Adaptation in Standard CMOS Processes with Floating Gate Structures and Techniques

We apply adaptation into ordinary circuits and systems to achieve high performance, high quality results. Mismatch in manufactured VLSI devices has been the main limiting factor in quality for many analog and mixed-signal designs. Traditional compensation methods are generally costly. A few examples include enlarging the device size, averaging signals, and trimming with laser. By applying floating gate adaptation to standard CMOS circuits, we demonstrate here that we are able to trim CMOS comparator offset to a precision of 0.7mV, reduce CMOS image sensor fixed-pattern noise power by a factor of 100, and achieve 5.8 effective number of bits (ENOB) in a 6-bit flash analog-to-digital converter (ADC) operating at 750MHz. The adaptive circuits generally exhibit special features in addition to an improved performance. These special features are generally beyond the capabilities of traditional CMOS design approaches and they open exciting opportunities in novel circuit designs. Specifically, the adaptive comparator has the ability to store an accurate arbitrary offset, the image sensor can be set up to memorize previously captured scenes like a human retina, and the ADC can be configured to adapt to the incoming analog signal distribution and perform an efficient signal conversion that minimizes distortion and maximizes output entropy

Calmodulin Regulates Ca2+-sensing Receptor-mediated Ca2+ Signaling and Its Cell Surface Expression*

The Ca2+-sensing receptor (CaSR) is a member of family C of the GPCRs responsible for sensing extracellular Ca2+ ([Ca2+]o) levels, maintaining extracellular Ca2+ homeostasis, and transducing Ca2+ signaling from the extracellular milieu to the intracellular environment. In the present study, we have demonstrated a Ca2+-dependent, stoichiometric interaction between CaM and a CaM-binding domain (CaMBD) located within the C terminus of CaSR (residues 871–898). Our studies suggest a wrapping around 1–14-like mode of interaction that involves global conformational changes in both lobes of CaM with concomitant formation of a helical structure in the CaMBD. More importantly, the Ca2+-dependent association between CaM and the C terminus of CaSR is critical for maintaining proper responsiveness of intracellular Ca2+ responses to changes in extracellular Ca2+ and regulating cell surface expression of the receptor