Flexible Silicon/Titanium Dioxide/Reduced Graphene Oxide Self-Standing Electrode with High Performance and High Stability for Lithium-Ion Batteries

The great volume expansion and unstable nature of the solid electrolyte interface film of silicon (Si) are central issues that obstruct the advancement of the Si-based electrode despite its high theoretical capacity and abundant resources. Here a kind of flexible silicon/titanium dioxide/reduced graphene oxide (Si/TiO2/rGO) self-standing electrode is constructed without the assistance of a binder and conductive agent. Briefly, the Si nanoparticle is coated with TiO2 via a sol–gel process, and then the core–shell structured Si/TiO2 is assembled with GO using chitosan as the cross-linker followed by freeze-drying, pressing, and annealing at an ammonia/argon (NH3/Ar) atmosphere. In this structure, TiO2 and rGO provide dual protection for Si, and a continuous conductive path is formed. Additionally, nitrogen doping by NH3 and chitosan further strengthens the lithium storage performance. The fabricated Si/TiO2/rGO film electrode demonstrates excellent rate performance over a broad range of current densities and keeps a reversible capacity of 1333.8 mAh g–1 after 200 cycles operated at 200 mA g–1

Huge bone resorption cavities in the cross section of peri-screw bone.

<p>A) irregular and bifurcated resorption cavity (arrow) in damaged bone; B) Huge resorption cavity (long arrow) with cutting zone (short arrow) in damaged bone and closing zone (arrow head) behind (1 month after surgery).</p

Comparison of bone resorption related parameters in peri-screw bone between different time points after surgery.

<p>Data expressed as mean (SD).</p><p>Intergroup comparison (p<0.05):</p>1<p>Compare with 1 day;</p>2<p>Compare with 2 weeks;</p>3<p>Compare with 1 month.</p

Microdamage in peri-screw bone stained with basic fuchsin.

<p>Diffuse damage was contacted with bone edge (large arrow), behind which larger linear cracks (small arrows) were visible. Linear cracks often mixed with diffuse damage (arrow heads) in the area adjacent to the bone-screw interface.</p

The morphology of microdamage and bone resorption cavities in peri-screw bone.

<p>A) microdamage adjacent to the bone-screw interface was composed of diffuse damage and linear cracks (1 day after surgery). The microcracks not only cut through osteocyte lacunae and canaliculi in bone matrix, but also destroyed the surface of Haversian canal (arrows); B) cutting cavities (arrows) in damaged bone (2 weeks after surgery); C) closing cavities (arrows) in damaged bone (2 months after surgery). Extensive osteocyte lacunar-canalicular network was visible in newly formed bone beneath the osteoid (top arrow).</p

Resorption cavities in peri-screw bone (1 month after surgery).

<p>A) cutting cavities (arrow) were covered by a thin layer of basic fuchsin stained tissue and contacted with microdamage; B) closing cavity (arrow) was covered by a thick seem of osteoid, on which there was a single layer of cuboidal osteoblasts attached.</p

Comparison of microdamage related parameters in peri-screw bone between different time points after surgery.

<p>Data expressed as mean (SD).</p><p>Intergroup comparison (p<0.05):</p>1<p>Compare with 1 day;</p>2<p>Compare with 2 weeks;</p>3<p>Compare with 1 month.</p

The variables for outcome assessment.

<p>*B.Ar: Area of peri-screw bone; DDx.Ar: Area of diffuse damage; DDx.L: Length of diffuse damage; BE.L: Length of bone edge; LCr.N: Number of linear cracks; LCr.L: Length of linear cracks; RC.N: Number of resorption cavities; RC.Ar: Area of resorption cavities.</p

Osteoblast-Secreted Factors Promote Proliferation and Osteogenic Differentiation of Bone Marrow Stromal Cells via VEGF/Heme-Oxygenase-1 Pathway

<div><p>The hypoxia-inducible factors (HIFα) are the critical factors that couple angiogenesis and osteogenesis by activating transcription of VEGF in osteoblasts. Mice lacking von Hippel–Lindau gene (<i>Vhl</i>), thus overexpressing HIFα in osteoblasts develop extremely dense and highly vascularized long bones. Here we provide evidence that osteoblasts lacking <i>Vhl</i> overexpress and secrete high levels of VEGF, which subsequently promotes the proliferation and osteogenic differentiation of bone marrow stromal cells (BMSC) by promoting expression of Heme oxygenase-1 (HO-1) in BMSC. Conditioned medium from osteoblasts <i>Vhl</i> (CM-CRE) promoted the proliferation and osteogenic differentiation of BMSC, in comparison with conditioned medium derived from normal osteoblasts (CM-GFP). Recombinant VEGF stimulated the proliferation and osteogenic differentiation of BMSC culturing in CM-GFP. By contrast, VEGF-neutralizing antibody inhibited the proliferation and osteogenic differentiation of BMSC culturing in CM-CRE. Treatment with a HO-1 inhibitor, SnPP, significantly inhibited VEGF-induced BMSC proliferation and osteogenic differentiation. On the contrary, activation of HO-1 with CoPP reversed the suppressing of VEGF-antibody on the proliferation and osteogesis of BMSC culturing in CM-CRE. These studies suggest that osteoblasts promote the proliferation and osteogenic differentiation of BMCS by VEGF/HO-1 pathway.</p></div

HSPA9 and TP53 interact in CD34+ cells and HSPA9 knockdown increases nuclear TP53 levels.

<p>(A) Representative immunoblots of TP53 and HSPA9 following immunoprecipitation with anti-TP53 or an IgG control. (B) Representative immunoblots of TP53 from the cytoplasmic and nuclear fractions of cell lysates following knockdown of HSPA9 in CD34+ cells grown in erythroid culture conditions for 5 days.</p