Flexible Polyimide Nanocomposites with dc Bias Induced Excellent Dielectric Tunability and Unique Nonpercolative Negative- k toward Intrinsic Metamaterials.

Intrinsic metamaterials with negative- k that originated from random-structured materials have drawn increasing attention. Currently, intrinsic negative- k was mainly achieved in percolative composites by tailoring the compositions and microstructures. Herein, plasmalike negative- k was successfully achieved in multiwalled carbon nanotubes (MWCNT)/polyimide (PI) nanocomposites via applying external dc bias which exhibited excellent capability in conveniently and accurately adjusting negative- k. Mechanism analysis indicated that the localized charges at the interfaces between MWCNT and PI became delocalized after gaining energy from the dc bias, resulting in elevated concentration of delocalized charges, and hence the enhanced negative- k. Furthermore, it is surprising to observe that negative- k also appeared in multilayer nanocomposites consisting of alternating BaTiO3/PI and PI layers, in which there was no percolative conducting network. On the basis of systematic analysis, it is proposed that the unique nonpercolative negative- k resulted from the mutual competition between plasma oscillations of delocalized charges and polarizations of localized charges. Negative- k appeared once the polarizations were overwhelmed by plasma oscillations. This work demonstrated that applying dc bias is a promising way to achieve highly tailorable negative- k. Meanwhile, the observation of unique nonpercolative negative- k and the clarification of underlying mechanisms offer new insights into negative- k metamaterials, which will greatly facilitate the exploration of high-performance electromagnetic metamaterials.

Mangiferin ameliorates insulin resistance by inhibiting inflammation and regulatiing adipokine expression in adipocytes under hypoxic condition.

Adipose tissue hypoxia has been recognized as the initiation of insulin resistance syndromes. The aim of the present study was to investigate the effects of mangiferin on the insulin signaling pathway and explore whether mangiferin could ameliorate insulin resistance caused by hypoxia in adipose tissue. Differentiated 3T3-L1 adipocytes were incubated under normal and hypoxic conditions, respectively. Protein expressions were analyzed by Western blotting. Inflammatory cytokines and HIF-1-dependent genes were tested by ELISA and q-PCR, respectively. The glucose uptake was detected by fluorescence microscopy. HIF-1α was abundantly expressed during 8 h of hypoxic incubation. Inflammatory reaction was activated by up-regulated NF-κB phosphorylation and released cytokines like IL-6 and TNF-α. Glucose uptake was inhibited and insulin signaling pathway was damaged as well. Mangiferin substantially inhibited the expression of HIF-1α. Lactate acid and lipolysis, products released by glycometabolism and lipolysis, were also inhibited. The expression of inflammatory cytokines was significantly reduced and the damaged insulin signaling pathway was restored to proper functional level. The glucose uptake of hypoxic adipocytes was promoted and the dysfunction of adipocytes was relieved. These results showed that mangiferin could not only improve the damaged insulin signaling pathway in hypoxic adipocytes, but also ameliorate inflammatory reaction and insulin resistance caused by hypoxia.