Search

This research explores the effects of income inequality and country risk on CO2 emissions and examines whether the effects change across countries with different development stages or income levels. A new panel quantile regression approach is used to conduct a comprehensive analysis of the impacts of affecting factors on CO2 emissions at various quantiles, while addressing econometric challenges such as endogeneity and heterogeneity. From a global perspective, we can conclude that the marginal impact of inequality on emissions drops constantly with decreasing country risk at 10th to 50th quantiles, which even performs negative, whereas at the other quantiles, the marginal impact of inequality always remains negative. When we focus on the different income groups, the nexus of inequality emissions is negative first and then positive with decrease of country risk in low-income countries but shows no significant in low-middle- and upper-middle-income countries. Additionally, we validate the detrimental impact of income inequality in upper-income countries. Besides, country risk adversely moderates the nexus of inequality and emissions in low- and upper-income countries. Empirical results confirm that the nexus of inequality emissions lies in country risk, income level, and existing emission degree. These findings provide some important recommendations for policy-makers. [ABSTRACT FROM AUTHOR]

This paper investigates the interaction effects of income inequality and democracy on CO2 emissions. The spatial panel model, which accounts for the spatial spillover effects across countries, is used. Using the panel data covering 41 Belt and Road initiative countries, the results indicate significant positive spatial spillovers effect to country-level CO2 emission activity. The Kuznets Curve hypothesis, which assumes that reverse U relation presents between income and CO2 emissions, is identified. Empirical results provide evidence that democracy levels promote the nonlinear nexus between income inequality and CO2 emissions. High levels of inequality, ceteris paribus, in conjunction with poor democratic institutions are likely to result in higher pollution. The findings are robust to various robustness tests. [ABSTRACT FROM AUTHOR]

The angiotensin II type 1 receptor (AT1R) antagonist losartan has been confirmed to have a moderate anti-inflammatory effect in vitro and in vivo. However, how it affects immune cells in Rheumatoid Arthritis (RA) is still unknown. We found that in human synovial tissues, AT1R is significantly expressed on T cells and B cells. Treatment with losartan (15 mg/kg) alone and in combination with a low dose of methotrexate (MTX 0.25 mg/kg/3 days) significantly suppressed the progression of CIA. Secondary paw swelling, joint destruction and the presence of pro-inflammatory cytokines (TNF-α and IFN-γ) in the serum were alleviated after treatment. The therapeutic effects of losartan were based on reduced T-cell and B-cell activation, specifically by decreased cell vitality and pro-inflammatory cytokine production. In addition, losartan combined with a low dose of MTX achieved a similar therapeutic effect, while protecting liver and kidney from MTX damage. Mechanistically, losartan inhibits the production of pro-inflammatory mediators, reduces the phosphorylation of p38, ERK, and p65, p50 nuclear transposition in T cells and B cells. Phosphorylation of JNK is not affected by losartan in the CIA rat model. losartan can be used as an effective RA treatment, which exhibits anti-arthritic effects potentially through down-regulating the phosphorylation of p38, ERK and signaling through NF-κB. While achieving similar anti-rheumatic effects, a combination therapy of losartan with a low dose of MTX, can protect from liver and renal damage caused by giving a high dose of MTX. [ABSTRACT FROM AUTHOR]

This paper empirically examines the effects of urbanization and income inequality on CO2 emissions in the BRICS economies (i.e., Brazil, Russia, India, China, and South Africa) during the periods 1994-2013. The method we used is the panel quantile regression, which takes into account the unobserved individual heterogeneity and distributional heterogeneity. Our empirical results indicate that urbanization has a significant and negative impact on carbon emissions, except in the 80th, 90th, and 95th quantiles. We also quantitatively investigate the direct and indirect effect of urbanization on carbon emissions, and the results show that we may underestimate urbanization’s effect on carbon emissions if we ignore its indirect effect. In addition, in middle- and high-emission countries, income inequality has a significant and positive impact on carbon emissions. The results of our study indicate that in the BRICS economies, there is an inverted U-shaped environmental Kuznets curve (EKC) between the GDP per capita and carbon emissions. The conclusions of this study have important policy implications for policymakers. Policymakers should try to narrow the income gap between the rich and the poor to improve environmental quality; the BRICS economies can speed up urbanization to reduce carbon emissions, but they must improve energy efficiency and use clean energy to the greatest extent in the process. [ABSTRACT FROM AUTHOR]

T helper 17 (Th17) cells are vital components of the adaptive immune system involved in the pathogenesis of most autoimmune and inflammatory syndromes, and adiponectin(ADN) is correlated with inflammatory diseases such as multiple sclerosis (MS) and type II diabetes. However, the regulatory effects of adiponectin on pathogenic Th17 cell and Th17-mediated autoimmune central nervous system (CNS) inflammation are not fully understood. In this study, we demonstrated that ADN could inhibit Th1 and Th17 but not Th2 cells differentiation in vitro. In the in vivo study, we demonstrated that ADN deficiency promoted CNS inflammation and demyelination and exacerbated experimental autoimmune encephalomyelitis (EAE), an animal model of human MS. Furthermore, ADN deficiency increased the Th1 and Th17 cell cytokines of both the peripheral immune system and CNS in mice suffering from EAE. It is worth mentioning that ADN deficiency predominantly promoted the antigen-specific Th17 cells response in autoimmune encephalomyelitis. In addition, in vitro and in vivo, ADN upregulated sirtuin 1 (SIRT1) and peroxisome proliferator-activated receptor γ (PPARγ) and inhibited retinoid-related orphan receptor-γt (RORγt); the key transcription factor during Th17 cell differentiation. These results systematically uncovered the role and mechanism of adiponectin on pathogenic Th17 cells and suggested that adiponectin could inhibit Th17 cell-mediated autoimmune CNS inflammation. [ABSTRACT FROM AUTHOR]

This paper describes a 10 bit 30 Msample/s (MSPS) CMOS analog-to-digital converter (ADC) for high-speed signal processing, especially for subsampling applications, for example digital video broadcasting over cable (DVB-C), terrestrial (DVB-T) and handheld (DVB-H) systems. The proposed pipelined ADC shows a good figure-of-merit (FoM). It adopts a power efficient amplifier sharing technique, a symmetrical gate-bootstrapping technique with modified timing for the bottom-sampling switch of a wideband sample-and-hold (S/H) circuit, a proposed stable high-swing bias circuit for a wide-swing gain-boosting telescopic amplifier. The measured differential and integral nonlinearities of the prototype in a 0.25-μm CMOS technology show less than 0.4 least significant bit (LSB) and 0.85 LSB respectively at full sampling rate. The ADC exhibits higher than 9 effective number of bits (ENOB) for input frequencies up to about 60 MHz, which is the fourfold Nyquist rate (fs/2), at 30 MSPS. The ADC consumes 60 mW from a 3-V supply and occupies about 1.36 mm2. [ABSTRACT FROM AUTHOR]