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Alzheimer's disease (AD) is the leading cause of dementia and presents a considerable disease burden. Its pathology involves substantial neuronal loss, primarily attributed to neuronal apoptosis. Although sirtuin 4 (SIRT4) has been implicated in regulating apoptosis in various diseases, the role of SIRT4 in AD pathology remains unclear. The study used APP/PS1 mice as an animal model of AD and amyloid-β (Aβ)1-42-treated HT-22 cells as an AD cell model. SIRT4 expression was determined by quantitative real-time polymerase chain reaction, Western blot, and immunofluorescence. A Sirt4 knockdown model was established by intracranial injection of lentivirus-packaged sh-SIRT4 and cellular lentivirus transfection. Immunohistochemistry and flow cytometry were used to examine Aβ deposition in mice and apoptosis, respectively. Protein expression was assessed by Western blot analysis. The UCSC and JASPAR databases were used to predict upstream transcription factors of Sirt4. Subsequently, the binding of transcription factors to Sirt4 was analyzed using a dual-luciferase assay and chromatin immunoprecipitation. SIRT4 expression was upregulated in both APP/PS1 mice and Aβ-treated HT-22 cells compared with their respective control groups. Sirt4 knockdown in animal and cellular models of AD resulted in reduced apoptosis, decreased Aβ deposition, and amelioration of learning and memory impairments in mice. Mechanistically, SIRT4 modulates apoptosis via the mTOR pathway and is negatively regulated by the transcription factor signal transducer and activator of transcription 2 (STAT2). Our study findings suggest that targeting the STAT2-SIRT4-mTOR axis may offer a new treatment approach for AD. NEW & NOTEWORTHY: The study reveals that in Alzheimer's disease models, SIRT4 expression increases, contributing to neuronal apoptosis and amyloid-β deposition. Reducing SIRT4 lessens apoptosis and amyloid-β accumulation, improving memory in mice. This process involves the mTOR pathway, regulated by STAT2 transcription factor. These findings suggest targeting the STAT2-SIRT4-mTOR axis as a potential Alzheimer's treatment strategy. [ABSTRACT FROM AUTHOR]

This paper takes the risk preference of modern listed companies as the research object, uses the financial data of Chinese listed companies combined with the literary inquisition file in Qing Dynasty to conduct an empirical study, and examines the influence of literary inquisition on the risk preference of modern corporate CEOs in Qing Dynasty. The study found that the literary inquisition incident in Qing Dynasty significantly affected and reduced the risk preference of modern enterprises. The competitive hypothesis of the influence of Confucian culture and China City Commercial Credit Environment Index (CEI) on CEOs' risk preference is excluded. In addition, through the study of heterogeneity, this paper also verifies that the influence of literary inquisition is more significant in areas with a higher degree of marketization, indicating that the influence of informal institutions depends on the establishment of formal institutions. Finally, in the mechanism study, this paper points out that the rulers' suppression of ideas will change long-term social capital and lead to the decrease of general trust in society, which will make the enterprise managers born in the region tend to be conservative in their risk preference. [ABSTRACT FROM AUTHOR]

As a result of high energy consumption and pollution from energy-intensive industries, the Chinese government has implemented a series of policies. A comprehensive assessment of these policies is necessary to guide the green transformation and upgrading of the industry, however, little research has been conducted on this issue. This article takes China's economic policy uncertainty (EPU) Index as a comprehensive and continuous policy shock and investigates the impact of EPU on the financial performance of energy-intensive firms. Based on 289 listed energy-intensive companies from 2003 to 2018, we find that EPU negatively affects the financial performance of firms, and the negative effect is robust after replacing the dependent variable and endogenous discussion. Further, the negative impacts are more pronounced for midwestern, non-SOE firms, as well as ferrous metal and chemical product manufacturers. Moreover, our results indicate that the negative impact of EPU on performance is mitigated for firms with high cash holdings and low debt ratios. [ABSTRACT FROM AUTHOR]

Chrysotile asbestos has excellent physical and chemical properties, but its high biotoxicity is very damaging to human health, due to its durability, high aspect ratio, and the exist of iron. By simple chemical treatment of chrysotile asbestos, silicon oxide nanofibers rich in hydroxyl groups on the surface can be prepared.

The nervous system possesses the remarkable ability to undergo changes in order to store information; however, it is also susceptible to damage caused by invading pathogens or neurodegenerative processes. As a member of nucleotide-binding oligomerization domain-like receptor (NLR) family, the NLRP6 inflammasome serves as a cytoplasmic innate immune sensor responsible for detecting microbe-associated molecular patterns. Upon activation, NLRP6 can recruit the adapter protein apoptosis-associated speck-like protein (ASC) and the inflammatory factors caspase-1 or caspase-11. Consequently, inflammasomes are formed, facilitating the maturation and secretion of pro-inflammatory cytokines such as inflammatory factors-18 (IL-18) and inflammatory factors-1β (IL-1β). Precise regulation of NLRP6 is crucial for maintaining tissue homeostasis, as dysregulated inflammasome activation can contribute to the development of various diseases. Furthermore, NLRP6 may also play a role in the regulation of extraintestinal diseases. In cells of the brain, such as astrocytes and neurons, NLRP6 inflammasome are also present. Here, the assembly and subsequent activation of caspase-1 mediated by NLRP6 contribute to disease progression. This review aims to discuss the structure and function of NLRP6, explain clearly the mechanisms that induce and activate NLRP6, and explore its role within the central and peripheral nervous system. [ABSTRACT FROM AUTHOR]

Recently, the World Health Organization noted the increasing signs of pandemic fatigue around the world and repeatedly warned the public to continue to stay cautious. The current study explores whether social media use plays a role in the formation and development of pandemic fatigue. Drawing on a survey of 849 social media users in China, the findings indicated that different social media behaviors play different roles in affecting pandemic fatigue. Specifically, social interaction use is negatively associated with pandemic fatigue, mediated by more social support and reduced hopelessness. Active content use contributes to pandemic fatigue development, an association explained by information overload and desensitization. Notably, passive content use is found to trigger reactance but is negatively associated with pandemic fatigue, which is fully mediated by reduced information overload. This study seeks to understand how pandemic fatigue is associated with social media use and to explicate the underlying mechanism. The implications of the findings and directions for future research are discussed. [ABSTRACT FROM AUTHOR]