Mesoporous delafossite CuCrO2 and spinel CuCr2O4: synthesis and catalysis.

Delafossite CuCrO2 and spinel CuCr2O4 with mesoporous structures have been successfully synthesized using nanocasting methods based on a KIT-6 template. The functional activity of the mesoporous materials was evaluated in applications as heterogeneous catalysts. The activity for photocatalytic hydrogen production of the delafossite structures with different morphologies was characterized and the oxidation state changes associated with photocorrosion of Cu(+) investigated using electron energy loss spectroscopy (EELS). Mg(2+) doping was found to facilitate the casting of ordered structures for CuCrO2 and improves the photocorrosion resistance of delafossite structures. The mesoporous spinel CuCr2O4 nanostructures were found to be active for low temperature CO oxidation.

Doxorubicin Induces Bone Loss by Increasing Autophagy through a Mitochondrial ROS/TRPML1/TFEB Axis in Osteoclasts.

Doxorubicin (DOX), a widely used chemotherapeutic agent, has been linked to an increased risk of bone damage in human patients and induces bone loss in mice. DOX induces autophagy, which contributes to bone homeostasis and excess autophagy in osteoclasts (OCs), resulting in bone loss. We hypothesized that DOX-induced bone loss is caused by the induction of autophagy in OCs. In vitro, DOX significantly increased the area of OCs and bone resorption activity, whereas it decreased OC number through apoptosis. DOX enhanced the level of LC3II and acidic vesicular organelles-containing cells in OCs, whereas an autophagy inhibitor, 3-methyladenine (3-MA), reversed these, indicating that enhanced autophagy was responsible for the effects of DOX. Increased mitochondrial reactive oxygen species (mROS) by DOX oxidized transient receptor potential mucolipin 1 (TRPML1) on the lysosomal membrane, which led to nuclear localization of transcription factor EB (TFEB), an autophagy-inducing transcription factor. In vivo, micro-computerized tomography analysis revealed that the injection of 3-MA reversed DOX-induced bone loss, and tartrate-resistant acid phosphatase staining showed that 3-MA reduced the area of OCs on the bone surface, which was enhanced upon DOX administration. Collectively, DOX-induced bone loss is at least partly attributable to autophagy upregulation in OCs via an mROS/TRPML1/TFEB axis.

High Cholesterol-Induced Bone Loss Is Attenuated by Arctiin via an Action in Osteoclasts.

High cholesterol-induced bone loss is highly associated with oxidative stress, which leads to the generation of oxysterols, such as 7-ketocholesterol (7-KC). Here, we conducted in vivo and in vitro experiments to determine whether arctiin prevents high cholesterol diet-induced bone loss by decreasing oxidative stress. First, arctiin was orally administered to atherogenic diet (AD)-fed C57BL/6J male mice at a dose of 10 mg/kg for 6 weeks. Micro-computerized tomography (µCT) analysis showed that arctiin attenuated AD-induced boss loss. For our in vitro experiments, the anti-oxidant effects of arctiin were evaluated in 7-KC-stimulated osteoclasts (OCs). Arctiin decreased the number and activity of OCs and inhibited autophagy by disrupting the nuclear localization of transcription factor EB (TFEB) and downregulating the oxidized TFEB signaling pathway in OCs upon 7-KC stimulation. Furthermore, arctiin decreased the levels of reactive oxygen species (ROS) by enhancing the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), catalase, and heme oxygenase 1 (HO-1), all of which affected OC differentiation. Conversely, silencing of Nrf2 or HO-1/catalase attenuated the effects of arctiin on OCs. Collectively, our findings suggested that arctiin attenuates 7-KC-induced osteoclastogenesis by increasing the expression of ROS scavenging genes in the Nrf2/HO-1/catalase signaling pathway, thereby decreasing OC autophagy. Moreover, arctiin inhibits the oxidation and nuclear localization of TFEB, thus protecting mice from AD-induced bone loss. Our findings thus demonstrate the therapeutic potential of arctiin for the prevention of cholesterol-induced bone loss.

Morin Disrupts Cytoskeleton Reorganization in Osteoclasts through an ROS/SHP1/c-Src Axis and Grants Protection from LPS-Induced Bone Loss.

Morin is a naturally occurring flavonoid with anti-inflammatory and antioxidative properties. Therefore, we hypothesized that morin may prevent inflammatory bone loss by reducing oxidative stress. To investigate the effect of morin on inflammatory bone loss, mice were injected with lipopolysaccharide (LPS). Osteoclasts (OCs) were analyzed by tartrate-resistant acid phosphatase (TRAP) staining and actin ring formation. Micro-computerized tomography analysis indicated that morin prevented LPS-induced bone loss in mice. In vivo TRAP staining indicated that morin decreased the number and surface of the OCs that were increased in LPS-treated mice. Furthermore, in vitro experiments indicated that morin decreased the number and activity of OCs upon LPS stimulation. Morin decreased actin ring-containing OCs with decreased activation of c-Src (Y416)/vav guanine nucleotide exchange factor 3/Ras-related C3 botulinum toxin substrate 1 compared with LPS alone. Morin decreased cytosolic reactive oxygen species (ROS), thus preventing the oxidation of Src homology region 2 domain-containing phosphatase 1 (SHP-1), followed by the inactivation of c-Src via direct interaction with SHP1. Conversely, SHP1 knockdown abolished the inhibitory effect of morin on OCs. Therefore, our findings suggest that morin disrupted cytoskeletal reorganization via an ROS/SHP1/c-Src axis in OCs, thereby granting protection from LPS-induced bone loss, which demonstrates its therapeutic potential against inflammatory bone loss.

Synthesis and characterization of sintering-resistant silica-encapsulated Fe3O4 magnetic nanoparticles active for oxidation and chemical looping combustion.

A nanocomposite catalyst composed of ferromagnetic magnetite cores (15.5 +/- 2.0 nm) and silica shells with a thickness of 4.5 +/- 1.0 nm (Fe(3)O(4)@SiO(2)) was prepared by a two-step microemulsion-based synthesis. X-ray photoelectron spectroscopy and Raman spectroscopy after oxidation support the presence of a stable Fe(3)O(4) core and a surface phase of gamma-Fe(2)O(3). The nanocomposite structure exhibited 100% conversion of CO in oxygen at a residence time of 0.1 s at 310 degrees C. When pre-oxidized, the Fe(3)O(4)@SiO(2) catalyst is shown to be a suitable solid oxygen carrier for chemical looping combustion of methane at 700 degrees C. The nanocomposites retain their magnetism following the reaction which provides the potential for use of magnetic separation and capture in moving bed reactor applications. The core magnetite within the silica shell is resistant to sintering and a bulk phase transition to temperatures as high as 700 degrees C. These catalysts can be of use in applications of high temperature applications where catalyst recovery by magnetic separation may be required.

Application of ordered nanoporous silica for removal of uranium ions from aqueous solutions.

Ordered nanoporous silica (MSU-H) with high surface area has been utilized as a solid substrate of a surface-modified hybrid sorbent for the application to the removal of U(VI). Carboxymethylated polyethyleneimine (CMPEI) with a strong complexing property has been introduced to the pore surface of MSU-H substrate. CMPEI-modified MSU-H (CMPEI/MSU-H) has been characterized by scanning electron microscopy and nitrogen sorption. In a kinetic experiment for 12.5 ppm U(VI) solution at pH 4.0, 99% U(VI) was removed from solution by the hybrid sorbent within less than 10 min, indicating that the sorption of U(VI) on the CMPEI/MSU-H proceeds very rapidly. It was evident that a U(VI) sorption capacity increased with pH in the range of 2.0 to 4.0. The CMPEI/MSU-H showed a high sorption capacity of 153 mg/g-sorbent at pH 4.0. In particular, the CMPEI/MSU-H showed a significantly high uranium loading stability. Only about 1% U(VI) was released out of CMPEI/MSU-H during 4 months, when the CMPEI/MSU-H was treated with polyacrylic acid.

Room-temperature heterogeneous hydroxylation of phenol with hydrogen peroxide over Fe2+, Co2+ ion-exchanged Na beta zeolite.

Ion-exchanged Na beta zeolite with Fe2+ and Co2+ cations shows high catalytic activity at room temperature in phenol hydroxylation with H2O2, where the conversion of phenol is ca. 21% and the selectivity of benzoquinone is below 3% at a molar ratio of phenol to H2O2 of 3 in the starting aqueous reaction medium.

Design of a highly nanodispersed Pd-MgO/SiO(2) composite catalyst with multifunctional activity for CH(4) reforming.

We describe a highly nanodispersed Pd-MgO/SiO(2) composite catalyst synthesized by an in situ, one-pot, reverse microemulsion method as a multifunctional catalyst for low-temperature CH(4) reforming. Experimental results suggested evidence for a synergistic interplay of each component and DFT calculations confirmed a multifunctional reaction mechanism of CH(4) reforming and the importance of the Pd-MgO interface. We find that the Pd nanoparticle binds and dissociates CH(4), that MgO activates CO(2) and increases coking resistance, and that SiO(2) prevents Pd sintering. CO spillover from Pd to MgO opens a faster pathway for CO production. A unique and ground-breaking feature of the present catalyst is the well-designed cooperation of each element that assures long-lasting, consistent, high- and low-temperature activity.