Effects of Osthole on Expressions of Apoptosis-Related Genes.

<p>SMMC-7721 cells were treated with osthole (123.0 µM) for 48 h. The expressions of apoptosis-related genes were analyzed using RT² Profiler PCR Arrays. Increased expressions of two folds or more were shown. Data shown were representatives of two experiments.</p

Additional file 1 of Fascin-1 limits myosin activity in microglia to control mechanical characterization of the injured spinal cord

Supplementary Material

Osthole Inhibited Cell Proliferation of HCC Cell Lines.

<p>(A) Chemical Structure of osthole (B) Viability of SK-HP-1, SMMC-7721, HepG-2 and Hepa1-6 cells treated with osthole. MTT assay was performed to measure cell growth inhibition rate at 48 h after osthole treatment. (C)(D) Viability of SMMC-7721 and Hepa1-6 cells treated with osthole. MTT assay was performed to measure cell growth inhibition rate at 24 h, 48 h and 72 h after osthole treatment. Data shown were representatives of three experiments.</p

Effects of Osthole on Cell Cycle of HCC Cells.

<p>Cell cycle analysis of SMMC-7721 and Hepa1-6 cells following 123.0 µM osthole treatment for 24 h by flow cytometry.</p

Effects of Osthole on apoptosis of HCC cells.

<p>(A) Induction of apoptosis of SMMC-7721 and Hepa1-6 cells after osthole treatment. SMMC-7721 and Hepa1-6 cells were treated with osthole at doses of 0, 41.0, 84.0, 123.0, 164.0 and 205.0 µM for 48 h. Apoptosis was measured by flow cytometry. (B) Statistical analysis of the percentages of the apoptotic cells. Data shown were representatives of three experiments.</p

Effect of Osthole Treatment on the Tumorigenicity of HCC Cells.

<p>A total of 2×10⁶ SMMC-7721 or Hepa1-6 cells were inoculated subcutaneously (s.c.) into the right flank of nude mice or C57/BL6 mice. Mice were randomized into five groups including osthole treatment (244 mg/kg, 122 mg/kg and 61 mg/kg), corn oil alone as the blank control and cisplatin (5 mg/kg) as the positive control on Day8 and were treated once every other day for 2 weeks. (A) The tumor volumes of the nude mice inoculated with SMMC-7721 cells were measured and calculated once every three days. The tumor sizes on day 21 were shown in the inserted figure. (B) Tumor weights of the nude mice inoculated with SMMC-7721 cells were measured on day21. (C) The tumor volumes of the C57/BL6 mice inoculated with Hepa1-6 cells were measured and calculated once every three days. (D) Tumor weights of the C57/BL6 mice inoculated with Hepa1-6 cells were measured on day21. (E) The body weights of nude mice inoculated with SMMC-7721 cells were weighed on day 21. The (F) spleen weights and (G) thymus weights of the C57/BL6 mice inoculated with Hepa1-6 cells were weighed on day21. Each data point represented the mean±S.D. of 10 mice. Data shown were the representatives of three experiments.</p

Effects of Osthole Treatment on Caspase-3 expression and NF-κB activation.

<p>(A) SMMC-7721 cells were treated with osthole (123.0 µM) for 12 h, 24 h and 48 h. The nuclear proteins were prepared and analyzed for NF-κB expression by EMSA. (B) SMMC-7721 cells were treated with osthole at doses of 0, 41.0, 82.0, 123.0, 164.0 and 205.0 µM for 24 h. The nuclear proteins were prepared and analyzed for NF-κB expression by EMSA. (C) SMMC-7721 cells were treated with osthole at doses of 0, 41.0, 82.0, 123.0, 164.0 and 205.0 µM for 48 h. The cell lysates were prepared and analyzed for caspase-3 expression by Western blot analysis. Equal loading was confirmed by stripping immunoblots and reprobing for β-actin. Data shown were representatives of three experiments. (D) Statistical analysis of caspase-3 quantification. * <i>p</i><0.05, ** <i>p</i><0.01.</p

Carbon Nanotube-Bridged Graphene 3D Building Blocks for Ultrafast Compact Supercapacitors

The main obstacles to achieving high electrochemical energy density while retaining high power density are the trade-offs of energy <i>versus</i> power and gravimetric <i>versus</i> volumetric density. Optimizing structural parameters is the key to circumvent these trade-offs. We report here the synthesis of carbon nanotube (CNT)-bridged graphene 3D building blocks <i>via</i> the Coulombic interaction between positively charged CNTs grafted by cationic surfactants and negatively charged graphene oxide sheets, followed by KOH activation. The CNTs were intercalated into the nanoporous graphene layers to build pillared 3D structures, which enhance accessible surface area and allow fast ion diffusion. The resulting graphene/CNT films are free-standing and flexible with a high electrical conductivity of 39 400 S m^–1 and a reasonable mass density of 1.06 g cm^–3. The supercapacitors fabricated using these films exhibit an outstanding electrochemical performance in an ionic liquid electrolyte with a maximum energy density of 117.2 Wh L^–1 or 110.6 Wh kg^–1 at a maximum power density of 424 kW L^–1 or 400 kW kg^–1, which is based on thickness or mass of total active material

Diffusion Mechanism of Lithium Ion through Basal Plane of Layered Graphene

Coexistence of both edge plane and basal plane in graphite often hinders the understanding of lithium ion diffusion mechanism. In this report, two types of graphene samples were prepared by chemical vapor deposition (CVD): (i) well-defined basal plane graphene grown on Cu foil and (ii) edge plane-enriched graphene layers grown on Ni film. Electrochemical performance of the graphene electrode can be split into two regimes depending on the number of graphene layers: (i) the corrosion-dominant regime and (ii) the lithiation-dominant regime. Li ion diffusion perpendicular to the basal plane of graphene is facilitated by defects, whereas diffusion parallel to the plane is limited by the steric hindrance that originates from aggregated Li ions adsorbed on the abundant defect sites. The critical layer thickness (<i>l</i>_c) to effectively prohibit substrate reaction using CVD-grown graphene layers was predicted to be ∼6 layers, independent of defect population. Our density functional theory calculations demonstrate that divacancies and higher order defects have reasonable diffusion barrier heights allowing lithium diffusion through the basal plane but neither monovacancies nor Stone-Wales defect

Data_Sheet_2_Analysis of shared ceRNA networks and related-hub genes in rats with primary and secondary photoreceptor degeneration.docx

IntroductionPhotoreceptor degenerative diseases are characterized by the progressive death of photoreceptor cells, resulting in irreversible visual impairment. However, the role of competing endogenous RNA (ceRNA) in photoreceptor degeneration is unclear. We aimed to explore the shared ceRNA regulation network and potential molecular mechanisms between primary and secondary photoreceptor degenerations.MethodsWe established animal models for both types of photoreceptor degenerations and conducted retina RNA sequencing to identify shared differentially expressed long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and messenger RNAs (mRNAs). Using ceRNA regulatory principles, we constructed a shared ceRNA network and performed function enrichment and protein–protein interaction (PPI) analyses to identify hub genes and key pathways. Immune cell infiltration and drug–gene interaction analyses were conducted, and hub gene expression was validated by quantitative real-time polymerase chain reaction (qRT-PCR).ResultsWe identified 37 shared differentially expressed lncRNAs, 34 miRNAs, and 247 mRNAs and constructed a ceRNA network consisting of 3 lncRNAs, 5 miRNAs, and 109 mRNAs. Furthermore, we examined 109 common differentially expressed genes (DEGs) through functional annotation, PPI analysis, and regulatory network analysis. We discovered that these diseases shared the complement and coagulation cascades pathway. Eight hub genes were identified and enriched in the immune system process. Immune infiltration analysis revealed increased T cells and decreased B cells in both photoreceptor degenerations. The expression of hub genes was closely associated with the quantities of immune cell types. Additionally, we identified 7 immune therapeutical drugs that target the hub genes.DiscussionOur findings provide new insights and directions for understanding the common mechanisms underlying the development of photoreceptor degeneration. The hub genes and related ceRNA networks we identified may offer new perspectives for elucidating the mechanisms and hold promise for the development of innovative treatment strategies.</p