ABSTRACT
The narrowband Internet-of-Things (NB-IoT) has been developed to provide low-power, wide-area IoT applications. The efficiency of a power amplifier (PA) in a transmitter is crucial for a longer battery lifetime, satisfying the requirements for output power and linearity. In addition, the design of an internal complementary metal-oxide semiconductor (CMOS) PA is typically required when considering commercial applications to include the operation of an optional external PA. This paper presents a dual-mode CMOS PA with an external PA driver for NB-IoT applications. The proposed PA supports an external PA mode without degrading the performances of output power, linearity, and stability. In the operation of an external PA mode, the PA provides a sufficient gain to drive an external PA. A parallel-combined transistor method is adopted for a dual-mode operation and a third-order intermodulation distortion (IMD3) cancellation. The proposed CMOS PA with an external PA driver was implemented using 40 nm-CMOS technology. The PA achieves a gain of 20.4 dB, a saturated output power of 28.8 dBm, and a power-added efficiency (PAE) of 57.8% in high-power (HP) mode at 920 MHz. With an NB-IoT signal (200 kHz π/4-differential quadrature phase shift keying (DQPSK)), the proposed PA achieves 24.2 dBm output power (Pout) with a 31.0% PAE, while satisfying -45 dBc adjacent channel leakage ratio (ACLR). More than 80% of the current consumption at 12 dBm Pout could be saved compared to that in HP mode when the proposed PA operates in low-power (LP) mode. The implemented dual-mode CMOS PA provides high linear output power with high efficiency, while supporting an external PA mode. The proposed PA is a good candidate for NB-IoT applications.
ABSTRACT
Ginsenosides, major active ingredients of Panax ginseng, are known to regulate excitatory ligand-gated ion channel activity such as nicotinic acetylcholine and NMDA receptor channel activity. However, it is not known whether ginsenosides affect inhibitory ligand-gated ion channel activity. We investigated the effect of ginsenosides on human recombinant GABA(A) receptor (alpha1beta1gamma2S) channel activity expressed in Xenopus oocytes using a two-electrode voltage-clamp technique. Among the eight individual ginsenosides examined, namely, Rb1, Rb2, Rc, Rd, Re, Rf, Rg1 and Rg2, we found that Rc most potently enhanced the GABA-induced inward peak current (I(GABA)). Ginsenoside Rc alone induced an inward membrane current in certain batches of oocytes expressing the GABA(A) receptor. The effect of ginsenoside Rc on I(GABA) was both dose-dependent and reversible. The half-stimulatory concentration (EC50) of ginsenoside Rc was 53.2 +/- 12.3 microM. Both bicuculline, a GABA(A) receptor antagonist, and picrotoxin, a GABA(A) channel blocker, blocked the stimulatory effect of ginsenoside Rc on I(GABA). Niflumic acid (NFA) and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), both Cl- channel blockers, attenuated the effect of ginsenoside Rc on I(GABA). This study suggests that ginsenosides regulated GABA(A) receptor expressed in Xenopus oocytes and implies that this regulation might be one of the pharmacological actions of Panax ginseng.
