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Addressing natural resource dependence is integral to achieving the Sustainable Development Goals by promoting economic diversification, environmental sustainability, and climate resilience. This study explores the effect of natural resource dependence on green development by adopting the balanced panel dataset from the "Belt and Road" countries from 2005 to 2019. Notably, the novelty of our analysis lies in the empirical analysis using instrument-based techniques that consolidate the "green development curse hypothesis" in the Belt and Road countries. The mechanism analysis reveals that natural resource dependence curbs green development by weakening innovative capability, disturbing institutional quality, reducing population density, and crowding out human capital. Further, the dynamic panel threshold model handling endogeneity verifies the nonlinear relationship between natural resource dependence and green development. Interestingly, digital trade offers greater "resilience" than traditional trade, correcting the resource curse dilemma. Finally, heterogeneity analyses indicate that the green development curse hypothesis only exists in countries with high-level environmental regulations and resource-based countries.

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Certain nations have opted for stimulus-based regulations to curtail emissions, build a liveable, environmentally friendly setting, and work towards aspirational mitigation targets. New Zealand (NZ) prefers an Emission Trading Scheme (ETS) to taxation, mitigating emissions on one hand while retaining incentives for economic growth on the other. As a result, NZ has initiated a legal framework since 2008 to allow its economic sectors to engage in ETS and minimize emissions. Yet, selecting the appropriate sectors and effectively adjusting sector-specific regulations remain critical and complex challenges in the global design of ETS since both excessive and insufficient intervention can lead to inefficiencies in the system's functioning. Therefore, this study begins validating the NZ ETS's abatement potential regarding sectoral carbon intensity by executing the double machine learning techniques, consolidating the ETS efficacy that has robustly mitigated sectoral carbon intensity in NZ during 2006-2020. However, this conclusion seems invalid at the disaggregated level when focusing on forward-backward linkages, where NZ's input-output tables furnish a compelling scenario of sectoral dependencies and the products (residuals) they provide. Altogether, the regulatory requirements are either too strict or too lax, leaving out five of the 24 (as a whole) key sectors. Rather, the ETS could be powerful, providing these five key sectors are well tackled, necessitating a reformulation of the ongoing ETS regulatory regime.

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Understanding the significance of financial clustering in the context of green development holds immense importance for China as it strives towards achieving high-quality green development. Using a balanced panel dataset encompassing China's 283 cities from 2009 to 2020, we aim to explore the impact of financial clustering on green development from both linear and nonlinear perspectives. Empirical evidence suggests that when the level of financial clustering increases by 1%, the city-level green development increases by 0.1012%. A mediation effect model certifies that there are three essential channels through which financial clustering robustly boosts green development: technical, structural and scale effects. Subsequently, a novel program handling endogeneity is designed and verifies the nonlinear nexus between financial clustering and green development. Moreover, the spatial Durbin model demonstrates that financial clustering significantly sustains local green development, despite its relatively weak spill over effects. Heterogeneity analysis presents that the promoting effect is particularly predominant in Central China, as well as in cities characterized by high levels of financial clustering and large population sizes.

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In the context of globalization, the role of the digital economy in carbon emissions may generate spatial spill over effects. This study comprehensively applies a spatial model to understand the nexus between the digital economy and carbon emissions in 67 economies from 2010 to 2019. Specifically, this study contributes by introducing a spatial panel threshold model, which helps to present the new evidence regarding decarbonization process. Empirical findings exemplify that the digital economy remarkably reduces local carbon emissions, with the positive spatial spill over effects being salient. The spatial moderating effect model uncover that globalization positively affects the nexus between the digital economy and carbon emissions. Interestingly, the spatial panel threshold model designates that the digital economy's reduction effect on local carbon emissions will be tightened, whereas the positive spatial spill over effects turn negative only when globalization surpasses a threshold. Our model has the potential to explain some results that traditional models cannot reach.

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BACKGROUND: Ruscogenin (Rus), a steroidal sapogenin extracted from Ophiopogon japonicus (L. f.) Ker-Gawl., has the effect of alleviating cerebral ischemia-reperfusion injury (IRI), acute lung injury. At present, the chronopharmacological effects of Rus are still unknown. PURPOSE: This study explored the alleviating effect and mechanism of Rus timing administration on mice cerebral IRI. METHODS: The animals in different groups were administrated Rus (10 mg/kg) by gavage at four time points (23:00-01:00, 05:00-07:00, 11:00-13:00, 17:00-19:00) respectively for 3 days. On the 4th day, middle cerebral artery occlusion (MCAO) surgery was operated during 5:00-7:00. Behavioral tests were executed and the brain was collected for infarct volume, qPCR and immunoblot detection. The levels of tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), interleukin-1beta (IL-1ß) and inducible nitric oxide synthase (iNOS) were detected by qPCR. Glutathione (GSH), superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in serum and cerebral cortex were detected. The clock genes were tested by western blot. Based on these results, 17:00-19:00 was selected to administrate Rus for further mechanism study and Nrf2 blocker group was administrated all-trans-retinoic acid (ATRA) at 14:00 for 3 days. RESULTS: Administration of Rus reduced cerebral infarcted volume, ameliorated the behavior score and upregulated the mRNA and protein expression of Per1, Bmal1, Clock, Rev-erbα, transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), quinone oxidoreductase 1 (NQO1). Administration of Rus during 17:00-19:00 had better preventive effect than other three time points. Combined administration of ATRA blunted the preventive effect of Rus. CONCLUSION: The preventive effect of Rus is affected by the time of administration, which was regulated by Nrf2 pathway. Taken together, we provide solid evidence to suggest that different administration time point affect the effectiveness of Rus in alleviating IRI.

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Backgrounds: The circadian clock protein Rev-erbα is a crucial regulator of circadian rhythms that affects multiple molecular, cellular, and physiology pathways that control susceptibility, injury, and recovery in the neurological disorders. Emerging evidence suggest that Rev-erbα plays a key role in the inflammation and oxidative stress, two pivotal mechanisms in the pathogenesis, progression, and recovery process of ischemic stroke. However, it remains inconclusive whether Rev-erbα activation is protective against ischemic brain damage. Nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, a master regulator of inflammatory and oxidative responses. Our study aimed to determine whether pharmacological activation of Rev-erbα by SR9009 protects against acute ischemic brain damage partly via Nrf2 pathway. Methods: Adult mice were pretreated with SR9009 or Nrf2 inhibitor all-trans-retinoic acid (ATRA) for 3 days prior to Sham or middle cerebral artery occlusion (MCAO) operation. After ischemia for 1 h and reperfusion for 24 h, the neurological function and cerebral infarction volume were determined, superoxide dismutase (SOD) activity, malondialdehyde (MDA) content and glutathione peroxidase (GSH-PX) activity in serum were detected by kit. The mRNA and/or protein level of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), inducible nitric oxide synthase (iNOS), Period (Per)1, Brain and muscle arnt-like1 (Bmal1), Circadian locomotor output cycles kaput (Clock), Rev-erbα, Nrf2, heme oxygenase-1 (HO-1) and quinone oxidoreductase 1 (NQO1) in cerebral cortex were detected by q-PCR and Western blot. Results: We confirmed that SR9009 activated Rev-erbα gene in the cerebral cortex under basal condition. At 24 h after reperfusion, SR9009 ameliorated acute neurological deficits, reduced infarct volume. Meanwhile, the inflammatory TNF-α, IL-1ß, iNOS and MDA content levels were significant decreased, SOD and GSH-PX activity were obviously increased, which were markedly blunted (or abolished) by ATRA. SR9009 enhanced the induction of Nrf2 and its downstream target genes HO-1 and NQO1 after ischemic insult. In addition, we found that SR9009 restored Rev-erbα, Bmal1, Clock, Per1 genes expression in the cerebral cortex under ischemic condition. Conclusion: Taken together, Rev-erbα activation by SR9009 protects against ischemic stroke damage, at least, partly through Nrf2 pathway.

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Based on an extended STIRPAT framework, this paper investigates the effects of financial development on carbon emission intensity in OECD countries from linear and non-linear perspectives, where financial development is proxied by three dimensions: financial deepening, financial deepening, and financial size, and financial efficiency. Fortunately, three types of financial development significantly alleviate carbon emission intensity. An extended moderation effect model is built to estimate the effect of financial development via information and communication technology on carbon emission intensity. The results reveal that internet-based information and communication technology and service-based information and communication technology are positively correlated with carbon emission intensity. To effectively handle the endogeneity issue triggered by causal relationships between variables and allow potential non-linear nexus, an advanced dynamic panel threshold model incorporating the generalised method of moments is employed to investigate how financial development affects carbon emission intensity under different types of information and communication technology. Empirical evidence demonstrates the significance of the non-linear nexus between financial development and carbon emission intensity. Lastly, heterogeneity analysis demonstrates the existence of heterogeneity associated with institutional quality, degree of economic development, and resource endowment concerning the effect of financial development on carbon emission intensity among the OECD countries.

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Public transportation is often considered as a green travel mode to alleviate the negative externalities such as traffic congestion and haze pollution generated from transport. However, is prioritizing urban public transportation actually conducive to haze emission reduction? In this study, considering special emphasis on the cumulative effect of haze, a dynamic panel model is constructed to analyze and quantify the impact of public transportation on haze pollution by using the data of 284 cities in China, and the heterogeneity of the impact in cities with different pollution levels is examined. Several interesting findings are derived from the empirical results. First, the development of urban public transportation can significantly alleviate urban haze pollution. Second, the haze reduction effect of public transportation in cities with different pollution levels is non-universal. Comparatively speaking, the haze reduction effect of public transportation in lightly polluted cities is more evident than that in heavily polluted cities. Therefore, in order to reduce haze pollution in a more effective manner, China should continue to promote urban public transportation priority strategy. Moreover, the government should also formulate differentiated traffic development strategies to effectively alleviate the urban traffic burdens.

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OBJECTIVES: The study explores the protective role of the peripheral serum of limb remote ischemic postconditioning (LRIP) in reducing the reactive oxygen species (ROS) levels and neutrophil activation, which are responsible for the deleterious reperfusion injury. METHODS: LRIP was induced in Sprague-Dawley rats by three cycles of 5 min occlusion /5 min reperfusion on the left hind limb. The blood samples were collected before LRIP or 0 and 1 h after LRIP (named SerumSham, SerumLRIP0, SerumLRIP1, respectively). The effects of LRIP serum on ROS level and neutrophils activation were determined. The expression of MyD88-TRAF6-MAPKs and PI3K/AKT pathways in neutrophils were examined. RESULTS: When compared with SerumSham, SerumLRIP0 and SerumLRIP1 significantly reduced the ROS released from neutrophils activated by fMLP. Meanwhile, the mRNA expression levels of NADPH oxidase subunit p22phox and multiple ROS-producing related key proteins, such as NADPH oxidase subunit p47phox ser 304, ser 345. MyD88, p-ERK, p-JNK and p-P38 expression of neutrophils were downregulated by SerumLRIP0 and SerumLRIP1. SerumLRIP1 also downregulated p47phox mRNA expression and tumor necrosis factor receptor-associated factor 6 (TRAF6) protein expression. CONCLUSION: LRIP serum protects against ROS level and neutrophils activation involving the MyD88-TRAF6-MAPKs. This finding provides new insight into the understanding of LRIP mechanisms.

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