Employing the "Green Credit Guidelines" implemented in 2012 as the basis for a quasi-natural experiment, this study applies the method of Difference-in-Differences(DID) to investigate the influence ...of the Green Credit Policy on both the quantity and quality of enterprise innovation. The outcomes of our analysis reveal that the policy has significantly boosted both the quantity and quality of innovation among enterprises identified as heavy polluters. It is noteworthy that the policy's positive impact on innovation quantity surpasses its positive effect on innovation quality. This substantiates that the Green Credit Policy effectively generates incentivizing outcomes for innovation among the heavy polluters, thereby verifying Porter's hypothesis within the domain of green credit in China. Furthermore, we find that the positive impact is more significant for enterprises with lower innovation capabilities, large-scale enterprises, state-owned enterprises, and those situated in both the Eastern and Western regions. Through these findings, this study illuminates a novel perspective on the interplay between the Green Credit Policy and enterprise innovation dynamics in China.
With the improvement of the requirements for lightweight automobiles, the research and development of a higher Al content of TRIP steel have received extensive attention. However, Al in molten steel ...is easy to react with SiO2 in mold slag, which is one of the restrictive factors of high Al-TRIP steel continuous casting quality control. Applying the double-film mass transfer theory, combined with the slag-steel reaction equilibrium test, a dynamic equilibrium model is established, and the crystalline phases composition before and after the reaction is analyzed. The results show that the melting process of mold flux samples A and B is uniform and meets the continuous casting control temperature. The main components of the two mold flux samples changed rapidly within 10 minutes of the initial reaction. When the reaction progressed to 20 minutes, the composition of the two mold flux samples had no obvious change trend, and the slag-steel reaction reached equilibrium. The main precipitated crystalline phases of the mold flux sample are LiAlO2, Ca3(BO3)2, NaAlO2, ZrO2, and CaZrO3 crystals. Mold slag A identified the mass transfer of Al in the steel as the limiting part of the reaction, while mold slag B identified the mass transfer of SiO2 in the slag as the limiting part of the reaction.
Cardiac hypertrophy is a major predictor of heart failure and a prevalent disorder with high mortality. Little is known, however, regarding mechanisms governing the transition from stable cardiac ...hypertrophy to decompensated heart failure. Here, we tested the role of autophagy, a conserved pathway mediating bulk degradation of long-lived proteins and cellular organelles that can lead to cell death. To quantify autophagic activity, we engineered a line of "autophagy reporter" mice and confirmed that cardiomyocyte autophagy can be induced by short-term nutrient deprivation in vivo. Pressure overload induced by aortic banding induced heart failure and greatly increased cardiac autophagy. Load-induced autophagic activity peaked at 48 hours and remained significantly elevated for at least 3 weeks. In addition, autophagic activity was not spatially homogeneous but rather was seen at particularly high levels in basal septum. Heterozygous disruption of the gene coding for Beclin 1, a protein required for early autophagosome formation, decreased cardiomyocyte autophagy and diminished pathological remodeling induced by severe pressure stress. Conversely, Beclin 1 overexpression heightened autophagic activity and accentuated pathological remodeling. Taken together, these findings implicate autophagy in the pathogenesis of load-induced heart failure and suggest it may be a target for novel therapeutic intervention.
Macroautophagy (hereafter termed autophagy) is a highly evolutionarily conserved pathway
that degrades intracellular components such as damaged organelles in lysosome. Autophagy occurs
at low basal ...levels in virtually all types of cells, which is required for the maintenance of cellular
homeostasis. Beclin 1 protein, encoded by the beclin 1 gene, plays a central role in the regulation of
autophagy. Beclin 1 primarily functions as a scaffolding protein assembling Beclin 1 interactome to
regulate Class III PI3K/VPS34 activity, which in turn, tightly controls autophagy at multiple stages. In
addition to autophagy, Beclin 1 participates in the regulation of other biological processes such as endocytosis,
apoptosis and phagocytosis. Fine-tuning of Beclin 1 protein levels, intracellular localization and the assembly
of its interactome is pivotal for the proper execution of these biological functions. Deregulation of Beclin 1 contributes to
the pathogenesis of a variety of human diseases. In this review, we summarize biology of Beclin 1 and its role in human
pathology, with an emphasis on heart disease.
Abstract
Phonons are the quantum mechanical descriptions of vibrational modes that manifest themselves in many physical properties of condensed matter systems. As the size of electronic devices ...continues to decrease below mean free paths of acoustic phonons, the engineering of phonon spectra at the nanoscale becomes an important topic. Phonon manipulation allows for active control and management of heat flow, enabling functions such as regulated heat transport. At the same time, phonon transmission, as a novel signal transmission method, holds great potential to revolutionize modern industry like microelectronics technology, and boasts wide-ranging applications. Unlike fermions such as electrons, polarity regulation is difficult to act on phonons as bosons, making the development of effective phonon modulation methods a daunting task. This work reviews the development of phonon engineering and strategies of phonon manipulation at different scales, reports the latest research progress of nanophononic devices such as thermal rectifiers, thermal transistors, thermal memories, and thermoelectric devices, and analyzes the phonon transport mechanisms involved. Lastly, we survey feasible perspectives and research directions of phonon engineering. Thermoelectric analogies, external field regulation, and acousto-optic co-optimization are expected to become future research hotspots.
Highlights
The latest theoretical and experimental progress in phonon engineering at the nanoscale is summarized comprehensively in this review, which proposes avenues for future research in related fields.
Phonon manipulation strategies and physical mechanisms of different thermophononic devices are sorted out and discussed in detail.
The experimental methods and technical means involved in this article can provide guidance for the fabrication of thermal functional devices, hence promoting phononics from fundamental research to practical applications.
Aging has often been linked to age-related vascular disorders. The elucidation of the putative genes and pathways underlying vascular aging likely provides useful insights into vascular diseases at ...advanced ages. Transcriptional regulatory network analysis is the key to describing genetic interactions between molecular regulators and their target gene transcriptionally changed during vascular aging.
A total of 469 differentially expressed genes were parsed into 6 modules. Among the incorporated sample traits, the most significant module related to vascular aging was associated with triglyceride and enriched with biological terms like proteolysis, blood circulation, and circulatory system process. The module associated with triglyceride was preserved in an independent microarray dataset, indicating the robustness of the identified vascular aging-related subnetwork. Additionally, Enpp5, Fez1, Kif1a, F3, H2-Q7, and their interacting miRNAs mmu-miR-449a, mmu-miR-449c, mmu-miR-34c, mmu-miR-34b-5p, mmu-miR-15a, and mmu-let-7, exhibited the most connectivity with external lipid-related traits. Transcriptional alterations of the hub genes Enpp5, Fez1, Kif1a, and F3, and the interacting microRNAs mmu-miR-34c, mmu-miR-34b-5p, mmu-let-7, mmu-miR-449a, and mmu-miR-449c were confirmed.
Our findings demonstrate that triglyceride and free fatty acid-related genes are key regulators of age-related vascular dysfunction in mice and show that the hub genes for Enpp5, Fez1, Kif1a, and F3 as well as their interacting miRNAs mmu-miR-34c, mmu-miR-34b-5p, mmu-let-7, mmu-miR-449a, and mmu-miR-449c, could serve as potential biomarkers in vascular aging.
The microarray gene expression profiles of aorta samples from 6-month old mice (n=6) and 20-month old mice (n=6) were processed to identify nominal differentially expressed genes. These nominal differentially expressed genes were subjected to a weighted gene co-expression network analysis. A network-driven integrative analysis with microRNAs and transcription factors was performed to define significant modules and underlying regulatory pathways associated with vascular aging, and module preservation test was conducted to validate the age-related modules based on an independent microarray gene expression dataset in mice aorta samples including three 32-week old wild-type mice (around 6-month old) and three 78-week old wild-type mice (around 20-month old). Gene ontology and protein-protein interaction analyses were conducted to determine the hub genes as potential biomarkers in the progress of vascular aging. The hub genes were further validated with quantitative real-time polymerase chain reaction in aorta samples from 20 young (6-month old) mice and 20 old (20-month old) mice.
The failure of gas turbines’ hot components due to fatigue significantly affects their efficient and stable operation. Conducting online damage assessment of components subjected to complex cyclic ...loads based on the working conditions of gas turbines can provide real-time reflection of component fatigue damage and achieve the purpose of predictive maintenance. In this study, we propose an online cycle counting method that considers temperature fluctuations during the cycle process. Our method is based on the four-point online rainflow counting method by coupling the counting variable with time, introducing the concept of the duration time for full cycles and half cycles, and incorporating a characteristic temperature that better represents the temperature information during the cycle process. With reference to the characteristic temperature, our proposed method comprehensively considers the form and parameters of subsequent life assessment models. This paper provides a detailed explanation of the proposed method and applies it to the fatigue damage assessment of turbine vanes in a micro gas turbine, thereby verifying its accuracy and applicability.
The therapeutic potential of doxorubicin (DOX) is limited by cardiotoxicity. Rubicon is an inhibitory interacting partner of autophagy protein UVRAG. Currently, the role of Rubicon in DOX-induced ...cardiotoxicity is unknown. In this study, we test the hypothesis that loss of Rubicon attenuates DOX-induced cardiotoxicity.
A mouse model of acute DOX-induced cardiotoxicity was established by a single intraperitoneal injection of DOX at a dose of 20 mg/kg. Rubicon expression was detected by Western blot. Cardiac damage was determined by measuring activities of lactate dehydrogenase and myocardial muscle creatine kinase in the serum, cytoplasmic vacuolization, collagen deposition, ROS levels, ATP content and mitochondrial damage in the heart. Cardiac morphometry and function were assessed by echocardiography. Markers for autophagy, mitophagy and mitochondrial dynamics were evaluated by Western blot and real time reverse transcription polymerase chain reaction.
Rubicon expression was reduced in the heart 16 h after DOX treatment. DOX induced accumulation of cytoplasmic vacuolization and collagen, increased serum activities of lactate dehydrogenase and myocardial muscle creatine kinase, enhanced ROS levels, reduced ATP content, pronounced mitochondrial damage and greater left ventricular wall thickness in wild type mice, which were mitigated by Rubicon deficiency. Mechanistically, loss of Rubicon improved DOX-induced impairment of autophagic flux, Parkin-mediated mitophagy and mitochondrial fission and fusion in the heart.
Loss of Rubicon ameliorates DOX-induced cardiotoxicity through enhancement of mitochondrial quality by improving autophagic flux, mitophagy and mitochondrial dynamics. Rubicon is a potential molecular target for prevention and therapy of DOX cardiotoxicity.
•Loss of Rubicon ameliorates DOX-induced cardiotoxicity.•DOX-induced mitochondrial damage in the heart is attenuated by Rubicon deficiency.•Loss of Rubicon mitigates DOX-induced impairment of autophagic flux, mitophagy and mitochondrial dynamics in the heart.
Internal Carbon Pricing (ICP) represents an innovative approach to carbon emission reduction. The implementation of the ICP involves enterprises and internal organizations, with its outcomes closely ...tied to government actions. In this study, a tripartite evolutionary game model comprising these subjects was constructed, and subsequent simulation analyses were conducted. The results revealed the following key findings: (1) When the combined total of carbon fees and governments' emission reduction subsidies surpasses the aggregate of carbon fees returned to internal organizations and ICP implementation costs, and when enterprises' revenues exceed governments' subsidies, all three parties will evolve towards ESS (1,1,1). This signifies that enterprises opt for the ICP, internal organizations actively reduce emissions, and governments engage in proactive regulation. (2) Reducing the cost of implementing ICP, increasing the carbon fee rebate ratio, raising governments' subsidies, and elevating the internal carbon price all contribute to promoting the attainment of the evolutionary game results ESS (1,1,1). However, it's important to note that higher governments' subsidies and carbon fee rebate ratios do not necessarily lead to a greater incentive for the three parties to reach the ESS(1,1,1). These findings provide a solid theoretical foundation for enterprises considering the implementation of the ICP in the future.
A missense mutation in the αB-crystallin (CryAB) gene triggers a severe form of desmin-related cardiomyopathy (DRCM) characterized by accumulation of misfolded proteins. We hypothesized that ...autophagy increases in response to protein aggregates and that this autophagic activity is adaptive. Mutant CryAB (CryABR¹²⁰G) triggered a >2-fold increase in cardiomyocyte autophagic activity, and blunting autophagy increased the rate of aggregate accumulation and the abundance of insoluble CryABR¹²⁰G-associated aggregates. Cardiomyocyte-restricted overexpression of CryABR¹²⁰G in mice induced intracellular aggregate accumulation and systolic heart failure by 12 months. As early as 2 months (well before the earliest declines in cardiac function), we detected robust autophagic activity. To test the functional significance of autophagic activation, we crossed CryABR¹²⁰G mice with animals harboring heterozygous inactivation of beclin 1, a gene required for autophagy. Blunting autophagy in vivo dramatically hastened heart failure progression with a 3-fold increase in interstitial fibrosis, greater accumulation of polyubiquitinated proteins, larger and more extensive intracellular aggregates, accelerated ventricular dysfunction, and early mortality. This study reports activation of autophagy in DRCM. Further, our findings point to autophagy as an adaptive response in this proteotoxic form of heart disease.
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