Broadband tunable terahertz metamaterial absorber having near-perfect absorbance modulation capability based on a patterned vanadium dioxide circular patch.

A new tunable broadband terahertz metamaterial absorber has been designed based on patterned vanadium dioxide (V O 2). The absorber consists of three simple layers, the top V O 2 pattern layer, the middle media layer, and the bottom metal layer. Based on phase transition properties of V O 2, the designed device has excellent absorption modulation capability, achieving the functional transition from broadband absorption to near-perfect reflection. When V O 2 is in the metallic state, there are two absorption peaks observed at frequencies of 4.16 and 6.05 THz, exhibiting near-perfect absorption characteristics; the combination of these two absorption peaks gives rise to the broadband phenomenon and the absorption bandwidth, where the absorbance exceeds 90% and spans from 3.40 to 7.00 THz, with a corresponding relative absorption bandwidth of 69.23%. The impedance matching theory, near-field patterns, and surface current distributions are provided to analyze the causes of broadband absorption. Furthermore, the broadband absorption could be completely suppressed when V O 2 presents the dielectric phase, and its absorbance could be dynamically adjusted from 100% to less than 0.70%, thereby achieving near-perfect reflection. Owing to its symmetrical structure, it exhibits excellent performance in different polarization directions and at large incidence angles. Our proposed absorber may have a wide range of promising applications and can be applied in a variety of fields such as communications, imaging, sensing, and security detection.

Triple-Band and Ultra-Broadband Switchable Terahertz Meta-Material Absorbers Based on the Hybrid Structures of Vanadium Dioxide and Metallic Patterned Resonators.

A bifunctional terahertz meta-material absorber with three layers is designed. The surface of the bifunctional meta-material absorber is a periodically patterned array composed of hybrid structures of vanadium dioxide (VO2) and metallic resonators; the middle layer is a nondestructive TOPAS film, and the bottom layer is a continuous metallic plane. Utilizing the phase-transition property of VO2, the responses of the meta-material absorber could be dynamically switched between triple-band absorption and ultra-broadband absorption. When VO2 is in the metallic state, an ultra-broadband absorption covering the bandwidth of 6.62 THz is achieved over the range from 4.71 THz to 11.33 THz. When VO2 is in the di-electric state, three absorption peaks resonated at 10.57 THz, 12.68 THz, and 13.91 THz. The physical mechanisms of the bifunctional meta-material absorber were explored by analyzing their near-field distributions. The effects of varying structural parameters on triple-band and ultra-broadband absorption were investigated. It is revealed that by optimizing the structure parameters, the number of absorption peaks could be increased for a certain sacrifice of absorption bandwidth. FDTD Solutions and CST Microwave Studio were used to simulate the data of the absorber, and similar results were obtained.

A 2 × 2 nonblocking Mach-Zehnder-based silicon switch matrix.

A 2 × 2 non-blocking switch matrix based on the Mach-Zehnder (MZ) interferometer was designed and fabricated on silicon-on-insulator (SOI) wafer through 0.8-µm standard commercial CMOS foundry. The two paired multimode-imaging (MMI) couplers in each MZ switching element were used as power splitters and combiners. Experimental results show that the switching elements are electrically driven with a switching speed of 17.4 ns and its cross-talk is lower than -16.1 dB under a common spectral bandwidth of 35 nm. The total switching power consumption varies from 4.55 mW to 22.4 mW for different switching paths.

[Mechanism underlying the inhibitory effects of peroxisome proliferator-activated receptor γ agonists on transforming growth factor ß1 in adult skin fibroblasts].

OBJECTIVE: To study the mechanism underlying the inhibitory effects of peroxisome proliferator-activated receptor γ (PPARγ) agonists on transforming growth factor ß1 (TGF-ß(1))-induced scarring of skin. METHODS: Fibroblasts isolated from healthy adult skin were cultured in vitro and divided into blank control group (serum-free DMEM culture), TGF-ß(1) group (with stimulation of 10 ng/mL TGF-ß(1) for 48 hours), troglitazone group (with the same treatment as in TGF-ß(1) group after stimulation of 10 µmol/L troglitazone for 2 hours), and 15-dioxygen prostaglandin J2 (15d-PGJ2) group (with the same treatment as in TGF-ß(1) group after stimulation of 10 µmol/L 15d-PGJ2 for 2 hours) according to the stimulation added into DMEM. The expression of connective tissue growth factor (CTGF) was determined with Western blot. The mRNA levels of CTGF, matrix metalloproteinase-1 (MMP-1) and platelet-derived growth factor (PDGF) were determined with real-time fluorescence RT-PCR. Data were processed with one-way analysis of variance. RESULTS: The expression of CTGF at mRNA and protein levels in skin fibroblasts were significantly increased in TGF-ß(1) group as compared with control group; while expression of CTGF at mRNA and protein levels in 15d-PGJ2 and troglitazone groups were significantly decreased as compared with that in TGF-ß(1) group. The mRNA level of MMP-1 in TGF-ß(1) group (0.193 ± 0.051) was obviously lower than that in blank control group (1.281 ± 0.195, F = 12.811, P < 0.01), while the mRNA levels of MMP-1 in troglitazone group (0.417 ± 0.043) and 15d-PGJ2 group (0.485 ± 0.027) were significantly increased as compared with that in TGF-ß(1) group (F = 12.811, P values all below 0.01). The mRNA level of PDGF in TGF-ß(1) group (1.044 ± 0.237) was obviously higher than that in control group (0.349 ± 0.057, F = 16.848, P < 0.01), while the levels in troglitazone group (0.677 ± 0.055) and 15d-PGJ2 group (0.511 ± 0.017) were significantly decreased as compared with that in TGF-ß(1) group (F = 16.848, P values all below 0.01). CONCLUSIONS: The inhibitory effect of activated PPARγ on the expression of CTGF induced by TGF-ß(1) may be the main mechanism of its inhibitory effect on TGF-ß(1)-induced scarring on skin, and its influence on MMP-1 and PDGF may also be one of the underlying mechanisms.