The integration of radiofrequency electronic methodologies on micro- as well as nanoscale platforms is crucial for information processing and data-storage technologies. In electronics, radiofrequency signals are controlled and manipulated by 'lumped' circuit elements, such as resistors, inductors and capacitors. In earlier work, we theoretically proposed that optical nanostructures, when properly designed and judiciously arranged, could behave as nanoscale lumped circuit elements--but at optical frequencies. Here, for the first time we experimentally demonstrate a two-dimensional optical nanocircuit at mid-infrared wavelengths. With the guidance of circuit theory, we design and fabricate arrays of Si3N4 nanorods with specific deep subwavelength cross-sections, quantitatively evaluate their equivalent impedance as lumped circuit elements in the mid-infrared regime, and by Fourier transform infrared spectroscopy show that these nanostructures can indeed function as two-dimensional optical lumped circuit elements. We further show that the connections among nanocircuit elements, in particular whether they are in series or in parallel combination, can be controlled by the polarization of impinging optical signals, realizing the notion of 'stereo-circuitry' in metatronics-metamaterials-inspired optical circuitry.

Mammalian target of rapamycin (mTOR) signaling has been suggested to be effective in modifying cognitive status in animal models of Alzheimer's disease (AD), but little is known about its role in AD patients. We hereby tested whether mTOR signaling was activated and whether activated mTOR signaling was related to the degree of cognitive deficits in patients with AD. Autopsy brain hippocampal tissues were obtained from controls and patients with AD and Western blots were performed using antibodies against mTOR signaling molecules and RagC, an upstream component of mTOR complex 1 (mTORC1) signaling. We found that expression of mTOR/p-mTOR and its downstream targets S6/p-S6 and Raptor/p-Raptor were expressed in the control and AD hippocampus. The expression levels of these signaling molecules were significantly increased in the hippocampus at the severe stages of AD, compared to controls and other stages of AD. Interestingly, Rictor expression level was unaltered. In addition, RagC was increased in the hippocampus at the early, moderate, and severe stages of AD. Our data indicate that mTORC1, but not mTORC2, was activated in the AD brains and that the level of mTOR signaling activation was correlated with cognitive severity of AD patients.

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