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The rising urban population and accelerated resource consumption pose major environmental challenges. Given that around 75% of global resources are consumed in urban areas, understanding the true association between urbanization (UR) and ecological quality is necessary for better urban strategies. Alongside this, eco-innovation (ECO) can limit environmental pollution and thus, it is the cornerstone of environmental policies. On that note, this research discloses the nexus between eco-innovation, economic growth (EGR), and ecological quality by considering the non-linear effects of UR in the emerging seven (E-7) nations from 1992 to 2018. Unlike previous literature, the newly developed indicator of ecological quality (the load capacity factor (LCF)) is adopted to understand the connection between UR, eco-innovation, and ecological quality since this new comprehensive indicator is based on both biocapacity and ecological footprint (EF). In the methodology, the "Continuously Updated-Fully Modified" (CuP-FM) test is used since this method offers diverse benefits for panel data estimation by accounting for major panel data estimation issues including autocorrelation, endogeneity, heteroscedasticity, fractional integration, and cross-sectional dependence. The empirical estimates unveiled that the current levels as well as high levels of UR limit the LCF. This evidence suggests that UR in the E-7 nations expands ecological degradation. This finding contradicts the assertions of ecological modernization theory that expanding urbanization brings some ecological benefits. Similarly, economic growth alleviates ecological quality. However, eco-innovation and agricultural land (AGL) contribute to enhancing the LCF and promoting ecological quality. Further, UR and eco-innovation Granger cause the LCF. Lastly, comprehensive urban environmental strategies are discussed to promote sustainable urbanization backed by eco-innovation. [ABSTRACT FROM AUTHOR]

Background: Flowering time is an important agronomic trait of crops and significantly affects plant adaptation and seed production. Flowering time varies greatly among maize (Zea mays) inbred lines, but the genetic basis of this variation is not well understood. Here, we report the comprehensive genetic architecture of six flowering time-related traits using a recombinant inbred line (RIL) population obtained from a cross between two maize genotypes, B73 and Abe2, and combined with genome-wide association studies to identify candidate genes that affect flowering time. Results: Our results indicate that these six traits showed extensive phenotypic variation and high heritability in the RIL population. The flowering time of this RIL population showed little correlation with the leaf number under different environmental conditions. A genetic linkage map was constructed by 10,114 polymorphic markers covering the whole maize genome, which was applied to QTL mapping for these traits, and identified a total of 82 QTLs that contain 13 flowering genes. Furthermore, a combined genome-wide association study and linkage mapping analysis revealed 17 new candidate genes associated with flowering time. Conclusions: In the present study, by using genetic mapping and GWAS approaches with the RIL population, we revealed a list of genomic regions and candidate genes that were significantly associated with flowering time. This work provides an important resource for the breeding of flowering time traits in maize. [ABSTRACT FROM AUTHOR]

Background: Flowering time is an important agronomic trait of crops and significantly affects plant adaptation and seed production. Flowering time varies greatly among maize (Zea mays) inbred lines, but the genetic basis of this variation is not well understood. Here, we report the comprehensive genetic architecture of six flowering time-related traits using a recombinant inbred line (RIL) population obtained from a cross between two maize genotypes, B73 and Abe2, and combined with genome-wide association studies to identify candidate genes that affect flowering time. Results: Our results indicate that these six traits showed extensive phenotypic variation and high heritability in the RIL population. The flowering time of this RIL population showed little correlation with the leaf number under different environmental conditions. A genetic linkage map was constructed by 10,114 polymorphic markers covering the whole maize genome, which was applied to QTL mapping for these traits, and identified a total of 82 QTLs that contain 13 flowering genes. Furthermore, a combined genome-wide association study and linkage mapping analysis revealed 17 new candidate genes associated with flowering time. Conclusions: In the present study, by using genetic mapping and GWAS approaches with the RIL population, we revealed a list of genomic regions and candidate genes that were significantly associated with flowering time. This work provides an important resource for the breeding of flowering time traits in maize. [ABSTRACT FROM AUTHOR]

Background: Breast cancer (BC) is one of the most prevalent malignancies among women globally. Emerging evidence indicates that long non-coding RNAs (lncRNAs) are associated with BC carcinogenesis. In the current study, we explored the mechanism by which LINC00662 regulates BC. Methods: Quantitative real-time PCR (qRT-PCR) assessed RNA expressions while western blot for protein levels. Kaplan Meier analysis evaluated overall survival (OS). Cytoplasmic/nuclear fractionation, RNA binding protein immunoprecipitation (RIP) and luciferase reporter assays probed into the underlying molecular mechanism of LINC00662 in BC. Xenograft model was established to explore the influence of LINC00662 on BC progression in vivo. R square graphs were utilized to represent RNA relationships. Results: LINC00662 is overtly overexpressed in BC tissues and cell lines. LINC00662 knockdown hampers cell proliferation, migration, invasion and stemness. LINC00662 expression is negatively correlated with OS of BC patients. LINC00662 up-regulates SOX2 expression by competitively binding to miR-144-3p, thereby modulating BC cell progression. Xenograft experiments verified that LINC00662 promotes BC tumor growth and cell stemness in vivo. Conclusion: LINC00662 enhances cell proliferation, migration, invasion and stemness in BC by targeting miR-144-3p/SOX2 axis. The findings in the present study suggested that LINC00662 could be a potential therapeutic target for BC treatment. [ABSTRACT FROM AUTHOR]