A Dual-Mode CMOS Power Amplifier with an External Power Amplifier Driver Using 40 nm CMOS for Narrowband Internet-of-Things Applications.

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.

Familial Risk of Gout and Interaction With Obesity and Alcohol Consumption: A Population-Based Cohort Study in Korea.

OBJECTIVE: Population-based studies of the familial aggregation of gout are scarce, and gene/environment interactions are not well studied. This study was undertaken to evaluate the familial aggregation of gout as well as assess interactions between family history and obesity or alcohol consumption on the development of gout. METHODS: Using the Korean National Health Insurance database, which includes information regarding familial relationships and risk factor data, we identified 5,524,403 individuals from 2002 to 2018. Familial risk was calculated using hazard ratios (HRs) with 95% confidence intervals (95% CIs) to compare the risk in individuals with and those without affected first-degree relatives. Interactions between family history and obesity/alcohol consumption were assessed on an additive scale using the relative excess risk due to interaction (RERI). RESULTS: Individuals with a gout-affected first-degree relative had a 2.42-fold (95% CI 2.39, 2.46) increased risk of disease compared to those with unaffected first-degree relatives. Having both a family history of gout and being either overweight or having moderate alcohol consumption was associated with a markedly increased risk of disease, with HRs of 4.39 (95% CI 4.29, 4.49) and 2.28 (95% CI 2.22, 2.35), respectively, which exceeded the sum of their individual risks but was only statistically significant in overweight individuals (RERI 0.96 [95% CI 0.85, 1.06]). Obese individuals (RERI 1.88 [95% CI 1.61, 2.16]) and heavy drinkers (RERI 0.36 [95% CI 0.20, 0.52]) had a more prominent interaction compared to overweight individuals and moderate drinkers, suggesting a dose-response interaction pattern. CONCLUSION: Our findings indicate the possibility of an interaction between gout-associated genetic factors and obesity/alcohol consumption.

Familial risk of seropositive rheumatoid arthritis and interaction with smoking: a population-based cohort study.

OBJECTIVES: We evaluated the familial risk of seropositive rheumatoid arthritis (RA) and examined interactions between family history and smoking. METHODS: Using the National Health Insurance and Health Screening Program databases, which include information on familial relationships and lifestyle factors, we identified 5 524 403 individuals with first-degree relatives (FDRs) from 2002-2018. We calculated familial risk using hazard ratios (HRs) with 95% CIs which compare the risk of individuals with and without affected FDRs. Interactions between smoking and family history were assessed on an additive scale using the relative excess risk due to interaction (RERI). RESULTS: Individuals with affected FDR had 4.52-fold (95% CI 3.98, 5.12) increased risk of disease compared with those with unaffected FDR. Familial risk adjusted for lifestyle factors decreased slightly (HR 4.49), suggesting that a genetic contribution is the predominant driver in the familial aggregation of RA. Smoking was associated with an increased risk of disease that was more pronounced among heavy (HR 1.92 95% CI 1.70, 2.18) compared with moderate (HR 1.15 95% CI 1.04, 1.28) smoking. In the interaction analysis, the risk associated with the combined effect of smoking and family history was higher than the sum of their individual effects, though statistically non-significant (RERI 1.30 95% CI ‒0.92, 3.51). Heavy smokers with a positive family history showed a prominent interaction (RERI 4.13 95% CI ‒0.88, 9.13) which exceeded moderate smokers (RERI 0.61 95% CI ‒1.90, 3.13), suggesting a dose-response interaction pattern. CONCLUSION: Our findings indicate the possibility of an interaction between RA-associated genes and smoking.

Socio-economic factors and outcomes in chronic lung disease of prematurity.

RATIONALE: Infants and children with chronic lung disease of prematurity (CLDP) are at increased risk for respiratory morbidities. We sought to determine (1) whether socio-economic status, race/ethnicity, and/or sex are risk factors for respiratory morbidities and (2) whether disparities in care existed for major therapy decisions such as home supplemental oxygen and gastrostomy tubes as well as initial length of stay in the neonatal intensive care unit. METHODS: Between January 2008 and February 2010 sociodemographic and respiratory morbidity data were collected on premature (<32 weeks gestation) infants and children (<3 years old) with CLDP. Associations between risk factors and respiratory morbidities and treatment parameters were examined using adjusted regression models. RESULTS: Data were collected on 135 subjects (gestational age: 26.2±2.0 weeks). Self-reported non-Whites were more likely to report rescue medication use in the past 7 days [adjusted OR: 2.87 (1.28-6.45), P=0.011] and the use of systemic steroids for respiratory symptoms since the last clinic visit [adjusted OR: 2.12 (1.02-4.43), P=0.045]. Lower median household income was associated with increased activity limitations [adjusted OR: 2.79 (1.16-6.70), P=0.022] and public insurance coverage was associated with a decreased risk for hospitalizations [adjusted OR: 0.36 (0.13-0.98), P=0.045]. Major therapy decisions were not associated with disparities of care. CONCLUSIONS: A key finding was that non-Whites were more likely to report rescue medication and systemic steroid use than Whites, but there was no difference in the frequency of respiratory symptoms or preventative inhaled corticosteroid use. Etiologies for these findings remain unclear and require further research.

Effects of ginsenosides on GABA(A) receptor channels expressed in Xenopus oocytes.

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.