ABSTRACT
Objective:To explore the correlation between the expression levels of serum estradiol and otolin-1 and the recurrence of postmenopausal benign paroxysmal positional vertigo (BPPV).Methods:A total of 116 postmenopausal female patients who were diagnosed with primary BPPV in the Vertigo Treatment Center of Beijing Geriatric Hospital from January 2018 to December 2019 were selected as the research objects. They were divided into recurrence group (27 cases) and the non-recurrence group (89 cases) according to the recurrence during follow-up. The basic data, laboratory indexes and complications of the two groups were compared. The serum estradiol level was detected by electrochemiluminescence and the serum otolin-1 level was detected by enzyme-linked immunosorbent assay. The receiver operating characteristic (ROC) curve was used to evaluate the predictive value of serum estradiol and otolin-1 in the recurrence of postmenopausal BPPV patients; Multivariate logistic regression was used to analyze the risk factors of recurrence in postmenopausal BPPV patients.Results:The proportion of severe cough in the recurrence group was higher than that in the non-recurrence group ( P<0.05); the level of estradiol in the recurrence group was significantly lower than that in the non-recurrence group ( P<0.05), and the level of otolin-1 was significantly higher ( P<0.05); ROC results showed that the areas under the curve (AUCs) of serum estradiol and otolin-1 for predicting the recurrence of postmenopausal BPPV patients were 0.852 (95% CI: 0.774-0.911) and 0.722 (95% CI: 0.631-0.801) respectively, and the cut-off values were 18.09 pg/ml and 361.79 pg/ml respectively; Multivariate logistic regression analysis showed that severe cough, estradiol ≤18.09 pg/ml, and otolin-1 >361.79 pg/ml were independent risk factors for recurrence in postmenopausal BPPV patients ( P<0.05). Conclusions:The serum estradiol level of patients with postmenopausal BPPV recurrence decreases, and the level of otolin-1 increases. The abnormal level is an independent risk factor affecting the recurrence of patients with postmenopausal BPPV.
ABSTRACT
<p><b>BACKGROUND</b>It is desirable to minimize the risk of adverse radiation effects associated with percutaneous coronary intervention. The aim of this study was to determine the impact of prolonging the interval between coronary angiography and percutaneous coronary intervention on X-ray-induced DNA double-strand breaks in blood lymphocytes using γ-H2AX immunofluorescence microscopy.</p><p><b>METHODS</b>Blood samples of eight patients were taken before the first exposure to ionizing radiation, 10 minutes, 20 minutes, 30 minutes, 1 hour, and 24 hours after the last exposure to determine the γ-H2AX foci repair kinetics. Fifty-eight patients undergoing percutaneous coronary intervention were randomized to an intermittent radiation exposure group and a continuous radiation exposure group. Blood samples were taken before coronary angiography and 15 minutes after the last exposure. By enumerating γ-H2AX foci, the impact of prolonging the interval on DNA double-strand breaks was investigated. Student t-test was used to compare the difference in DNA double-strand breaks between the two groups.</p><p><b>RESULTS</b>An increase in foci was found in all patients received percutaneous coronary intervention. The maximum number of γ-H2AX foci was found 10-20 minutes after the end of the last exposure. There was no statistically significant difference between the two groups in γ-H2AX foci at baseline. On average there were (0.79 ± 0.15) γ-H2AX foci induced by interventional X-rays per lymphocyte in the continuous radiation exposure group and (0.66 ± 0.21) in the intermittent radiation exposure group after exposure (P < 0.05).</p><p><b>CONCLUSIONS</b>A significant number of γ-H2AX foci develop following the percutaneous coronary intervention procedures. The number of X-ray-induced DNA double-strand breaks may be decreased by prolonging the interval time between coronary angiography and percutaneous coronary intervention to 30 minutes.</p>
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Coronary Angiography , DNA Breaks, Double-Stranded , Radiation Effects , Dose-Response Relationship, Radiation , Lymphocytes , Metabolism , Radiation Effects , Percutaneous Coronary InterventionABSTRACT
Objective To investigate the protective effect of adiponectin on angiotesin Ⅱ (Ang Ⅱ)-mediated cardiomyocyte apoptosis,and explore the related mechanism. Methods Cardiomyocytes isolated from neonatal rats were cultured in vitro. The identity of cardiomyocytes was confirmed by morphological examination and staining with anti-sarcomeric ?-actin antibody,and most (more than 95%) of the cells were identified as neonatal rat ventricular myocytes. After being placed in a serum-free medium for 24 hours,the ventricular myocytes were randomly grouped and received the following treatments respectively:placebo,or Ang Ⅱ (1?mol/L),or Ang Ⅱ (1?mmol/L) plus adiponectin (30mg/L). The protein levels of Bcl-2 and Bax were detected by Western blotting. The apoptotic rate and the levels of intracellular reactive oxygen species (ROS) in the ventricular myocytes were determined by flow cytometry. The survival rate of ventricular myocytes was evaluated by trypan blue staining. Results As compared with placebo group,the apoptosis of neonatal rat ventricular myocytes was significantly promoted in 1?mol/L angiotesin Ⅱ group,the survival rate of cardiomyocytes was significantly reduced,with the protein expression of Bax and the ROS level increased,and the protein expression of Bcl-2 decreased (P
