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  • Autor: Ayşe Emre x
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Effects of Smoking during Pregnancy on DNA Damage and ROS Level Consequences in Maternal and Newborns’ Blood

Some of the genotoxic/carcinogenic substances or metabolites in cigarette smoke are capable of passing through the placenta and harming a newborn’s health. Smoking is also known as a factor in the formation of oxidative damage and the main mechanism involved in the carcinogenic process. Predetermining this genotoxic risk can be successfully achieved by measuring certain parameters of oxidative stress. The comet assay is considered an important biomarker for the evaluation of genotoxic substances and is effective for detecting DNA damage caused by smoking. This study examined third trimester bloods and the cord blood of 28 actively smoking and 22 non-smoking mothers in terms of DNA damage and oxidative stress parameters. Cu/Zn superoxide dismutase (CuZn-SOD), malondialdehyde (MDA), catalase (CAT), plasma nitrite/nitrates (NO2 -/NO3 -), selenium-dependent glutathione peroxidase (Se-GPx), Cu, and Zn levels were measured as indicators of oxidative damage. There were no significant increases in DNA damage of the actively smoking pregnant group in comparison with the non-smoking pregnant group, either in the third trimester or cord blood. Oxidative stress parameters of smoker and non-smoker groups were statistically different for MDA (p<0.05), CuZn-SOD (p<0.01), Se-GPx (p<0.05) values while the difference was not significant for NO2 -/NO3 -, CAT, Zn, and Cu values. The same values were also investigated in cord blood, and only NO2/NO3 -(p<0.01), Se-GPx (p<0.01 and CAT (p<0.001) values were found statistically different. Smoking mothers may have been exposed to more oxidative stress than non-smoking mothers.

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Mean Platelet Volume Predicts Short-term Prognosis in Young Patients with St-segment Elevation Myocardial Infarction


Background: Acute ST-elevation myocardial infarction (STEMI) is an uncommon diagnosis in patients less than 40 years of age. Over the last two decades, there is an increase in the frequency of cardiovascular events among young adults. However, at present there is only limited clinical data on the clinical characteristics and outcomes of STEMI in young patients who were treated with primary percutaneous coronary intervention (pPCI). Plaque erosion is the underlying pathological mechanism leading to STEMI in the vast majority of young adults. Thrombi that complicate superficial erosion seem more platelet-rich than the fibrinous clots precipitated by plaque rupture. Mean platelet volume (MPV) is recognized as a marker of the platelet activation process and may be a better indicator of short-term prognosis than the inflammatory markers in young patients with STEMI. Therefore, we aimed to investigate clinical and angiographic characteristics, risk factors and the independent value of MPV on predicting short-term major adverse cardiovascular events (MACEs) in young adults with STEMI. Methods: A total of 349 patients aged 40 years or younger who underwent pPCI at our center between 2010–2015 with the diagnosis of STEMI were retrospectively analyzed. Results: The mean age of the patients was 36.4 ± 3.6 years and 90% of them were men. Smoking was by far the most frequent cardiovascular risk factor. MACEs were observed in 23 patients (6.6%), and according to the multivariate regression analysis, Killip IIIIV (OR 7.52, 95% CI 1.25–45.24, p = 0.03), lower admission SBP (OR 0.94, 95% CI 0.90–0.98, p <0.01) and increased MPV (OR 1.67, 95% CI 1.05–2.67, p = 0.03) were found to be independently correlated with MACE in the study population. Conclusion: Our results indicate that MPV is an independent predictor of MACEs at the short-term follow-up in young patients with STEMI undergoing pPCI. Accordingly, we suggested that MPV, a marker of platelet activation, could play a significant role in predicting clinical evolution in young patients with STEMI.

Open access