Three layers of periodic artificial metamaterial sensing structure (including the upper metal particles, intermediate dielectric layer, and the lower reflective layer) with ultra-narrow band absorption were designed. The resonance characteristics and sensing properties were analyzed by the finite difference time domain (FDTD) method. The effect of localized surface plasmon resonance (LSPR) was obviously observed at the resonance wavelength of 911 nm, and it achieves nearly perfect absorption of exceeding 98% with a full width at half maximum (FWHM) of 3.5 nm. In addition, a wavelength sensitivity of 542 nm/RIU with a figure of merit (FOM) of 155 was obtained in the refractive index (RI) range from 1.00 to 1.35, which has a wide range of applications. The results show that the proposed structure has high absorption and RI sensitivity, which is suitable for bioengineering and medical detection.
The SH2/SH3 adapter Nck has an evolutionarily conserved role in neurons, linking the cell surface signals to actin cytoskeleton-mediated responses. The mechanism, however, remains poorly understood. We have investigated the role of Nck/Nckalpha/Nck1 versus Grb4/Nckbeta/Nck2 side-by-side in the process of mammalian neuritogenesis. Here we show that permanent genetic silencing of Nckbeta, but not Nckalpha, completely blocked nerve growth factor-induced neurite outgrowth in PC12 cells and dramatically disrupted the axon and dendrite tree in primary rat cortical neurons. By screening for changes among the components reportedly present in complex with Nck, we found that the steady-state level of paxillin was significantly reduced in Nckbeta knockdown, but not Nckalpha knockdown, neurons. Interestingly, Nckbeta knockdown did not affect the paxillin level in glial cells and several other cell types of various tissue origins. Genetic silencing of paxillin blocked neuritogenesis, just like Nckbeta knockdown. Reintroducing a nondegradable Nckbeta into Nckbeta short interfering RNA-expressing PC12 cells rescued paxillin from down-regulation and allowed the resumption of neuritogenesis. Forced expression of paxillin in Nckbeta knockdown PC12 also rescued its capacity for neuritogenesis. Finally, Nckbeta, but not Nckalpha, binds strongly to paxillin and treatment of the neurons with proteosome inhibitors prevented paxillin down-regulation in Nckbeta knockdown neurons. Thus, Nckbeta maintains paxillin stability during neuritogenesis. 相似文献
The aryl hydrocarbon receptor (AhR) binds with high affinity to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related halogenated aromatics, but also binds with lower affinity to structurally diverse exogenous and endogenous chemicals. One study reported that 3-methylcholanthrene (3MC) activated the estrogen receptor (ER) through the AhR, which acts as co-regulatory protein, whereas a recent report showed that 3MC directly bound and activated ERalpha. This study also shows that the AhR agonists benzo[a]pyrene, 3,3',4,4'-tetrachlorobiphenyl, chrysin, 6-methyl-1,3,8-trichlorodibenzofuran, and 3,3'-diindolylmethane also induce ERalpha-dependent transactivation. Moreover, in chromatin immunoprecipitation assays, these compounds induce binding of AhR and ERalpha to the CYP1A1 and pS2 gene promoters, which is consistent with their activities as both selective AhR modulators (SAhRMs) and selective ER modulators (SERMs). 相似文献
17beta-Estradiol (E2) induces and represses gene expression in breast cancer cells; however, the mechanisms of gene repression are not well understood. In this study, we show that E2 decreases vascular endothelial growth factor receptor 2 (VEGFR2) mRNA levels in MCF-7 cells, and this gene was used as a model for investigating pathways associated with E2-dependent gene repression. Deletion analysis of the VEGFR2 promoter indicates that the proximal GC-rich motifs at -58 and -44 are critical for the E2-dependent decreased response in MCF-7 cells. Mutation or deletion of these GC-rich elements results in loss of hormone responsiveness and shows that the -60 to -37 region of the VEGFR2 promoter is critical for both basal and hormone-dependent decreased VEGFR2 expression in MCF-7 cells. Western blot, immunofluorescent staining, RNA interference, and EMSAs support a role for Sp proteins in hormone-dependent down-regulation of VEGFR2 in MCF-7 cells, primarily through estrogen receptor (ER)alpha/Sp1 and ERalpha/Sp3 interactions with the VEGFR2 promoter. Using chromatin immuno-precipitation and transient transfection/RNA interference assays we show that the ERalpha/Sp protein-promoter interactions are accompanied by recruitment of the co-repressors SMRT (silencing mediator of retinoid and thyroid hormone receptor) and NCoR (nuclear receptor corepressor) to the promoter and that SMRT and NCoR knockdown reverse E2-mediated down-regulation of VEGFR2 expression in MCF-7 cells. This study illustrates that both SMRT and NCoR are involved in E2-dependent repression of VEGFR2 in MCF-7 cells. 相似文献
Conversion of fructose and glucose into 5-hydroxymethylfurfural (HMF) was investigated in various imidazolium ionic liquids, including 1-butyl-3-methylimidazolium chloride (BmimCl), 1-hexyl-3-methylimidazolium chloride (HmimCl), 1-octyl-3-methylimidazolium chloride (OmimCl), 1-benzyl-3-methylimidazolium chloride (BemimCl), 1-Butyl-2,3-dimethylimidazolium chloride (BdmimCl), and 1-butyl-3-methylimidazolium p-toluenesulfonate (BmimPS). The acidic C-2 hydrogen of imidazolium cations was shown to play a major role in the dehydration of fructose in the absence of a catalyst, such as sulfuric acid or CrCl3. Both the alkyl groups of imidazolium cations and the type of anions affected the reactivity of the carbohydrates. Although, except BmimCl and BemimCl, other four ionic liquids could only achieve not more than 25% HMF yields without an additional catalyst, 60–80% HMF yields were achieved in HmimCl, BdmimCl, and BmimPS in the presence of sulfuric acid or CrCl3 in sufficient quantities. 相似文献