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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.

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.

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.

Peste des petits ruminants (PPR) is a highly infectious transboundary disease of small ruminants caused by peste-des-petits-ruminants virus. It is one of the most destructive diseases in sheep industry in Africa, Asia and the Middle East. In Pamir Plateau, India, Pakistan, Afghanistan, Tajikistan, Kazakhstan and other countries bordering Tibet and Xinjiang of China are all PPR epidemic areas. Within this region, there are many big population size wild small ruminants, moving freely across the border. The time-honored transboundary nomadic lifestyle results in transboundary migration of livestock too. China has experienced two national epidemics, which can be sourced back to Tibet and Xinjiang. In order to reach the China National Plan for the Eradication of Peste des Petits Ruminants and construct a national wide free zone without immunization in 2020, effective control of transboundary spreading and imported cases is an unavoidable choice. For the countries in the pan Pamir Plateau, the spatial risk distribution of PPR were predicted by a variety of eco-geographical, anthropoid and meteorological variants first time; by the resistance surface analysis, maximum available transboundary paths for PPR spreading by small ruminants were calculated. Finally, 5 paths were obtained, respectively from Kazakhstan, Tajikistan, Pakistan and Kashmir to enter Xinjiang and Tibet of China through different channels. This study not only confirmed the fact of transboundary communication of small ruminants for the first time, but also provided specific objectives for PPR prevention. This research can also provide new methods for the prevention and control of other transboundary infectious diseases.

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 (120 μl) 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 2 days starting from 6 h 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.

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 PPARγin 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 PPARγin 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 PPARγin 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 PPARγexpression in the vessel wall could be underlying mechanisms.

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 real‑time 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