In this study, the equilibrium data of the hydrates forming in tetra-n-butylphosphonium bromide (TBPB) aqueous solution with and without carbon dioxide (CO2) are measured at mass fractions w = (0.10, 0.20, 0.35, and 0.50) in the pressure range of (0.4 to 4.0) MPa and in the temperature range of (281.0 to 292.0) K. Meanwhile, the crystal morphologies of TBPB hydrates with and without CO2 are visually observed. The equilibrium data and morphologies of TBPB hydrates are compared with those of tetra-n-butylammonium bromide (TBAB) hydrates.

These results indicate that TMP could protect ischemic brain damage, and promote cell proliferation and differentiation stimulated by ischemia, which might be related to the reduction of nNOS expression after treatment with TMP in rat cerebral ischemia model.

Studies have shown that long noncoding ribonucleic acids (lncRNAs) play critical roles in multiple biologic processes. However, the Small Nucleolar RNA Host Gene 1 (SNHG1) function and underlying molecular mechanisms in ischemic stroke have not yet been reported. In the present study, we found that SNHG1 expression was remarkably increased both in isolated cerebral micro-vessels of a middle cerebral artery occlusion (MCAO) mice model, and in oxygen-glucose deprivation (OGD)-cultured mice brain micro-vascular endothelial cells (BMECs), meanwhile, the SNHG1 level was negatively correlated with miR-18a in MCAO mice. Mechanistically, SNHG1 inhibition presents larger brain infarct size and worsens neurological scores in MCAO mice. Consistent with the in vivo findings, SNHG1 inhibition also significantly increased caspase-3 activity and cell apoptosis in OGD-cultured BMECs. Furthermore, we found that SNHG1 functions as a competing endogenous RNA (ceRNA) for miR-18a, thereby regulating the de-repression of its endogenous target HIF-1α and promoting BMEC survival through HIF-1α/VEGF signaling. This study found a neuroprotective effect of SNHG1 mediated by HIF-1α/VEGF signaling through acting as a ceRNA for miR-18a. These findings reveal a novel function of SNHG1, which contributes to an extensive understanding of ischemic stroke and provides novel therapeutic options for this disease.

No abstract

Astrocytes have now been well accepted to play important roles in epileptogenesis by controlling gliotransmitter release and neuronal excitability, contributing to blood-brain barrier dysfunction and involving in brain inflammation. Recent studies indicate that abnormal expression of gap junction protein connexin (Cx) may also be a contributing factor for seizure generation. To further address this issue, we investigated the progressive changes of Cx 43 and Cx 40 in the mouse hippocampus at 4 h, 1 day, 1 week and 2 months during and after pilocarpine-induced status epilepticus (PISE). The co-localization of Cx 43 and Cx 40 with glial fibrillary acidic protein (GFAP) was also examined. We observed that Cx 43 and Cx 40 protein expression remained unaltered at 4 h during and at 1 day (acute stage) after PISE. However, their expression was significantly increased in CA1 and CA3 areas and in the dentate gyrus at 1 week (latent stage) and 2 months (chronic stage) after PISE. Double immunofluorescence labeling indicated the localization of Cx 43 and Cx 40 in astrocytes. Combined with progressive neuronal loss in the mouse hippocampus, our results suggest that the increase in gap junctions in the neuronoglial syncytium of reactive astrocytes may be implicated in synchronization of hippocampal hyperactivity leading to neuronal loss and epileptogenesis.