Purpose: Circular RNAs (circRNAs) have been reported to regulate the incidence of tumor by regulating the transcriptional level and post-transcriptional level of tumor-related genes, and are significantly correlated with tumor metastasis and progression. CircRNA_100395 (circ_100395) has been reported to suppress lung cancer cell proliferation, and might act as an oncogene in deveopment of various cancers. However, the expression and function of circ_100395 in ovarian cancer has not been systematically researched. Methods: The expression of circ_100395 in ovarian cancer tissues was detected by Real-time Quantitative polymerase chain reaction (RT-qPCR), while the relationship between circ_100395 expression and clinicopathological characteristics was further analyzed. After increasing the expression of circ_100395 by plasmid transfection in ovarian cancer cells, we further investigated the cell proliferation, invasion and migration by cell counting kit-8 (CCK-8), and Transwell assays. Epithelial-mesenchymal transition (EMT) pathway was also measured by western blotting. In addition, the relationship among circ_100395, miR-1228 and p53 in ovarian cancer, was explored by luciferase reporter assay. Results: The expression of circ_100395 was found to be significantly down-regulated in ovarian cancer, while low expression of circ_100395 was highly correlated with the poor outcomes. In addition, upregulation of circ_100395 could significantly inhibit tumor growth, metastasis and EMT signaling pathway in ovarian cancer. Furthermore, the expression level of circ_100395 was negatively correlated with the expression of miR-1228, and with the addition of miR-1228 could reverse anti-cell proliferation effect induced by circ_100395 in ovarian cancer cells. In addition, p53 might be the key target of circ_100395 / miR-1228 axis in ovarian cancer. Conclusion: CircRNA_100395 could inhibit cell growth and metastasis of ovarian cancer cells via regulating the miR-1228/p53/EMT axis.

The lower uterine segment scar becomes stable at 3 years after cesarean delivery, and by 9 years, the scar is mature.

BackgroundThe purpose of this study was to evaluate the efficacy of prenatal ultrasonography and Doppler sonography in detecting isolated ventricular septal defects (VSDs) in a late-second-trimester population.MethodsFetal echocardiography, Doppler ultrasound, and biometry were used to evaluate 2,661 singleton fetuses (1,381 male fetuses and 1,280 female fetuses) between 1 August 2006 and 31 May 2010. The efficacy of each fetal biometry, Doppler ultrasound, and nasal bone length (NBL) measurement was evaluated in all of the fetuses. A standard fetal echocardiographic evaluation, including two-dimensional gray-scale imaging and color and Doppler color flow mapping, was performed on all fetuses.ResultsWe detected isolated VSDs in 124 of the 2,661 singleton fetuses between 19 and 24 weeks of gestation. The prevalence of isolated VSDs in the study population was 4.66%. A multiple logistic regression analysis indicated that short fetal NBL (odds ratio = 0.691, 95% confidence interval: 0.551 to 0.868) and the pulsatility index (PI) of the umbilical artery (odds ratio = 8.095, 95% confidence interval: 4.309 to 15.207) and of the middle cerebral artery (odds ratio = 0.254, 95% confidence interval: 0.120 to 0.538) are significantly associated with isolated VSDs.ConclusionLate-second-trimester fetal NBL, umbilical artery PI, and middle cerebral artery PI are useful parameters for detecting isolated VSDs, and can be used to estimate the a priori risk of VSDs in women at high risk and at low risk of isolated VSDs.

Objectives. Hyponatremia is a common complication of diabetes. However, the relationship between serum sodium level and diabetic peripheral neuropathy (DPN) is unknown. This study was aimed at investigating the relationship between low serum sodium level and DPN in Chinese patients with type 2 diabetes mellitus. Methods. A retrospective study was performed on 1928 patients with type 2 diabetes between 2010 and 2018. The multivariate test was used to analyze the relationship between the serum sodium level and the nerve conduction function. A restricted cubic spline was used to flexibly model and visualize the relationship between the serum sodium level and DPN, followed by logistic regression with adjustment. Results. As the serum sodium level increased, the prevalence of DPN had a reverse J-curve distribution with the serum sodium levels (69.6%, 53.7%, 49.6%, 43.9%, and 49.7%; P = 0.001 ). Significant differences existed between the serum sodium level and the motor nerve conduction velocity, sensory nerve conduction velocity, part of compound muscle action potential, and sensory nerve action potential of the participants. Compared with hyponatremia, the higher serum sodium level was a relative lower risk factor for DPN after adjusting for several potential confounders ( OR = 0.430 , 95 % CI = 0.220 – 0.841 ; OR = 0.386 , 95 % CI = 0.198 – 0.755 ; OR = 0.297 , 95 % CI = 0.152 – 0.580 ; OR = 0.376 , 95 % CI = 0.190 – 0.743 ; all P < 0.05 ). Compared with low-normal serum sodium groups, the high-normal serum sodium level was also a risk factor for DPN ( OR = 0.690 , 95 % CI = 0.526 – 0.905 , P = 0.007 ). This relationship was particularly apparent in male participants, those aged <65 years, those with a duration of diabetes of <10 years, and those with a urinary   albumin − to − creatinine   ratio   UACR < 30   mg / g . Conclusions. Low serum sodium levels were independently associated with DPN, even within the normal range of the serum sodium. We should pay more attention to avoid the low serum sodium level in patients with type 2 diabetes mellitus.