A series of single-composition emission-tunable Ca9Y(PO4)7:Eu2+,Mn2+ phosphors were synthesized by solid-state reaction. The energy transfer from Eu2+ to Mn2+ in Ca9Y(PO4)7 host matrix was studied and demonstrated to be a resonant type via a dipole−quadrupole mechanism with the critical distance of ∼ 11 Å. The wavelength-tunable white light can be realized by coupling the emission bands centered at 486 and 638 nm ascribed to the contribution from Eu2+ and Mn2+, respectively. By properly tuning the relative composition of Eu2+/Mn2+, chromaticity coordinates of (0.31, 0.33) can be achieved under excitation at 250−440 nm. Moreover, white-light-emitting diodes were fabricated through the integration of 365 nm chips and single composition white-light-emitting phosphors (Ca0.975Eu0.01Mn0.015)9Y(PO4)7 into a single package shows a cool white light of 7200 K, color rendering index of 76, and color coordinates of (0.30, 0.31) close to that of ideal white light can be achieved.

The levels of adiponectin were higher in umbilical cord serum than in maternal serum. Moreover, the adiponectin levels in umbilical cord serum were found to correlate positively with neonatal birthweights. Therefore, fetal adiponectin, not maternal serum adiponectin, may be involved in fetal development during late pregnancy.

Hepatocellular carcinoma (HCC) has been known as one of the most lethal human malignancies, due to the difficulty of early detection, chemoresistance, and radioresistance, and is characterized by active angiogenesis and metastasis, which account for rapid recurrence and poor survival. Its development has been closely associated with multiple risk factors, including hepatitis B and C virus infection, alcohol consumption, obesity, and diet contamination. Genetic alterations and genomic instability, probably resulted from unrepaired DNA lesions, are increasingly recognized as a common feature of human HCC. Dysregulation of DNA damage repair and signaling to cell cycle checkpoints, known as the DNA damage response (DDR), is associated with a predisposition to cancer and affects responses to DNA-damaging anticancer therapy. It has been demonstrated that various HCC-associated risk factors are able to promote DNA damages, formation of DNA adducts, and chromosomal aberrations. Hence, alterations in the DDR pathways may accumulate these lesions to trigger hepatocarcinogenesis and also to facilitate advanced HCC progression. This review collects some of the most known information about the link between HCC-associated risk factors and DDR pathways in HCC. Hopefully, the review will remind the researchers and clinicians of further characterizing and validating the roles of these DDR pathways in HCC.

The crystal structure of Eu(2+)-activated Sr(8)ZnSc(PO(4))(7):Eu(2+) phosphor was refined and determined from XRD profiles by the Rietveld refinement method using a synchrotron light source. This phosphor crystallizes in the monoclinic structure with the I2/a space group. The SZSP:xEu(2+) phosphors showed a broad yellow emission band centered at 511 and 571 nm depending on the concentration of Eu(2+), and the composition-optimized concentration of Eu(2+) in the Sr(8)ZnSc(PO(4))(7):Eu(2+) phosphor was determined to be 2 mol %. The estimated crystal-field splitting and CIE chromaticity coordinates of Sr(8)ZnSc(PO(4))(7):xEu(2+) (x = 0.001-0.05 mol) were 20181-20983 cm(-1) and (0.3835, 0.5074) to (0.4221, 0.5012), respectively, and the emission band showed a redshift from 547 to 571 nm with increasing Eu(2+) concentration. The nonradiative transitions between the Eu(2+) ions in the Sr(8)ZnSc(PO(4))(7) host were attributable to dipole-dipole interactions, and the critical distance was approximately 19.8 Å. The combination of a 400 nm NUV chip with a blend of Sr(8)ZnSc(PO(4))(7):0.02Eu(2+) and BAM:Eu(2+) phosphors (light converters) gave high color rendering indices between 79.38 and 92.88, correlated color temperatures between 4325 and 7937 K, and tuned CIE chromaticity coordinates in the range (0.381, 0.435) to (0.294, 0.310), respectively, depending on the SZSP:0.02Eu(2+)/BAM:Eu(2+) weight ratio. These results suggest that the Sr(8)ZnSc(PO(4))(7):0.02Eu(2+)/BAM:Eu(2+) phosphor blend has potential applications in white NUV LEDs.

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Novel single-phased white light-emitting KCaY(PO(4))(2):Eu(2+),Mn(2+) phosphors for light-emitting diode (LED) applications were synthesized by conventional solid-state reaction. The emission hue could be controlled by tuning the Eu(2+)/Mn(2+) ratio via the energy transfer; the the emission hue of KCaY(PO(4))(2):Eu(2+),Mn(2+) varied from blue (0.1853, 0.2627) to white-light (0.3350, 0.3203) and eventually to purple (0.3919, 0.2867). The mechanism of energy transfer from a sensitizer Eu(2+) to an activator Mn(2+) in KCaY(PO(4))(2):Eu(2+),Mn(2+) phosphors was demonstrated to be an electric dipole-quadrupole interaction. Combining a NUV 405-nm chip and a white-emitting KCaY(PO(4))(2):1%Eu(2+),4%Mn(2+) phosphor produced a white-light NUV LED, demonstrating CIE chromaticity coordinates of (0.314, 0.329) and a color temperature of 6507 K.

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Background: Constitutive activation of signal transducer and activator of transcription 3 at tyrosine residue 705 (p-STAT3 (tyr705)) has been associated with many types of human cancers. However, its potential roles and biological effects in hepatocellular carcinoma (HCC) are not well established. Aim: To explore whether an altered p-STAT3 (tyr705) expression is associated with angiogenesis or proliferation and thereby plays a part in HCC development. Methods: Paraffin-wax-embedded sections from 69 patients with HCC were collected in this study. Using a semiquantitative immunohistochemical staining method, the expression patterns of p-STAT3 (tyr705) in both HCC lesions and the adjacent non-tumorous liver parenchyma were analysed. The results obtained were further correlated with intratumour microvessel density (MVD), Ki-67 expression, clinicopathological parameters and overall survival. Results: A strong p-STAT3 (tyr705) nuclear staining was observed in 49.3% of HCC lesions, but was reported only in 5.8% of the adjacent non-tumorous liver parenchyma (p,0.001). The expression of p-STAT3 (tyr705) in HCC lesions was significantly and positively correlated with the intratumour MVD (p = 0.002), but not with Ki-67 expression. No significant correlation of p-STAT3 (tyr705) was found in addition to histological grading (p = 0.019). Multivariate Cox regression analysis showed that p-STAT3 (tyr705) expression was a significant predictor of overall survival for HCC (p = 0.036), although the Kaplan-Meier survival curves showed no significant difference between the high and low p-STAT3 (tyr705) expression subgroups. Conclusions:The results showed that p-STAT3 (tyr705) expression was closely correlated with histological grading and intratumour MVD in HCC. Thus, the potential role of p-STAT3 (tyr705) in HCC development may be through these correlations.