We present, in this paper, a new full-wave CMOS rectifier dedicated for wirelessly-powered low-voltage biomedical implants. It uses bootstrapped capacitors to reduce the effective threshold voltage of selected MOS switches. It achieves a significant increase in its overall power efficiency and low voltage-drop. Therefore, the rectifier is good for applications with low-voltage power supplies and large load current. The rectifier topology does not require complex circuit design. The highest voltages available in the circuit are used to drive the gates of selected transistors in order to reduce leakage current and to lower their channel on-resistance, while having high transconductance. The proposed rectifier was fabricated using the standard TSMC 0.18 μm CMOS process. When connected to a sinusoidal source of 3.3 V peak amplitude, it allows improving the overall power efficiency by 11% compared to the best recently published results given by a gate cross-coupled-based structure.

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We present in this paper a new topology of inductively-coupled links based on a monolithic multi-coils receiver. A model is built to characterize the proposed structure using Matlab and is verified employing simulation tools under ADS electromagnetic environment. This topology accounts for the losses associated with the receiver micro-coil including substrate and oxide layers. The geometry of micro-coils significantly desensitizes the link to both angular and side misalignments. A custom fabrication process using 1 micron metal thickness is also presented by which two sets of micro-coils varying in the number of coils are realized. The first set possesses one coil 4 mm of diameter and represents a power efficiency close to 4% while the second set possesses multi-coils with an efficiency of 18%. The resulting optimized link can deliver up to 50 mW of power to power up an implantable device either sensor or stimulator. The experimental results for the prototypes are remarkably in agreement with those obtained from simulated models and circuits.

Several studies have recently reported strong association between type 2 diabetes and variation in the transcription factor 7-like 2 (TCF7L2) gene, which has been confirmed by several other genome-wide studies. However, the physiological implications of this transcription factor on the pathogenesis of type 2 diabetes is not yet known. The aim of this study was to investigate the alteration in TCF7L2 gene expression in human pancreatic cell line in response to various factors in vitro. MIA Paca-2 cell line (Human Pancreas cell line) was cultured in the presence of curcumin, lipopolysaccaride and glucose (low and high concentration). TCF7L2 gene expression was determined using quantitative real-time RT-PCR. Treatment with curcumin significantly increased TCF7L2 gene expression to 3.24 fold (1.7-log fold) (P = 0.003) compared to the controls while treatment with LPS decreased TCF7L2 gene expression to 0.88-fold (-0.18-log). On the other hand, glucose increased TCF7L2 gene expression in pancreatic cell line. Our data suggest a role for TCF7L2 in glucose homeostasis. The contrary effect of curcumin and LPS on expression of TCF7L2 in pancreatic cells supports a role for TCF7L2 in their survival and function in inflammatory conditions.

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