Process, voltage, and temperature (PVT) variations in chip fabrication or operation pose a significant challenge to the robustness of analog integrated circuits. Existing design techniques for mitigating PVT variations involve analyzing offsets of DC operating points, but this approach often leads to compromises in circuit performance. To address this challenge, we developed a ‘PVT-Transfer’ framework to facilitate knowledge transfer with evolutionary design. Specifically, by cross-operating the circuit parameters under variations, design knowledge is transferred through parameter migration, thus enhancing the robustness of the resultant circuit. In addition, we leverage data-driven learning to discover potential similarities among PVT variations, thereby mitigating negative knowledge transfer. The PVT-Transfer Framework is evaluated on three integrated voltage references and compared with four state-of-the-art circuit sizing methods. Based on post-layout Monte-Carlo simulations, this framework is verified to offer superior performance to existing methods, yielding a 60% reduction in power consumption, an 80% increase in temperature resilience, and up to 70 $\times$ enhancement in the figure of merit. Further, it leads to a 60% reduction in the number of required circuit simulations and is suitable for parallel computation.

A UHF RFID indoor positioning system based on phase difference is presented in this paper. An additional auxiliary tag and the target tag make up a double tag array to eliminate the phase ambiguity. To quantify the phase offset caused by the interference between tags, a mathematical model is built. Based on the double tag array and the interference model, a hyperbolic positioning algorithm, combining the genetic algorithm, is implemented to improve the positioning accuracy. Compared with other RFID positioning systems, proposed system achieves a better positioning accuracy of 0.2217m.

This paper presents a compact dual-band rectenna for GSM900 and GSM1800 energy harvesting. The monopole antenna consists of a longer bent Koch fractal element for GSM900 band and a shorter radiation element for GSM1800. The rectifier is composed of a multisection dual-band matching network, two rectifying branches, and filter networks. Measured peak efficiency of the proposed rectenna is 62% at 0.88 GHz 15.9 μW/cm² and 50% at 1.85 GHz 19.1 μW/cm², respectively. When the rectenna is 25 m away from a cellular base station, measurement result shows that the harvested power is able to power a batteryless LCD watch and achieve 1.275 V output voltage. The proposed rectenna is compact, efficient, low cost, and easy to fabricate, and it is suitable for RF energy harvesting and various wireless communication scenarios.

Aristolochic acids (AAs) are a family of structurally related nitrophenanthrene carboxylic acids that are present in medicinal herbs such as Aristolochia species. The organic anion transporters (OATs) of the solute carrier (SLC22) gene family located in the renal proximal tubules play a key role in the excretion of a variety of exogenous and endogenous compounds. However, it is unclear how AAs permeate into renal epithelial cells. In this regard, we investigated the role of rat OAT1 ([rOAT1] SLC22A6) in the cellular uptake of AAI in vitro and in vivo. A concentration- and time-dependent intracellular accumulation of AAI was observed in rOAT1-transfected human embryonic kidney 293 (HEK293) cells, which was 2- to 6-fold higher than the control cells. There was a significantly increased rate of cellular apoptosis in rOAT1-transfected HEK293 cells than control cells after AAI treatment. Para-aminohippuric acid (PAH) significantly reduced the intracellular accumulation of AAI in rOAT1-transfected HEK293 cells. Administration of AAI for 35 days in rats caused significantly reduced expression of OAT1 in basolateral membrane and declined renal clearance of PAH as well as renal proximal tubule injuries. These findings indicate that AAI is taken up by OAT1, which then exert its intracellular toxic effects on renal proximal tubule cells, which in turn damage functional OAT1 and may further disturb the transport of its substrates.