Multilayer Photonic Crystal for Spectral Narrowing of Emission

Multilayer colloidal crystal has been prepared by the layer-by-layer deposition of silica microspheres on a glass slide. Each layer is a slab consisting of a fcc close-packed colloidal arrays. By properly choosing the sizes of spheres, the whole spectral feature of multilayer colloidal crystal can be tuned. Here, we engineered a multilayer superlattice structure with an effective passband (380 nm) between two stop bands (366 nm and 400 nm). This gives a strong narrowing effect on emission spectrum (378 nm). With the stop bands at the shortwave and longwave edges of emission spectrum, the passband in the central wavelength region can be regarded as a strong decrease of suppression effect and enhancement of a narrow wavelength region of emission. The FWHM values of stop band modified emission spectrum were narrowed from 59 nm to 22 nm. The spectral narrowing modification effect of suitably engineered colloidal crystals shows up their importance in potential application as optical filters and lasing devices

Cancer-associated exportin-6 upregulation inhibits the transcriptionally repressive and anticancer effects of nuclear profilin-1

Aberrant expression of nuclear transporters and deregulated subcellular localization of their cargo proteins are emerging as drivers and therapeutic targets of cancer. Here, we present evidence that the nuclear exporter exportin-6 and its cargo profilin-1 constitute a functionally important and frequently deregulated axis in cancer. Exportin-6 upregulation occurs in numerous cancer types and is associated with poor patient survival. Reducing exportin-6 level in breast cancer cells triggers antitumor effects by accumulating nuclear profilin-1. Mechanistically, nuclear profilin-1 interacts with eleven-nineteen-leukemia protein (ENL) within the super elongation complex (SEC) and inhibits the ability of the SEC to drive transcription of numerous pro-cancer genes including MYC. XPO6 and MYC are positively correlated across diverse cancer types including breast cancer. Therapeutically, exportin-6 loss sensitizes breast cancer cells to the bromodomain and extra-terminal (BET) inhibitor JQ1. Thus, exportin-6 upregulation is a previously unrecognized cancer driver event by spatially inhibiting nuclear profilin-1 as a tumor suppressor

Methyl jasmonate inhibits lamina joint inclination by repressing brassinosteroid biosynthesis and signaling in rice

Lamina joint inclination or leaf angle (the angle between the leaf blade and vertical culm) is a major trait of rice plant architecture. The plant hormone brassinosteroid (BR) is the main regulator of this trait, while other plant hormones, including ethylene, gibberellin, and auxin, also influence leaf angle. In this study, we found that methyl jasmonate (MeJA) also participates in regulating lamina joint inclination. MeJA decreased lamina joint inclination and inhibited the BR-induced increase in lamina joint inclination. Furthermore, addition of a BR synthesis inhibitor increased the extent of change in lamina joint inclination in response to treatment with a low concentration of MeJA (0.05 or 0.5 mg L-1), but it did not alter the lamina joint inclination of plants treated with a high concentration of MeJA (5 mg L-1). Further studies showed that MeJA treatment significantly repressed the expression of BR biosynthesis-related genes and decreased endogenous BRs levels. In addition, the lamina joint inclination in the OsBRI1 mutant d61-1 was less sensitive to MeJA compared with its wild type counterpart, and lithium chloride-induced inactivation of GSK3-like kinase, a negative regulator of BR signaling, partly rescued the MeJA-induced reduction in lamina joint inclination. Further studies showed that MeJA treatment reduced the mRNA levels of BR signaling and target genes. These results indicate that MeJA-inhibition of lamina joint inclination may depend on BR biosynthesis and the BR signaling pathway. (C) 2015 Elsevier Ireland Ltd. All rights reserved

Association between life’s essential 8 and biological ageing among US adults

Abstract Background Biological ageing is tightly linked to cardiovascular disease (CVD). We aimed to investigate the relationship between Life’s Essential 8 (LE8), a currently updated measure of cardiovascular health (CVH), and biological ageing. Methods This cross-sectional study selected adults ≥ 20 years of age from the 2005–2010 National Health and Nutrition Examination Survey. LE8 scores (range 0–100) were obtained from measurements based on American Heart Association definitions, divided into health behavior and health factor scores. Biological ageing was assessed by different methods including phenotypic age, phenotypic age acceleration (PhenoAgeAccel), biological age and biological age acceleration (BioAgeAccel). Correlations were analyzed by weighted linear regression and restricted cubic spline models. Results Of the 11,729 participants included, the mean age was 47.41 ± 0.36 years and 5983 (51.01%) were female. The mean phenotypic and biological ages were 42.96 ± 0.41 and 46.75 ± 0.39 years, respectively, and the mean LE8 score was 67.71 ± 0.35. After adjusting for potential confounders, higher LE8 scores were associated with lower phenotypic age, biological age, PhenoAgeAccel, and BioAgeAccel, with nonlinear dose–response relationships. Negative associations were also found between health behavior and health factor scores and biological ageing, and were stronger for health factors. In health factor-specific analyses, the β negativity was greater for blood glucose and blood pressure. The inverse correlations of LE8 scores with phenotypic age and biological age in the stratified analyses remained solid across strata. Conclusions LE8 and its subscale scores were strongly negatively related to biological ageing. Encouraging optimal CVH levels may be advantageous in preventing and slowing down ageing