Highly transparent cerium doped gadolinium gallium aluminum garnet ceramic prepared with precursors fabricated by ultrasonic enhanced chemical co-precipitation.

Cerium doped gadolinium gallium aluminum garnet (GGAG:Ce) ceramic precursors have been synthesized with an ultrasonic chemical co-precipitation method (UCC) and for comparison with a traditional chemical co-precipitation method (TCC). The effect of ultra-sonication on the morphology of powders and the transmittance of GGAG:Ce ceramics are studied. The results indicate that the UCC method can effectively improve the homogenization and sinterability of GGAG:Ce powders, which contribute to obtain high transparent GGAG ceramic with the highest transmittance of 81%.

A novel banded structure ceramic phosphor for high-power white LEDs.

A novel banded structure ceramic phosphor has been fabricated in this research. This structure provides a convenient and effective method for regulating the full spectrum. It has the advantage of being able to adjust the intensity of all three primary colors independently, regardless of the mutual absorption among different active ions.

Effect of Yb(3+) on the Crystal Structural Modification and Photoluminescence Properties of GGAG:Ce(3+).

Gadolinium gallium aluminum garnet (GGAG) is a very promising host for the highly efficient luminescence of Ce(3+) and shows potential in radiation detection applications. However, the thermodynamically metastable structure would be slanted against it from getting high transparency. To stabilize the crystal structure of GGAG, Yb(3+) ions were codoped at the Gd(3+) site. It is found that the decomposition of garnet was suppressed and the transparency of GGAG ceramic was evidently improved. Moreover, the photoluminescence of GGAG:Ce(3+),xYb(3+) with different Yb(3+) contents has been investigated. When the Ce(3+) ions were excited under 475 nm, a typical near-infrared region emission of Yb(3+) ions can be observed, where silicon solar cells have the strongest absorption. Basing on the lifetimes of Ce(3+) ions in the GGAG:Ce(3+),xYb(3+) sample, the transfer efficiency from Ce(3+) to Yb(3+) and the theoretical internal quantum efficiency can be calculated and reach up to 86% and 186%, respectively. This would make GGAG:Ce(3+),Yb(3+) a potential attractive downconversion candidate for improving the energy conversion efficiency of crystalline silicon (c-Si) solar cells.

Intracellular signaling pathways involved in cell growth inhibition of human umbilical vein endothelial cells by melatonin.

Melatonin, an indolamine mainly produced in the pineal gland, has received a great deal of attention in the last decade because of its oncostatic effects, which are due to its immunomodulatory, antiproliferative, antioxidant and its possible antiangiogenesis properties. Herein, we document its antiproliferative action on human umbilical vein endothelial cells (HUVECs). Moreover, the possible cell signaling pathways when melatonin inhibited HUVEC proliferation were explored in this study. Primary HUVECs were isolated, cultured, purified and identified before the studies were performed. HUVECs were found to possess G-protein-coupled membrane receptors for melatonin (MT1 and MT2) and also nuclear melatonin receptors (RORalpha and RORbeta, especially RORbeta). No obvious expression of RORgamma was found. We investigated the membrane receptors and several intracellular signaling pathways including mitogen-activated protein kinases (MAPK)/extracellular signal-related kinases (ERK), phosphoinositol-3-kinase (PI3K)/Akt and protein kinases C (PKC) involved in antiproliferative action of melatonin on HUVECs. The blockade of these pathways using special inhibitors decreased cell growth. Furthermore, the constitutive activation of nuclear factor kappa B (NF-kappaB) contributed to the proliferation of HUVECs. High concentrations of melatonin inhibited both NF-kappaB expression and its binding ability to DNA, possibly through inactivation of ERK/Akt /PKC pathways. Taken together, high concentrations of melatonin markedly reduced HUVEC proliferation; the antiproliferative action of melatonin was closely correlated with following pathway: melatonin receptors/ERK/PI3K/Akt/PKC/ NF-kappaB.

Effect and mechanism of melatonin's action on the proliferation of human umbilical vein endothelial cells.

Melatonin is the major secretory product of the pineal gland and is considered an important natural oncostatic agent. The anticancer activity of melatonin is due to its immunomodulatory, anti-proliferative and antioxidative effects. At present there are no direct data available as to melatonin's possible influence on angiogenesis, which is a major biological mechanism responsible for tumor growth and dissemination. The current study investigated the influence of melatonin on angiogenesis. Human umbilical vein endothelial cells (HUVECs) were cultured, identified, and purified. Cell growth and viability, DNA fragmentation and cell cycle analyses were determined. To elucidate the mechanism of action of melatonin, Western blot analyses for P53, Bax and Bcl-2 expression were carried out. The results demonstrate the anti-proliferative and apoptosis-inducing effects of melatonin; these changes were associated with cell cycle arrest, upregulation of P53 and Bax and downregulation of Bcl-2. Taken together, our data showed that melatonin in high concentrations markedly reduces HUVECs proliferation, induces cellular apoptosis, and modulates cell cycle length. P53 and Bax/Bcl-2 expression changes may be involved in these actions of melatonin.

Effects of human connective tissue growth factor gene transfection on migration of human umbilical vein endothelial cell.

Connective tissue growth factor (CTGF) is a 38-kDa cysteine-rich protein and an important regulator of angiogenesis. In order to study the role CTGF gene playing in angiogenesis, the eukaryotic expression vector of CTGF gene was constructed in this study, and the role of endogenous CTGF on migration of human umbilical vein endothelial cell (HUVECs) was investigated. According to human CTGF cDNA sequence, a pair of specific primers containing digestion sites of Xba I and Hind III on the 5' end respectively were designed. Reverse transcript polymerase chain reaction (RT-PCR) was used to amplify CTGF cDNA from HUVECs. The eukaryotic expression vector pcDNA3.1(-)/CTGF containing the entire coding region was constructed successfully. Compared with CTGF sequence of GenBank, DNA sequence analysis showed that this reformed plasmid contained the same full length of CTGF cDNA. The results of Western blotting demonstrated that CTGF was over-expressed at 48 h after transfection. Migration of HUVECs transfected with CTGF vector increased significantly compared with those transfected with vector control. In conclusion, the eukaryotic expression vector pcDNA3.1(-)/CTGF was constructed successfully and the endogenous CTGF promoted the migration of HUVECs. This study lays a foundation for further study on the role CTGF gene playing in angiogenesis.