A Fully-Integrated Quad-Band GSM/GPRS CMOS Power Amplifier

Concentric distributed active transformers (DAT) are used to implement a fully-integrated quad-band power amplifier (PA) in a standard 130 nm CMOS process. The DAT enables the power amplifier to integrate the input and output matching networks on the same silicon die. The PA integrates on-chip closed-loop power control and operates under supply voltages from 2.9 V to 5.5 V in a standard micro-lead-frame package. It shows no oscillations, degradation, or failures for over 2000 hours of operation with a supply of 6 V at 135° under a VSWR of 15:1 at all phase angles and has also been tested for more than 2 million device-hours (with ongoing reliability monitoring) without a single failure under nominal operation conditions. It produces up to +35 dBm of RF power with power-added efficiency of 51%

Activated β-catenin in Foxp3+ regulatory T cells links inflammatory environments to autoimmunity.

Foxp3+ regulatory T cells (Treg cells) are the central component of peripheral immune tolerance. Whereas a dysregulated Treg cytokine signature has been observed in autoimmune diseases, the regulatory mechanisms underlying pro- and anti-inflammatory cytokine production are elusive. Here, we identify an imbalance between the cytokines IFN-γ and IL-10 as a shared Treg signature present in patients with multiple sclerosis and under high-salt conditions. RNA-sequencing analysis on human Treg subpopulations revealed β-catenin as a key regulator of IFN-γ and IL-10 expression. The activated β-catenin signature was enriched in human IFN-γ+ Treg cells, as confirmed in vivo with Treg-specific β-catenin-stabilized mice exhibiting lethal autoimmunity with a dysfunctional Treg phenotype. Moreover, we identified prostaglandin E receptor 2 (PTGER2) as a regulator of IFN-γ and IL-10 production under a high-salt environment, with skewed activation of the β-catenin-SGK1-Foxo axis. Our findings reveal a novel PTGER2-β-catenin loop in Treg cells linking environmental high-salt conditions to autoimmunity