DataSheet1_Can performance-based budgeting reform improve corporate environment in ESG? Evidence from Chinese-listed firms.docx

Finance is a pillar industry of national governance. It also provides a solid guarantee for achieving the official Double Carbon target. The question of how to forefront the role of environmental governance in the reform of fiscal and taxation systems, whilst also motivating enterprises to enhance Environment in Environmental, Social, and Governance (EESG) considerations is worth investigating in depth. This study takes A-share listed companies in China from 2001 to 2020 as examples. The effect of Performance-Based Budgeting (PBB) reform on the EESG of these enterprises is empirically examined through quasi-natural experiments using a multi-time difference-in-difference model. We find that PBB significantly optimizes the EESG of the enterprises. The placebo test, the difference-in-difference method, and a series of other robustness tests all support this conclusion. Furthermore, it is suggested that the environmental governance effect of PBB is more significant in areas with heavy financial pressure and stronger government audit. The environmental governance effect of the PBB reform is significant for enterprises with government contracts, strong green innovation capabilities, or high financing constraints. The mechanism test is performed, and the results suggest that the influence mechanism of this environmental governance role lies in the fact that PBB has improved environmental protection subsidies and enhanced fiscal transparency. Through the economic consequences test, we find that enterprise EESG can bring economic benefits to enterprises, which is reflected in the improvement of enterprise return on total assets, price-to-book ratio, and total patent authorization. This study enriches literature on the economic consequences of PBB, and has significance in deepening current fiscal and tax system reform, vigorously optimizing the major strategy of carbon peak and carbon neutrality.</p

Image_1_Real-time detection of Seneca Valley virus by one-tube RPA-CRISPR/Cas12a assay.pdf

IntroductionSenecavirus A (SVA) is a highly contagious virus that causes vesicular disease in pigs. At present, laboratory detection methods, such as virus isolation and polymerase chain reaction (PCR), required precision instruments and qualified personnel, making them unsuitable for point-of-care tests (POCT). Fortunately, the emergence of CRISPR/Cas system has provided new opportunities for fast and efficient pathogen detection.MethodsThis study successfully developed a precise and sensitive detection platform for diagnosing SVA by combining the CRISPR system with recombinase polymerase amplification (RPA). ResultsThe minimum detection limit of the assay was 10 copies of the SVA genome. Meanwhile, the assay demonstrated high specificity. To validate the effectiveness of this system, we tested 85 swine clinical samples and found that the fluorescence method had a 100% coincidence rate compared to RT-qPCR. DiscussionOverall, the RPA-CRISPR/Cas12a assay established in our study is a highly effective method for detecting SVA and holds great potential for practical applications in the resource-limited settings.</p

Image_1_Autophagy Benefits the Replication of Egg Drop Syndrome Virus in Duck Embryo Fibroblasts.TIF

<p>Egg drop syndrome virus (EDSV) is an economically important pathogen with a broad host range, and it causes disease that leads to markedly decreased egg production. Although EDSV is known to induce apoptosis in duck embryo fibroblasts (DEFs), the interaction between EDSV and its host needs to be further researched. Here, we provide the first evidence that EDSV infection triggers autophagy in DEFs through increases in autophagosome-like double-membrane vesicles, the conversion of LC3-I to LC3-II, and LC3 colocalization with viral hexon proteins. Conversely, P62/SQSTM1 degradation, LC3-II turnover, and colocalization of LAMP and LC3 confirmed that EDSV infection triggers complete autophagy. Furthermore, we demonstrated that inhibition of autophagy by chloroquine (CQ) and 3-methyladenine (3MA) or RNA interference targeting ATG-7 decreased the yield of EDSV progeny. In contrast, induction of autophagy by rapamycin increased the EDSV progeny yield. In addition, we preliminarily demonstrated that the class I phosphoinositide 3-kinase (PI3K)/Akt/mTOR pathway contributes to autophagic induction following EDSV infection. Altogether, these finding lead us to conclude that EDSV infection induces autophagy, which benefits its own replication in host cells. These findings provide novel insights into EDSV–host interactions.</p

Effects of metalloporphyrins on Cisplatin induced DNA fragmentation.

<p>Cisplatin induced significant DNA fragmentation and the effect was attenuated by FeTMpyP or MnTBAP treatments. Results are mean ± S.E.M. n = 4/group. *p<0.05 versus vehicle; and ^#p<0.05 versus cisplatin.</p

Protective Effect of Metalloporphyrins against Cisplatin-Induced Kidney Injury in Mice

<div><p>Oxidative and nitrative stress is a well-known phenomenon in cisplatin-induced nephrotoxicity. The purpose of this work is to study the role of two metalloporphyrins (FeTMPyP and MnTBAP), water soluble complexes, in cisplatin-induced renal damage and their ability to scavenge peroxynitrite. In cisplatin-induced nephropathy study in mice, renal nitrative stress was evident by the increase in protein nitration. Cisplatin-induced nephrotoxicity was also evident by the histological damage from the loss of the proximal tubular brush border, blebbing of apical membranes, tubular epithelial cell detachment from the basement membrane, or intra-luminal aggregation of cells and proteins and by the increase in blood urea nitrogen and serum creatinine. Cisplatin-induced apoptosis and cell death as shown by Caspase 3 assessments, TUNEL staining and DNA fragmentation Cisplatin-induced nitrative stress, apoptosis and nephrotoxicity were attenuated by both metalloporphyrins. Heme oxygenase (HO-1) also plays a critical role in metalloporphyrin-mediated protection of cisplatin-induced nephrotoxicity. It is evident that nitrative stress plays a critical role in cisplatin-induced nephrotoxicity in mice. Our data suggest that peroxynitrite is involved, at least in part, in cisplatin-induced nephrotoxicity and protein nitration and cisplatin-induced nephrotoxicity can be prevented with the use of metalloporphyrins.</p></div

Effects of metalloporphyrins on Cisplatin induced kidney tubular damage in mice.

<p>Histological examination (Panel A) and quantification (Panel B) revealed necrosis, protein cast, vacuolation, and desquamation of epithelial cells in the renal tubules of the cisplatin-treated group. Cisplatin administration resulted in severe tubular damage. Cisplatin induced damages were attenuated by FeTMPyP and MnTBAP treatments (n = 4–5/each group; p<0.01). Results are mean ± S.E.M. n = 4–5/group. *p<0.05 versus vehicle; and ^#p<0.05 versus cisplatin.</p

Effects of metalloporphyrins on Cisplatin induced HO-1 mRNA.

<p>Metallophorphyrins induced HO-1 mRNA by itself ($ p<0.05 vs vehicle). Cisplatin induced significant HO-1 mRNA level and the induction was attenuated by FeTMpyP or MnTBAP treatments. Results are mean ± S.E.M. n = 4/group. *p<0.05 versus vehicle; and ^#p<0.05 versus cisplatin.</p

Machine Learning-Guided Adaptive Parametrization for Coupling Terms in a Mixed United-Atom/Coarse-Grained Model for Diphenylalanine Self-Assembly in Aqueous Ionic Liquids

Precise regulation of the peptide self-assembly into ordered nanostructures with intriguing properties has attracted intense attention. However, predicting peptide assembly at atomic resolution is a challenge due to both the structural flexibility of peptides and the associated huge computational costs. A machine learning-guided adaptive parametrization method was proposed for developing a mixed atomic and coarse-grained (CG) model through a multiobjective optimization strategy. Our model incorporates the united-atom (UA) model for diphenylalanine (P) and the polarizable electrostatic-variable coarse-grained (VaCG) model for aqueous ionic liquid [BMIM]+[BF4]− solution. In this mixed model, the coupling van der Waals (vdW) interaction is addressed by introducing virtual sites (VS) in the UA model to interact with solvent CG beads. The coupling parameters, including the electrostatic parameter and vdW parameters, are automatically optimized through ML-guided adaptive parametrization. The performance of this model was tested by some microstructural properties, e.g., the average number of P–P intermolecular hydrogen bonds (HBs) and radius distribution functions (RDFs) between P and different fragments of IL, in comparison with all-atom (AA) simulations. The computational cost is significantly reduced using such a parametrization scheme, which could search tens of thousands of force-field parameter sets, while needing only a small fraction of them to be assessed with molecular dynamics (MD) simulations. We used such a mixed resolution model to investigate the self-assembly in IL–water mixtures with variants of IL concentration (X). The long-range-ordered fibril structure is formed in a pure water system (X = 0). With an increase of IL concentrations, the formation of an ordered self-assembly nanostructure is prohibited, instead forming branched fibril at X = 2 mol % or amorphous aggregates when X > 10 mol %, resulting from the interplay between π-stacking and HB interactions between P and IL. The qualitative agreement between the simulated structures and the observed morphologies in experiments indicates the applicability of ML-guided parametrization strategy in the study of complex systems, such as polymers, lipid bilayers, and polysaccharides

Effects of metalloporphyrins on Cisplatin induced early apoptosis marker Caspase 3.

<p>Histological examination (Panel A) demonstrated cisplatin induced cleaved caspase 3 staining in kidney and the caspase 3 staining were significantly attenuated with pretreatments of FeTMPyP or MnTBAP. Panel B: caspase 3 activity were measured and similar trend was observed. Results are mean ± S.E.M. n = 4–5/group. *p<0.05 versus vehicle; and ^#p<0.05 versus cisplatin.</p

Schematic diagram of protection mechanism of metalloporphyrins in Cisplatin induced kidney injury.

<p>Metalloporphyrins induce HO-1 resulting in antioxidant defense and autophagy during cisplatin induced kidney injury. Metalloporphyrins also neutralize superoxide or scavenge peroxynitrite generated during cisplatin exposure. All combitorial effects leads to reduced inflammation and cell death, thus protecting against cisplatin induced kidney injury.</p