Noise suppression of on-chip mechanical resonators by chaotic coherent feedback

We propose a method to decouple the nanomechanical resonator in optomechanical systems from the environmental noise by introducing a chaotic coherent feedback loop. We find that the chaotic controller in the feedback loop can modulate the dynamics of the controlled optomechanical system and induce a broadband response of the mechanical mode. This broadband response of the mechanical mode will cut off the coupling between the mechanical mode and the environment and thus suppress the environmental noise of the mechanical modes. As an application, we use the protected optomechanical system to act as a quantum memory. It's shown that the noise-decoupled optomechanical quantum memory is efficient for storing information transferred from coherent or squeezed light

Poly[(6-carboxy­picolinato-κ3 O 2,N,O 6)(μ3-pyridine-2,6-dicarboxyl­ato-κ5 O 2,N,O 6:O 2′:O 6′)dysprosium(III)]

In the title complex, [Dy(C7H3NO4)(C7H4NO4)]n, one of the ligands is fully deprotonated while the second has lost only one H atom. Each DyIII ion is coordinated by six O atoms and two N atoms from two pyridine-2,6-dicarboxyl­ate and two 6-carboxy­picolinate ligands, displaying a bicapped trigonal-prismatic geometry. The average Dy—O bond distance is 2.40 Å, some 0.1Å longer than the corresponding Ho—O distance in the isotypic holmium complex. Adjacent DyIII ions are linked by the pyridine-2,6-dicarboxyl­ate ligands, forming a layer in (100). These layers are further connected by π–π stacking inter­actions between neighboring pyridyl rings [centroid–centroid distance = 3.827 (3) Å] and C—H⋯O hydrogen-bonding inter­actions, assembling a three-dimensional supra­molecular network. Within each layer, there are other π–π stacking inter­actions between neighboring pyridyl rings [centroid–centroid distance = 3.501 (2) Å] and O—H⋯O and C—H⋯O hydrogen-bonding inter­actions, which further stabilize the structure

Poly[diaqua­bis(μ3-1H-benzimidazole-5,6-dicarboxyl­ato-κ4 N 3:O 5,O 5′:O 6)bis­(μ2-1H,3H-benzimidazolium-5,6-dicarboxyl­ato-κ3 O 5,O 5′:O 6)digadolinium(III)]

In the title complex, [Gd2(C9H4N2O4)2(C9H5N2O4)2(H2O)2]n, two of the benzimidazole-5,6-dicarboxyl­ate ligands are pro­ton­ated at the imidazole groups. Each GdIII ion is coordinated by six O atoms and one N atom from five ligands and one water mol­ecule, displaying a distorted bicapped trigonal-prismatic geometry. The GdIII ions are linked by the carboxyl­ate groups and imidazole N atoms, forming a layer parallel to (001). These layers are further connected by O—H⋯O and N—H⋯O hydrogen bonds into a three-dimensional supra­molecular network

Effect of polygonimitin C on bone formation and resorption in human osteoblast-like MG63 cells

Purpose: To investigate the effect of polygonimitin C (PC) on bone formation and resorption in human osteoblast-like MG63 cells.Methods: MG63 cells were treated with PC at doses of 0, 20, 40 or 80 μg/mL for 48 h, with an untreated group as control. The effect of PC on alkaline phosphatase (ALP) activity in MG63 cells was investigated by p-nitrophenyl phosphate disodium hexahydrate assay. Western blot assay was used to evaluate the effect of PC on the expressions of osterix (OSX), bone morphogenetic protein-2 (BMP-2), runt-related transcription factor 2 (RUNX-2), osteocalcin (OC), fibronectin (FN), type I collagen (COL I), osteoprotegerin (OPG) and receptor activator of NF-κB ligand (RANKL) proteins in MG63 cells.Results: ALP relative activity in MG63 cells treated with PC at 20, 40 or 80 μg/mL (123.58, 137.74 or 159.62 %, respectively) was significantly (p < 0.05 or 0.01) higher than that in control group (99.37 %). Expressions of OSX, BMP-2, RUNX-2, OC, FN, COL I and OPG proteins in MG63 cells treated with PC at 20, 40 or 80 μg/mL were significantly (p < 0.01) higher than those in control group. However, there were no statistically significant differences in RANKL protein expression between PC-treated MG63 cells and control group.Conclusion: These results show that PC exerts protective effects against osteoporosis by promoting bone formation and inhibiting bone resorption. Thus, PC may be useful in the development of new antiosteoporosis drugs.Keywords: Polygonimitin C, MG63 cells, Bone formation, Bone resorption, Osteoporosi

Graphene Field-Effect Transistor for Terahertz Modulation

The real-world applications of terahertz (THz) technology necessitate versatile adaptive optical components, for example, modulators. In this chapter, we begin with a brief review on different techniques for THz modulation. After that, we introduce the extraordinary features of graphene along with its advantages and disadvantages as channel materials for field effect transistor (FET). We then discuss two types of graphene FET-based THz modulators, one is rigid and another is flexible. The feasibility of the high-quality THz modulators with different graphene FET structures has been successfully demonstrated. It is observed that by tuning the carrier concentration of graphene by electrical gating, the THz modulation can be obtained with relatively large modulation depth, broad width band, and moderate speed. This chapter helps the reader in obtaining guidelines for the proper choice of a specific structure for THz modulator with graphene FET

Axin downregulates TCF-4 transcription via β-catenin, but not p53, and inhibits the proliferation and invasion of lung cancer cells

<p>Abstract</p> <p>Background</p> <p>We previously reported that overexpression of Axin downregulates T cell factor-4 (TCF-4) transcription. However, the mechanism(s) by which Axin downregulates the transcription and expression of TCF-4 is not clear. It has been reported that β-catenin promotes and p53 inhibits TCF-4 transcription, respectively. The aim of this study was to investigate whether β-catenin and/or p53 is required for Axin-mediated downregulation of TCF-4.</p> <p>Results</p> <p>Axin mutants that lack p53/HIPK2 and/or β-catenin binding domains were expressed in lung cancer cells, BE1 (mutant p53) and A549 (wild type p53). Expression of Axin or AxinΔp53 downregulates β-catenin and TCF-4, and knock-down of β-catenin upregulates TCF-4 in BE1 cells. However, expression of AxinΔβ-ca into BE1 cells did not downregulate TCF-4 expression. These results indicate that Axin downregulates TCF-4 transcription via β-catenin. Although overexpression of wild-type p53 also downregulates TCF-4 in BE1 cells, cotransfection of p53 and AxinΔβ-ca did not downregulate TCF-4 further. These results suggest that Axin does not promote p53-mediated downregulation of TCF-4. Axin, AxinΔp53, and AxinΔβ-ca all downregulated β-catenin and TCF-4 in A549 cells. Knock-down of p53 upregulated β-catenin and TCF-4, but cotransfection of AxinΔβ-ca and p53 siRNA resulted in downregulation of β-catenin and TCF-4. These results indicate that p53 is not required for Axin-mediated downregulation of TCF-4. Knock-down or inhibition of GSK-3β prevented Axin-mediated downregulation of TCF-4. Furthermore, expression of Axin and AxinΔp53, prevented the proliferative and invasive ability of BE1 and A549, expression of AxinΔβ-ca could only prevented the proliferative and invasive ability effectively.</p> <p>Conclusions</p> <p>Axin downregulates TCF-4 transcription via β-catenin and independently of p53. Axin may also inhibits the proliferation and invasion of lung cancer cells via β-catenin and p53.</p

Systemically administered liposome-encapsulated Ad-PEDF potentiates the anti-cancer effects in mouse lung metastasis melanoma

BACKGROUND: The use of adenoviral vector for gene therapy is still an important strategy for advanced cancers, however, the lack of the requisite coxsackie-adenovirus receptor in cancer cells and host immune response to adenovirus limit the application of adenoviral vector in vivo. METHOD: We designed the antiangiogenic gene therapy with recombinant PEDF adenovirus (Ad-PEDF) encapsulated in cationic liposome (Ad-PEDF/Liposome), and investigated the anti-tumor efficacy of Ad-PEDF/Liposome complex on inhibition of tumor metastasis. RESULTS: We found that systemic administration of Ad-PEDF/liposome was well tolerated and resulted in marked suppression of tumor growth, and was more potent than uncoated Ad-PEDF to induce apoptosis in B16-F10 melanoma cells and inhibit murine pulmonary metastases in vivo. After Ad-luciferase was encapsulated with liposome, its distribution decreased in liver and increased in lung. The anti-Ad IgG level of Ad-PEDF/Liposome was significantly lower than Ad-PEDF used alone. CONCLUSION: The present findings provide evidences of systematic administration of cationic liposome-encapsulated Ad-PEDF in pulmonary metastatic melanoma mice model, and show an encouraging therapeutic effect for further exploration and application of more complexes based on liposome-encapsulated adenovirus for more cancers