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As the global economic landscape evolves, the low technological content and persistent lack of international competitiveness in China’s manufacturing exports have become increasingly apparent, underscoring the urgent need for a transition from “quantity” to “quality” in the sector. Administrative approval reform, a key pillar of institutional innovation in the new era, plays a critical role in enhancing the technological complexity of manufacturing exports and strengthening international competitiveness. Using data from 2001 to 2013, this study investigates the impact of administrative approval reform on the technological complexity of manufacturing exports and explores its underlying mechanisms from both theoretical and empirical perspectives. Theoretical model analysis suggests that administrative approval reform effectively increases technological complexity by reducing the marginal and fixed costs associated with adjusting product complexity. Empirical findings provide robust evidence that administrative approval reform significantly enhances technological complexity, with results holding across various sensitivity tests. At the micro level, the reduction of institutional transaction costs emerges as a key channel through which the reform exerts its impact. Additionally, increasing investment in research and development, fixed assets, and technological innovation are identified as critical pathways influencing technological complexity. The reform’s effects are particularly pronounced for non-state-owned enterprises and firms located in coastal and port cities, as revealed by a heterogeneity analysis. Furthermore, a decomposition of city-level export technological complexity using the DOP method shows that improved inter-firm resource allocation—by shifting market share from firms with lower technological complexity to those with higher technological complexity—serves as the primary mechanism driving the observed improvements at the city level. This study contributes to the literature by providing empirical evidence on the role of administrative approval reform in fostering the technological upgrading of manufacturing exports, highlighting its differentiated impact across firm types and regions. The findings offer valuable insights for policymakers seeking to enhance the technological complexity and international competitiveness of manufacturing exports in China.

Caspase-mediated cleavage of gasdermin D, previously shown to mediate pyroptosis, acts by inducing oligomerization and pore formation in cell membranes. Gasdermin-induced cell death Pyroptosis, an inflammatory form of programmed cell death that is part of the innate immune response, is triggered by caspase-mediated cleavage of the inflammasome protein gasdermin D. Judy Lieberman and colleagues examine the underlying molecular mechanism for gasdermin functioning in pyroptosis. They present evidence that caspase 11 cleavage of gasdermin D, previously shown to mediate pyroptosis, induces oligomerization of the N-terminal domain and pore formation. Also in this issue of Nature , Feng Shao and colleagues show that the N-terminal domains of gasdermins D, A and A3 are cytotoxic because they disrupt cell membranes in both mammalian cells and artificially transformed bacteria through the formation of membrane pores. Inflammatory caspases (caspases 1, 4, 5 and 11) are activated in response to microbial infection and danger signals. When activated, they cleave mouse and human gasdermin D (GSDMD) after Asp276 and Asp275, respectively, to generate an N-terminal cleavage product (GSDMD-NT) that triggers inflammatory death (pyroptosis) and release of inflammatory cytokines such as interleukin-1β 1 , 2 . Cleavage removes the C-terminal fragment (GSDMD-CT), which is thought to fold back on GSDMD-NT to inhibit its activation. However, how GSDMD-NT causes cell death is unknown. Here we show that GSDMD-NT oligomerizes in membranes to form pores that are visible by electron microscopy. GSDMD-NT binds to phosphatidylinositol phosphates and phosphatidylserine (restricted to the cell membrane inner leaflet) and cardiolipin (present in the inner and outer leaflets of bacterial membranes). Mutation of four evolutionarily conserved basic residues blocks GSDMD-NT oligomerization, membrane binding, pore formation and pyroptosis. Because of its lipid-binding preferences, GSDMD-NT kills from within the cell, but does not harm neighbouring mammalian cells when it is released during pyroptosis. GSDMD-NT also kills cell-free bacteria in vitro and may have a direct bactericidal effect within the cytosol of host cells, but the importance of direct bacterial killing in controlling in vivo infection remains to be determined.

Based on the vertical connection between upstream and downstream industries, a unique theoretical model is constructed to analyse the impact mechanism of the opening of producer services on downstream manufacturing wage growth. The empirical tests are carried out using the data of China’s manufacturing listed companies from 1999 to 2020. Our findings indicate that the opening of producer services has an inverted-U-shaped impact on downstream manufacturing wage growth, and the average level of the opening of producer services in the sample period is lower than the corresponding threshold. Overall, it is in the stage of promoting the wage growth of the downstream manufacturing industry. The opening of producer services mainly affects the wage growth of the downstream manufacturing industry through two channels: labour productivity and labour income share. The results of heterogeneity analysis show that the wages of capital and technology-intensive and low-competitive manufacturing industries are relatively strongly promoted by the opening of producer services. Therefore, promoting the orderly opening of producer services and strengthening the technological links between industries will help promote the wage growth of downstream manufacturing industries.

Background People who have experienced the Chinese Great Famine (1959–1961) in their fetal period are getting old. It is particularly important for China’s response to the ageing of this cohort to study the impact of the Holodomor on disability. Method This paper presents an empirical analysis that utilizes the survey data from the 2018 China Health and Retirement Longitudinal Study (CHARLS), employing a cohort Difference-in-Differences (DID) modeling approach. It integrates the excess mortality rate (EDR) from China’s Great Famine with the 2018 CHARLS survey data, selecting suitable control and experimental groups for a comprehensive study. The empirical analysis is conducted using the cohort DID model, comprising a total of 11,567 samples. Results This study found that the experience of famine would increase the level of disability in the population, with each 0.1% increase in excess mortality increasing the level of IADL by approximately 0.019. This experience during the fetal period will increase the incidence of handicaps, mainly in the brain and hearing. This thesis finds strong heterogeneity across gender and between urban and rural areas. Conclusions China’s long-term care capacity should be improved, with attention paid to the rural disabled population and to the health of pregnant women and fetuses.

Gasdermins, a family of five pore-forming proteins (GSDMA–GSDME) in humans expressed predominantly in the skin, mucosa and immune sentinel cells, are key executioners of inflammatory cell death (pyroptosis), which recruits immune cells to infection sites and promotes protective immunity 1 , 2 . Pore formation is triggered by gasdermin cleavage 1 , 2 . Although the proteases that activate GSDMB, C, D and E have been identified, how GSDMA—the dominant gasdermin in the skin—is activated, remains unknown. Streptococcus pyogenes , also known as group A Streptococcus (GAS), is a major skin pathogen that causes substantial morbidity and mortality worldwide 3 . Here we show that the GAS cysteine protease SpeB virulence factor triggers keratinocyte pyroptosis by cleaving GSDMA after Gln246, unleashing an active N-terminal fragment that triggers pyroptosis. Gsdma1 genetic deficiency blunts mouse immune responses to GAS, resulting in uncontrolled bacterial dissemination and death. GSDMA acts as both a sensor and substrate of GAS SpeB and as an effector to trigger pyroptosis, adding a simple one-molecule mechanism for host recognition and control of virulence of a dangerous microbial pathogen. The Streptococcus pyogenes virulence factor SpeB triggers pyroptosis in keratinocytes by catalysing cleavage of host gasdermin A, a key event triggering the immune response to S. pyogenes infection.

Cytosolic sensing of pathogens and damage by myeloid and barrier epithelial cells assembles large complexes called inflammasomes, which activate inflammatory caspases to process cytokines (IL-1β) and gasdermin D (GSDMD). Cleaved GSDMD forms membrane pores, leading to cytokine release and inflammatory cell death (pyroptosis). Inhibiting GSDMD is an attractive strategy to curb inflammation. Here we identify disulfiram, a drug for treating alcohol addiction, as an inhibitor of pore formation by GSDMD but not other members of the GSDM family. Disulfiram blocks pyroptosis and cytokine release in cells and lipopolysaccharide-induced septic death in mice. At nanomolar concentration, disulfiram covalently modifies human/mouse Cys191/Cys192 in GSDMD to block pore formation. Disulfiram still allows IL-1β and GSDMD processing, but abrogates pore formation, thereby preventing IL-1β release and pyroptosis. The role of disulfiram in inhibiting GSDMD provides new therapeutic indications for repurposing this safe drug to counteract inflammation, which contributes to many human diseases. Disulfiram is an FDA-approved drug for treating alcoholism. Wu and colleagues show that disulfiram can be repurposed to efficiently inhibit pyroptosis by specifically blocking gasdermin-mediated pore formation.

Efficient extraction of uranium from seawater is expected to provide virtually infinite fuel sources to power nuclear reactors and thus enable sustainable development of nuclear energy. The extraction efficiency for uranium greatly depends on the availability of active adsorption sites on the adsorbents. Maximization of the utilization rate of the binding sites in the adsorbent is vital for improving adsorption capacity. Herein, micro-redox reactors functioned by Cu(I)/Cu(II) conversion are constructed internally in an adsorbent bearing both amidoxime and carboxyl groups to induce active regeneration of the inactivated binding sites to enhance uranium capture. This adsorbent has high adsorption capacity (962.40 mg-U/g-Ads), superior anti-fouling ability as well as excellent uranium uptake (14.62 mg-U/g-Ads) in natural seawater after 56 days, placing it at the top of high-performance sorbent materials for uranium harvest from seawater. Extraction of uranium from seawater could help with sustainable development of nuclear energy. Here the authors incorporated Cu(I)/Cu(II) microredox reactors in a seaweed-like adsorbent to enhance uranium capture by taking advantage of its adsorption and reduction effects.

MicroRNA-34a (miR-34a) was closely associated with liver steatosis. However, the link between changes in miR-34a and the progression of liver steatosis remained unclear. In the work, sixty mice were randomly and equally selected into six groups: normal control group (NC), normal exercise group (NE), high-fat diet group (HFD), high-fat diet plus exercise group (HFE), miR-34a overexpression group (OE), and miR-34a overexpression plus exercise group (OEE). Live morphology showed that treadmill exercise intervention for 8 weeks reduced high-fat diet-induced liver steatosis in mice. 8-week treadmill exercise directly decreased mir-34a expression of mice in HFD group, confirmed in OE group. More, treadmill exercise enhanced the expression of PPARα and SIRT1, thereby affecting the downstream hepatic steatosis-associated target genes, including CPT1(Carnitine palmitoyltransferase 1), CPT2(Carnitine palmitoyltransferase 2), SLC27A1(Solute carrier family 27 member 1), SLC27A4(Solute carrier family 27 member 4), in addition to activating the expression of the central metabolic sensor AMPK. Following aerobic exercise intervention, miR-34a was downregulated, thereby affecting the expression of genes associated with hepatic steatosis, and this mechanism was confirmed in miR-34a overexpression mice. This study contributed to our understanding of the pathogenesis of hepatic steatosis and may provide new therapeutic approaches.

With an increasing number of heterogeneous shareholders participating in corporate governance in reality, the assumption of shareholder homogeneity in agency theory is gradually relaxing in the modern field of corporate governance. The policy of mixed ownership reform in China provides empirical evidence for studying heterogeneous shareholder governance. To fully understand the governance effects of non-state shareholders, we employ the ownership proportion held by non-state shareholders among the top ten shareholders and the appointment of directors as measures for non-state shareholder governance. Using a panel fixed-effect model from the perspective of state-owned enterprises (SOEs) party organizations, we examine the impact of non-state shareholder governance on the governance level of SOEs. The study reveals that non-state shareholder governance positively affects the governance level of SOEs, with board resolutions playing a crucial role in this relationship. When party members serve as directors, the governance effect of non-state shareholders is more significant. Based on the aforementioned research findings, we recommend further refining corporate governance measures for SOEs within the context of SOE reforms. It is advisable to optimize the party organizational governance structure and leverage the synergistic effects of non-state shareholder governance and party organizational governance. Advancing reforms along the Pareto improvement path will contribute to establishing a distinctive corporate governance system for Chinese SOEs.

Animal husbandry is a vital sector in China’s agriculture sector, contributing to over one-third of its agricultural output, and more than 40% of farmers’ income. However, this industry is vulnerable to risks arising from production and operation, such as disease outbreaks, natural disasters, and market fluctuations. Livestock insurance can help mitigate these risks, but the lack of reliable data on shed environments has hindered its effectiveness. The objective of this study is to propose a livestock shed environmental regulatory platform that utilizes blockchain and the Internet of Things to ensure data authenticity, real-time monitoring, and transparency in the regulatory process. The platform also automates the insurance process, reducing costs and improving efficiency. The proposed platform employs blockchain to ensure data authenticity and devices to monitor and collect real-time environmental data. It also utilizes smart contracts to automate the insurance process, from negotiating and signing contracts to making insurance claims. The system’s design rationale, architecture, and implementation are detailed. The proposed platform has been implemented and currently manages over 300,000 livestock animals with more than 350,000 insurance contracts signed. The use of blockchain and the Internet of Things has ensured data authenticity, real-time monitoring, and transparency in the regulatory process, while the automation of the insurance process has reduced costs and improved efficiency. The proposed livestock shed environmental regulatory platform has the potential to improve the effectiveness of livestock insurance in China by addressing the critical issue of data reliability. The use of blockchain and the Internet of Things has enabled real-time monitoring, data authenticity, and transparency in the regulatory process, while the automation of the insurance process has improved efficiency and reduced costs. This platform could serve as a model for other countries looking to improve the effectiveness of their livestock insurance programs.