Efficient Energy Transfer from Trap Levels to Eu3+ Leads to Antithermal Quenching Effect in High-Power White Light-Emitting Diodes.

The most critical aspect in the assembly of phosphor-converted white light-emitting diodes (pc-WLEDs) is how to stabilize the device in a practical environment. The high applied currents can generate enormous heat up to more than 100 °C, and such a continuous illumination process will lead to serious effects concerning the stability of the device. Therefore, the new search for examples to fully suppress thermal quenching effect is a real challenge. In this study, a novel Eu3+-activated CaMgGeO4 (CMGO) phosphor of olivine type is developed via a conventional solid-state reaction. The results reveal that Eu3+ occupies the low symmetric Ca2+ site of this host. Upon visible-light sensitization at 464 nm, a dominant red emission band with maximum at 612 nm is witnessed. Its full width at half-maximum (fwhm) is merely ∼4.37 nm, and a high color purity of around 94% is achieved. Their corresponding Commission Internationale de L'Eclairage (CIE) coordinates are very close to standard red color coordinates (0.666, 0.333). The influence of concentration and temperature on the optical property has been explored. It has been discovered that the optimized sample (CMGO:0.01Eu3+) is not influenced by the thermal quenching effect and its fluorescent intensity is improved even up to 473 K, which is mainly attributed to the incorporation of abundant trap sites generated by the nonequivalent substitution Eu3+ for Ca2+. After it is integrated into commercially available YAG:Ce3+ phosphor-based pc-WLEDs, the excellent optical parameters of the fabricated WLEDs are evaluated. The correlated color temperature (CCT) varies from cool white (6458 K) to warm (4370 K), and the color rendering index (CRI) increases from 78 to 86 under a high flux operating current of 200 mA. Furthermore, the chromaticity coordinates remain almost stable with the increasing drive current from 200 mA to 1000 mA. It is highly expected that CaMgGeO4:0.01Eu3+ will become a suitable red phosphor for the preparation of white LEDs with high efficiency.

Hetero-metal encapsulation induced ratiometric recognition of fluoride.

Emissive lanthanide ions are considered as luminescent species or optical probes for the analytes in ambient conditions or even cellular environment. But a variety of factors determine the stability of photo-luminescent signals due to the excitation sources, statistical errors or the selection of solvents. In this way, ratiometric assays effectively circumvent such problem and lead to more sensitive and reliable results. Herein, an organic-inorganic hybrid material has been developed with the europium complex as the core and the terbium species can be attached onto the surface of silica host. As for the evaluation of the internal structure, the terbium complex has been integrated into the hybrid network via weak forces and its sensitizing moiety will be easily attacked by Lewis acid-base interactions. In a different manner, the europium complex has been shielded from perturbation due to the protection of the outside silica shells. Such sharp difference in response to fluoride induces drastic signal changes and the conversion of binding process between fluoride and molecular receptors (boronic group) into readable optical outputs has afforded the lower detection limit for F- as 0.17 µM. In addition, the intracellular uptake and distribution of the hybrid material have been explored.

Tunable photoluminescence studies based on blue-emissive carbon dots and sequential determination of Fe(III) and pyrophosphate ions.

Fluorescence has been well documented and the optical feature of carbon dots generates considerable interests. Here the nitrogen-doped carbon dots with a relative quantum yield of 25% have been prepared. It displays stable blue emission based on the excitation at 355 nm. The carbon nanomaterial is highly dispersible in aqueous solution and can be employed as an effective optical probe for label-free detection of Fe3+ (0.87 µM) via a switched off change. Additionally, such sensing nanoplatform can be recovered in the presence of pyrophosphate (PPi) and an "off-on" process has been identified. It is expected that this on-off-on strategy will allow new possibilities for developing efficient sensors in industrial fields.

IL-1ß promotes the nuclear translocaiton of S100A4 protein in gastric cancer cells MGC803 and the cell's stem-like properties through PI3K pathway.

It has been shown that nuclear expression of S100A4 is significantly correlated with increased metastasis and reduced survival in patients with gastric cancer and many other cancers. However, the factors which could influence the nuclear contents of S100A4 in cancer cells are not clear. It has also been reported that Interleukin-1ß (IL-1ß) promotes the nuclear translocation of S100A4 in chondrocytes. Previous studies have shown that IL-1ß promotes the stemness of colon cancer cells, and S100A4 is also involved in maintaining cancer-initiating cells in head and neck cancers. We speculate that IL-1ß might promote the nuclear translocation of S100A4 protein in MGC803 gastric cancer cells and therefore enhance their stem-like properties. The results from Western-blot and qRT-PCR analysis showed that IL-1ß increased the nuclear and total cellular content of S100A4 protein and S100A4 mRNA level in MGC803 cells. LY294002, a pharmacological inhibitor of Phosphoinositide 3-kinase (PI3K) reversed the above effects. Functional studies indicated that IL-1ß promoted the colony-forming and spheroid-forming capabilities of the cells and the expression of SOX2 and NANOG gene. PI3K or S100A4 inhibition reversed the IL-1ß-mediated increase in colony and spheroid-forming capabilities of the cells. LY294002 also reversed the elevated SOX2 and NANOG expression induced by IL-1ß. Our study demonstrated that IL-1ß promote the nuclear translocation of S100A4 protein in gastric cancer cells MGC803, which are PI3K dependent, suggesting the existence of IL-1ß-PI3K-S100A4 pathway for the first time. The study also showed that IL-1ß promoted stem-like properties of the cells through the new pathway.

FAM107B is regulated by S100A4 and mediates the effect of S100A4 on the proliferation and migration of MGC803 gastric cancer cells.

FAM107B expression was decreased in stomach cancer and many other kinds of cancer. The forced expression of FAM107B in HeLa cells diminished proliferation in response to growth factors, suggesting that FAM107B might play important roles in many types of cancers. But the mechanisms underlying the decreased expression of FAM107B in cancers are not clear, the functional significance needs to be further clarified. Our previous findings from cDNA microarray showed that there are 179 differentially expressed genes after S100A4 inhibition in gastric cancer cells MGC803. FAM107B was an upregulated one among them. In the present study, we confirmed that FAM107B expression was upregulated in MGC803 cells after S100A4 inhibition by qRT-PCR. We demonstrated for the first time that FAM107B was downregulated by S100A4. The results from CCK-8 and transwell assay showed that FAM107B inhibition by siRNA led to significantly increased proliferation and migrating abilities of MGC803 cells, respectively, indicating that FAM107B plays important roles in inhibiting the proliferation and migration of MGC803 cells. The rescue experiment showed that FAM107B-siRNA transfection reversed the reduced proliferation and migration abilities induced by S100A4 inhibition in the cells. These findings suggest that, as a downstream effector, FAM107B at least partly mediates the effect of S100A4 on the proliferation and migration of MGC803 cells. In conclusion, we first provide experimental evidence suggesting that FAM107B was downregulated by S100A4 in gastric cancer MGC803 cells. And FAM107B at least partially mediates the biological effect of S100A4 in the cells.

S100A4 influences cancer stem cell-like properties of MGC803 gastric cancer cells by regulating GDF15 expression.

Many studies have revealed that S100A4 is involved in cancer progression by affecting a variety of biological functions. Our previous study showed that S100A4 influences many biological properties of gastric cancer cells; however, the underlying mechanisms are far from clear. In this study, we used cDNA microarray analysis to investigate the global alterations in gene expression in MGC803 gastric cancer cells after siRNA-mediated S100A4 inhibition. Among the total genes investigated, 179 differentially expressed genes (38 upregulated and 141 downregulated) were detected in S100A4-siRNA transfected MGC803 cells compared with NC-siRNA transfected cells. We focused on the GDF15 gene, which was significantly downregulated after S100A4 inhibition. ChIP studies showed that the S100A4 protein binds to the GDF15 promoter, implicating S100A4 in GDF15 regulation at the transcriptional level. GDF15 overexpression promoted CSC-like properties of MGC803 cells, such as spheroid and soft-agar colony forming abilities. S100A4 inhibition suppressed the CSC-like properties of the cells, whereas, GV141-GDF15 vector transfection reversed these effects. Our results suggest that S100A4 influences the CSC-like properties of MGC803 gastric cancer cells by regulating GDF15 expression.

S100A4 interacts with mutant p53 and affects gastric cancer MKN1 cell autophagy and differentiation.

The acquired p53 mutations are the most common genetic alterations in human cancers. Mutant p53 proteins tend to accumulate, augmenting their oncogenic potential. However, the mechanisms for mutant p53 accumulation are not known. Previous studies have shown that S100A4 interacts with wild­type p53. The present study marks the first time the effect of S100A4 on mutant p53 levels in gastric cancer MKN1 cells, which harbor mutant p53V143A, and the functional consequences have been investigated. S100A4 interacted with mutant p53V143A in the cells, and S100A4 inhibition decreased mutant p53V143A levels, indicating that S100A4 promoted mutant p53 accumulation through their interaction. We also found that S100A4 inhibition altered the expression of the mutant p53V143A target genes [c-Myc and inhibitor of DNA binding 2 (Id2)]. Moreover, we demonstrated that S100A4 knockdown increased mutant p53-related autophagy and cell differentiation. In conclusion, our data suggest a novel mechanism for mutant p53V143A accumulation and add a new facet to the role of S100A4 in cancer.

Activation of cannabinoid receptor 2 enhances osteogenic differentiation of bone marrow derived mesenchymal stem cells.

Bone marrow derived mesenchymal stem cells (BM-MSCs) are considered as the most promising cells source for bone engineering. Cannabinoid (CB) receptors play important roles in bone mass turnover. The aim of this study is to test if activation of CB2 receptor by chemical agonist could enhance the osteogenic differentiation and mineralization in bone BM-MSCs. Alkaline phosphatase (ALP) activity staining and real time PCR were performed to test the osteogenic differentiation. Alizarin red staining was carried out to examine the mineralization. Small interference RNA (siRNA) was used to study the role of CB2 receptor in osteogenic differentiation. Results showed activation of CB2 receptor increased ALP activity, promoted expression of osteogenic genes, and enhanced deposition of calcium in extracellular matrix. Knockdown of CB2 receptor by siRNA inhibited ALP activity and mineralization. Results of immunofluorescent staining showed that phosphorylation of p38 MAP kinase is reduced by knocking down of CB2 receptor. Finally, bone marrow samples demonstrated that expression of CB2 receptor is much lower in osteoporotic patients than in healthy donors. Taken together, data from this study suggested that activation of CB2 receptor plays important role in osteogenic differentiation of BM-MSCs. Lack of CB2 receptor may be related to osteoporosis.

EZH2 Mediates the Regulation of S100A4 on E-cadherin Expression and the Proliferation, Migration of Gastric Cancer Cells.

BACKGROUND/AIMS: Several reports have showed the inverse correlation between S100A4 and E-cadherin expression, but the exact molecular mechanism remained unclear. It has been reported that EZH2 mediates transcriptional silencing of E-cadherin by trimethylating lysine 27 of histone H3 (H3K27me3). Therefore, we hypothesized that EZH2 might mediate the inhibition of S100A4 on E-cadherin and further affect the functions of S100A4 in gastric cancer cells. METHODOLOGY: RT-PCR and Western Blot were used to detect the expression of EZH2 and E-cadherin after inhibiting or increasing S100A4 expression. MTT and Transwell assay were performed to detect the proliferation and migration of gastric cancer cells. RESULTS: Inhibition or overexpression of S100A4 led to decreased or increased EZH2 expression, and increased or decreased E-cadherin expression. The SET domain was important for EZH2 in rescuing the decreased proliferation and migration of the cells after S100A4 inhibition. CONCLUSION: As a novel downstream target of S100A4, EZH2 mediates the inhibition of S100A4 on E-cadherin. The SET domain is important for EZH2 in mediating the cellular function of S100A4.