Dynamics of the Deformable Fluid Interface Interacting with an Approaching Solid under the Electrostatic Field.

A theoretical model was developed to describe the dynamics of a deformable fluid interface interacting with an approaching solid without contact by both the attractive electrostatic and van der Waals (i.e., vdW) interaction, analogous to the situation in the experiments by electric force microscopy (i.e., EFM) or electric-surface force apparatus (i.e., E-SFA) involved in the soft fluid interface. On the basis of this model, a numerical study of the deformation of the fluid interface, the force-vs-separation behavior, and the critical limiting conditions of contact has systematically been carried out. Our results show that the surface pressure induced by the electrostatic interaction plays a more prominent role in the deformation of the fluid interface than the vdW interaction does, and there exists a principal length scale associated with the relative strength of the electrostatic field to the surface tension, affecting the fluid interface shape under the electrostatic field. It was also shown that both the force-distance curves and the corresponding curves of fluid interface deformation peak versus distance for various electrostatic fields satisfy the universal scaling power law. Moreover, an analytical solution to the Euler-Lagrange differential equation governing the deformation of the fluid interface under the external electric field is obtained, and two extended formulas for explicitly describing the principal length scales that respectively characterize the lateral and longitudinal deformations of the fluid interface were determined.

Non-criteria and criteria antiphospholipid antibodies and their association with pregnancy outcomes in women with a history of miscarriage: A retrospective study.

INTRODUCTION: The objective of this study was to investigate both antiphospholipid antibodies (aPLs) and non-criteria aPLs (NC-aPLs) in relation with pregnancy outcomes. METHODS: We retrospectively analyzed 1574 pregnant women with experienced at least one miscarriage who were tested for aPLs and NC-aPLs, and compared their clinical characteristics, immune biomarkers, and pregnancy outcomes. The χ2 test or Fisher's exact test compared pregnancy outcomes among patients negative for all aPLs, positive for NC­aPLs subtypes, and positive for criteria aPLs subtypes. RESULTS: Multivariate logistic regression analysis indicated that positive aPLs (OR = 2.216, 95 % CI 1.381-3.558), and positive NC-aPLs (OR = 1.619, 95 % CI 1.245-2.106) are linked to adverse outcomes. For fetal loss, positive aPLs (OR = 2.354, 95 % CI 1.448-3.829), NC-aPLs (OR = 1.443, 95 % CI 1.076-1.936) were significant. Premature delivery was associated with positive NC-aPLs (OR = 2.102, 95 % CI 1.452-3.043). In the NC-aPLs positive group, the rate of adverse outcomes was higher in the multiple-positive subgroup (77.8 %) compared to the double-positive (52.3 %) and single-positive (37.0 %) subgroups. The rates of fetal loss and premature delivery were also higher in the multiple-positive NC-aPLs subgroup compared to the single-positive subgroup (48.1 % vs. 22.6 % for fetal loss and 57.1 % vs. 16.5 % for premature delivery). DISCUSSION: Our findings suggest that both aPLs and NC-aPLs are associated with an increased incidence of adverse pregnancy outcomes, and patients presenting with multiple NC-aPLs positivity were found to have a higher incidence of adverse outcomes compared to their single-positive counterparts.

[LncRNA SNHG8 inhibits miR-494-3p expression to alleviate cerebral ischemia-reperfusion injury in mice].

OBJECTIVE: To explore the mechanism by which LncRNA SNHG8 regulates miR-494-3p expression to alleviate cerebral ischemia-reperfusion injury. METHODS: A mouse model of cerebral ischemia-reperfusion injury was established, and TTC staining was used to determine the infarct area; ELISA was used to detect the contents of the inflammatory factors IL-1ß, IL-6 and TNF-α in the brain tissue, and RT-qPCR was performed to detect the expression levels of LncRNA MALAT1 and miR-155-5p. A microglial cell model overexpressing LncRNA SNHG8 was exposed to oxygen-glucose deprivation/reoxygenation (OGD/R), and inflammatory reaction and apoptosis of the cells were detected using ELISA and flow cytometry. A luciferase reporter assay was used to detect the targeting relationship between LncRNA SNHG8 and miR-494-3p. We further constructed a microglial cell model overexpressing both LncRNA SNHG8 the miR-494-3p, and examined inflammatory reactions and apoptosis of the cells following OGD/R exposure. RESULTS: In the mouse model of cerebral ischemia-reperfusion injury, the contents of inflammatory factors IL-1ß, IL-6 and TNF-α increased significantly in the brain tissue (P < 0.001), where LncRNA SNHG8 expression was lowered (P < 0.01) and miR-494-3p expression increased significantly (P < 0.01). In the microglial cells, overexpression of LncRNA SNHG8 significantly inhibited the inflammatory reaction and apoptosis following OGD/R exposure (P < 0.01), and overexpression of LncRNA SNHG8 strongly inhibited the expression of miR-494-3p (P < 0.01). Overexpression of miR-494-3p in microglia overexpressing SNHG8 partially promoted inflammatory reaction and cell apoptosis in response to OGD/R (P < 0.05). CONCLUSION: LncRNA SNHG8 can improve cerebral ischemia-reperfusion injury in mice by inhibiting the expression of miR-494-3p and suppressing inflammatory reactions and apoptosis of the microglia.