Solar-assisted high-efficient cleanup of viscous crude oil spill using an ink-modified plant fiber sponge.

Rapid and efficient clean-up of viscous crude oil spills is still a global challenge due to its high viscous and poor flowability at room temperature. The hydrophobic/oleophilic absorbents with three-dimensional porous structure have been considered as a promising candidate to handle oil spills. However, they still have limited application in recovering the high viscous oil. Inspired by the viscosity of crude oil depended on the temperature, a solar-heated ink modified plant fiber sponge (PFS@GC) is fabricated via a simple and environmentally friendly physical foaming strategy combined with in-situ ink coating treatment. After wrapping by the polydimethylsiloxane (PDMS), the modified PFS@GC (PFS@GC@PDMS) exhibits excellent compressibility, high hydrophobic (141° in water contact angle), solar absorption (> 96.0%), and oil absorptive capacity (12.0-27.8 g/g). Benefiting from the favorable mechanical property and photothermal conversion capacity, PFS@GC@PDMS is demonstrated as a high-performance absorbent for crude oil clean-up and recovery. In addition, PFS@GC@PDMS can also be applied in a continuous absorption system for uninterrupted recovering of oil spills on the water surface. The proposed solar-heated absorbent design provides a new opportunity for exploring biomass in addressing large-scale oil spill disasters.

Effective silencing of miR-126 after ischemic stroke by means of intravenous α-tocopherol-conjugated heteroduplex oligonucleotide in mice.

Brain endothelial cells (BECs) are involved in the pathogenesis of ischemic stroke. Recently, several microRNAs (miRNAs) in BECs were reported to regulate the endothelial function in ischemic brain. Therefore, modulation of miRNAs in BECs by a therapeutic oligonucleotide to inhibit miRNA (antimiR) could be a useful strategy for treating ischemic stroke. However, few attempts have been made to achieve this strategy via systemic route due to lack of efficient delivery-method toward BECs. Here, we have developed a new technology for delivering an antimiR into BECs and silencing miRNAs in BECs, using a mouse ischemic stroke model. We designed a heteroduplex oligonucleotide, comprising an antimiR against miRNA-126 (miR-126) known as the endothelial-specific miRNA and its complementary RNA, conjugated to α-tocopherol as a delivery ligand (Toc-HDO targeting miR-126). Intravenous administration of Toc-HDO targeting miR-126 remarkably suppressed miR-126 expression in ischemic brain of the model mice. In addition, we showed that Toc-HDO targeting miR-126 was delivered into BECs more efficiently than the parent antimiR in ischemic brain, and that it was delivered more effectively in ischemic brain than non-ischemic brain of this model mice. Our study highlights the potential of this technology as a new clinical therapeutic option for ischemic stroke.

Modulation of blood-brain barrier function by a heteroduplex oligonucleotide in vivo.

The blood-brain barrier (BBB) is increasingly regarded as a dynamic interface that adapts to the needs of the brain, responds to physiological changes, and gets affected by and can even promote diseases. Modulation of BBB function at the molecular level in vivo is beneficial for a variety of basic and clinical studies. Here we show that our heteroduplex oligonucleotide (HDO), composed of an antisense oligonucleotide and its complementary RNA, conjugated to α-tocopherol as a delivery ligand, efficiently reduced the expression of organic anion transporter 3 (OAT3) gene in brain microvascular endothelial cells in mice. This proof-of-concept study demonstrates that intravenous administration of chemically synthesized HDO can remarkably silence OAT3 at the mRNA and protein levels. We also demonstrated modulation of the efflux transport function of OAT3 at the BBB in vivo. HDO will serve as a novel platform technology to advance the biology and pathophysiology of the BBB in vivo, and will also open a new therapeutic field of gene silencing at the BBB for the treatment of various intractable neurological disorders.

[Effect of icariin on hypoxia induced vascular endothelial cells injury].

OBJECTIVE: To study the effect of icariin on vascular endothelial cells (VECs) injury induced by hypoxia. METHODS: The hypoxia-ischemia model was established. The effect of icariin on injury of VECs activity induced by hypoxia was determined by MTT assay. The levels of malondialdehyde (MDA), superoxide dismutase (SOD) and lactate dehydrogenase (LDH) activity in cell homogenate were measured with corresponding kit. Effect of icariin on cells apoptosis induced by hypoxia was determined by Hoechst 33342 fluorescent staining, cell ultrastructure observation under transmission electron microscopy and analysis on gene fragmentation by flow cytometry and DNA gel electrophoresis. RESULTS: ICA could inhibit the hypoxia induced VECs reduction, suppress LDH activity, reduce the MDA production, and enhance SOD activity under hypoxia. Hypoxia could induce VECs apoptosis, revealed chromation condensed in nuclei with the fragments arranged along the nuclear membrane. DNA gel electrophoresis showed typical ladder strands of DNA. Cells displayed a typical sub-diploid peak in flow cytometry. ICA could significantly inhibit the hypoxia induced apoptosis of VECs. CONCLUSION: ICA has the protective effect on hypoxia injured VECs, which may be related to its effect of anti-apoptosis, anti-lipid peroxidation and SOD activity enhancing.