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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]

Parkinson's disease remains one of the leading neurodegenerative diseases in developed countries. Despite well-defined symptomology and pathology, the complexity of Parkinson's disease prevents a full understanding of its etiological mechanism. Mechanistically, α-synuclein misfolding and aggregation appear to be central for disease progression, but mitochondrial dysfunction, dysfunctional protein clearance and ubiquitin/proteasome systems, and neuroinflammation have also been associated with Parkinson's disease. Particularly, neuroinflammation, which was initially thought to be a side effect of Parkinson's disease pathogenesis, has now been recognized as driver of Parkinson's disease exacerbation. Next-generation sequencing has been used to identify a plethora of long noncoding RNAs (lncRNA) with important transcriptional regulatory functions. Moreover, a myriad of lncRNAs are known to be regulators of inflammatory signaling and neurodegenerative diseases, including IL-1β secretion and Parkinson's disease. Here, LncZFAS1 was identified as a regulator of inflammasome activation, and pyroptosis in human neuroblast SH-SY5Y cells following MPP+ treatment, a common in vitro Parkinson's disease cell model. Mechanistically, TXNIP ubiquitination through MIB1 E3 ubiquitin ligase regulates NLRP3 inflammasome activation in neuroblasts. In contrast, MPP+ activates the NLPR3 inflammasome through miR590-3p upregulation and direct interference with MIB1-dependent TXNIP ubiquitination. LncZFAS overexpression inhibits this entire pathway through direct interference with miR590-3p, exposing a novel research idea regarding the mechanism of Parkinson's disease. [ABSTRACT FROM AUTHOR]