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Radon observation is an important measurement item of seismic precursor network observation. The radon detector calibration is a key technical link for ensuring radon observation accuracy. At present, the radon detector calibration in seismic systems in China is faced with a series of bottleneck problems, such as aging and scrap, acquisition difficulties, high supervision costs, and transportation limitations of radon sources. As a result, a large number of radon detectors cannot be accurately calibrated regularly, seriously affecting the accuracy and reliability of radon observation data in China. To solve this problem, a new calibration method for radon detectors was established. The advantage of this method is that the dangerous radioactive substance, i.e., the radon source, can be avoided, but only “standard instruments” and water samples with certain dissolved radon concentrations can be used to realize radon detector calibration. This method avoids the risk of radioactive leakage and solves the current widespread difficulties and bottleneck of radon detector calibration in seismic systems in China. The comparison experiment with the traditional calibration method shows that the error of the calibration coefficient obtained by the new method is less than 5% compared with that by the traditional method, which meets the requirements of seismic observation systems, confirming the reliability of the new method. This new method can completely replace the traditional calibration method of using a radon source in seismic systems. [ABSTRACT FROM AUTHOR]

Objectives: To investigate the correlations of initial lab and imaging findings in COVID-19 patients of different clinical types. Methods: We retrospective analyzed patients confirmed with COVID-19 in the Fifth Medical Center of the People’s Liberation Army (PLA) General Hospital between February to April 2020, selected a total of 58 (N) patients with lab and imaging examinations that met the study criteria, using Artificial intelligence (AI) software to calculate the percentage of COVID-19 lesions in the volume of the whole lung, then the correlations of general information, initial chest CT examination after admission and laboratory examinations were analyzed. Results: The 58 (N) COVID-19 patients were divided into mild group [41(n) cases] and severe group [17(n) cases] according to patient’s condition. CT findings of the severe group and mild group mainly included single or multiple ground glass opacity (GGO), with lesions mainly distributed in the periphery of lungs or GGO mixed with consolidation, with lesions involved in peripheral and central areas of both lungs, accompanied other signs. A significant difference in CRP, IL-6, D-D, GGT was observed between the two groups (p < 0.05). The ratios regarding lymphocyte abnormality and neutrophil abnormality in the severe group were higher than those in the mild group (p < 0.05). Conclusion: The CT features at initial diagnosis of COVID-19 were mainly characterized by multiple GGO with or without partial consolidation in both lungs, with the lesions mainly distributed at the subpleural regions. Some lab test indexes were correlated with the clinical types of COVID-19. [ABSTRACT FROM AUTHOR]

Viral infection of cells is sensed by pathogen recognition receptors that trigger an antiviral innate immune response, and consequently viruses have evolved countermeasures. Vaccinia virus (VACV) evades the host immune response by expressing scores of immunomodulatory proteins. One family of VACV proteins are the BTB-BACK (broad-complex, tram-trac, and bric-a-brac [BTB] and C-terminal Kelch [BACK]) domain-containing, Kelch-like (BBK) family of predicted cullin-3 E3 ligase adaptors: A55, C2, and F3. Previous studies demonstrated that gene A55R encodes a protein that is nonessential for VACV replication yet affects viral virulence in vivo. Here, we report that A55 is an NF-κB inhibitor acting downstream of IκBα degradation, preventing gene transcription and cytokine secretion in response to cytokine stimulation. A55 targets the host importin α1 (KPNA2), acting to reduce p65 binding and its nuclear translocation. Interestingly, while A55 was confirmed to coprecipitate with cullin-3 in a BTB-dependent manner, its NF-κB inhibitory activity mapped to the Kelch domain, which alone is sufficient to coprecipitate with KPNA2 and inhibit NF-κB signaling. Intradermal infection of mice with a virus lacking A55R (vΔA55) increased VACV-specific CD8+ T-cell proliferation, activation, and cytotoxicity in comparison to levels of the wild-type (WT) virus. Furthermore, immunization with vΔA55 induced increased protection to intranasal VACV challenge compared to the level with control viruses. In summary, this report describes the first target of a poxvirus-encoded BBK protein and a novel mechanism for DNA virus immune evasion, resulting in increased CD8+ T-cell memory and a more immunogenic vaccine. [ABSTRACT FROM AUTHOR]

Deep eutectic solvents (DESs) offer attractive options for the "green" dissolution of cellulose. However, the protic hydroxyl group causes weak dissolving ability of DESs, requiring the substitution of hydroxyl groups in the cation. In this study, a novel allyl-functionalized DES was synthesized and characterized, and its possible effect on improved dissolution of cellulose was investigated. The DES was synthesized by a eutectic mixture of allyl triethyl ammonium chloride ([ATEAm]Cl) and oxalic acid (Oxa) at a molar ratio of 1:1 and a freezing point of 49 °C. The [ATEAm]Cl- Oxa exhibited high polarity (56.40 kcal/mol), dipolarity/polarizability effects (1.10), hydrogen-bond donating acidity (0.41), hydrogen-bond basicity (0.89), and low viscosity (76 cP at 120 °C) owing to the p-p conjugative effect induced by the allyl group. The correlation between temperature and viscosity on the [ATEAm]Cl-Oxa fit the Arrhenius equation well. The [ATEAm]Cl-Oxa showed low pseudo activation energy for viscous flow (44.56 kJ/mol). The improved properties of the [ATEAm]Cl-Oxa noticeably promoted the solubility (6.48 wt.%) of cellulose. [ABSTRACT FROM AUTHOR]

A series of choline chloride-based deep eutectic solvents (ChCl-DESs) were synthesized and characterized, and their performance in the dissolution of cellulose was investigated. The hydrogen-bond donors significantly (β-value) affected the properties of ChCl-DESs, causing differentiated dissolution performances. ChCl- imidazole (Im) showed the highest Hammett acidity function (1.869), hydrogen bond basicity (0.864), and dipolarity/polarizability effect (0.382) among the ChCl-DESs. The ChCl-Im showed the lowest pseudo-activation energy for viscous flow (31.76 kJ mol-1) among the ChCl-DESs. The properties of ChCl-Im caused the highest solubility of cellulose (2.48 wt.%) relative to the other ChCl-DESs. Polyethylene glycol (PEG), as a co-solvent, significantly (β-value) enhanced the accessibility of ChCl-Im to cellulose by breaking the supramolecular structure of cellulose, promoting its dissolution. The decrystallization of ChCl-Im-coupled PEG approximately doubled the dissolving capabilities, and the solubility increased by more than 80% in comparison with only ChCl-Im. The cellulose was directly dissolved by ChCl-Im-coupled PEG, and no other derivatives were produced. [ABSTRACT FROM AUTHOR]

With the distributed generation technology widely applied, some system problems such as overvoltages and undervoltages are gradually remarkable, which are caused by distributed generations like wind energy system (WES) and photovoltaic system (PVS) because of their probabilistic output power which relied on natural conditions. Since the impacts of WES and PVS are important in the distribution systemvoltage quality, we study these in this paper using newmodels with the probability density function of node voltage and the cumulative distribution function of total losses. We apply these models to solve the IEEE33 distribution system to be chosen in IEEE standard database. We compare our method with the Monte Carlo simulation method in three different cases, respectively. In the three cases, these results not only can provide the important reference information for the next stage optimization design, system reliability, and safety analysis but also can reduce amount of calculation. [ABSTRACT FROM AUTHOR]

Presents a study which cloned two cDNA of metallothionein in a freshwater crucian carp. Methodology; Results; Discussion.

To utilize the multiple functions and give full play of ginsenosides, a variety of ginsenosides with different structures were prepared into liposomes and evaluated for their effect on the stability, pharmacokinetics and tumor targeting capability of liposomes. The results showed that the position and number of glycosyl groups of ginsenosides have significant effect on the in vitro and in vivo properties of their liposomes. The pharmacokinetics of ginsenosides liposomes indicated that the C-3 sugar group of ginsenosides is beneficial to their liposomes for longer circulation in vivo. The C-3 and C-6 glycosyls can enhance the uptake of their liposomes by 4T1 cells, and the glycosyls at C-3 position can enhance the tumor active targeting ability significantly, based on the specific binding capacity to Glut 1 expressed on the surface of 4T1 cells. According to the results in the study, ginsenoside Rg3 and ginsenoside Rh2 are potential for exploiting novel liposomes because of their cholesterol substitution, long blood circulation and tumor targeting capabilities. The results provide a theoretical basis for further development of ginsenoside based liposome delivery systems. [ABSTRACT FROM AUTHOR]

Vaccinia virus (VACV) is a large DNA virus that encodes scores of proteins that modulate the host immune response. VACV protein C4 is one such immunomodulator known to inhibit the activation of both the NF-κB signaling cascade and the DNA-PK-mediated DNA sensing pathway. Here, we show that the N-terminal region of C4, which neither inhibits NF-κB nor mediates interaction with DNA-PK, still contributes to virus virulence. Furthermore, this domain interacts directly and with high affinity to the C-terminal domain of filamin B (FLNB). FLNB is a large actin-binding protein that stabilizes the F-actin network and is implicated in other cellular processes. Deletion of FLNB from cells results in larger VACV plaques and increased infectious viral yield, indicating that FLNB restricts VACV spread. These data demonstrate that C4 has a new function that contributes to virulence and engages the cytoskeleton. Furthermore, we show that the cytoskeleton performs further previously uncharacterized functions during VACV infection. [ABSTRACT FROM AUTHOR]

The dissolution of cellulose is an important pretreatment method required for some of its catalytic conversion processes. Morpholinium-based ionic liquids (ILs) are challenging solvent choices available for "greener" and "cheaper" dissolution of cellulose. In this study, morpholinium-based ILs were prepared, and their influencing factors were experimentally investigated. The unique bipolar chemical structure derived from oxygen (electron-rich center) and nitrogen (electron-poor center) considerably enhanced the Hammett acidity function (H0) of task-ILs. N-Methyl-N-allylmorpholinium acetate IL showed the highest H0 (2.324) and polarizability power (1.096). The anion of ILs determined the hydrogen bond basicity (β). The acetate anion contributed to β (0.88) values. As to fluid properties, the morpholinium-based ILs exhibited much lower viscosity. The properties of ILs improved the dissolution efficiency. The cellulose was directly dissolved in morpholinium-based Ils, and no other derivatives were formed. The cations and the anions of ILs studied reacted with oxygen and hydrogen atoms on the hydroxyl groups of cellulose, respectively. [ABSTRACT FROM AUTHOR]

RIG-I is an intracellular RNA virus sensor that mediates a signaling pathway that triggers the alpha/beta interferon (IFN-α/β) immune defenses. However, the mechanism for regulation of RIG-I activity remains largely unknown. Here we show that RIG-I activity is regulated by phosphorylation and dephosphorylation in its repressor domain (RD). Threonine at amino acid (aa) 770 and serine at aa 854 to 855 of RIG-I are phosphorylated by casein kinase II (CK2) in the resting state of the cell and dephosphorylated when cells are infected by RNA virus. Mutation at aa position 770 or 854 to 855 of RIG-I renders it constitutively active. Pharmacological inhibition of CK2 enhances virus-induced expression of IFN-β and suppresses virus proliferation, while inhibition of phosphatase reduces virus-induced expression of IFN-β. Overexpression of CK2 suppresses RIG-I-mediated signaling, while silencing of CK2 results in the increased suppression of virus proliferation. Our results reveal a novel mechanism of the regulation of RIG-I activity during RNA virus infection. [ABSTRACT FROM AUTHOR]

Vaccinia virus (VACV) protein N1 is an intracellular virulence factor and belongs to a family of VACV B-cell lymphoma (Bcl)-2-like proteins whose members inhibit apoptosis or activation of pro-inflammatory transcription factors, such as interferon (IFN) regulatory factor-3 (IRF-3) and nuclear factor-κB (NF-κB). Unusually, N1 inhibits both apoptosis and NF-κB activation. To understand how N1 exerts these different functions, we have mutated residues in the Bcl-2-like surface groove and at the interface used to form N1 homodimers. Mutagenesis of the surface groove abolished only the N1 anti-apoptotic activity and protein crystallography showed these mutants differed from wild-type N1 only at the site of mutation. Conversely, mutagenesis of the dimer interface converted N1 to a monomer and affected only inhibition of NF-κB activation. Collectively, these data show that N1 inhibits pro-inflammatory and pro-apoptotic signalling using independent surfaces of the protein. To determine the relative contribution of each activity to virus virulence, mutant N1 alleles were introduced into a VACV strain lacking N1 and the virulence of these viruses was analysed after intradermal and intranasal inoculation in mice. In both models, VACV containing a mutant N1 unable to inhibit apoptosis had similar virulence to wild-type virus, whereas VACV containing a mutant N1 impaired for NF-κB inhibition induced an attenuated infection similar to that of the N1-deleted virus. This indicates that anti-apoptotic activity of N1 does not drive virulence in these in vivo models, and highlights the importance of pro-inflammatory signalling in the immune response against viral infections. [ABSTRACT FROM AUTHOR]

It is well known that aged or senescent cells develop a complex senescence-associated secretory phenotype (SASP), which is observed both in culture and in vivo. However, the mechanisms underlying the induction of the SASP are largely unknown. We demonstrate that retinoic-acid-inducible gene-I (RIG-I) is induced through the ataxia telangiectasia mutated-interferon regulatory factor 1 (ATM-IRF1) axis in senescent cells and that RIG-I signalling mediates the expression of two important mediators of inflammation, interleukin-6 (IL-6) and IL-8. Klotho has been associated with ageing. We show here that the intracellular, but not the secreted, form of klotho interacts with RIG-I and that this interaction inhibits RIG-I-induced expression of IL-6 and IL-8 both in vitro and in vivo. Our study uncovers a mechanism in which klotho functions as an anti-ageing factor through the suppression of RIG-I-mediated inflammation. [ABSTRACT FROM AUTHOR]

Objectives: To discuss the value of applying magnetic resonance diffusion-weighted imaging (DWI) to evaluate inflammatory activity from chronic viral hepatitis B. Methods: One hundred forty-two patients with chronic viral hepatitis B who received treatment at The Fifth Medical Center of Chinese PLA General Hospital from January 2014 to December 2015 and 20 healthy persons in the control group who were scheduled to undergo nuclear magnetic resonance scanning and DWI examinations (b value = 0, 800 s/mm²), and the apparent diffusion coefficients (ADCs) were measured and compared with the biopsy results of hepatic tissue. Results: The ADC value of the group with hepatitis B was lower than that of the healthy group (P<0.05), and the ADC value of the group with mild inflammation (G1) significantly differed from that of the group with moderate inflammation (G2) and that of the group with severe inflammation (G3-G4) (P<0.05). Conclusions: Magnetic resonance diffusion-weighted imaging technology has high clinical value for evaluating the inflammatory activity from chronic hepatitis B, and the measured ADC value corresponds to the pathological grade well, so this method is worth clinical promotion and application. [ABSTRACT FROM AUTHOR]

• BBB damage and astrocyte activation are important cause of recurrent epilepsy. • Losartan treatment reduced astrocyte activation and BBB damage after SE. • Losartan has a direct antiepileptic effect. • Losartan may be a useful antiepileptic agent in the clinic. Blood-brain barrier (BBB) damage and astrocyte activation are important cause of recurrent epilepsy. There is experimental evidence for increased angiotensin receptor type 1 (AT1) expression during BBB breakdown and brain injury, and that blocking the AT1 receptor (e.g., with losartan) can improve microcirculation, attenuate inflammation and oxidative stress, and exhibit neuroprotective effects. Thus, in the present study, we examined the effects of losartan on status epilepticus-induced astrocyte activation and BBB damage in the lithium–pilocarpine model of epilepsy in rats. We found that losartan treatment reduced astrocyte activation and BBB damage. However, under physiological condition, losartan have not effect on BBB permeability and astrocyte activation. Further, losartan exhibited a direct antiepileptic effect, which was mediated, at least in part by normalizing AQP4 expression after SE. As the changes of AQP4 expression were closely related to astrocyte activation and BBB permeability, the antiepileptic action of losartan likely relates to its effects on astrocyte activation and BBB permeability. Overall, these data suggest that losartan may be a useful antiepileptic agent in the clinic, either alone or in combination with other antiepileptic drugs. [ABSTRACT FROM AUTHOR]

Exponential consensus of non-linear stochastic multi-agent systems is investigated. The authors consider a class of non-linear stochastic multi-agent systems that are subject to time-varying delays, randomly occurring uncertainties and randomly occurring non-linearities. Impulsive pinning control algorithms are proposed to ensure that follower agents track the leader under a fixed topology. On the basis of the Lyapunov function and the Halanay differential inequality of impulsive dynamical systems, we derive sufficient conditions for the globally exponential consensus of the multi-agent systems. Finally, numerical simulations demonstrate the effectiveness of the proposed theoretical results. [ABSTRACT FROM AUTHOR]

Cement-emulsified asphalt mortar (CAM) is a critically important engineering material for a slab ballastless track. Segregation, which results in a density difference between the upper and lower part of the hardened CAM, is the most important factor that affects construction quality in practice. With the aim of decreasing the segregation of CAM, a minute amount of associative thickener, in which the mass ratio of the thickener to emulsified asphalt was 0, 0.2, 0.4, 0.6, 0.8, and 1.0%, respectively, has been incorporated into CAM, and the effects were systematically studied in terms of rheological behavior, segregation, microstructure, and construction quality of CAM. The results showed that the segregation resistance of hardened CAM was dramatically improved by increasing the thickener, whereas the rheological behavior characterized by the workability and fluidity indexes was prone to worsen. Considering the technical and economic aspects, an optimum mass ratio of the associative thickener to emulsified asphalt of 0.4% was recommended. Simultaneously, the microstructure analysis indicated the proper amount of thickener takes an active role in the compacting matrix and in refining the pores of the hardened CAM. Furthermore, in the practical application, the thickener could increase both the surface hardness and homogeneity of CAM. [ABSTRACT FROM AUTHOR]

During the Wenchuan Fault Scientific Drilling Project, we determined the values of total mercury (HgT) and gaseous elemental mercury (GEM) from drilled cores and drilling mud, respectively. Geochemical analysis shows HgT values ranging from 0.24 to 6.45 ng/g for the Penguan complex and from 2.90 to 137.54 ng/g for T3 sediment. The average levels of HgT for the Penguan complex and T3 sediments are 1.81 ± 0.26 ng/g and 23.96 ± 4.80 ng/g, respectively. Major anomalous peaks of HgT appear at depth of 614,731,993 and 1,107 m, which correspond to the long-term high seismic activity during crustal deformation in response to tectonic stresses. Gaseous elemental mercury dissolved in drilling mud was also analyzed. We found fluid inflow zones with high GEM at depths of 590-750 m, suggesting that fluid-filled ruptures exist in the LMS fault zone. It indicates that mercury provides geochemical evidence for inflow zones and ruptures/fault zones in the Wenchuan Ms 8.0 earthquake fault. [ABSTRACT FROM AUTHOR]

As the energy conservation and emission reduction and sustainable development have become the hot topics in the world, low carbon issues catch more and more attention. Logistics, which is one of the important economic activities, plays a crucial role in the low carbon development. Logistics leads to some significant issues about consuming energy and carbon emissions. Therefore, reducing energy consumption and carbon emissions has become the inevitable trend for logistics industry. Low carbon logistics is introduced in these situations. In this paper, from the microcosmic aspects, we will bring the low carbon idea in the path optimization issues and change the amount of carbon emissions into carbon emissions cost to establish the path optimization model based on the optimization objectives of the lowest cost of carbon emissions. According to different levels of air pollution, we will establish the double objectives path optimization model with the consideration of carbon emissions cost and economy cost. Use DNA-ant colony algorithm to optimize and simulate the model. The simulation indicates that DNA-ant colony algorithm could find a more reasonable solution for low carbon logistics path optimization problems. [ABSTRACT FROM AUTHOR]

The transcription factor NF-κB is essential for immune responses against pathogens and its activation requires the phosphorylation, ubiquitination and proteasomal degradation of IκBα. Here we describe an inhibitor of NF-κB from vaccinia virus that has a closely related counterpart in variola virus, the cause of smallpox, and mechanistic similarity with the HIV protein Vpu. Protein A49 blocks NF-κB activation by molecular mimicry and contains a motif conserved in IκBα which, in IκBα, is phosphorylated by IKKβ causing ubiquitination and degradation. Like IκBα, A49 binds the E3 ligase β-TrCP, thereby preventing ubiquitination and degradation of IκBα. Consequently, A49 stabilised phosphorylated IκBα (p-IκBα) and its interaction with p65, so preventing p65 nuclear translocation. Serine-to-alanine mutagenesis within the IκBα-like motif of A49 abolished β-TrCP binding, stabilisation of p-IκBα and inhibition of NF-κB activation. Remarkably, despite encoding nine other inhibitors of NF-κB, a VACV lacking A49 showed reduced virulence in vivo. [ABSTRACT FROM AUTHOR]

A correction to the article "Klotho suppresses RIG-I-mediated senescence-associated inammation" that was published online on February 20, 2011 is presented.

Recognition of viruses by pattern recognition receptors (PRRs) causes interferon-β (IFN-β) induction, a key event in the antiviral innate immune response, and also a target of viral immune evasion. Here the vaccinia virus (VACV) protein C6 is identified as an inhibitor of PRR-induced IFN-β expression by a functional screen of select VACV open reading frames expressed individually in mammalian cells. C6 is a member of a family of Bcl-2-like poxvirus proteins, many of which have been shown to inhibit innate immune signalling pathways. PRRs activate both NF-κB and IFN regulatory factors (IRFs) to activate the IFN-β promoter induction. Data presented here show that C6 inhibits IRF3 activation and translocation into the nucleus, but does not inhibit NF-κB activation. C6 inhibits IRF3 and IRF7 activation downstream of the kinases TANK binding kinase 1 (TBK1) and IκB kinase-ε (IKKε), which phosphorylate and activate these IRFs. However, C6 does not inhibit TBK1-and IKKε-independent IRF7 activation or the induction of promoters by constitutively active forms of IRF3 or IRF7, indicating that C6 acts at the level of the TBK1/IKKε complex. Consistent with this notion, C6 immunoprecipitated with the TBK1 complex scaffold proteins TANK, SINTBAD and NAP1. C6 is expressed early during infection and is present in both nucleus and cytoplasm. Mutant viruses in which the C6L gene is deleted, or mutated so that the C6 protein is not expressed, replicated normally in cell culture but were attenuated in two in vivo models of infection compared to wild type and revertant controls. Thus C6 contributes to VACV virulence and might do so via the inhibition of PRR-induced activation of IRF3 and IRF7. [ABSTRACT FROM AUTHOR]

gC1qR is one of the C1q receptors implicated in the regulation of innate and adaptive immunity. We found that gC1qR inhibits RIG-I and MDA5-dependent antiviral signaling. Double stranded RNA and virus trigger the translocation of gC1qR to the mitochondrial outer membrane leading to the interaction of gC1qR with the RIG-I and MDA5 adaptor. VISA/MAVS/IPS-1/Cardif. The interaction of gC1qR with VISA/MAVS/IPS-1/Cardif at mitochondria results in the disruption of RIG-I and MDA5 signaling and the promotion of virus replication. Knockdown of endogenous gC1qR enhances RIG-I- dependent antiviral signaling, and augments the inhibition of virus proliferation. Therefore, gC1qR is a physiological inhibitor of the RIG-I and MDA5-mediated antiviral signaling pathway. These data uncover a new viral mechanism used to negatively control antiviral signaling in host cells. [ABSTRACT FROM AUTHOR]