Background and Purpose-Aortic stenosis, causing flow abnormalities, disturbs the normal hemodynamics in the common carotid arteries. The aim of the present study was to investigate the remodeling process of the common carotid arteries after surgical correction of aortic stenosis. Methods-Eleven subjects with aortic stenosis were studied before and 1 and 6 months after aortic valve replacement.Arterial diameter, intima-media thickness (IMT), and flow velocity were measured by echo-Doppler examination. Shear stress, blood flow, and pulsatility index were calculated. Blood viscosity and hematocrit were measured by standard methods. A control group was also enrolled. Results-Before surgery, compared with controls, patients had lower systolic peak velocity but higher mean and end-diastolic velocity. Arterial diameter, IMT, and blood flow were comparable in the 2 groups. Blood viscosity, hematocrit, wall shear stress, and pulsatility index were markedly lower in patients. After surgery, IMT was reduced (0.741Ϯ0.152 versus 0.627Ϯ0.108 mm before and 6 months after surgery, respectively; PϽ0.0001), and hematocrit and blood viscosity increased, leading to increased wall shear stress (mean wall shear stress, 7.83Ϯ1.97 versus 9.65Ϯ3.12 dyne/cm 2 before and 6 months after surgery, respectively; PϽ0.02). Conclusions-The present results demonstrate that aortic valve replacement, in subjects with aortic stenosis, leads to reduction of the common carotid artery IMT. Wall shear stress is increased after the intervention and probably mediates the remodeling process.
Human Papillomavirus (HPV) is the main cause of cervical cancer and its precursor lesions. Transformation may be induced by several mechanisms, including oncogene activation and genome instability. Individual differences in DNA damage recognition and repair have been hypothesized to influence cervical cancer risk. The aim of this study was to evaluate whether the double strand break gene polymorphisms XRCC2 R188H G>A (rs3218536), XRCC3 T241M C>T (rs861539) and R243H G>A (rs77381814) are associated to cervical cancer in Argentine women. A case control study consisting of 322 samples (205 cases and 117 controls) was carried out. HPV DNA detection was performed by PCR and genotyping of positive samples by EIA (enzyme immunoassay). XRCC2 and 3 polymorphisms were determined by pyrosequencing. The HPV-adjusted odds ratio (OR) of XRCC2 188 GG/AG genotypes was OR = 2.4 (CI = 1.1-4.9, p = 0.02) for cervical cancer. In contrast, there was no increased risk for cervical cancer with XRCC3 241 TT/CC genotypes (OR = 0.48; CI = 0.2-1; p = 0.1) or XRCC3 241 CT/CC (OR = 0.87; CI = 0.52-1.4; p = 0.6). Regarding XRCC3 R243H, the G allele was almost fixed in the population studied. In conclusion, although the sample size was modest, the present data indicate a statistical association between cervical cancer and XRCC2 R188H polymorphism. Future studies are needed to confirm these findings.
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