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To explore the effect and mechanism of APRPG-modified nanoliposomes loaded with miR-146a-5p inhibitor (ANL-miR-146a-5p inhibitor) on endothelial cell proliferation, migration, tube formation, and choroidal neovascularization (CNV) in mice.
ANL-miR-146a-5p inhibitors were generated by thin film hydration; invitro, endothelial cell uptake experiment was used to detect the targeting effect of ANL-miR-146a-5p inhibitor; endothelial cells proliferation, migration, and tube formation were detected, respectively, by CCK8 assay, scratch assay, and Matrigel tube formation assay. In vivo, the mice CNV models were established by 810 nm laser photocoagulation. Mice choroidal flatmounts were performed to detect the volume of CNV after intravitreal injection of L-miR-146a-5p inhibitor, ANL-miR-146a-5p inhibitor, or normal saline; the vascular endothelial growth factor (VEGF) expression of mice choroidal tissue was detected by ELISA; HE section and electrophysiology (ERG) were performed to check the toxicity of ANL-miR-on, and mice CNV formation.As a chronic inflammatory disease, coronary artery disease (CAD) is a common cause of death worldwide. Dysregulation of microRNA expression levels in peripheral blood mononuclear cells (PBMCs) may contribute to CAD and serve as a potential diagnostic biomarker. Here, we evaluated PBMC expression of two CAD-related inflammatory miRNAs, miR-196a and miR-100, in PBMCs of CAD patients with significant stenosis (CAD, n 72), patients with insignificant coronary stenosis (ICAD, n 30), and controls (n 74) and checked whether they can segregate study groups. MiRNA expression was evaluated using the standard stem-loop RT-qPCR method. MiR-196a expression was downregulated in ICAD compared to CADs and healthy groups. MiR100 expression levels were not different between groups. The receiver operating characteristic (ROC) curve analysis acquainted that miR-196a expression levels in PBMC could segregate CAD individuals or any of its clinical manifestations (i.e. unstable angina, stable angina, acute myocardial infarction) from ICADs. In conclusion, this study reported a distinct miR-196a expression pattern in PBMCs of all patient groups and recommended a biomarker potential for miR-196a in discriminating ICADs from CADs or healthy controls.
Hypertensive disorders are a common cause of maternal mortality. Whether interpregnancy BMI (body mass index kg/m
) gain is associated with hypertensive disorders in a subsequent pregnancy is not unclear.
To examine the association between interpregnancy BMI and hypertensive disorders in women without a history of hypertensive disorders in pregnancy.
This was a retrospective cohort study of all women who had more than one singleton pregnancy at 23 weeks' gestation or greater at a single academic institution. Only the second pregnancy in the dataset was analyzed. We excluded women who had any hypertensive disorder in the index pregnancy. Interpregnancy BMI change was calculated by the change of early pregnancy BMI (within 14 weeks' gestation) measured in the office between the index pregnancy compared to that of the subsequent pregnancy. Women were categorized according to interpregnancy BMI change (BMI loss greater than 2 kg/m
, BMI change ±2 kg/m
, and BMI gain greater than 2 kg/m
). The primary ouds ratio 0.58 [95% confidence interval 0.32-1.05]).
Compared to interpregnancy BMI change ±2 kg/m
, interpregnancy BMI gain greater than 2 kg/m
was associated with increased odds of any hypertensive disorder. Weight control after pregnancy could be a potentially modifiable factor that may reduce the risk of hypertensive disorders.
Compared to interpregnancy BMI change ±2 kg/m2, interpregnancy BMI gain greater than 2 kg/m2 was associated with increased odds of any hypertensive disorder. Weight control after pregnancy could be a potentially modifiable factor that may reduce the risk of hypertensive disorders.
To determine the relationship between gestational diabetes mellitus (GDM) and coagulation/fibrinolysis abnormality in antenatal Chinese women.
Case control study 50 women had GDM and 132 did not (the NGDM group) grouping by the International Association of Diabetes and Pregnancy Study Groups (IADPSG) criteria. Maternal plasma biochemistry and previous medical history were collected from perinatal health records. Antenatal coagulation/fibrinolysis activity (CFA) parameters were assessed using thromboelastography and routine CFA parameters, respectively. Univariate and multiple regression analyses were used to evaluate the associations between GDM and CFA parameters. Maternal age, platelet, ALT, ALP, urea nitrogen, and previous history of abortion were taken as the covariables.
The women with GDM were significantly older than those without GDM (30.3 vs. 28.6 years,
= .012). Compared with the NGDM group, the GDM group had a significantly higher prevalence of cesarean delivery (56.0 vs. 37.9%,
= .027) and higher values of fibrinogen (FIB; 4.7 vs. 4.3 g/L,
= .001), activated partial thromboplastin time (APTT; 30.9 vs. 29.5 s,
= .010).There were no significant differences in the prevalence of maternal thrombotic events or neonatal events. GDM was significantly associated with higher APTT (
=1.41 s, 95% CI 0.29-2.53), higher FIB (
= 0.38 g/L, 95% CI 0.14-0.61), and higher percentage reduction in clot lysis after 30 min (LY30;
= 1.14%, 95% CI 0.15-2.13) after adjustment for potential confounding factors.
GDM is significantly associated with hypercoagulability and hyperfibrinolysis in these antenatal Chinese women.
GDM is significantly associated with hypercoagulability and hyperfibrinolysis in these antenatal Chinese women.
To evaluate first trimester maternal weight as a spina bifida screening marker.
Case-control study of spina bifida and unaffected pregnancies; cases were from national records and controls from women referred to prenatal screening centers in the Ukraine. The median and inter-quartile range of weight, body mass index (BMI) and the obesity rate (BMI ≥ 30 kg/m
) were compared. Discriminatory power was assessed by logistic regression. selleck chemicals Gaussian modeling was used to predict the additional spina bifida detection when weight was included as a screening marker risk in addition to first trimester biparietal diameter (BPD) and serum α-fetoprotein (AFP).
There were 97 cases and 274 controls. The distribution of maternal weight was increased in cases by 3 kg, on average, about 5% (
< .05); BMI was increased about 8% (
< .005). Some 15% of cases were obese compared with 6.9% of controls (
< .02). In logistic regression including BMI and maternal age, 29% cases and 9.8% controls had high risk of spina bifida.
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