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The main challenges in clinical applications of mesenchymal stem cells (MSCs) are attributed to their heterogeneity. It is believed that preconditioning of MSCs with active compounds may enhance the expression of potentially therapeutic molecules and thus achieve stable and effective therapeutic outcomes. In the present study, we investigated the mechanism by which pyrogallol increased the therapeutic efficacy of human umbilical cord mesenchymal stem cells (hUCMSCs) against LPS-induced acute lung injury (ALI). hUCMSCs with pyrogallol treatment increased expression of HO-1 at both mRNA and protein levels, accompanied by Kelch-Like ECH-Associated Protein 1 (Keap1) degradation, and upregulation of the Nrf2 protein levels as well as nuclear translocation of Nrf2. Moreover, the modulation of Keap1 and Nrf2 as well as HO-1 upregulation by pyrogallol was reversed by pretreatment with N-acetylcysteine (NAC) and a P38 kinase inhibitor (SB203580). Whereas, NAC pretreatment abrogated pyrogallol-mediated activation of P38 kinase, indicating that pyrogallol-derived ROS led to P38 kinase activation, thus promoting Nrf2/HO-1 signaling. Additionally, we found that the induction of p62 by the pyrogallol-mediated ROS/P38/Nrf2 axis interacted with Keap1 and resulted in autophagic degradation of Keap1, which created a positive feedback loop to further release of Nrf2. Furthermore, the increased expression of HO-1 in pyrogallol-pretreated hUCMSCs led to enhanced inhibitory effects on LPS-mediated TLR4/P-P65 signaling in BEAS-2B cells, resulting in increasing suppression of LPS-indued expression of a series of pro-inflammatory mediators. Compared to untreated hUCMSCs, Sprague-Dawley (SD) rats with pyrogallol-primed hUCMSCs transplantation showed enhanced improvements in LPS-mediated lung pathological alterations, the increased lung index (lung/body ratio), apoptosis of epithelial cells, the activation of TLR4/NF-κB signaling as well as the release of pro-inflammatory mediators. Together, these results suggested that hUCMSCs with pyrogallol pretreatment enhanced the therapeutic efficacy of hUCMSCs, which may provide a promising therapeutic strategy to maximize the therapeutic efficacy of hUCMSC-based therapy for treating LPS-associated ALI.

The roles of Caveolin-1 (Cav-1) and Wnt/β-catenin signaling pathways in cerebral ischemia-reperfusion (I/R) injury are well established. Translocation of β-catenin into the nucleus is critical in regulating the apoptosis, repair, and nerve regeneration of neurons in the ischemic brain. Caveolin (Cav)-1 scaffold domain (residues 95-98) has been reported to interact with β-catenin (residues 330-337). However, the contribution of the Cav-1/β-catenin complex to I/R injury is currently unknown. To investigate the mechanism underlying the involvement of the Cav-1/β-catenin complex in the subcellular translocation of β-catenin and its subsequent effects on cerebral I/R injury, we treated ischemic brains with ASON (Cav-1 antisense oligodeoxynucleotides) or FTVT (a competitive peptide antagonist of the interaction Cav-1 and β-catenin). Our study showed that the binding of Cav-1 to β-catenin after I/R injury prevented the nuclear accumulation of β-catenin. The disruption of the Cav-1/β-catenin complex with ASON or FTVT after I/R injury significantly increased nuclear β-catenin. ASON and FTVT reduced the Ser33, Ser37 Thr41 phosphorylation of β-catenin, contributing to its proteasomal degradation; however, it increased the Tyr333 phosphorylation relating to its nuclear translocation. The above results indicated that the formation of the Cav-1/ β-catenin complex anchored the cytoplasmic β-catenin after I/R injury. Besides, both ASON and FTVT could attenuate neuronal death in ischemic brains. Our study suggests that targeting the interaction of Cav-1 with β-catenin could be a novel therapeutic strategy to protect against neuronal damage during cerebral injury.

In 2017, the Polar Code, negotiated under the auspices of the IMO, came into force. Later that same year, Canada issued new regulations applicable to navigation in the Canadian Arctic. In this pape...

Linyan Huang1 &ast;, Li Zhang1,2 &ast;, Shuiping Jiang,1 Baozhu Liang,1 Ningning Xu,1 Jingxin Li,1 Xiaoyan Zhang,1,3 Zhen Zhang1 1Department of Endocrinology, Zhujiang Hospital, Southern Medical University, Guangzhou, People’s Republic of China; 2Department of Endocrinology, People’s Hospital of Dehong, Yunnan, People’s Republic of China; 3Department of Pediatrics, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, Guangzhou, People’s Republic of China&ast; These authors contributed equally to this workCorrespondence: Zhen Zhang, Department of Endocrinology, Zhujiang Hospital, Southern Medical University, 253 Industrial Avenue, Guangzhou, Guangdong, 510282, People’s Republic of China, Tel +86-15913162742, Email zzhen311@163.comBackground: The coronavirus disease 2019 (COVID-19) outbreak has seriously affected people’s lives, especially those with chronic diseases. Diabetes self-management, which plays an important role in glycaemic control and reducing the risk of acute and long-term complications, may be discouraged by social distancing.Purpose: To evaluate the level of self-management activities in Chinese patients with type 2 diabetes mellitus (T2DM) during the COVID-19 pandemic.Patients and Methods: A survey of with 872 patients with T2DM in the inpatient and outpatient departments through face-to-face interviews was conducted from 1 July, 2020 to 30 September, 2020. The main outcome measures were glycaemic control status and level of self-management activities during the pandemic.Results: In terms of glycaemic control, the data showed that patients with fasting plasma glucose (FPG) < 7.0 mmol/L (36.4%), postprandial plasma glucose (PPG) < 10.0 mmol/L (26.3%), or glycosylated haemoglobin (HbA1c) < 7.0% (18.6%) in our investigation has well-controlled blood glucose level, and 11.9% of patients experienced blood glucose < 3.9 mmol/L during the outbreak. The diabetes self-management of Chinese patients decreased and the final diabetes self-management score of the Chinese patients was 3.4 ± 1.45. Patients with higher education, diabetes education, comorbidities, and online consultations had higher diabetes self-management scores (P < 0.05). Adherence to diabetes self-management in the normal glycaemic control group was higher than that in the substandard glycaemic control group (P< 0.05). Among all participants, 72.1% of the patients reduced the frequency of hospital visits, and 44.8% considered that they had diabetes-related stress during the pandemic. The mean anxiety level score rated by 286 patients was 5.3± 2.8.Conclusion: The COVID-19 pandemic has affected diabetes self-management, including substandard glycemic control, increased diabetes-related stress, limited exercise range and medical visits. Therefore, future interventions should focus on the online management of chronic diseases and support online consultation’ development and promotion, which can overcome physical distance and provide personalized services conveniently.Keywords: coronavirus disease 2019, diabetes self-management, online consultation, type 2 diabetes mellitus

Since 2011, freight transport rail links between China and Europe have been rapidly multiplying. Against all expectations, this commercial initiative, under the aegis of the Deutsche Bahn, has expanded significantly. The number of origin-destination pairs has increased, the number of trains has risen sharply, and both Chinese and European partners have far-reaching ambitions. The railways’ market share of trans-Asian freight is still low. However, rail link development projects have received a spectacular boost from the Belt and Road Initiative (BRI), resulting in the rapid expansion of volume, services offered, and the emergence of new rail infrastructure. Does this development, which needs to be examined more closely, represent a political tool for China? To what extent does the development of these rail links rely on a buoyant market? This article studies the development of rail services and infrastructure by means of a cross-analysis of a body of technical reports and publications by the transport sector’s professional press.

In vertebrates, the hypothalamus-pituitary-adrenal gland (HPA) axis is the main endocrine pathway regulating the stress response, thus also called the stress axis. It has been well-accepted that the stress axis is tightly controlled by both hypothalamic stimulators and inhibitors [e.g. corticotropin (ACTH)-releasing inhibitory factor (CRIF)]. However, the identity of authentic CRIF remains unclear for decades. Recently, neuropeptide W (NPW) was proved to be the physiological CRIF in chickens. Together with its functional receptor (NPBWR2), they play critical roles in attenuating the activity of the chicken stress axis. Because increasing pieces of evidence suggested that sex steroids could regulate the stress axis, using chicken as a model, we investigated whether the newly identified CRIF and its receptor are under the control of sex steroids in this study. Our results showed that: (1) expression of NPW-NPBWR2 in the hypothalamus-pituitary axis was sexually dimorphic and developmental stage-dependent; (2) progesterone (P

The association of herb medicine Cortex Dictamni (CD) with severe even fatal hepatotoxicity has been widely reported. Recently, we demonstrated that the metabolic activation of at least ten furanoids in CD was responsible for the liver injury caused by the ethanol extract of CD (ECD) in mice. Protein adduction by reactive metabolites is considered to initiate the process of liver injury. Unlike single chemicals, the mode of and the details of protein modification by multiple components in an herb is unclear. This study aimed to characterize protein adductions derived from the reactive metabolite of furanoids in ECD-treated mice and define the association of protein adduction with liver injury. The hepatic cysteine- and lysine-based protein adducts derived from epoxide or cis-enedione of at least six furanoids were identified in mice. The furanoids with an earlier serum content T

BackgroundNeural stem cell proliferation is a critical process in endogenous neurogenesis after ischemic/reperfusion injury. Ischemic succinate accumulation causes cerebral damage due to excess reactive oxygen species production. However, it remains elusive whether ischemic succinate accumulation affects neural stem cell proliferation.MethodsIn this study, we established rat middle cerebral artery occlusion model to mimic ischemic/reperfusion injury in vivo. Primary neural stem cell and neural stem cell line C17.2 were challenged with oxygen-glucose deprivation and reoxygenation. The level of succinate was assessed by liquid chromatography–mass spectrometry analysis. Cell proliferation was tested by cell counting kit 8. The infarct volume was measured by 2,3,5-Triphenyltetrazolium chloride staining. G protein coupled receptor GPR91 was detected by immunofluorescence. Sirtuin 5 knockdown was performed with Sirt 5 siRNA transfection. Cdc42 GTPase activity and succinylation were evaluated by co-immunoprecipitation.ResultsWe showed that succinate increased in the serum and brain (cortex and hippocampus) in middle cerebral artery occlusion rats. oxygen-glucose deprivation also induced abundant succinate in neural stem cell. Diethyl succinate inhibited C17.2 cell proliferation. Intraperitoneal administration of DS (800mg/kg) increased the infarct volume in middle cerebral artery occlusion rats. Besides, Diethyl succinate increases Cdc42 succinylation but represses Rho family GTPase Cdc42 activity, without affecting the level of its receptor G protein-coupled receptor-91 in neural stem cells. Increasing Cdc42 succinylation by desuccinylacylase Sirt5 knockdown inhibited GTPase Cdc42 activity. Accordingly, Cdc42 inhibtor ML141 also inhibited C17.2 proliferation.ConclusionsOur observations showed that accumulation of succinate inhibited neural stem cell proliferation by inducing Cdc42 succinylation, which reduced Cdc42 GTPase activity and was detrimental for neurogenesis after ischemic/reperfusion injury. Our data revealed a new mechanism that ischemic succinate accumulation aggrevated cerebral ischemic/reperfusion injury.

Our study objective was to explore whether abnormalities in the subtypes of T cells and B cells were present in peripheral blood of patients with osteoarthritis (OA) and healthy controls (HCs).Demographic and clinical variables and blood were collected. OA severity was measured using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) questionnaire. Flow cytometry was used to establish the frequencies of lineage subsets. Monoclonal antibodies against 21 surface markers were used to distinguish and evaluate T cells' and B cells' subpopulation. The proportion of each subset was compared and correlations between age, immune cells, and clinical data were analyzed.A total of 30 OA patients (male/female = 9/21) and 45 HCs (male/female = 14/31) were included. Median WOMAC pain was 3.0 (2.0). There was no difference in the proportion of T cells, CD8+ T cells, and B cells (p 0.05). The proportion of CD4+ T cells was higher in OA groups, together with an increased CD4 to CD8 ratio (p = 0.016). CD8+CD45RA+ T cells were reduced after adjustment for age, while CD8+CD45RA- T cells were elevated in OA (p 0.05). CD4+CD45RA-CCR7+ T cells and CD4+CD45RA-CCR7- T cells were increased (p 0.004). The proportion of T helper (Th) 17 and T follicular helper (Tfh) 2 cells was higher, but cytotoxic T (Tc) 17 cells were fewer in OA (p 0.05). CD3-CD19+IgD-IgM-CD27+CD38+ B cells were decreased in OA (p ≤ 0.001). The WOMAC pain score correlated with CD3+CD4+CXCR5-PD-1+ T cells positively (B = 0.404, p = 0.027). CD3-CD19+CD27-IgD+ cells correlated negatively with erythrocyte sedimentation rate (ESR) (B = -0.550, p = 0.005).The T cell and B cell profiles were proved to have alteration suggesting that acquired immune system may play a substantial role in the pathogenesis of OA.Key Points• The T cell and B cell profiles were proved to have alteration suggesting that acquired immune system may play a substantial role in the pathogenesis of OA.• The WOMAC pain score correlated with CD3+CD4+CXCR5-PD-1+ T cells and T helper 17 cells positively.• Memory T cells were increased in OA patients, suggesting they could play an important role in OA.

The coordinated proliferation and apoptosis of granulosa cells plays a critical role in follicular development. To identify the exact mechanisms of how stress-driven glucocorticoid production suppresses reproduction, granulosa cells were isolated from chicken follicles at different developmental stages and then treated with corticosterone. Using CCK-8, EDU and TUNEL assays, we showed that corticosterone could trigger both anti-proliferative and pro-apoptotic effects in granulosa cells from 6 to 8 mm follicles only, while depicting no influence on granulosa cells from any preovulatory follicles. High-throughput transcriptomic analysis identified 1362 transcripts showing differential expression profiles in granulosa cells from 6 to 8 mm follicles after corticosterone treatment. Interestingly, Kyoto Encyclopedia of Genes and Genomes enrichment analysis revealed that 17 genes were enriched in the TGF-β signaling pathway, and 13 showed differential expression patterns consistent with corticosterone-induced effects. The differential expression profiles of these 13 genes were examined by quantitative real-time PCR in cultured chicken ovarian granulosa cells at diverse developmental stages following corticosterone challenge for a short (8 h) or long period (24 h). After 24 h of treatment, INHBB, FST, FMOD, NOG, ACVR1, SMAD1 and ID3 were the genes that responded consistently with corticosterone-induced proliferative and apoptotic events in all granulosa cells detected. However, only ACVR1, SMAD1 and ID3 could initiate coincident expression patterns after being treated for 8 h, suggesting their significance in corticosterone-mediated actions. Collectively, these findings indicate that corticosterone can inhibit proliferation and cause apoptosis in chicken ovarian prehierarchical, but not preovulatory granulosa cells, through impeding ACVR1-SMAD1-ID3 signaling presumptively.

As an educational system to train high-quality citizens, higher education system plays an important role in the overall layout of the country. In order to assess the health of a country's higher education system, a variety of factors must be fully taken into account. In order to quantitatively analyze and evaluate the health status of higher education in a country, we must choose an appropriate model to solve this problem. In this paper, the analytic hierarchy process comprehensively reflects the influence of various factors on the index. In this paper, in order to build a model that can evaluate the health status of the higher education system in any country, taking into account the huge differences between countries in the world, we select the common characteristics of all countries from massive data. At the same time, in order to eliminate the numerical differences of various indicators caused by the differences in the size of different countries, and try to reflect the quality of education rather than the scale, it is necessary to preprocess the relevant data.

Growth hormone (GH) participates in many physiological processes through the activation of its membrane-anchored receptor (GHR) in vertebrates. Because of its pivotal role in regulating growth and development, a large number of studies examining GH-GHR have been conducted in mammals, birds and fish. However, whether a functional GH-GHR pair exists in the Chinese soft-shelled turtle (st-) has not been previously studied. Here, the full-length cDNA encoding GH was cloned from Chinese soft-shelled turtle (Trionyx sinensis) pituitary. The results revealed that it consisted of 784 bp and encoded a precursor of 217 amino acids. Furthermore, recombinant stGH was prepared and purified from Escherichia coli (E. coli) strain BL21. Using the 5×STAT5-Luciferase reporter system, we found that stGHR expressed in human hepatocellular carcinoma cells could be activated in a dose-dependent manner by recombinant stGH, thereby triggering the intracellular JAK2-STAT5 signaling pathway, suggesting stGH is a functional ligand for stGHR. Quantitative real-time PCR revealed that GH mRNA was predominantly and abundantly expressed in pituitary, while GHR exhibited ubiquitous expression in all tissues examined, including pituitary and liver. Collectively, our data indicate a conserved GH-GHR pair might function in reptiles including Chinese soft-shelled turtle, as that in mammals, birds and fishes.

KRAB domain-associated protein 1 (KAP1) is highly expressed in atherosclerotic plaques. Here, we studied the role of KAP1 in atherosclerosis development using a cell model of endothelial dysfunction induced by oxidative low-density lipoprotein (OxLDL). The phosphorylation and protein levels of KAP1 were similar between OxLDL-treated and non-treated endothelial cells (ECs). KAP1 depletion significantly inhibited the production of OxLDL-enhanced reactive oxygen species and the expression of adhesion molecules in ECs. Treatment with OxLDL promoted the proliferation and migration of ECs, which was also confirmed by the elevated levels of the proliferative markers c-Myc and PCNA, as well as the migratory marker MMP-9. However, these effects were also abrogated by KAP1 depletion. Moreover, the depletion of KAP1 in OxLDL-treated ECs resulted in decreases in the LOX-1 level and increases in eNOS expression. Generally, the data suggest that strategies targeting KAP1 depletion might be particularly useful for the prevention or treatment of atherosclerosis.

Background Stroke is the leading cause of long-term motor disability and cognitive impairment. Recently, neurogenesis has become an attractive strategy for the chronic recovery of stroke. It is important to understand the molecular mechanism that promotes neural stem cell (NSC) neurogenesis for future NSC-based therapies. Our previous study showed that Momordica charantia polysaccharides (MCPs) exerted neuroprotective effects on stroke via their anti-oxidant and anti-inflammation activities. However, it remains unknown whether MCPs promote NSC neurogenesis after cerebral ischemic/reperfusion injury (IRI). Methods We investigated MCPs’ function in differentiation of neural stem cells (NSCs) in vivo and in vitro experiments. Based on a middle cerebral artery occlusion (MCAO) rat model, the effect of MCPs on neuronal differentiation after MCAO was analyzed. Primary NSCs and neural stem cell line C17.2 were cultured and subjected to glutamate stimulation to establish the cell model of IRI. We evaluated the effect of MCPs on NSC differentiation in IRI cell model by Western blot and immunofluorescence staining. The SIRT1 activity of NSCs post glutamate stimulation was also evaluated by CELL SIRT1 COLORIMETRY ASSAY KIT. In addition, molecular mechanism was clarified by employing the activator and inhibitor of SIRT1. Results MCPs had no effects on the differentiation of neural stem cells under physiological conditions while shifted NSC differentiation potential from the gliogenic to neurogenic lineage under pathological conditions. Activation of SIRT1 with MCPs was responsible for the neuronal differentiation of C17.2-NSCs. The neuronal differentiation effect of MCPs was attributed to upregulation SIRT1-mediated deacetylation of β-catenin. MCP-induced deacetylation via SIRT1 promoted nuclear accumulation of β-catenin in NSCs. Conclusion Our findings indicate that the deacetylation of β-catenin by SIRT1 represents a critical mechanism of action of MCPs in promoting NSC neuronal differentiation. It provides an improved understanding of molecular mechanism underlying neuroprotective effects of MCPs in IRI, indicating its potential role on treating ischemic stroke especially chronic recovery.

Many furan containing compounds have been reported to be toxic resulted from the metabolic activation of the furan ring to reactive metabolite (RM). Cortex Dictamni (CD), a widely used herbal medicine, has been reported to cause severe even fatal hepatotoxicity. The injurious components and mechanism of CD-induced liver injury remain unclear. Our preliminary study showed that dictamnine, one major furanoid in CD, caused mouse liver injury via its reactive epoxide metabolite. Besides dictamnine, the major components of CD are series of bioactivation-alerting furanoids. Thus, we hypothesize that series of furanoids in CD may undergo metabolic activation and play a key role in CD-induced liver injury. Here, a single oral dose of 60 g/kg ethanol extract of CD (ECD) caused severe hepatocellular necrosis in mice at 24 h post-dose. ECD-induced liver injury showed a dose- and time-dependent manner. The hepatotoxic effects could be completely abolished by P450 nonselective inhibitor 1-aminobenzotriazole (ABT) and strongly modulated by other P450 modulators. The furanoids-concentrated fraction of ECD was responsible for the hepatotoxicity. At least ten furanoids with high abundance in ECD, such as obakunone, dictamnine, fraxinellone, limonin, were found to be metabolized to reactive epoxide or cis-enedione. The RM levels were consistent with the liver injury degree. Multiple furanoids, rather than single one, cooperatively contributed to the hepatotoxicity. ECD-induced liver injury could be reproduced by a mixture of pure furanoids. In summary, this study provides toxic component profiles of CD and demonstrates that P450-mediated bioactivation of multiple furanoids is responsible for CD-induced liver injury.

Additional file 1.

Arecoline is the primary active and toxic constituent of areca nut. Arecaidine and arecoline N-oxide are two major active metabolites of arecoline. In this work, an accurate and simple high performance liquid chromatography tandem mass spectrometry method for simultaneous quantification of arecoline, arecaidine and arecoline N-oxide in rat plasma was developed and fully validated to study their pharmacokinetic behaviors in rats. After extracted from rat plasma by protein precipitation with methanol and then concentrated, the analytes were chromatographic separated on a Sepax Sapphire C18 analytical column. The mobile phase consisted of methanol and 2 mM ammonium acetate buffer solution containing 0.2% (v/v) formic acid (8:92, v/v) under isocratic elution. The analytes were detected by multiple reaction monitoring (MRM) with an electrospray ionization source in the positive ion mode. The transitions of m/z 156.2 → 53.2, m/z 142.2 → 44.2 and m/z 172.2 → 60.2 were selected for arecoline, arecaidine and arecoline N-oxide, respectively. The method was linear over the concentration range of 0.5–100 ng/mL for arecoline, 5–5000 ng/mL for arecaidine and arecoline N-oxide with no carry-over effect. The accuracies and intra- and inter-batch precisions were all within the acceptance limits. No matrix effect and potential interconversion between the analytes and other metabolites were observed in this method. The validated method was further employed to a preclinical pharmacokinetic study of arecoline, arecaidine and arecoline N-oxide after oral treatment with 20 mg/kg arecoline to rats.

NixCo1-xFe2Oz composite oxide nanosphere was successfully prepared, to degrade 2-monochlorobiphenly (CB-1) in continuous-flow fixed-bed microreactor at GHSV of 20000 h−1. The five cycles of temperature-dependent run experiments between 150 and 350 °C showed its superior activity with a CB-1 conversion of more than 95% above 300 °C over Ni0.5Co0.5Fe2Oz. Importantly, the sustainable higher reactivity could be observed over prolonged 600 min reaction times after the 5th run test. The degradation products detected as biphenyl and monochlorobenzene with yield ratio of 129, account for 0.24% and 0.0011% of initial CB-1 respectively. This indicated the weak occurrence of hydrodechlorination and breakage of C C bridge bond during the degradation of CB-1. The possibly dominant occurrence of oxidative degradation probably follows Mars–van Krevelen mechanism, resulting in the generation of the formic, acetic, propanoic and butyric acids and so on. Due to the high oxygen mobility over Ni0.5Co0.5Fe2Oz nanosphere, the consumed oxygen species could be compensated rapidly by the gas phase oxygen via O2 → O2− → 2O− → 2O2−. The interaction among different elements in Ni0.5Co0.5Fe2Oz nanosphere confirmed by the derivation of the electron cloud, enhanced the mobility of the reactive oxygen species, which would be beneficial for the oxidation of chlorinated biphenyls.

The cloud-free monthly composite of global nighttime light (NTL) data of the Suomi National Polar-orbiting Partnership with the Visible Infrared Imaging Radiometer Suite (NPP-VIIRS) day/night band (DNB) provides indispensable indications of human activities and settlements. However, the coarse spatial resolution (15 arc sec) of NTL imagery greatly restricts its application potential. This study proposes a feasible framework to downscale NPP-VIIRS NTL using muti-source spatial variables and geographically weighted regression (GWR) method. High-resolution auxiliary variables were acquired from the Landsat 8 OLI/ TIRS and social media platforms. GWR-based downscaling procedures were consequently implemented to obtain NTL at a 100-m resolution. The downscaled NTL data were validated against Loujia1-01 imagery based on the coefficient of determination (R2) and root-mean-square error (RMSE). The results suggest that the data quality was suitably improved after downscaling, yielding higher R2 (0.604 vs. 0.568) and lower RMSE (8.828 vs. 9.870 nW/cm2/sr) values than those of the original NTL data. Finally, the NTL was extendedly applied to detect impervious surfaces, and the downscaled NTL had higher accuracy than the original NTL. Therefore, this study facilitates data quality improvement of NPP-VIIRS NTL imagery by downscaling, thus enabling more accurate applications.

Enzyme-aided Cl 2 bleaching is widely considered as promising replacements for conventional Cl 2 bleaching in wood pulp and paper mills. However, the effects of using enzyme-aided bleaching on the formation of polychlorinated dibenzo- p -dioxins and dibenzofurans (PCDD/Fs) in the non-wood pulp and paper mills are unclear. A field study was performed to investigate PCDD/F formation when enzyme-aided Cl 2 bleaching was used to replace conventional Cl 2 bleaching in non-wood pulp and paper mills. Unexpectedly, the PCDD/F toxic equivalents (TEQs) in solid samples were higher when using enzyme-aided bleaching (0.49–5.4 pg TEQ/g) than that using conventional Cl 2 bleaching (0.15–2.44 pg TEQ/g). Large amounts of octachlorodibenzo- p -dioxin were formed during the enzyme-aided bleaching process. This could have been because enzyme strongly promoted the release of organic molecules bound to lignin and thus accelerated the formation of octachlorodibenzo- p -dioxin through organic molecular precursors. Although enzyme-aided Cl 2 bleaching was previously considered to be efficient for reducing PCDD/F releases and to be the best available technologies and best environmental practices for wood pulp and paper mills, the results obtained in this study suggested the necessity and urgency to evaluate the suitability of enzyme-aided Cl 2 bleaching for non-wood pulp and paper mills that intensively practiced in developing countries.

We present novel evidence showing that people prefer searching for an exit and avoiding smoke rather than following the crowd regardless whether with intuition or deliberation when the crisis situation was activated. Intuition leads to more obvious preferences on escape judgment and decision-making than does deliberation under unconscious priming condition. People are more cautious with decision-making than judgment across two experiments. Priming method was adopted because the same primes tend to activate different associative links for different people (Cameron et al., 2012). Across two experiments, reliable and consistent evidence shows that when facing a crisis (e.g., fire), searching for an exit and avoiding smoke are preferred by people rather than following the crowd. In Experiment 1, we demonstrated that searching for an exit and avoiding smoke were judged as more helpful than following the crowd by both intuition and deliberation regardless whether the situation is simple or complex. In Experiment 2, we found that intuition has a more significant influence on judgment and decision-making than deliberation under both simple and complex situations. Our findings contribute to the crisis literature by demonstrating that people less prefer to follow the crowd when escaping from crisis situations, and that intuition is more effective under unconscious priming condition.

Climate change in the Arctic is leading to the fast recession of sea ice in the summer. This evolution leads several observers, scientists, media and government officials, to consider the possibility of developing new shipping routes along Arctic routes, as these routes are much shorter between Europe and Asia. The literature displays a strong discourse about interest from Asian countries for these potential shipping routes. This paper tackles with this idea and examines to what extent Asian shipping companies, the ultimate economic agents, are really interested in Arctic shipping routes. The image the research portrayed is that only a minority of Asian shipping companies are indeed interested, and those that are interested stress the destinational dimension of Arctic shipping, not transit shipping.

Degradation reaction of decachlorobiphenyl (PCB-209) was investigated over the synthesized Ca species-doped Fe2O3 at 300 °C. The 1%Ca–Fe2O3 exhibited the highest activity among the four catalysts prepared with the pseudo-first order reaction at kobs = 0.103 min−1. PCB-207, PCB-197, PCB-176, PCB-184, PCB-150, PCB-136, PCB-148, PCB-104, PCB-96, PCB-54, PCB-19, PCB-4 and PCB-1 were identified as the dominant isomers in their respective nonachlorobiphenyl (NonaCB) to monochlorobiphenyl (MonoCB) homologue groups. Analysis of the hydrodechlorination products indicated that dechlorination was much more favored on meta- and para-than on ortho-positions. The formation of significantly predominant NonaCB and octachlorobiphenyl (OctaCB) isomers was attributed to lower energy principles and to the 90° dihedral angles of two aromatic rings which prevented the hydrodechlorination at ortho-positions. When the number of chlorine atoms is not more than 7, the steric effect supports the formation of predominant PCB isomers having chlorines at four ortho-positions. During the dechlorination of tetrachlorobiphenyl (TetraCB) formed to generate monochlorobiphenyl (MonoCB) isomers, the chlorine atoms fully substituted at the ortho-positions have to be successively removed, with the first two dechlorinations preferentially occurring at the two different benzene rings. This is dissimilar to that of octachloronaphthalene (PCN-75) in which the hydrodechlorination reaction happened preferentially at ortho-position due to the existence of steric effects. The opposite roles of the steric effect in ortho-position between PCB-209 and PCN-75 might be due to the difference of the π-conjugated plane caused by the dihedral angle of 90° and 0° of the two aromatic rings.

Dans un contexte de bouleversements climatiques dans l’Arctique, la fonte rapide du pergélisol, le recul des glaciers et la fonte de la banquise créent des occasions stratégiques et économiques qui n’ont pas échappé aux États riverains. L’intérêt pour la région ne se limite pas aux pays directement concernés. La Chine, par exemple, sans accès direct à l’Arctique, a adopté une attitude officielle très prudente ; cependant, ses efforts diplomatiques, économiques, politiques et scientifiques dans cette région suscitent des réactions négatives de la part des médias occidentaux. Ils dressent souvent un portrait d’une Chine ambitieuse et arrogante, prête à bousculer la souveraineté des pays arctiques pour défendre ses intérêts dans cette région. Dans cette optique, il paraît pertinent d’analyser les activités de la Chine en Arctique et de tenter d’identifier quelle est la stratégie de Pékin dans cette zone polaire. In a context of climatic upheavals in the Arctic, the fast melting of permafrost, the decline of glaciers and the melting of sea ice created strategic and economic opportunities which did not escape the riparian States. The interest for the region goes beyond its shores. China, for example, without direct access to the Arctic, adopted a very careful official attitude ; however, its diplomatic, economic, political and scientific efforts in this region arouse negative reactions among western media. They often draw up a portrait of an ambitious and arrogant China, ready to push aside the sovereignty of the Arctic countries to defend its interests in the Arctic. From this perspective, it seems relevant to analyze China’s activities in the region and try to assess Beijing’s strategy in the Arctic.

In recent years, China’s urbanization process has increased year by year, and the environmental problems brought by it have become increasingly prominent. The urban ecological environment and urban green space are closely connected. The improvement and reconstruction of the ecological environment need to be realized through the urban green space system planning. Therefore, it is imperative to apply landscape ecology in the urban green space system planning. This paper first outlines the important role of urban green space systems in restoring ecological and environmental problems. Second, based on the research on the landscape ecological progress of urban green space systems at home and abroad, through in-depth investigation of some representative urban green space systems in China, the current domestic Problems existing in urban green space system planning. Finally, based on the principles of landscape ecology, an optimization strategy for landscape ecological planning in urban green space systems was proposed. The results show that the use of landscape ecology can rationally plan the landscape space, green space corridors, green space patches and other factors in the green space system, thereby achieving the purpose of improving the urban environment and promoting ecological balance.

Chinese shipping industry has experienced a rapid growth in the past three decades. With the analysis of the Chinese fleet capacity and the evolution of its market share in Chinese freight market, this paper reveals that foreign shipping companies took a majority share of ocean shipping while Chinese state-owned shipping companies have the upper hand in coastal and river shipping markets. Chinese private shipping companies were squeezed to either be a subcontractor or be confined in a niche market. This paper collects data from Chinese official shipping report and Chinese academic publications. It reveals that the prosperity of China's shipping market has not enabled the emergence of strong and very competitive Chinese shipping companies when facing foreign competitors.

Cortex Dictamni is extensively used as an herbal medicine worldwide, but is believed to induce hepatotoxicity and even causes mortality in many Asian and European countries. As the most abundant furoquinoline alkaloid ingredient of Cortex Dictamni, dictamnine (DIC) can be metabolically activated by CYP3A to an epoxide metabolite, which possesses the potential to induce hepatotoxicity by covalent binding with proteins. As yet, the hepatotoxicity of DIC and the role played by metabolic activation remain unknown. Here, we found that DIC caused acute liver injury in a time- and dose-dependent manner in mice. The hepatic and urinary DIC epoxide intermediates were observed in DIC-treated mice. Ketoconazole, a CYP3A inhibitor, significantly reduced the hepatotoxicity of DIC and inhibited the formation of reactive metabolites of DIC. Moreover, treatment with 2,3-dihydro-DIC, a DIC analog synthesized by selective reduction of the furan moiety, produced no hepatotoxicity in mice, and no reactive metabolite was formed, suggesting a structural necessity of furan moiety in DIC hepatotoxicity. A time course of gradual hepatic glutathione consumption was observed in DIC-treated mice, while depletion of hepatic glutathione by L-buthionine-S,R-sulfoximine enhanced the hepatotoxicity of DIC. Collectively, this study demonstrates that DIC induces acute hepatocellular injury in mice, and that metabolic activation of furan plays a crucial role in DIC-induced hepatotoxicity.

The simple circuit characteristic tester system is based on circuit construction and design. The system uses the f407 of the STM32 chip as the main control chip, and combines the test circuit and the basic operational amplifier circuit (voltage follower), RC filter circuit, relay control. The circuit and the triode regulator circuit are tested. The system uses a single-chip microcomputer to generate a sine wave (DAC) with amplitude of 0-3.3VPWM and amplitude of 0.1-1V, and then attenuates ten times as an input by the op amp, and performs ADC sampling comparison on a specific part of the circuit to complete the input resistance and output resistance of the circuit. And the gain and frequency characteristic curve at the frequency of 1KHZ. Finally, the system can automatically measure and measure the fault of a given component through programming. The system analyzes and compares the output waveform at a specific circuit as a single-chip microcomputer. The input is then judged by the processing of the microcontroller. In the process of system operation, the OPA2314 operational amplifier is used. The triode adopts the Model 9013. A small capacitor with a value of 100nF is added between the power supply and the ground, which enables the system test to be successfully completed.

Clostridium difficile is the leading cause of pseudomembranous colitis in hospitalized patients. C. difficile enterotoxins TcdA and TcdB promote this inflammatory condition via a cytotoxic response on intestinal epithelial cells (IECs), but the underlying mechanisms are incompletely understood. Additionally, TcdA and TcdB engage the Pyrin inflammasome in macrophages, but whether Pyrin modulates CDI pathophysiology is unknown. Here we show that the Pyrin inflammasome is not functional in IECs and that Pyrin signaling is dispensable for CDI-associated IEC death and for in vivo pathogenesis. Instead, our studies establish that C. difficile enterotoxins induce activation of executioner caspases 3/7 via the intrinsic apoptosis pathway, and demonstrate that caspase-3/7-mediated IEC apoptosis is critical for in vivo host defense during early stages of CDI. In conclusion, our findings dismiss a critical role for inflammasomes in CDI pathogenesis, and identify IEC apoptosis as a host defense mechanism that restricts C. difficile infection in vivo., The enterotoxins TcdA and TcdB induce cytotoxicity of epithelial cells during Clostridium difficile infection. Here the authors show that bacterial induced epithelial cell death occurs via activation of caspases 3 and 7, resulting in apoptotic cell death.