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Purposes In the in-situ mining of oil shale, poor heat transfer efficiency and pronounced anisotropic differences present challenges. Methods In this study, standard samples from Xinjiang's Barikun oil shale are adopted to explore heat transfer variations in horizontal and vertical bedding at different temperatures through indoor experiments, and in-situ mining simulation was conducted. Findings The experimental results show that: 1) With the increase of temperature, the heat conduction coefficient of each bedding direction shows a "decreasing" trend, but the heat conduction coefficient of parallel bedding direction is greater than that of vertical bedding direction; 2) With the increase of temperature, the specific heat capacity first increases and then decreases. When the temperature is 400 ℃, the specific heat capacity is the maximum; 3) Combined with the micro-CT image, with the increase of temperature, the influence of increasing cracks on the heat conduction in the vertical bedding direction is greater than that in the parallel bedding direction. On the basis of the above experimental parameters, the "heat-solid" coupling model of in-situ electric heating of oil shale reservoir is established by COMSOL software. The simulation results show that: With the increase of heating time, anisotropic heat transfer difference gradually appears. When heating duration reaches 600 d, the heat transfer area in parallel bedding direction is obviously larger than that in vertical bedding direction, showing an "ellipse" shape. When heating duration reaches 1 440 d, the heat transfer area increases slightly, and the pyrolysis of the shale in the heating well control area is basically completed.

Abstract Background How physical activity (PA) and different sleep traits and overall sleep pattern interact in the development of Parkinson’s disease (PD) remain unknown. Objective To prospectively investigate the joint associations of PA and sleep pattern with risk of PD. Methods Included were 339,666 PD-free participants from the UK Biobank. Baseline PA levels were grouped into low (

Abstract Apoptosis releases numerous apoptotic vesicles that regulate processes such as cell proliferation, immunity, and tissue regeneration and repair. Now, it has also emerged as an attractive candidate for biotherapeutics. However, apoptotic vesicles encompass a diverse range of subtypes, and it remains unclear which specific subtypes play a pivotal role. In this study, we successfully isolated different apoptotic vesicle subtypes based on their sizes and characterized them using NTA and TEM techniques, respectively. We compared the functional variances among the distinct subtypes of apoptotic vesicles in terms of stem cell proliferation, migration, and differentiation, as well as for endothelial cell and macrophage function, effectively identifying subtypes that exhibit discernible functional differences. ApoSEV (with diameter 1000 nm) played the opposite effect on cell function and tissue regeneration. Lastly, employing protein analysis and gene sequencing techniques, we elucidated the intrinsic mechanisms underlying these differences between different subtypes of apoEVs. Collectively, this study identified that apoptotic vesicle subtypes possessed distinct bio‐functions in regulating stem cell function and behaviour and modulating tissue regeneration, which primarily attribute to the distinct profiling of protein and mRNA in different subtypes. This comprehensive analysis of specific subtypes of apoEVs would provide novel insights for potential therapeutic applications in cell biology and tissue regeneration.

As a new type of economic format, digital economy has three major characteristics: technical, innovative, energy-saving and environmentally friendly. Acting on various sectors of the national economy, it is beneficial for improving carbon emission efficiency and is of great significance for achieving China's two major goals of carbon peak and carbon neutrality. Firstly, theoretical analysis of the impact mechanism of digital economy on carbon emission efficiency, proposing research hypotheses on the direct effect, mediating effect, and spatial effect of digital economy on carbon emission efficiency. Secondly, based on panel data from 279 cities in China from 2011 to 2020, the econometric models are constructed to empirically analyze the direct, mediating, and spatial effects of digital economy on carbon emission efficiency. The results show that: 1) Digital economy can improve carbon emission efficiency; 2) The impact of digital economy on carbon emission efficiency has a "U"-shaped relationship, which is consistent with the "Environmental Kuznets Curve" hypothesis; 3) The impacts of digital economy on carbon emission efficiency exist in urban heterogeneity, specifically manifested as regional heterogeneity and urban scale heterogeneity; 4) Technological innovation is an important mediator for improving carbon emission efficiency in digital economy, and promoting technological innovation in digital economy can improve carbon emission efficiency; 5) Digital economy has spatial effect on carbon emission efficiency, which can improve the carbon emission efficiency of neighboring cities. Finally, based on the above results, suggestions are proposed from three aspects: promoting important industries and key areas for deep cultivation of carbon emission in digital economy, emphasizing regional balance in the development of digital economy, and strengthening regional cooperation in the development of digital economy, in order to continue to play a positive role in improving carbon emission efficiency through digital economy.

With the high pervasiveness of viral diseases, the battle against viruses has never ceased. Here we discuss five cellular processes, namely “autophagy”, “programmed cell death”, “immune response”, “cell cycle alteration”, and “lipid metabolic reprogramming”, that considerably guide viral replication after host infection in an orchestrated manner. On viral infection, “autophagy” and “programmed cell death” are two dynamically synchronized cell survival programs; “immune response” is a cell defense program typically suppressed by viruses; “cell cycle alteration” and “lipid metabolic reprogramming” are two altered cell housekeeping programs tunable in both directions. We emphasize on their functionalities in modulating viral replication, strategies viruses have evolved to tune these processes for their benefit, and how these processes orchestrate and govern cell fate upon viral infection. Understanding how viruses hijack host networks has both academic and industrial values in providing insights toward therapeutic strategy design for viral disease control, offering useful information in applications that aim to use viral vectors to improve human health such as gene therapy, and providing guidelines to maximize viral particle yield for improved vaccine production at a reduced cost.

Canine parvovirus (CPV) has been used in cancer control as a drug delivery vehicle or anti-tumor reagent due to its multiple natural advantages. However, potential host cell cycle arrest induced by virus infection may impose a big challenge to CPV associated cancer control as it could prevent host cancer cells from undergoing cell lysis and foster them regain viability once the virotherapy was ceased. To explore CPV-induced cell cycle arrest and the underlying mechanism toward improved virotherapeutic design, we focus on epidermal growth factor receptor (EGFR), a cellular receptor interacting with TfR that mediates CPV-host interactions, and alterations on its tyrosine phosphorylation sites in response to CPV infection. We found that CPV could trigger host G1/S cell cycle arrest via the EGFR (Y1086)/p27 and EGFR (Y1068)/STAT3/cyclin D1 axes, and EGFR inhibitor could not reverse this process. Our results contribute to our understandings on the mechanism of CPV-induced host cellular response and can be used in the onco-therapeutic design utilizing CPV by preventing host cancer cells from entering cell cycle arrest.

Fatty acyl reductase (FAR) is a crucial enzyme that catalyzes the NADPH-dependent reduction of fatty acyl-CoA or acyl-ACP substrates to primary fatty alcohols, which in turn acts as intermediate metabolites or metabolic end products to participate in the formation of plant extracellular lipid protective barriers (e.g., cuticular wax, sporopollenin, suberin, and taproot wax). FARs are widely present across plant evolution processes and play conserved roles during lipid synthesis. In this review, we provide a comprehensive view of FAR family enzymes, including phylogenetic analysis, conserved structural domains, substrate specificity, subcellular localization, tissue-specific expression patterns, their varied functions in lipid biosynthesis, and the regulation mechanism of FAR activity. Finally, we pose several questions to be addressed, such as the roles of FARs in tryphine, the interactions between transcription factors (TFs) and FARs in various environments, and the identification of post-transcriptional, translational, and post-translational regulators.