Structural Electromagnetic Absorber Based on MoS2 /PyC-Al2 O3 Ceramic Metamaterials.

Limited by the types of suitable absorbents as well as the challenges in engineering the nanostructures (e.g., defects, dipoles, and hetero-interface) using state-of-the-art additive manufacturing (AM) techniques, the electromagnetic (EM) wave absorption performance of the current ceramic-based materials is still not satisfying. Moreover, because of the high residual porosity and the possible formation of cracks during sintering or pyrolysis, AM-formed ceramic components may in many cases exhibit low mechanical strength. In this work, semiconductive MoS2 and conductive PyC modified Al2 O3 (MoS2 /PyC-Al2 O3 ) ceramic-based structural EM metamaterials are developed by innovatively harnessing AM, precursor infiltration and pyrolysis (PIP), and hydrothermal methods. Three different meta-structures are successfully created, and the ceramic-based nanocomposite benefit from its optimization of EM parameters. Ultra-broad effective absorption bandwidth (EAB) of 35 GHz is achieved by establishment of multi-loss mechanism via nanostructure engineering and fabrication of meta-structures via AM. Due to the strengthening by the PyC phase, the bending strength of the resulting ceramics can reach ≈327 MPa, which is the highest value measured on 3D-printed ceramics of this type that has been reported so far. For the first time, the positive effect deriving from the engineering of the microscopic nano/microstructure and of the macroscopic meta-structure of the absorber on the permittivity and EM absorption performance is proposed. Integration of outstanding mechanical strength and ultra-broad EAB is innovatively realized through a multi-scale design route. This work provides new insights for the design of advanced ceramic-based metamaterials with outstanding performance under extreme environment.

Natural wood templated hierarchically cellular NbC/Pyrolytic carbon foams as Stiff, lightweight and High-Performance electromagnetic shielding materials.

Hierarchically cellular, stiff, and lightweight niobium carbide (NbC)-pyrolytic carbon (PyC) monolithic foam composites possessing excellent electromagnetic interference shielding effectiveness (EMI SE) were developed via a natural wood template-based method. Pyrolytic carbon derived from the decomposed cellulose in the wood worked as the carbon source for the growth of NbC phase, and the NbC-PyC heterogeneous nano-interface formed between the residual PyC and the freshly formed NbC. Multi-loss mechanisms (e.g. conductive loss, dipole polarization loss, and especially interface polarization loss) were established by controlling the NbC content and residual PyC phase in the NbC-PyC foams, which significantly improved the absorption capability. Compared to 28.0 dB of PyC monolith, the EMI SE of NbC-PyC foam can reach 54.8 dB when the thickness is 0.5 mm, which outperforms the other porous-based shielding materials. Due to the highly porous structure of pristine wood, the resulting NbC-PyC foam exhibited a low density of 0.48 g/cm3, which is ~ 1/16 of dense NbC (7.78 g/cm3). Generally, this work introduces innovative ideas for designing novel and advanced transition metal carbide-carbon composite materials.

[Effect of paeonol on protecting endothelial cells of diabetic rats].

OBJECTIVE: To study the effect of paeonol on protecting endothelial cells of diabetic rats. METHODS: Streptozocin was used on rats to make diabetic models. Different dosages of paeonol were fed on all the model rats. PGI, TXA2, ET, CRP, ICAM-1, VCAM-1 and NO were tested after 30 day's therapy. RESULTS: Compared with control group PGI increased from 89.75 +/- 2.75, 89.97 +/- 7.28, 89.97 +/- 11.36 to 120.03 +/- 13.85, 108.34 +/- 11.25, 105.32 +/- 8.85, respectively. TXA2 decreased from 157.64 +/- 10.36, 156.64 +/- 11.35, 153.33 +/- 19.40 to 124.46 +/- 18.67, 136.40 +/- 18.15, 138.40 +/- 22.20, respectively. ET decreased from 181.68 +/- 5.10, 181.27 +/- 4.76, 181.04 +/- 4.19 to 140.55 +/- 3.01, 150.51 +/- 2.22, 161.02 +/- 3.76, respectively. CRP decreased from 41.63 +/- 7.37, 44.83 +/- 7.80, 42.06 +/- 7.21 to 28.62 +/- 5.45, 30.00 +/- 10.73, 37.09 +/- 4.94, respectively. ICAM-1 decreased from 225.77 +/- 11.96, 222.78 +/- 14.46, 225.17 +/- 10.03 to 190.93 +/- 12.67, 197.42 +/- 14.56, 200.64 +/- 15.36, respectively. VCAM-1 decreased from 566.72 +/- 24.46, 560.61 +/- 25.67, 359.61 +/- 42.75 to 506.26 +/- 37.26, 516.83 +/- 28.17, 527.02 +/- 43.47, respectively. NO had no change. CONCLUSIONS: Paeonol can protect the endothelial cells of diabetic rats.

[Effect of cortex moutan on PGI2, TXA2, ET and NO in diabetic rats].

OBJECTIVE: To study the effect of Paeonol on PGI2, TXA2, ET and NO in diabetic rats. METHODS: Streptozocin was used on rats to make diabetic animal models. Different dosage of Paeonol were used on diabetic animal models. PGI2, TXA2, ET and NO were tested after 30 days therapy. RESULTS: Compared with those in the control group, the level of PGI2 increased and the contents of TXA2 and ET decreased in treatment group. Among them, the high dosage group was more obvious (P < 0.01). But the level of No Had no change. CONCLUSION: Paeonol can decrease the ET and TXA2 in diabetic rats, and increase PGI2 in diabetic rats.

[The effect of "Jian Pi Dao Zhi Fang" on human gastric carcinoma cells].

OBJECTIVE: To study the effect of Traditional Chinese medicine "Jian Pi Dao Zhi Fang" (JPDZF) with invigorating the spleen and purgative function on the growth of gastric carcinoma cells and the expression of VEGF and P53 in gastric carcinoma cells. METHODS: Gastric carcinoma cells were cultured in the RPMI-1640 media with 10% serum containing JPDZF for 48 hours. The cell cycle were tested with flow cytometer. Expression of P53, VEGF and its receptor Fit were evaluated by immunohistochemistry. RESULT: The cell cycle of gastric carcinoma cells cultured in the media with JPDZF were different from the control. The expression of P53, VEGF, Flt decreased with the dosage increasing of JPDZF. CONCLUSION: Traaditional Chinese medicine JPDZF can inhibit the growth of gastric carcinoma cells and the expression of P53, VEGF, Flt.