA method, to evaluate the in vivo level of platelet activation, both in healthy and SP MS subjects. We found a statistically significant increase in P-selectin expression, GP IIb/IIIa activation, and formation of PMPs and PA, as well as in unstimulated and agonist-stimulated (ADP, collagen) platelets in whole blood samples from patients with SP MS in comparison to the control group. We also determined the higher sP-selectin level in plasma of SP MS subjects than in the control group. Based on the obtained results, we might conclude that during the course of SP MS platelets are chronically activated and display hyperreactivity to physiological agonists, such as ADP or collagen.
Accumulating data suggests that miRNAs might play a major role in neuroinflammatory processes. Therefore, our study aimed to first estimate the levels of miR-155, miR-326, and miR-301a in serum of RR-MS patients in the remission phase and then compare the levels of the examined miRNAs at different times after relapse. In this study, 36 RR-MS patients in the remission phase took part. We analyzed two subgroups of RR-MS: one, 1 to 2 months after completing steroid treatment during relapse (post-acute; n = 13) and the other, over 2 years without any relapse (stable; n = 23). Moreover, we made correlations between these biochemical results and clinical parameters of cognitive impairment, depression, and disability. The obtained results presented downregulation of miR-155 and miR-301a (in 94% and 51% samples, respectively) and overexpression of miR-326 (in 72% samples) in RR-MS patients. Moreover, we observed a positive correlation between the relative expression of miRNAs and BDI (Beck Depression Index) for miR-326 (rho = 0.385459, p = 0.022210; Spearman's rank correlation) and miR-301a (rho = 0.435131, p = 0.008991; Spearman rank correlation). We also observed the differences in expression levels between the post-acute and stable phases of RR-MS. The expression levels of miR-301a and miR155 were higher in the post-acute vs. stable phase of remission (2.385 vs. 0.524 and 0.594 vs. 0.147; respectively). Our study, for the first time, presents miRNA expression differences in two stages of remission: post-acute and stable.
Poststroke depression, the second most serious psychosomatic complication after brain stroke, leads to delay of the rehabilitation process and is associated with an increased disability and cognitive impairment along with increase in term mortality. Research into the biochemical changes in depression is still insufficiently described. The aim of our study was therefore to evaluate the possible association between plasma protein oxidative/nitrative damages and the development of poststroke depression. We evaluated oxidative/nitrative modifications of specific proteins by measurement of 3-nitrotyrosine and carbonyl groups levels using ELISA test. Additionally, we checked differences in proteins thiol groups by spectrophotometric assay based on reaction between DTNB and thiols. We also evaluated catalase activity in erythrocytes measured as ability to decompose H2O2. Correlation analysis was performed using Spearman's rank. We observed significant (P < 0.001) differences in all oxidative/nitrative stress parameters in brain stroke patients compared to healthy group. Our research shows that oxidative damage of proteins is correlated with the degree of poststroke depression, while nitrative changes do not show any relationship. We demonstrate a positive correlation between the concentration of carbonyl groups and the Geriatric Depression Scale and a negative correlation between the degree of depression and the concentration of -SH groups or catalase activity.
Objective The goal of this study was to describe muscle function deficit in patients after stroke as well as to define the relationship between maximal muscle power (Pmax) and optimal shortening velocity (υopt) with functional efficiency in stroke survivors. Material and Methods A total of 134 participants were enrolled in the study, including 67 patients after a stroke and 67 volunteers, matched for age and sex (controls). Functional performance was measured with the timed Up and Go test (TUG) and additionally with Rivermead Motor Assessment (RMA) and Barthel Index (BI) in stroke survivors. To assess Pmax and υopt of the knee extensor muscles, a specially equipped Monark cycle ergometer was used. Results The power generated by stroke survivors was 49.6% that of their peers and muscle contraction velocity was 65.5%. Pmax/kg and υopt were associated with TUG outcomes in both groups. Pmax/kg and υopt were associated with age in the control group, but not in patients after stroke. In multivariate analysis in patients after stroke, TUG was better predicted by Pmax/kg or υopt than by the age. In stroke survivors, both Pmax/kg and υopt were related to the BI and to the RMA total results. Both BI and RMA total were not determined by age. Conclusions Muscle power and muscle contraction velocity in patients who have had a stroke within three months have reduced markedly. These factors significantly affect functional performance. Muscle power and optimal shortening velocity are more important determinants of functional status than age in these stroke survivors.
Our results indicate that impaired red-ox balance can significantly promote neurodegeneration in secondary progressive MS.
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