Association of placenta-derived extracellular vesicles with pre-eclampsia and associated hypercoagulability: a clinical observational study.

Objective: Pre-eclampsia (PE) is a pregnancy-associated condition initiated by placental factors. We have demonstrated that placental extracellular vesicles (pcEVs) cause hypertension and proteinuria in pregnant and non-pregnant mice.

Study Design: An observational study with both case-control and longitudinal designs.

Placenta-derived extracellular vesicles induce preeclampsia in mouse models.

Preeclampsia is a pregnancy-induced condition that impairs the mother's health and results in pregnancy termination or premature delivery. Elevated levels of placenta-derived extracellular vesicles (pcEV) in the circulation have been consistently associated with preeclampsia, but whether these vesicles induce preeclampsia or are the product of preeclampsia is not known. Guided by a small cohort study of preeclamptic patients, we examined the impact of pcEV on the pathogenesis of preeclampsia in mouse models.

Correlation of Circulating T Lymphocytes and Intracranial Hypertension in Intracerebral Hemorrhage.

Background: The close correlation between intracerebral pressure (ICP) and immunologic responses has been well described, but the role of T lymphocytes in this process remains unknown. This study targeted the relationship of circulating T lymphocytes and ICP in patients with intracerebral hemorrhage (ICH).

Methods: Between October 2015 and October 2016, consecutive patients age 18-65 years with ICH were enrolled.

MicroRNA-204 suppresses epileptiform discharges through regulating TrkB-ERK1/2-CREB signaling in cultured hippocampal neurons.

MicroRNAs (miRs) have been increasingly recognized as post-transcriptional regulators involved in the pathogenesis of epilepsy. Extensive evidence suggests that inhibition of tropomyosin related kinase type B (TrkB) signaling limits epileptogenesis. It has been reported that miR-204 directly targeted and downregulated TrkB protein in a variety of cancers to suppress tumorigenesis, but its effect on epileptogenesis is unknown.

MicroRNA-132 aggravates epileptiform discharges via suppression of BDNF/TrkB signaling in cultured hippocampal neurons.

MicroRNAs (miRs) are increasingly recognized as targets to prevent or disrupt epilepsy as well as serve as diagnostic biomarkers of epileptogenesis. Brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin related kinase type B (TrkB) also contribute to the pathophysiology of epilepsy. However, the possible involvement of miRs in BDNF-mediated molecular basis for epileptogenesis is less understood.