Background: Stroke patients have a redox imbalance, a consequence of both the cerebrovascular event and the associated pathological conditions. Our study was aimed to investigate the dynamic of some oxidative and nitrosative markers during the convalescent phase of postacute stroke patients undergoing rehabilitation. Methods: We assessed thiol, advanced oxidation protein product, protein carbonyl, 3-nitro-L-tyrosine, ceruloplasmin and oxidized LDL concentrations, as well as gamma-glutamyltranspeptidase (GGT) activity in 20 patients at the beginning of the hospitalization and at the discharge moment, respectively, and 24 apparently healthy controls. Results: We found significantly increased values for GGT (P ¼ 0.04), ceruloplasmin (P ¼ 0.01) and protein carbonyl (P ¼ 0.04) in stroke patients at the hospitalization moment when compared with healthy controls, while total thiols were significantly decreased (P ¼ 0.002). Rehabilitation was associated with a significant decrease of protein carbonyl (P ¼ 0.03) and oxidized LDL particle concentrations (P ¼ 0.03), as well as GGT activity (P ¼ 0.02). At the hospitalization moment, both GGT and ceruloplasmin were significantly negatively correlated with non-proteic thiols (r ¼ 20.44, P ¼ 0.049, and r ¼ 20.53, P ¼ 0.015, respectively) and significantly positively with protein carbonyls (r ¼ þ0.80, P , 0.001, and r ¼ þ0.69, P , 0.001, respectively) suggesting putative roles of GGT and ceruloplasmin in the redox imbalance. Conclusions: These results highlight the existence of a redox imbalance in postacute stroke patients, and the possible benefits of an antioxidant-based therapy for the recovery of these patients.
Stroke is a pathological condition associated with an enhanced inflammatory response that has a multifactorial etiology. We evaluated the dynamic of plasma concentrations of IL-1α, IL-6, IL-8, TNF-α, soluble form of intercellular adhesion molecule 1, and lipoprotein (a) [Lp(a)] during the rehabilitation of post-acute stroke patients (n = 20), in parallel with control subjects (n = 24). Stroke patients had significantly increased concentrations of IL-6, TNF-α, and Lp(a) when compared to healthy controls. It was found that the changes in the IL-6, IL-8, and TNF-α concentrations associated with the pathological condition were statistically significant (χ2 = 4.81, p = 0.028, χ2 = 10.40, p = 0.005 and χ2 = 6.73, p = 0.034, respectively). The decrease of Lp(a) during the rehabilitation had statistical significance (p = 0.043), while the decrease of IL-1α had marginal significance (p = 0.071). IL-1α, TNF-α, and Lp(a) concentrations were significantly negatively correlated with the Barthel index values, suggesting that the decrease of these inflammatory markers was beneficial for patients' recovery.
Objective. Estrogen receptor alpha (ESR1) polymorphisms (XbaI and PvuII) and vitamin D receptor (VDR) polymorphisms (FokI, BsmI, ApaI and TaqI) are the most frequently studied regarding the correlations with the infertility in males, but the results are controversial.The purpose of this study is to evaluate possible correlations between hormonal markers, VDR and ESR1 genotypes and semen analysis, in order to bring new data for a better understanding of male infertility.Subjects and Methods. 42 infertile men and 28 controls were enrolled. The polymorphisms of VDR gene (ApaI, TaqI, BsmI and FokI) and ESR1 (XbaI and PvuII) were performed by PCR-RFLP, along with hormonal markers.Results. An important correlation between PvuII polymorphism and infertility status was revealed. A significant difference between control and infertility group regarding the presence of BsmI (A>G) and ApaI (G>T) polymorphisms was observed in infertile group, prolactin and DHEA were found to correlate significantly statistic with BsmI GG genotype, whereas ApaI AA genotype correlates with prolactin and SHBG levels.Conclusions. By a multivariate analysis, we demonstrated a cumulative effect of some genetic variants in the hormonal status of infertile patients. Therefore, we show that specific genetic variants of ESR1 and VDR genes may jointly influence human spermatogenesis.
Background. Genetic variants of the endothelial nitric oxide synthase (eNOS) gene have been reported to be associated with cardiovascular disease. We hypothesized that G894T polymorphism might trigger many of the endocrine-metabolic changes related to metabolic syndrome (MetS).Study Design. 148 subjects with MetS and 142 healthy control subjects aged 23-60 years were studied. Fasting serum levels of insulin, cortisol, 17-OH Progesterone, DHEA, androstendione, IGF1, GH, PRL, CRP, resistin and biochemical profile were evaluated. G894T (eNOS) polymorphism was assayed by using PCR-RFLP technique.Results. The frequencies of genotypes and alleles of G894T polymorphism did not deviate from the Hardy-Weinberg equilibrium. In the MetS group the percentages of both GT (51.35 vs. 39.44; OR=2.09; CI=1.27-3.45; p= 0.003) and TT (16.22 vs. 8.45; OR=3.08; CI=1.41-6.74; p=0.003) genotypes and T allele (41.9 vs. 28.2; OR=1.83; CI=1.3-2.6; p=0.0005) significantly increased compared to control group. The G894T polymorphism was more significantly associated with the MetS in the presence of cortisol, 17-OH Progesterone, PRL, IGF1 and CRP (OR= 8.20; p=0.001) and significantly stronger in the presence of IGF1, PRL, 17OHP, resistin and CRP (OR= 10.21; 95%CI=2.42-43.05; p=0.002). The T allele carriers had higher values of waist circumference, systolic and diastolic blood pressure, cortisol, 17-OHP, androstendione, PRL, resistin and lower values of glucose, HOMA-IR in MetS group; The TT genotype carriers had higher values of triglyceride in both control and MetS group.Conclusion. Our results show an interaction between the G894T polymorphism and its phenotypes in conferring a higher susceptibility to the endocrine changes involved in pathogenesis of MetS suggesting a role of the eNOS gene in the modulation of the molecular endocrine mechanisms.
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