Carbon tax-driven technological innovation may accelerate the directional recovery of waste cooking oil into bio-jet fuel: An evolutionary game approach.

Biofuel production from waste cooking oil (WCO) offers an alternative to fossil fuels, especially for high-value bio-jet fuel. However, this industry is hindered by informal recyclers who covertly divert large amounts of WCO to illegal gutter oil production. Investigating the dynamic evolution of stakeholder behavior will help explore solutions. Thus, this study presents a tripartite evolutionary game model that includes the government, formal recyclers, and informal recyclers, aims to redesign the government intervention strategy to promote the directional flow of WCO from restaurant trash cans to bio-jet fuel production. We find that the evolutionary game model exists eight possible evolutionary stability strategies (ESSs), and the choice of each ESS depends mainly on the trade-off between costs and revenues for each stakeholder. The numerical study results reveal that formal recyclers are driven to carry out technological innovation by government support, profiting from bio-aviation kerosene products, and income from carbon emission reduction. These factors also have an indirect impact on the transformation of informal recyclers. Therefore, the government should provide adequate support for technological innovation to formal recyclers and increase their profitability of products to enable them to actively implement innovative strategies. This can be achieved by expanding the sales channels of bio-jet fuel products, implementing patent protection measures, and improving the carbon reduction trading mechanism. Furthermore, the government's high tax rate on formal recyclers and the significant profits earned by informal recyclers through illegal gutter oil production may dissuade them from transitioning their businesses. Above findings are in line with the actual issues of WCO recycling and provide a new dynamic decision-making method for enterprises and government managers.

How do information strategy and information technology governance influence firm performance?

Organizations today engage in turbulent competition to seize opportunities and cope with challenges by making strategy planning, increasing information technology (IT) investment, and other means. Based on survey data through questionnaires, this paper constructs models to explore the synergistic effects of information strategy (IS) and IT governance (ITG) on firm performance. The results show that, first, ITG and IS as explanatory variables have a significant influence on firm performance. Second, ITG has a positive effect on the relationship between IS and firm performance. This study extends existing research on IS and ITG by exploring the synergistic effects of IS and ITG on firm performance. The conclusion provides management insight and practical guidance for enterprises by actively implementing IS to improve firm performance to transform from the inherent pattern of traditional governance to the new technology governance.

Modeling the environmental suitability for Bacillus anthracis in the Qinghai Lake Basin, China.

Bacillus anthracis is a gram-positive, rod-shaped and endospore-forming bacterium that causes anthrax, a deadly disease to livestock and, occasionally, to humans. The spores are extremely hardy and may remain viable for many years in soil. Previous studies have identified East Qinghai and neighbouring Gansu in northwest China as a potential source of anthrax infection. This study was carried out to identify conditions and areas in the Qinghai Lake basin that are environmentally suitable for B. anthracis distribution. Anthrax occurrence data from 2005-2016 and environmental variables were spatially modeled by a maximum entropy algorithm to evaluate the contribution of the variables to the distribution of B. anthracis. Principal Component Analysis and Variance Inflation Analysis were adopted to limit the number of environmental variables and minimize multicollinearity. Model performance was evaluated using AUC (area under the curve) ROC (receiver operating characteristics) curves. The three variables that contributed most to the suitability model for B. anthracis are a relatively high annual mean temperature of -2 to 0°C, (53%), soil type classified as; cambisols and kastanozems (35%), and a high human population density of 40 individuals per km2 (12%). The resulting distribution map identifies the permanently inhabited rim of the Qinghai Lake as highly suitable for B. anthracis. Our environmental suitability map and the identified variables provide the nature reserve managers and animal health authorities readily available information to devise both surveillance strategy and control strategy (administration of vaccine to livestock) in B. anthracis suitable regions to abate future epidemics.

Spatial modeling and ecological suitability of monkeypox disease in Southern Nigeria.

The reemergence of monkeypoxvirus (MPXV) in 2017 after about 39 years of no reported cases in Nigeria, and the recent incidence in countries such as the United States of America, United Kingdom, Singapore, and Israel which have been reportedly linked with travelers from Africa, have heightened concern that MPXV may have emerged to occupy the vacant ecological and immunological niche created by the extinct smallpox virus. This study was carried out to identify environmental conditions and areas that are environmentally suitable (risky areas) for MPXV in southern Nigeria. One hundred and sixteen (116) spatially unique MPXV occurrence data from 2017-2021 and corresponding environmental variables were spatially modeled by a maximum entropy algorithm to evaluate the contribution of the variables to the distribution of the viral disease. A variance inflation analysis was adopted to limit the number of environmental variables and minimize multicollinearity. The five variables that contributed to the suitability model for MPXV disease are precipitation of driest quarter (47%), elevation (26%), human population density (17%), minimum temperature in December (7%), and maximum temperature in March (3%). For validation, our model had a high AUC value of 0.92 and standard deviation of 0.009 indicating that it had excellent ability to predict the suitable areas for monkeypox disease. Categorized risk classes across southern states was also identified. A total of eight states were predicted to be at high risk of monkeypox outbreak occurrence. These findings can guide policymakers in resources allocation and distribution to effectively implement targeted control measures for MPXV outbreaks in southern Nigeria.

Environmental suitability of Yersinia pestis and the spatial dynamics of plague in the Qinghai Lake region, China.

Plague, a highly infectious disease caused by Yersinia pestis, has killed millions of people in history and is still active in the natural foci of the world nowadays. Understanding the spatiotemporal patterns of plague outbreaks in history is critically important, as it may help facilitate the prevention and control for potential future outbreaks. This study's objective was to estimate the effect of the topography, vegetation, climate, and other environmental factors on the Y. pestis ecological niche. A maximum entropy algorithm spatially modelled plague occurrence data from 2004-2018 and the environmental variables to evaluate the contribution of the variables to the distribution of Y. pestis. Our results found that the average minimum temperature in September (-8 °C to +5 °C) and the sheep population density (250 sheep per km2) were influential in characterising the niche. The rim of Qinghai Lake showed more favourable conditions for Y. pestis presence than other areas within the study area. Identifying various factors will assist any future modelling efforts. Our suitability map identifies hotspots and will help public health officials in resource allocation in their quest to abate future plague outbreaks.

Transboundary spread of peste des petits ruminants virus in western China: A prediction model.

In pan Pamir Plateau countries, Peste des petits ruminants (PPR) has brought huge losses to the livestock industry and threaten the endangered wildlife. In unknown regions, revealing PPRV transmission among countries is the premise of effective prevention and control, therefore calls for quantified monitoring on disease communication among countries. In this paper, a MaxEnt model was built for the first time to predict the PPR risk within the research area. The least cost path (LCP) for PPR transboundary communication were calculated and referred to as the maximum available paths (MAP). The results show that there are many places with high-risk in the research area, and the domestic risk in China is lower than that in foreign countries and is mainly determined by human activities. Five LCPs representing corridors among Kazakhstan, Tajikistan, Pakistan, India and China were obtained. This study proves for the first time that there is the possibility of cross-border transmission of diseases by wild and domestic animals. In the future, it will play an important role in monitoring the PPR epidemic and blocking-up its cross-border transmission.

Using conflict negativity to index psychological tension between impartiality and status-upholding principles.

People often endorse the moral principle that all human lives are equally valuable. At the same time, people often privilege high-status individuals over low-status individuals. These two inclinations come into conflict in a scenario involving the potential killing of a high-status person to save the lives of multiple low-status people. In the present study, participants viewed a series of sacrificial dilemmas in which the social status of the victims and beneficiaries was varied. We measured participants' choice (sacrifice vs. don't sacrifice), response time, and electroencephalographic activity, with an emphasis on conflict negativity (CN). Overall, we found no effects of victim/beneficiaries status on choice and response time. However, participants displayed a more pronounced CN effect when contemplating a high-status victim/low-status beneficiaries tradeoff than a low-status-victim/high-status beneficiaries tradeoff. Further analyses revealed that this effect was primarily driven by participants who endorsed deontological principles (e.g., "Some rules must never be broken, no matter the consequences"). In contrast, those who endorsed utilitarian principles displayed equivalent levels of conflict negativity, regardless of the social status of victims and beneficiaries. These findings shed light on the role of conflict in the phenomenology of moral decision making.

Vascular Remodeling, Oxidative Stress, and Disrupted PPARγ Expression in Rats of Long-Term Hyperhomocysteinemia with Metabolic Disturbance.

Hyperhomocysteinemia, a risk factor for vascular disease, is associated with metabolic syndrome. Our study was aimed at exploring the effect of long-term hyperhomocysteinemia with metabolic disturbances on vascular remodeling. We also studied oxidative stress and expression of PPARγ in the coronary arteriole as a possible mechanism underlying vascular remodeling. Rats were treated with standard rodent chow (Control) or diet enriched in methionine (Met) for 48 weeks. Plasma homocysteine, blood glucose, serum lipids, malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO) levels were measured. Coronary arteriolar and carotid arterial remodeling was assessed by histomorphometric techniques and the expression of PPARγ in vessel wall was investigated. In Met group, an increase in the level of fasting blood glucose, serum triglyceride, total cholesterol, MDA, and NO, a decline in the serum SOD level, and increased collagen deposition in coronary and carotid arteries were found. Moreover, we detected decreased expression of PPARγ in the coronary arterioles in Met group. In summary, our study revealed metabolic disturbances in this model of long-term hyperhomocysteinemia together with vascular remodeling and suggested that impaired oxidative stress, endothelium dysfunction, and decreased PPARγ expression in the vessel wall could be underlying mechanisms.

Mild hypothermia protects rat neuronal injury after intracerebral hemorrhage via attenuating endoplasmic reticulum response induced neuron apoptosis.

BACKGROUND AND PURPOSE: Mild hypothermia has been proved to reduce global and focal cerebral ischemic injury in rodents by preventing cellular apoptosis through several pathways. However, whether hypothermia will be beneficial for intracerebral hemorrhage (ICH) and its underlying mechanisms haven't reached a consensus. It has been implicated that endoplasmic reticulum (ER) stress plays a role in the secondary injury after ICH in rats. In this study, we aimed to investigate whether mild hypothermia would attenuate ICH induced neuronal injury via regulating ER stress. METHODS: The model of ICH was induced by injecting autologous blood (120µl) into the rat striatum. Rats were divided into sham, normothermic (NT) and hypothermic (HT) groups. HT group were subjected to mild hypothermia (33°C-35°C) for 2days starting from 6h after ICH. Neurological deficits were evaluated. The ER stress related proteins (GRP78, CHOP and p-eIF2α) and the apoptosis associated indicators (cleaved caspase3, Bcl-2 and Bim) around hematoma were assessed by western blot, qRT-PCR (quantificational real-time polymerase chain reaction), immunofluorescence and TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling) assay. RESULTS: Neurological deficits following ICH were reduced in HT group compared to NT group. Protein levels of GRP78, CHOP and p-eIF2α significantly increased after ICH in both NT and HT group compared to sham group, which was consistent with the trend of cleaved-caspase3 at protein level, and Bim, Bcl-2 at gene level. In comparison to NT group, GRP78, CHOP, p-eIF2α, cleaved caspase-3 and Bim all decreased, while Bcl-2 increased in HT group. Additionally, apoptotic cells detected by TUNEL staining significantly decreased in the HT group. CONCLUSION: Mild hypothermia could attenuate ICH caused neuron injury by decreasing ER response-induced neuron apoptosis.

Desflurane preconditioning protects human umbilical vein endothelial cells against anoxia/reoxygenation by upregulating NLRP12 and inhibiting non-canonical nuclear factor-κB signaling.

Volatile anesthetics modulate endothelial cell apoptosis and inhibit nuclear factor-κB (NF-κB) signaling. In this study, we aimed to assess whether desflurane preconditioning protects human umbilical vein endothelial cells (HUVECs) agaist anoxia/reoxygenation (A/R) injury. HUVECs were pre-conditioned with desflurane (1.0 MAC) for 30 min, followed by a 15-min washout, then exposed to 60 min anoxia and 60 min reoxygenation (A/R), and incubated with 10 ng/ml tumor necrosis factor (TNF)-α for 60 min. HUVEC viability and apoptosis were measured by MTT assay and annexin V staining, and immunoblot analysis was used to measure the levels of Smac and cellular inhibitor of apoptosis 1 (cIAP1). NF-κB activation was assessed using the NF-κB signaling pathway real­time PCR array, and the levels of NF-κB inducing kinase (NIK), p52, IκB kinase (IKK)α, p100, RelB and NLR family, pyrin domain containing 12 (NLRP12) were assessed by immunoblot analysis. Desflurane preconditioning attenuated the effects of A/R and/or A/R plus TNF-α on cell viability, decreasing the levels of Smac and enhancing the levels of of cIAP1 (P<0.05). Preconditioning with desflurane also enhanced the mRNA levels of interleukin (IL)-10 and NLRP12 in the cells exposed to A/R by 2.40- and 2.16­fold, respectively. The HUVECs exposed to A/R had greater levels of NIK and p100 and reduced levels of p52 and IKKα. Desflurance preconditioning further increased p100 levels, decreased the level of NIK, further decreased p52 levels and further reduced IKKα levels. A/R in combination with TNF-α increased the NIK, IKKα, p100 and RelB levels, and this increase was significantly attenuated by desflurance preconditioning (all P<0.05). Desflurane preconditioning enhanced HUVEC survival and protected the cells against A/R injury, and our results suggested that this process involved the upregulation of NLRP12 and the inhibition of non-canonical NF-κB signaling.