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Advances in financial inclusions have contributed to economic growth and poverty alleviation, addressing environmental implications and implementing measures to mitigate climate change. Financial inclusions force advanced countries to progress their policies in a manner that does not hinder developing countries' current and future development. Consequently, this research examined the asymmetric effects of information and communication technology (ICT), financial inclusion, consumption of primary energy, employment to population ratio, and human development index on CO2 emissions in oil-producing countries (UAE, Nigeria, Russia, Saudi Arabia, Norway, Kazakhstan, Kuwait, Iraq, USA, and Canada). The study utilizes annual panel data spanning from 1990 to 2021. In addition, this study investigates the validity of the Environmental Kuznets Curve (EKC) trend on the entire sample, taking into account the effects of energy consumption and population to investigate the impact of financial inclusion on environmental degradation. The study used quantile regression, FMOLS, and FE-OLS techniques. Preliminary outcomes revealed that the data did not follow a normal distribution, emphasizing the need to use quantile regression (QR). This technique can effectively detect outliers, data non-normality, and structural changes. The outcomes from the quantile regression analysis indicate that ICT consistently reduces CO2 emissions in all quantiles (ranging from the 1st to the 9th quantile). In the same way, financial inclusion, and employment to population ratio constrains CO2 emissions across each quantile. On the other side, primary energy consumption and Human development index were found to increase CO2 emissions in each quantile (1st to 9th). The findings of this research have implications for both the academic and policy domains. By unraveling the intricate interplay between financial inclusion, ICT, and environmental degradation in oil-producing nations, the study contributes to a nuanced understanding of sustainable development challenges. Ultimately, the research aims to guide the formulation of targeted policies that leverage financial inclusion and technology to foster environmentally responsible economic growth in oil-dependent economies. [ABSTRACT FROM AUTHOR]

In light of the carbon neutrality goals set post-Paris Climate Conference (COP21), this study delves into the relationship between green technology innovations, energy consumption, and CO2 emissions in China, spanning the period of 1990 to 2021. The objective of this paper is to creatively present the idea of a low-carbon digital economy from the viewpoint of digital technology. Utilizing the Stochastic Impacts by Regression on Population, Affluence, and Technology (STIRPAT) model, we scrutinize this relationship, employing unit-root testing to verify the integrative attributes of the variables, inclusive of structural break data. Further analysis using the bootstrap Autoregressive Distributed Lag (ARDL) bound testing method corroborates the relationship between these key variables. The study reveals unidirectional co-integration over time among green technology innovations, renewable and non-renewable energy, per capita income, population, and CO2 emissions as per the Granger causality test. Interestingly, our findings suggest that while green technology innovation, per capita income, and renewable energy contribute to the reduction of CO2 emissions, non-renewable energy consumption and population growth exacerbate them. These insights offer valuable guidance for policymakers in formulating comprehensive strategies to enhance environmental quality through the promotion of renewable energy and green technology innovations, with a specific emphasis on the Chinese context. [ABSTRACT FROM AUTHOR]

Summary: Programmed cell death (PCD) is a highly conserved cellular suicide process important in developmental processes and elimination of damaged cells upon environmental stresses. Among the important regulators of PCD, much interest has been centered on BCL2-associated x protein (BAX) as the pro-PCD factor. On the other hand, BAX inhibitor-1 (BI-1) has been implicated as an anti-PCD factor that balances out the activity of BAX in the developmental processes and responses to environment. A cDNA clone coding a BI-1 gene was isolated from a cDNA library of heat-stressed hot pepper (Capsicum annuum) and named as CaBI-1. This gene contains an open reading frame (ORF) of 248 amino acids encoding a BI-1 protein. Genomic DNA-blot analysis for CaBI-1 suggested one or two loci in the C. annuum genome. Transcription of CaBI-1 was induced in response to high or low temperatures, drought, high salinity, flooding and heavy metal stresses, and ABA. We introduced the ORF of CaBI-1 under the control of the CaMV 35S promoter (P35S) into tobacco (Nicotiana tabacum cv. Wisconsin 38) genome by Agrobacterium-mediated transformation. The P35S:CaBI-1 transgenic plants displayed markedly improved tolerance to high temperature, water deficit, and high salinity in comparison to the control plants. The results indicate that CaBI-1 is a BI-1 gene of which expression induced under various abiotic stresses and endows tolerance to several types of environmental stresses. [Copyright &y& Elsevier]

The myosin light chain kinase ( MYLK) gene encodes both smooth muscle and nonmuscle cell isoforms. Recently, polymorphisms in MYLK have been reported to be associated with several diseases. To examine the genetic effects of polymorphisms on the risk of asthma and related phenotypes, we scrutinized MYLK by re-sequencing/genotyping and statistical analysis in Korean population (n = 1,015). Seventeen common polymorphisms located in or near exons, having pairwise r values less than 0.25, were genotyped. Our statistical analysis did not replicate the associations with the risk of asthma and log-transformed total IgE levels observed among African descendant populations. However, two SNPs in intron 16 (+ 89872C > G and + 92263T > C), which were in tight LD (|D′| = 0.99), revealed significant association with log-transformed blood eosinophil level even after correction multiple testing (P = 0.002/P= 0.01 and P = 0.002/P = 0.01, respectively). The log-transformed blood eosinophil levels were higher in individuals bearing the minor alleles for + 89872C > G and + 92263T > C, than in those bearing other allele. In additional subgroup analysis, the genetic effects of both SNPs were much more apparent among asthmatic patients and atopic asthma patients. Among atopic asthma patients, the log-transformed blood eosinophil levels were proportionally increased by gene-dose dependent manner of in both + 89872C > G and + 92263T > C (P = 0.0002 and P = 0.00007, respectively). These findings suggest that MYLK polymorphisms might be among the genetic factors underlying differential increases of blood eosinophil levels among asthmatic patients. Further biological and/or functional studies are needed to confirm our results. [ABSTRACT FROM AUTHOR]