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For improving the emergency capacities during road transportation accidents of dangerous goods, this paper divides the accident emergency procedure into four subsystems: accident information processing, personnel rescue and evacuation, vehicle evacuation, and rescue materials delivery. On this basis, the causal mechanism and the loop diagrams of the emergency process are established by using the System Dynamics Method and Vensim software. First, six factors including transportation distance, the degree of mechanical modernization, delay time of personnel control, delay time of traffic information release, command level coefficient, and delay time of department arrival are selected as parameters to test the model's sensitivity analysis. Then, the influences of the abovementioned factors on the observed value, such as the demand gap of on-site materials, number of people in safe area, number of vehicles in safe area, amount of disposal information, and the dynamic evolution behavior of the system, are analyzed. The results show that the transportation distance is shortened by half, and the time to fill the demand gap is reduced by 39%. The level of mechanical modernization is doubled, the peak inventory of materials in transit will increase by 9.2%, and the time to reach the peak will be shortened by 6.8%. If the delay time of personnel control is shortened by 480 s, the number of people to be evacuated in accident area will be reduced by 56. The delay time of traffic information release is shortened by 480 s, the number of vehicles to be evacuated is reduced by 74, and the time when the vehicle stops entering accident area is 1646 s in advance. The command level coefficient increases by 9.5%, and the speed of action execution increases by 9.6%. [ABSTRACT FROM AUTHOR]

Brain 'Computer Interface (BCI) is an emerging technology for communication between human brain and external devices. The traditional feature extraction method based on time-frequency characteristics cannot reflect the nonlinear characteristics of EEG signals. In order to further improve the accuracy of classification, the pretreatment method of wave threshold denossing is firstly used to improve the signal-to-noise ratio of EEG signals. Then, the feature extraction of the three kinds of imaginary motion EEG signal is carried out by the parameter-sample entropy of nonlinear dynamics, and the nonlinear features of EEG signal are preserved. Among them, the research of Motor-Imagery (MI) EEG has always been the focus of BCI that is a highspeed development field. This paper studies three classifiers including support vector machine, LVQ neural network and BP neural network. The experimental results show that BP neural network has higher recognition rate for classification and recognition of EEG signal. [ABSTRACT FROM AUTHOR]

To seek out novel promising biomarkers for predicting lung adenocarcinoma (LUAD) prognosis, we conducted this study. First, 279 upregulated and 37 downregulated differentially expressed genes were obtained from LUAD and para‐carcinoma tissues by the Affymetrix GeneChip Human Transcriptome Array. Then, we randomly classified samples of LUAD data set GSE31210 as training and testing sets in a 1:1 ratio. Alcohol dehydrogenase 1C (ADH1C) and secreted phosphoprotein 1 (SPP1) were finally identified correlating with the LUAD survival through least absolute shrinkage and selection operator penalized Cox proportion hazards regression model, and applied to build a 2‐gene signature related to prognosis in training set. Univariate and multivariable survival analyses suggested that overall survival (OS) and relapse‐free survival (RFS) in the 2‐gene signature low‐risk group were better than the high‐risk group. Kaplan–Meier curves proved that elevated ADH1C expression and reduced SPP1 expression were related to better OS and RFS. Besides, the SPP1 expressed higher in LUAD than para‐carcinoma tissues using quantitative reverse transcription polymerase chain reaction assay. Finally, the association between the two genes and clinicopathological parameters in 80 LUAD were analyzed, it is suggested that SPP1 was relevant to epidermal growth factor receptor mutation. These findings indicated that ADH1C and SPP1 might be novel promising biomarkers for predicting LUAD prognosis. [ABSTRACT FROM AUTHOR]

Cryptotanshinone (CTS), a major constituent extracted from the medicinal herb Salvia miltiorrhiza Bunge, has well-documented antioxidative and anti-inflammatory effects. In the present study, the pharmacological effects and underlying molecular mechanisms of CTS on lipopolysaccharide (LPS)-induced inflammatory responses were investigated. By enzyme-linked immunosorbent assay, we observed that CTS reduced significantly the production of proinflammatory mediators (tumor necrosis factor-α and interleukin-6) induced by LPS in murine macrophage-like RAW264.7 cells. Mechanistically, CTS inhibited markedly the phosphorylation of mitogen-activated protein kinases (MAPKs), including ERK1/2, p38MAPK, and JNK, which are crucially involved in regulation of proinflammatory mediator secretion. Moreover, immunofluorescence and western blot analysis indicated that CTS abolished completely LPS-triggered nuclear factor-κB (NF-κB) activation. Taken together, these data implied that NF-κB and MAPKs might be the potential molecular targets for clarifying the protective effects of CTS on LPS-induced inflammatory cytokine production in macrophages. [ABSTRACT FROM AUTHOR]

The potential relationship between the establishment of Foot-and-mouth disease virus (FMDV) persistent infection and gene variation was identified by investigating the variation of VP1 and 3ABC genes from yellow cattle persistent infection isolates. Five yellow cattle were inoculated on their tongue with 1.0×104 ID50/ml of FMDV O/Akesu/58 strain. After displaying clinical or subclinical signs, they probably became asymptomatic carriers. Oesophageal-pharyngeal fluids were collected monthly from the carriers with a probang and inoculated into a baby hamster kidney cell line (BHK-21); 12 FMDV isolates were obtained. The VP1 and 3ABC genes of the 12 isolates were then amplified by reverse-transcriptase polymerase chain reaction (RT-PCR). Cloning and sequencing revealed that the homology of the VP1 nucleotide and amino-acid sequence of all the isolates was above 98%, with no base deletion or insertion. When compared with the O/Akesu/58 FMDV strain, the homology of the VP1 nucleotide sequence of the isolates was only 85%, and that of the deduced amino-acid sequence only 90%.There were several nucleotide mutations in the VP1 gene of the isolates, including 16 consistent nucleotide mutations, with only two of them leading to a change in amino acid (I56→T, A210→E). Moreover, it was found that four nucleotide points and three amino-acid points had transversions among all isolates. The 3ABC gene had only 13 nucleotide transversions and five amino-acid mutations. It was presumed that persistent FMDV infection might have little connection with variation in the VP1 and 3ABC genes, and was probably related to other structural protein gene and key factors. [ABSTRACT FROM AUTHOR]

As a special type of lung cancer, multiple primary lung cancer (MPLC) has unique biological characteristics, and its research remains limited. The aim of our research was to identify prognostic factors and construct a prognostic nomogram of dual primary lung cancer (DPLC). A population cohort study of patients with DPLC was conducted using the extracted data from the Surveillance, Epidemiology, and End Results (SEER) database. Relevant survival variables were identified using the Cox proportional hazard model. Prognostic nomogram was performed and its predictive performance was validated via the modeling and validating cohort data. Additionally, propensity score matching (PSM) was also applied to evaluate whether surgery affected the OS of this study population. 5411 eligible DPLC patients were included in this study cohort, with 41.0% of 3-year OS rate and 27.7% of 5-year OS rate. Age, sex, race, grade, stage, lymph node (LN) metastasis, histological type, primary site, and surgery were considered to be prognostic factors of OS. The C-indexes of the established nomogram were 0.70 (95% CI (0.69, 0.71)) in the modeling group and 0.70 (95% CI (0.68, 0.72)) in the validation group, which showed an ideal model discrimination ability. AUC and calibration plots of 3- and 5-year OS also proved the good performance of the established nomogram. After 1 : 1 PSM, surgery can potentially reduce the risk of OS (HR = 0.63, 95% CI: 0.56–0.72) of DPLC. The prognostic nomogram with reliable performance was developed to predict 3- and 5-year OS rates, which could assist clinicians to make more reasonable survival prediction for DPLC patients. For patients without absolute surgical contraindications, surgery should be actively considered. [ABSTRACT FROM AUTHOR]

Abstract: Microbial polyhydroxyalkanoates (PHA) including poly(3-hydroxybutyrate-co-3-hydroxyhexanoate) (PHBHHx) were found to induce chondrogenesis of mesenchymal stem cells (MSCs) and preserve chondrocytic phenotype as well as support chondrocytes-specific extracellular matrix (ECM) secretion. In this study, mouse MSCs cultured on the PHBHHx films for 24 h showed up-regulated expression of chondrogenic marker genes including aggrecan, col2, sox9, col10 and pthrp. To further illustrate this phenomonon, chondrogenesis-related microRNA expression profiling was examined by quantitative real-time PCR (RT-PCR) based on results of microRNA array obtained from comparison between mouse MSCs and mature mouse chondrocytes. Among 44 microRNAs related to chondrogenesis on microrray studies, considering only broadly-conserved microRNAs, seven differentially-expressed microRNAs were selected to study their target genes related to chondrogenesis. Two microRNAs out of the seven, namely, miR-29a and miR-29b, were revealed to directly target 3′ UTR of col2a1 encoding type II collagen by dual-luciferase assay, and their activity was under the regulation of Sox9, the SRY-related high mobility group-box gene 9. For the first time microRNAs were shown to regulate the stem cell differentiation processes mediated by cell–material interactions. [Copyright &y& Elsevier]

Abstract: Mercaptoacetic acid-stabilized CdSe nanocrystals (NCs) coated with SiO2 shell have been prepared in aqueous solution at room temperature. The results showed that the characteristic UV–Vis absorption peak disappeared, the band-edge photoluminescent (PL) emission greatly increased and the surface state emission decreased after the CdSe core overcoating with SiO2 shell. The absorption spectra of the CdSe/SiO2 composites did not obviously change but the PL spectra continually varied with reaction time during, about, a month. The quantum yield of the CdSe/SiO2 composites was enhanced compared to the CdSe cores. Transmission electron microscopy (TEM) images revealed that multiple nanocores were incorporated in the spheres ranging in diameter mainly from 50 to 100nm. Very aggregated spheres might be caused by the further hydrolysis of tetraethyl orthosilicate (TEOS). The X-ray diffraction (XRD) patterns also implied that the CdSe NCs had been incorporated in the SiO2 matrix. [Copyright &y& Elsevier]

Ethnopharmacological relevance Jiang-Xian HuGan (JXHG) formulated by five natural products including Freshwater clam (Corbicula fluminea) , Curcuma longa L., Ligustrum lucidum , Eclipta prostrata (L.) L. and Paeonia lactiflora Pall. , has exhibited a great hepatoprotective effect. Aim of this study We investigated the effect of JXHG on concanavalin A (ConA)-induced acute live injury in mice, and to elucidate its underlying molecular mechanisms. Materials and methods Jiangkanling Capsule (900 mg/kg), low-dose JXHG (LJXHG, 700 mg/kg), high-dose JXHG (HJXHG, 1400 mg/kg) were administered to mice by oral gavage daily for 20 days prior to a single intravenous injection of ConA (20 mg/kg). Liver injury was evaluated by measuring the serum levels of enzymes and cytokines as well as liver histological analysis. We also measured the hepatic expression of cytokines at mRNA levels and the proteins related to NF-κB and Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) signaling pathways. Result Our results showed that JXHG pretreatment significantly alleviated ConA-induced live injury as evidenced by decreased serum levels of glutamic-pyruvic transaminase (ALT) and glutamic oxalacetic transaminase (AST), and reduced hepatocyte apoptosis and mortality. Furthermore, JXHG was able to significantly reduce the serum levels of proinflammatory cytokines, down-regulate the mRNA expression of interleukin-6 (IL-6) and interferon-γ (IFN-γ), and up-regulate IL-10 as well as superoxide-dimutase-1 (SOD1), glutathione reductase (GSR) and Glutathione peroxidase 2 (GPX2) mRNA in the liver tissues after Con A injection. In addition, JXHG pretreatment dramatically suppressed the phosphorylation of NF-κB p65 (p65), increased Nrf2 expression, and decreased the expression ratio of cleaved caspase-3/caspase-3 in liver tissues. Conclusion These results suggest that JXHG protects against ConA-induced acute live injury through inhibiting NF-κB mediated inflammatory pathway and promoting Nrf2 mediated anti-oxidative stress signaling pathway. [ABSTRACT FROM AUTHOR]

Myocardial infarction is the highest cause of cardiovascular death. Previous studies found that patients with myocardial infarction have elevated serum IL-37 and IL-37 treatment significantly alleviates adverse remodeling in myocardial infarction mice. However, the underlying mechanism of IL-37 in myocardial infarction is still unknown. Here we explored the underlying mechanism of IL-37 in attenuating myocardial infarction. The myocardial infarction mice model was constructed by left anterior descending ligation and then submitted to recombinant IL-37 administration. The histology and cardiac function were detected by HE & Masson staining and echocardiography, respectively. The macrophage phenotypes were analyzed by flow cytometry and real-time PCR. The cytokines in serum and cell culture supernatant were determined by ELISA. In addition, THP-1 cells were used in vitro to investigate the underlying mechanisms. Infarcted mice showed increased inflammatory cell infiltration and impaired cardiac function. IL-37 treatment alleviated pro-inflammatory macrophage infiltration, tissue injury, and collagen deposition in hearts on day 3 and 7 after infarction in mice. In addition, IL-37 application modulated the balance between M1 and M2 macrophages in infarcted hearts. In vitro, THP-1 cell line polarization was also regulated by IL-37, companied by YAP phosphorylation and NLRP3 inactivation. Verteporfin, a YAP inhibitor, could abolish IL-37-induced NLRP3 inhibition and M2 macrophage polarization. Our results demonstrated that IL-37 achieves a favorable therapeutical function on myocardial infarction by modulating YAP-NLRP3 mediated macrophage programming, providing a promising drug for the treatment of myocardial infarction. [ABSTRACT FROM AUTHOR]

Background and Purpose: Sirtuin 6 (SIRT6) is involved in regulation of glucose and fat metabolism. However, its possible contribution to cardiac dysfunction remains to be determined. In the present study, the effect of SIRT6 on cardiac hypertrophy induced by angiotensin II (AngII) and the underlying molecular mechanisms were investigated.Experimental Approach: The expression and deacetylase activity of SIRT6 were measured in hypertrophic cardiomyocytes induced by AngII. After SIRT6 overexpression by transfection, or depletion by RNA interference in neonatal rat cardiomyocytes, cellular hypertrophy was monitored by measuring cell surface area and the mRNA levels of hypertrophic biomarkers. Further, the interaction between SIRT6 and the transcription factor NF-κB was investigated by co-immunoprecipitation, confocal immunofluorescence microscopy and luciferase reporter gene assay. The expression and deacetylase activity of SIRT6 were measured in vivo, using the abdominal aortic constriction (AAC) model of cardiac hypertrophy in rats.Key Results: In AngII-induced hypertrophic cardiomyocytes and also in AAC-induced hypertrophic hearts, the expression of SIRT6 protein was upregulated, while its deacetylase activity was decreased. Overexpression of wild-type SIRT6 but not its catalytically inactive mutant, attenuated AngII-induced cardiomyocyte hypertrophy. We further demonstrated a physical interaction between SIRT6 and NF-κB catalytic subunit p65, whose transcriptional activity could be repressed by SIRT6 overexpression.Conclusions and Implications: Our findings suggest that SIRT6 suppressed cardiomyocyte hypertrophy in vitro via inhibition of NF-κB-dependent transcriptional activity and that this effect was dependent on its deacetylase activity. [ABSTRACT FROM AUTHOR]

BACKGROUND AND PURPOSE Sirtuin 6 (SIRT6) is involved in regulation of glucose and fat metabolism. However, its possible contribution to cardiac dysfunction remains to be determined. In the present study, the effect of SIRT6 on cardiac hypertrophy induced by angiotensin II (AngII) and the underlying molecular mechanisms were investigated. EXPERIMENTAL APPROACH The expression and deacetylase activity of SIRT6 were measured in hypertrophic cardiomyocytes induced by AngII. After SIRT6 overexpression by transfection, or depletion by RNA interference in neonatal rat cardiomyocytes, cellular hypertrophy was monitored by measuring cell surface area and the mRNA levels of hypertrophic biomarkers. Further, the interaction between SIRT6 and the transcription factor NF-κB was investigated by co-immunoprecipitation, confocal immunofluorescence microscopy and luciferase reporter gene assay. The expression and deacetylase activity of SIRT6 were measured in vivo, using the abdominal aortic constriction (AAC) model of cardiac hypertrophy in rats. KEY RESULTS In AngII-induced hypertrophic cardiomyocytes and also in AAC-induced hypertrophic hearts, the expression of SIRT6 protein was upregulated, while its deacetylase activity was decreased. Overexpression of wild-type SIRT6 but not its catalytically inactive mutant, attenuated AngII-induced cardiomyocyte hypertrophy. We further demonstrated a physical interaction between SIRT6 and NF-κB catalytic subunit p65, whose transcriptional activity could be repressed by SIRT6 overexpression. CONCLUSIONS AND IMPLICATIONS Our findings suggest that SIRT6 suppressed cardiomyocyte hypertrophy in vitro via inhibition of NF-κB-dependent transcriptional activity and that this effect was dependent on its deacetylase activity. [ABSTRACT FROM AUTHOR]

Background: The efflux of cellular cholesterol mediated by apolipoprotein (apo)A-I and ATP-binding cassette transporter A1 (ABCA1) is a major pathway of reverse cholesterol transport. We investigated the effect of aspirin on this process. Methods: The expression levels of ABCA1 in RAW264.7 cells were determined using reverse transcription polymerase chain reaction and Western blot analysis. 3H-cholesterol efflux was measured by scintillation counting. Results: 0.5 mmol/l aspirin increased apoA-I-mediated cholesterol efflux and increased the expression of ABCA1. By increasing the dose of aspirin higher than 0.5 mmol/l, ABCA1 expression and function were significantly decreased. In cells transfected with a specific peroxisome proliferator-activated receptor (PPAR)-α small interfering RNA, the induction of ABCA1 expression and apoA-I-mediated 3H-cholesterol efflux by aspirin were substantially suppressed. Conclusions: The data demonstrate that low-dose aspirin increases ABCA1 expression via a PPAR-α-dependent mechanism and increases apoA-I-mediated cholesterol efflux. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The following sections are included: Introduction Conventional Meson Spectrum Glueball Spectrum Hybrid Mesons Multiquarks Molecular States [ABSTRACT FROM AUTHOR]

The following sections are included: Baryons as qqq States Outstanding Problems in Baryon Spectroscopy Baryon Spectroscopy at BESI and BESII Prospects for Baryon Spectroscopy at BESIII [ABSTRACT FROM AUTHOR]

The following sections are included: Partially Conserved Vector Current (PCAC) and Soft Pions Beyond the Breit–Wigner Description of a Broad Resonance Final State Interaction Theorem and Omnés Solution On the Nature of the Lightest Scalar Resonances [ABSTRACT FROM AUTHOR]

The following sections are included: Introduction Experimental Status of Two-Photon Processes Measurement of Two-Photon Processes at BES-III Summary [ABSTRACT FROM AUTHOR]