Nano-silica anti-icing coatings for protecting wind-power turbine fan blades.

Wind power is a promising electricity source. Nevertheless, wind turbine blade icing can cause severe problems in turbine operation. In this study, SiO2 spherical nanoparticles (∼90 nm), produced by RF (radio frequency) plasma spheroidization, were mixed with E51, PDMS, and ethyl acetate, and sprayed on the surface of aluminum plates and regular power windmill fan blades which were already coated with polyurethane primer. XPS and IR spectroscopies revealed the development of SiC and SiPh (Ph = phenolic ring) bonds, whose formation should be favored by the ultrasound and curing processes at 50 °C. The integrity of the coating/substrate interface, whose strength is ascribed to hydrogen bonds, was maintained after 100 icing-melting cycles. The coatings display superhydrophobic behavior and excellent anti-icing performance, along with stability in abrasion, sunlight and self-cleaning ability towards solid pollutants.

A novel strategy to motivate the luminescence efficiency of a phosphor: drilling nanoholes on the surface.

A facile approach to fabricate nanoholes on the surface of a phosphor via a carbothermal reaction between C and BaMgAl10O17 was adopted. Drilling nanoholes greatly enhanced excitation light absorption and consequently increased the quantum efficiency, which provided new insight to help improve the luminescence efficiency of oxygen-containing phosphors.

Transition of Emission Colours as a Consequence of Heat-Treatment of Carbon Coated Ce3+-Doped YAG Phosphors.

To modify the luminescence properties of Ce3+-doped Y3Al5O12 (YAG) phosphors, they have been coated with a carbon layer by chemical vapor deposition and subsequently heat-treated at high temperature under N2 atmosphere. Luminescence of the carbon coated YAG:Ce3+ phosphors has been investigated as a function of heat-treatment at 1500 and 1650 °C. The 540 nm emission intensity of C@YAG:Ce3+ is the highest when heated at 1650 °C, while a blue emission at 400-420 nm is observed when heated at 1500 °C but not at 1650 °C. It is verified by X-ray diffraction (XRD) that the intriguing luminescence changes are induced by the formation of new phases in C@YAG:Ce3+-1500 °C, which disappear in C@YAG:Ce3+-1650 °C. In order to understand the mechanisms responsible for the enhancement of YAG:Ce3+ emission and the presence of the blue emission observed for C@YAG:Ce3+-1500 °C, the samples have been investigated by a combination of several electron microscopy techniques, such as HRTEM, SEM-CL, and SEM-EDS. This local and cross-sectional analysis clearly reveals a gradual transformation of phase and morphology in heated C@YAG:Ce3+ phosphors, which is related to a reaction between C and YAG:Ce3+ in N2 atmosphere. Through reaction between the carbon layer and YAG host materials, the emission colour of the phosphors can be modified from yellow, white, and then back to yellow under UV excitation as a function of heat-treatment in N2 atmosphere.

Insight the Luminescence Properties of AlON: Eu, Mg Phosphor under VUV Excitation.

Owing to high quantum efficiency, adjustable composition and antioxidation properties of oxynitride phosphors, extensive investigations have focused on their photoluminescence properties under low-energy light excitation (UV or blue light). However, the vacuum ultraviolet (VUV) luminescence properties of oxynitride phosphors are rarely researched. Present work studies the structure and VUV luminescence properties of an oxynitride phosphor: AlON: Eu, Mg, which is synthesized by solid-state reaction. Under 147 nm excitation, it was found that AlON: Eu, Mg phosphor shows a blue emission band centered at about 470 nm. The first principle calculation is used to analyze the origin of the VUV absorption. Compared with BaMgAl10O17: Eu2+ phosphor, AlON: Eu, Mg phosphor shows better thermal stability.

Bone morphogenetic protein 9 stimulates callus formation in osteoporotic rats during fracture healing.

Fracture healing involves the coordinated actions of multiple cytokines. Bone morphogenetic protein 9 (BMP9) is an important factor in bone formation. The present study aimed to investigate the osteogenic potential of bone marrow stem cells (BMSCs) in response to adenoviral (Ad)BMP9, and the early fracture repair properties of AdBMP9 in surgically­created fractures in osteoporotic rats. Alkaline phosphatase (ALP) activity was assayed and matrix mineralization was examined by Alizarin Red S staining. mRNA and protein expression levels of BMP9, runt­related transcription factor 2 (RUNX2) and type 1 collagen (COL­1) were detected in vitro and in vivo. Femoral bone mineral density was assessed for osteoporosis in ovariectomized rats. An open femora fracture was subsequently created, and gelatin sponges containing AdBMP9 were implanted. The femora were harvested for radiographical, micro­computed tomography, biomechanical and histological analysis 4 weeks later. BMP9 successfully increased ALP activity and induced mineralized nodule formation in BMSCs. BMP9 in gelatin sponges demonstrated marked effects on microstructural parameters and the biomechanical strength of bone callus. In addition, it upregulated the expression levels of RUNX2 and COL­1. AdBMP9 in gelatin sponges significantly mediated callus formation, and increased bone mass and strength in osteoporotic rats with femora fractures. The results of the present study suggested that BMP9 enhanced callus formation and maintained early mechanical stability during fracture healing in osteoporotic rats, implicating it as a potential novel therapeutic target for fracture healing.

Adenovirus-mediated expression of vascular endothelial growth factor-a potentiates bone morphogenetic protein9-induced osteogenic differentiation and bone formation.

Mesenchymal stem cells (MSCs) are suitable seed cells for bone tissue engineering because they can self-renew and undergo differentiation into osteogenic, adipogenic, chondrogenic, or myogenic lineages. Vascular endothelial growth factor-a (VEGF-a), an angiogenic factor, is also involved in osteogenesis and bone repair. However, the effects of VEGF-a on osteogenic MSCs differentiation remain unknown. It was previously reported that bone morphogenetic protein9 (BMP9) is one of the most important osteogenic BMPs. Here, we investigated the effects of VEGF-a on BMP9-induced osteogenesis with mouse embryo fibroblasts (MEFs). We found that endogenous VEGF-a expression was undetectable in MSCs. Adenovirus-mediated expression of VEGF-a in MEFs potentiated BMP9-induced early and late osteogenic markers, including alkaline phosphatase (ALP), osteocalcin (OCN), and osteopontin (OPN). In stem cell implantation assays, VEGF-a augmented BMP9-induced ectopic bone formation. VEGF-a in combination with BMP9 effectively increased the bone volume and osteogenic activity. However, the synergistic effect was efficiently abolished by the phosphoinositide 3-kinase (PI3K)/AKT inhibitor LY294002. These results demonstrated that BMP9 may crosstalk with VEGF-a through the PI3K/AKT signaling pathway to induce osteogenic differentiation in MEFs. Thus, our findings demonstrate the effects of VEGF-a on BMP9-induced bone formation and provide a new potential strategy for treating nonunion fractures, large segmental bony defects, and/or osteoporotic fractures.

Gut-derived serotonin induced by depression promotes breast cancer bone metastasis through the RUNX2/PTHrP/RANKL pathway in mice.

Breast cancer metastasizes to the bone in a majority of patients with advanced disease resulting in bone destruction. The underlying mechanisms are complex, and both processes are controlled by an interaction between locally and systemically derived signals. Clinically, breast cancer patients with depression have a higher risk of bone metastasis, yet the etiology and mechanisms are yet to be elucidated. MDA­MB­231 breast cancer cells were used to establish a bone metastasis model by using intracardiac injection in nude mice. Chronic mild stress (CMS) was chosen as a model of depression in mice before and after inoculation of the cells. Knockdown of the RUNX­2 gene was performed by transfection of the cells with shRNA silencing vectors against human RUNX­2. A co­culture system was used to test the effect of the MDA­MB­231 cells on osteoclasts and osteoblasts. RT­PCR and western blotting were used to test gene and protein expression, respectively. We confirmed that depression induced bone metastasis by promoting osteoclast activity while inhibiting osteoblast differentiation. Free serotonin led to an increase in the expression of RUNX2 in breast cancer cells (MDA­MB­231), which directly inhibited osteoblast differentiation and stimulated osteoclast differentiation by the PTHrP/RANKL pathway, which caused bone destruction and formed osteolytic bone lesions. Additionally, the interaction between depression and breast cancer cells was interrupted by LP533401 or RUNX2 knockdown. In conclusion, depression promotes breast cancer bone metastasis partly through increasing levels of gut­derived serotonin. Activation of RUNX2 in breast cancer cells by circulating serotonin appears to dissociate coupling between osteoblasts and osteoclasts, suggesting that the suppression of gut­derived serotonin decreases the rate of breast cancer bone metastasis induced by depression.

IGF1 potentiates BMP9-induced osteogenic differentiation in mesenchymal stem cells through the enhancement of BMP/Smad signaling.

Engineered bone tissue is thought to be the ideal alternative for bone grafts in the treatment of related bone diseases. BMP9 has been demonstrated as one of the most osteogenic factors, and enhancement of BMP9-induced osteogenesis will greatly accelerate the development of bone tissue engineering. Here, we investigated the effect of insulin-like growth factor 1 (IGF1) on BMP9-induced osteogenic differentiation, and unveiled a possible molecular mechanism underling this process. We found that IGF1 and BMP9 are both detectable in mesenchymal stem cells (MSCs). Exogenous expression of IGF1 potentiates BMP9-induced alkaline phosphatase (ALP), matrix mineralization, and ectopic bone formation. Similarly, IGF1 enhances BMP9-induced endochondral ossification. Mechanistically, we found that IGF1 increases BMP9-induced activation of BMP/Smad signaling in MSCs. Our findings demonstrate that IGF1 can enhance BMP9-induced osteogenic differentiation in MSCs, and that this effect may be mediated by the enhancement of the BMP/Smad signaling transduction triggered by BMP9. [BMB Reports 2016; 49(2): 122-127].

Evodiamine inhibits the proliferation of human osteosarcoma cells by blocking PI3K/Akt signaling.

Osteosarcoma (OS) is the most common non-hematologic primary malignancy of bone, and multiple chemotherapeutic agents have been applied in the treatment of OS for over 40 years. Nevertheless, due to the poor prognosis of OS, it is essential to develop a novel treatment strategy. Evodiamine (EVO), a quinolone alkaloid extracted from the fruit of Evodia rutaecarpa, has been demonstrated to inhibit tumor cell proliferation. Thus, the main aim of the present study was to investigate the anti-proliferative and apoptosis-inducing effects of evodiamine (EVO) on human OS 143B cells, but also the possible mechanisms underlying these effects. The results of crystal violet staining, flow cytometry, western blot analysis and an in vivo experiment demonstrated that EVO exhibits significant inhibitory effects on cell proliferation, exhibits apoptosis-inducing effects and arrests the cell cycle in 143B cells. According to our findings of polymerase chain reaction (PCR), western blot analysis and recombinant adenoviral transfection, we confirmed that EVO upregulates both the protein and gene levels of phosphatase and tensin homolog (PTEN) in a concentration-dependent manner in 143B cells. Overexpression of PTEN reinforced the anti-proliferative effect of EVO in the 143B cells, while knockdown of PTEN upregulated PI3K/Akt signaling transduction and reversed the inhibitory effect of EVO on 143B cell proliferation. Further analysis indicated that EVO upregulated the expression of PTEN by inactivating PI3K/Akt signaling by decreasing phosphorylated Akt1/2. Based on the above results, we conclude that PTEN/PI3K/Akt signaling is involved in the inhibitory effect on human OS 143B cell proliferation by EVO.

Oridonin inhibits the proliferation of human osteosarcoma cells by suppressing Wnt/ß-catenin signaling.

It has been reported that oridonin (ORI) can inhibit proliferation and induce apoptosis in various types of cancer cell lines. However, the exact mechanism for this function remains unclear. In this study, we investigated the proliferation inhibitory effect of ORI on human osteosarcoma (OS) 143B cells and dissected the possible molecular mechanism(s) underlying this effect. We demonstrated that ORI can inhibit proliferation, induce apoptosis and arrest the cell cycle in 143B cells. Using luciferase reporter assay, we found that the Wnt/ß-catenin signaling was inhibited in 143B cells by ORI. Accordingly, the total protein levels and nuclear translocation of ß-catenin were reduced by ORI treatment. ORI increased glycogen synthase kinase 3ß (GSK3ß) activity and upregulated Dickkopf-1 (Dkk-1) expression. We found that Dkk-1 overexpression or ß-catenin knockdown can potentiate the proliferation inhibitory effect of ORI in 143B cells, while ß-catenin overexpression attenuated this effect. Using the xenograft tumor model of human OS, we demonstrated that ORI effectively inhibited the growth of tumors. Histological examination showed that ORI inhibited cancer cell proliferation, decreased the expression of PNCA and ß-catenin. Our findings suggest that ORI can inhibit 143B OS cell proliferation by downregulating Wnt/ß-catenin signal transduction, which may be mediated by upregulating the Dkk-1 expression and/or enhancing the function of GSK3ß. Therefore, ORI can be potentially used as an effective adjuvant agent for the clinical management of OS.

The PTEN/PI3K/Akt and Wnt/ß-catenin signaling pathways are involved in the inhibitory effect of resveratrol on human colon cancer cell proliferation.

Colon cancer is one of the most common malignancies and the treatments for colon cancer have been developed substantially in the last decades, but there is still a great clinical need to explore new treatment regimens due to the undesirable prognosis. In this investigation, we demonstrated the anti-proliferative and apoptosis-inducing activities of resveratrol (Res) in human colon cancer cells, and the possible mechanisms underlying these effects. We used crystal violet staining, flow cytometry and western blotting to validate the anti-proliferative and apoptosis-inducing effects of Res on HCT116 cells. A xenograft tumor model was used to confirm the anti-proliferative effects of Res. We employed polymerase chain reaction, western blotting, recombinant adenovirus and luciferase reporter assay to explore the possible mechanism(s) of action. We found that Res inhibits significantly the proliferation and promotes apoptosis in HCT116 cells, as well as inhibits the xenograft tumor growth of colon cancer. Res upregulates the expression of phosphatase and tensin homolog (PTEN) and decreases the phosphorylation of Akt1/2. The exogenous expression of PTEN inhibits the PI3K/Akt signal and promotes the anti-proliferative effects of Res in HCT116 cells, while knockdown of PTEN increases PI3K/Akt signal but reduces the anti-proliferative function of Res. The protein and mRNA expression of ß-catenin are all decreased by Res concentration-dependently. Thus, our findings strongly suggest that the anti-proliferative effects of Res in human colon cancer cells may be mediated by regulating separately the PTEN/PI3K/Akt and Wnt/ß-catenin signaling.

BMP9 and COX-2 form an important regulatory loop in BMP9-induced osteogenic differentiation of mesenchymal stem cells.

Mesenchymal stem cells (MSCs) can self-renew and differentiate into osteogenic, chondrogenic, adipogenic and myogenic lineages. It's reported that bone morphogenetic protein 9 (BMP9) is one of the most potent osteogenic BMPs to initiate the commitment of MSCs to osteoblast lineage. Cyclooxygenase-2 (COX-2) is critical for bone fracture healing and osteogenic differentiation in MSCs. However, the relationship between COX-2 and BMP9 in osteogenesis remains unknown. Herein, we investigate the role of COX-2 in BMP9-induced osteogenesis in MSCs. We demonstrate that COX-2 is up-regulated as a target of BMP9 in MSCs. Both COX-2 inhibitor (NS-398) and COX-2 knockdown siRNAs can effectively decrease alkaline phosphatase (ALP) activities induced by BMP9 in MSCs. NS-398 also down-regulates BMP9-induced expression of osteopontin and osteocalcin, so does the matrix mineralization. The in vivo studies indicate that knockdown of COX-2 attenuates BMP9-induced ectopic bone formation. In perinatal limb culture assay, NS-398 is shown to reduce the hypertropic chondrocyte zone and ossification induced by BMP9. Mechanistically, knockdown of COX-2 significantly inhibits the BMP9 up-regulated expression of Runx2 and Dlx-5 in MSCs, which can be rescued by exogenous expression of COX-2. Furthermore, knockdown of COX-2 apparently reduces BMP9 induced BMPR-Smad reporter activity, the phosphorylation of Smad1/5/8, and the expression of Smad6 and Smad7 in MSCs. NS-398 blocks the expression of BMP9 mediated by BMP9 recombinant adenovirus. Taken together, our findings suggest that COX-2 plays an important role in BMP9 induced osteogenic differentiation in MSCs; BMP9 and COX-2 may form an important regulatory loop to orchestrate the osteogenic differentiation in MSCs.

[Gly374Arg mutation in Fgfr3 causes achondroplasia in mice].

OBJECTIVE: To establish the mouse model of Gly374Arg mutation in fibroblast growth factor receptor 3(Fgfr3) and to analyze the phenotype of the mutant mice. METHODS: The double PCR was used to introduce Gly374Arg point mutation into mouse Fgfr3. The electroporation of embryonic stem(ES) cells was carried out with targeting vector. The targeted ES cells were screened by Positive-Negative Selection of G418 and Ganciclovir, and Southern blot. The correct targeted ES cells were microinjected into blastula. Finally, mutant mice were obtained by crossing between EIIa-Cre transgenic mice and mice carrying recombined mutant Fgfr3 allele. The mice were genotyped by PCR, and phenotype was observed by skeleton staining, histology, etc. RESULTS: Fgfr3-Gly374Arg mutant mice exhibited small size, short tail, macrocephaly and had dome-shaped heads, the epiphyseal growth plates of mutant mice were narrower, and the hypertrophic chondrocyte zone was also obviously decreased. Meanwhile, the majority of female mice were infertile, and the uterus, ovary and mammal gland in mutant female mice were also smaller and underdeveloped. CONCLUSION: The model of Fgfr3-Gly374Arg mutation causing achondroplasia in mice has been established successfully.