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The melon fly Zeugodacus cucurbitae Coquillett (Diptera: Tephritidae) is an agricultural quarantine pest threatening fruit and vegetable production. Heat shock cognate 70 (Hsc70), which is a homolog of the heat shock protein 70 (Hsp70), was first discovered in mice testes and plays an important role in spermatogenesis. In this study, we identified and cloned five Hsc70 genes from melon fly, namely ZcHsc70_1/2/3/4/5. Phylogenetic analysis showed that these proteins are closely related to Hsc70s from other Diptera insects. Spatiotemporal expression analysis showed that ZcHsc70_1 and ZcHsc70_2 are highly expressed in Z. cucurbitae testes. Fluorescence in situ hybridization further demonstrated that ZcHsc70_1 and ZcHsc70_2 are expressed in the transformation and maturation regions of testes, respectively. Moreover, RNA interference-based suppression of ZcHsc70_1 or ZcHsc70_2 resulted in a significant decrease of 74.61% and 63.28% in egg hatchability, respectively. Suppression of ZcHsc70_1 expression delayed the transformation of sperm cells to mature sperms. Meanwhile, suppression of ZcHsc70_2 expression decreased both sperm cells and mature sperms by inhibiting the meiosis of spermatocytes. Our findings show that ZcHsc70_1/2 regulates spermatogenesis and further affects the male fertility in the melon fly, showing potential as targets for pest control in sterile insect technique by genetic manipulation of males. [Display omitted] • Two heat shock cognate 70 genes were identified to be highly expressed in the testis of melon fly. • FISH results demonstrated that ZcHsc70_1/2 are expressed in the transformation and maturation regions of the testis. • RNAi-mediated suppression of ZcHsc70_1/2 resulted in a reduction of spermatid production and then affected male fertility. [ABSTRACT FROM AUTHOR]

Propylene glycol (PG) and vegetable glycerin (VG) are the most common solvents used in electronic cigarette liquids. No long-term inhalation toxicity assessments have been performed combining conventional and multi-omics approaches on the potential respiratory effects of the solvents in vivo. In this study, the systemic toxicity of aerosol generated from a ceramic heating coil-based e-cigarette was evaluated. First, the aerosol properties were characterized, including carbonyl emissions, the particle size distribution, and aerosol temperatures. To determine toxicological effects, rats were exposed, through their nose only, to filtered air or a propylene glycol (PG)/ glycerin (VG) (50:50, %W/W) aerosol mixture at the target concentration of 3 mg/L for six hours daily over a continuous 28-day period. Compared with the air group, female rats in the PG/VG group exhibited significantly lower body weights during both the exposure period and recovery period, and this was linked to a reduced food intake. Male rats in the PG/VG group also experienced a significant decline in body weight during the exposure period. Importantly, rats exposed to the PG/VG aerosol showed only minimal biological effects compared to those with only air exposure, with no signs of toxicity. Moreover, the transcriptomic, proteomic, and metabolomic analyses of the rat lung tissues following aerosol exposure revealed a series of candidate pathways linking aerosol inhalation to altered lung functions, especially the inflammatory response and disease. Dysregulated pathways of arachidonic acids, the neuroactive ligand-receptor interaction, and the hematopoietic cell lineage were revealed through integrated multi-omics analysis. Therefore, our integrated multi-omics approach offers novel systemic insights and early evidence of environmental-related health hazards associated with an e-cigarette aerosol using two carrier solvents in a rat model. [Display omitted] • Aerosol generated from e-cigarettes loaded with PG/VG was characterized. • Clinical observations, blood analyses and histopathology did not identify toxicity. • Transcriptome, proteomics and metabolomics on rat lung tissues were analyzed. [ABSTRACT FROM AUTHOR]

The outer membrane (OM) of Gram-negative bacteria is asymmetric, with lipopolysaccharides (LPSs) on the outer surface and phospholipids (PLs) on the inner surface. This unique organization of OM makes Gram-negative bacteria resistant to many toxic chemicals. How this asymmetric distribution of lipids is maintained has been studied for decades with previous reports of an Mla (M aintenance of OM L ipid A symmetry) system to be involved. Furthermore, the OM of Gram-negative bacteria is about 20 nm away from inner membrane (IM) where the lipids are synthesized. Therefore, how nascent lipids travel across the periplasmic space and arrive at the inner surface of OM is another interesting question. YebT is a homologue of MlaD in the Mla pathway, but its role in lipid distribution of the OM and IM is largely unknown. Here we report the first high-resolution (~3.0 Å) cryo-EM structure of full-length E. coli YebT in a substrate-bound state. Our structure with details of lipid interaction indicates that YebT is a lipid transporter spanning between IM and OM. We also demonstrate the symmetry mismatch in YebT and the existence of many other conformations of YebT revealing the intrinsic dynamics of this lipid channel. And a brief discussion on possible mechanisms of lipid transport is also included. Image 1 • YebT hexamer is a highly dynamic complex with many conformations. • YebT has a hydrophobic central channel for lipid transport. • Lipid binding sites of YebT locate between MCE5 and MCE6. • YebT bound with lipid has a symmetry mismatch. [ABSTRACT FROM AUTHOR]

Abstract In unstructured mobile peer-to-peer systems (MP2P), the frequent link breakages lead frequent topology mismatching problems and data transmission failures due to high mobility of nodes. The overhead of data transmission and synchronization cannot be neglected. In order to keep the data consistent, flooding is a fundamental and straightforward data synchronization mechanism since a mobile node does not know which else has the same shared data item. However, data flooding causes the broadcast storm problem. In this paper, we propose a mobility-aware data update approach (MADU) to improve the data dissemination and to reduce the overhead of maintaining the consistency of shared data items in an MP2P network. We use safe-time which is derived from the neighbor's location and speed to determine the time for a node to do the checking and updating between the neighbor nodes and itself. We also consider the network connectivity of a mobile node and access frequency of a data item as the factors to trigger the update process. By combining the mobility information of nodes, network connectivity, and access frequency of data items, we set a reasonable data update mechanism, which can significantly decrease the number of retransmissions and redundant messages so as to reduce the overhead of maintaining the data consistency. [ABSTRACT FROM AUTHOR]

Abstract Ionic rare earth mining is of strategic importance in China; however, the heavy metal pollution it causes is of great concern, both at home and abroad. Data on Pb speciation at a rare earth mine were used to analyse the migration capacity of Pb during the process of ore leaching. The major factors thought to influence the migration capacity of Pb, including the clay mineral content, soil pH, oxidation-reduction potential, organic matter content, and cation exchange capacity (CEC), were quantified. Entropy and fuzzy clustering methods were used to identify the most predictive factors. The results showed that the clay mineral content of the soil exerts the strongest influence on the migration capacity of Pb in rare earth mines; the other factors demonstrated relatively weak influences on the transport processes. The results obtained from the classification of Pb per the potential migration index (PMI) approximated those obtained from fuzzy clustering, and the results of entropy analyses were consistent with those of fuzzy clustering. Thus, the methods upon which the proposed model is based are suitable for predicting the migration capacity of Pb in ore during the mining of ionic rare earth minerals. Highlights • In-situ leaching during rare earth mining can lead to Pb pollution. • Acid soluble and reducible forms of Pb showed a high capacity for migration. • The entropy weight–fuzzy clustering model can effectively predict Pb migration. • Clay mineral content was found to be play an important role in Pb migration. [ABSTRACT FROM AUTHOR]

Highlights • Multi-controller coordinated deployment problem in software defined optical networks is studied in this paper. • A load balancing strategy named switch migration based controller placement algorithm (SMBCP) is proposed for multi-controller deployment. • Simulation results show SMBCP algorithm can significantly improve the load balancing and reduce the cost of switch migration. Abstract In software defined optical networks (SDON), a single controller can hardly manage all the optical devices especially in the large-scale networks, while multiple controllers deployed in the network can solve it. Recently, more and more attention has been paid to the multi-controller architecture, and the deployment of controllers is an important issue in large software defined optical networks. However, the existing architectures focus on static mapping of controllers and switches and do not consider load balance among different controllers. It is worth further studying the cooperation of multiple controllers. This paper presents a multi-controller coordinated deployment strategy (Switch Migration Based Controller Placement, SMBCP) based on load balancing. Simulation results show that SMBCP can significantly reduce the load difference among different controllers in SDON and reduce the migration cost of switches, thus improving the load balance of the controller. [ABSTRACT FROM AUTHOR]

MoS 2 is recognized as competitive low-cost and efficient electrocatalyst for water electrolysis application, and its catalytic activity needs further improving. Nitrogen doped MoS 2 nanosheets assembled flowers have been firstly synthesized as hydrogen evolution reaction (HER) catalyst. N-doping is determined by XPS characterization, which achieves boosting effect on HER activity. Edge terminated feature supplies exposed active sites for catalytic reaction. N-MoS 2 exhibits excellent HER activity with a low overpotential of 114 mV to afford a current density of 10 mA cm −2 and high stability, making it good candidate as advanced HER electrocatalyst. [ABSTRACT FROM AUTHOR]

This series of nine papers described the operation and pre-clinical assessment of a tobacco heating product THP1.0. This last paper contextualises the pre-clinical assessment data on THP1.0 with data from other next generation products relative to cigarette smoke. The tobacco and nicotine risk continuum is a concept that ranks products according to their potential harm, with cigarettes at the highest risk extreme and Nicotine Replacement Therapy at the least risky extreme. Data generated in pre-clinical studies on THP1.0 and a range of Next Generation Products (NGPs) may provide some initial indication of potential ranking of these products, although importantly, data from such studies are limited and cannot take into consideration several important aspects for risk such as long term product use patterns. In each of the studies, the responses to the emissions from THP1.0 were substantially reduced relative to cigarette smoke. Additionally, responses from THP1.0 were very similar to those from the other NGP emissions. A comparison of the results clearly showed the emissions from all the NGPs were considerably lower than those from cigarettes and all in around the same emissions level. These results show that THP1.0 could have the potential to be a reduced risk product compared to cigarettes, though further studies assessing the exposure, individual and population risk reduction profile would be required to substantiate this potential. [ABSTRACT FROM AUTHOR]

Recently, long non-coding RNAs (lncRNAs) have been shown to have critical regulatory roles in tumourigenesis. Increasing evidence has suggested that lncRNA NEAT1 has been implicated in various types of human cancer. However, the potential biological roles and regulatory mechanisms of NEAT1 in pancreatic cancer (PC) remains unclear. Here, we found that the expression level of NEAT1 was higher in PC tissues compared to the corresponding non-tumor tissues. Besides, our findings indicate that high NEAT1 expression level is closely correlated with tumor progression and poor survival in PC patients. Furthermore, we also found that knockdown of NEAT1 remarkably suppressed cell proliferation by inducing cell cycle arrest and apoptosis promotion in PC cells. Moreover, bioinformatics analysis and luciferase reporter assay revealed that NEAT1 directly bound to the miR-506-3p, which has been reported to act as a tumor suppressor in diverse cancers. Additionally, our results confirmed that the tumor-promoting effects of NEAT1 in PC cells is at least partly through negative modulation of miR-506-3p. Overall, our results suggested that NEAT1 functions as an oncogenic lncRNA in PC, which could be a novel diagnostic and therapeutic target for PC. [ABSTRACT FROM AUTHOR]

Abstract: Peroxiredoxins (Prx), a family of small non-seleno peroxidases, are important regulators for cellular reactive oxygen species (ROS), which contribute to many signaling pathways and pathogenesis of diseases. Targeting redox homeostasis is being developed as a promising therapeutic strategy for many diseases such as cancers. This mini-review attempts to focus on our recent discoveries on adenanthin as the first natural molecule to specifically target the resolving cysteines of Prx I and Prx II and thus inhibit their peroxidase activities, and its role in differentiation induction in vitro and in vivo of acute myeloid leukemic cells. [Copyright &y& Elsevier]

Abstract: One critical issue in wireless sensor networks is how to gather sensed information in an energy-efficient way since the energy is a scarce resource in a sensor node. Cluster-based architecture is an effective architecture for data-gathering in wireless sensor networks. However, in a mobile environment, the dynamic topology poses the challenge to design an energy-efficient data-gathering protocol. In this paper, we consider the cluster-based architecture and provide distributed clustering algorithms for mobile sensor nodes which minimize the energy dissipation for data-gathering in a wireless mobile sensor network. There are two steps in the clustering algorithm: cluster-head election step and cluster formation step. We first propose two distributed algorithms for cluster-head election. Then, by considering the impact of node mobility, we provide a mechanism to have a sensor node select a proper cluster-head to join for cluster formation. Our clustering algorithms will achieve the following three objectives: (1) there is at least one cluster-head elected, (2) the number of cluster-heads generated is uniform, and (3) all the generated clusters have the same cluster size. Last, we validate our algorithms through an extensive experimental analysis with Random Walk Mobility (RWM) model, Random Direction Mobility (RDM) model, and a Simple Mobility (SM) model as well as present our findings. [Copyright &y& Elsevier]

Spontaneous refolding of GdnHCl denatured bovine carbonic anhydrase II (BCA II) shows at least three phases: a burst phase, a fast phase, and a slow phase. The fast and slow phases are both controlled by proline isomerization. However, we find that in trigger factor (TF)-assisted BCA II folding, only the fast phase is catalyzed by wild-type TF, suggesting that certain proline residues are accessible in folding intermediates. The refolding yields of BCA II assisted by wild-type TF and TF mutants which lack PPIase activity are about the same, which provides further experimental evidence that the PPIase and chaperone activities of TF are independent. The binding of TF to folding intermediates during BCA II refolding was characterized by chemical crosslinking and Western blotting. A scheme for TF-assisted BCA II folding is proposed and the possible role of the TF dimer as a “binding” chaperone in vivo is discussed. [Copyright &y& Elsevier]

Ethylene signaling was addressed, for the first time, in plant responses to nitrogen dioxide (NO 2) by comparatively analyzing the performance of Arabidopsis ethylene insensitive 2 (ein2-1) with wild-type (WT) plants. Following NO 2 fumigation, severe leaf wilting and chlorosis occurred in WT plants, but much less symptoms were observed in ein2-1. The activities of superoxide dismutase (SOD), peroxidase (PRX) and catalase (CAT) were 39%, 92%, and 11% higher, respectively, in ein2-1 than in WT following NO 2 exposure. Although glutathione contents and the ratio of its reduced form (GSH) to oxidized form (GSSG) were decreased by NO 2 , an obviously alleviated degree was detected in ein2-1 relative to WT. Correspondingly, the contents of hydrogen peroxide (H 2 O 2) and malondialdehyde (MDA), and electrolyte leakage were 25%, 24%, and 29% lower, respectively, in ein2-1 than in WT. The difference of oxidative stress between two tested genotypes was also revealed by the leaf staining regarding the production and distribution of H 2 O 2 , superoxide anion (O 2 ˙ˉ), and cell death. The genes involved in antioxidation or oxidation-reduction processes mostly presented a stronger expression in ein2-1 than in WT under NO 2 stress. The photosynthesis-related parameters including chlorophyll and soluble sugar contents, net photosynthetic rate (P n), and ribulose bisphosphate carboxylase/oxygenase (Rubisco) activity and gene expression, and chlorophyll fluorescence parameters were affected, generally, to a lesser degree in ein2-1 than in WT following NO 2 fumigation. The enzymatic activities and gene expressions of invertases mostly displayed a higher level in ein2-1 relative to WT following NO 2 fumigation. For example, the activities of cytoplasmic, cell wall and vacuolar invertases were 76%, 26%, and 26% higher, respectively, in ein2-1 than in WT. Together, these data suggest that ethylene signal insensitivity efficiently improves plant tolerance to NO 2 exposure, and the possible mechanisms might be correlated with leaf antioxidative defense, photosynthesis-related processes, and sucrose metabolisms. • Ethylene insensitive mutation improves NO 2 tolerance. • The mechanism is correlated with antioxidative defense by regulating gene expression. • Differential cleavage of sucrose by invertases may play an important role. • The tolerance was positively correlated with photosynthesis efficiency. [ABSTRACT FROM AUTHOR]

Abstract Oxidized low-density lipoprotein (ox-LDL)-induced endothelial cell (EC) apoptosis is the initial step of atherogenesis and associated with Ca2+ overload. Mitochondria-associated endoplasmic reticulum (ER) membrane (MAM), regulated by tethering proteins such as phosphofurin acidic cluster sorting protein 2 (PACS2), is essential for mitochondrial Ca2+ overload by mediating ER-mitochondria Ca2+ transfer. In our study, we aimed to investigate the role of PACS2 in ox-LDL-induced apoptosis in human umbilical vein endothelial cells (HUVECs) and the underlying mechanisms. Ox-LDL dose- and time-dependently increased cell apoptosis concomitant with mitochondrial Ca2+ elevation, mitochondrial membrane potential (MMP) loss, reactive oxygen species (ROS) production, and cytochrome c release. Silencing PACS2 significantly inhibited ox-LDL-induced cell apoptosis at 24 h in addition to the effects of ox-LDL on mitochondrial Ca2+, MMP, and ROS at 2 h. Besides, ox-LDL promoted PACS2 localization at mitochondria as well as ER-mitochondria contacts at 2 h. Not only that, ox-LDL upregulated PACS2 expression at 24 h. Furthermore, silencing PACS2 inhibited ox-LDL-induced mitochondrial localization of PACS2 and MAM formation at 24 h. Altogether, our findings suggest that PACS2 plays an important role in ox-LDL-induced EC apoptosis by regulating MAM formation and mitochondrial Ca2+ elevation, implicating that PACS2 may be a promising therapeutic target for atherosclerosis. Graphical abstract Schematic illustration of how PACS2 mediates ox-LDL-increased ER-mitochondria Ca 2+ transfer and subsequent EC apoptosis. In resting ECs, there are a few ER-mitochondria contacts (MAMs) mediating ER-mitochondria Ca2+ transfer. However, ox-LDL significantly increases mitochondrial localization of PACS2, leading to elevated MAM formation to facilitate ER-mitochondria Ca2+ transfer. Subsequently, ox-LDL-induced mitochondrial Ca2+ elevation caused MMP loss and ROS production, resulting in cytochrome c release and EC apoptosis. Image 1 Highlights • PACS2 is required for oxidized low-density lipoprotein (oxLDL)-induced endothelial cell apoptosis. • Mitochondrial Ca2+ elevation is critical for oxLDL-induced mitochondrial dysfunction and endothelial cell apoptosis. • PACS2 regulates mitochondrial Ca2+ elevation by promoting MAM formation following oxLDL treatments. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) can negatively impact systemic organs, which can lead to more death and disability. However, the mechanism underlying the effect of TBI on systemic organs remains unclear. In previous work, we found that brain-derived extracellular vesicles (BDEVs) released from the injured brain can induce systemic coagulation with a widespread fibrin deposition in the microvasculature of the lungs, kidney, and heart in a mouse model of TBI. In this study, we investigated whether BDEVs can induce heart, lung, liver, and kidney injury in TBI mice. The results of pathological staining and related biomarkers indicated that BDEVs can induce histological damage and systematic dysfunction. In vivo imaging system demonstrated that BDEVs can gather in systemic organs. We also found that BDEVs could induce cell apoptosis in the lung, liver, heart, and kidney. Furthermore, we discovered that BDEVs could cause multi-organ endothelial cell damage. Finally, this secondary multi-organ damage could be relieved by removing circulating BDEVs. Our research provides a novel perspective and potential mechanism of TBI-associated multi-organ damage. • BDEVs can mediate multi-organ damage after injury. • BDEVs can induce endothelial cell injury in vivo and in vitro. • Removing circulating BDEVs can alleviate multi-organ damage after injury. [ABSTRACT FROM AUTHOR]

The ultra-long V 2 O 5 nanobelts were prepared by the improved PVD method. The performance of V 2 O 5 nanobelts photodetectors modified with Pt NPs was investigated from visible to near-infrared region, and the mechanism of enhancing the performance of V 2 O 5 nanobelts photodetectors modified by Pt NPs was revealed. [Display omitted] • Large-scale and ultra-long V 2 O 5 nanobelts have been prepared. • The property of the V 2 O 5 nanobelt photodetector is enhanced by modification with Pt NPs. • The mechanism of the formation of Schottky barrier by Pt modification is revealed. • The Pt NPs-modified V 2 O 5 nanobelt photodetector exhibits excellent performance. Schottky-contacted nanosensors have attracted extensive attention due to their high sensitivity and fast response time. In this article, we proved that the construction of Schottky contact by Pt nanoparticles (NPs) decoration can effectively improve the performance of V 2 O 5 nanobelts photodetectors. After modified by Pt NPs, the photocurrent of V 2 O 5 nanobelts is increased by more than two orders of magnitude, and the photoresponse speed is improved by at least three orders of magnitude. Detailed studies have shown that the performance enhancement is attributed to the formation of the Schottky contact at the electrode-semiconductor interface due to the decrease of surface gas adsorption and the increase of V 2 O 5 work function after Pt NPs modification. The strong built-in field in the Schottky barrier region will quickly separate photogenerated carriers, thereby reducing the electron-hole recombination rate, resulting in the fast response time and an increase in the free carrier density. Moreover, it is found that this enhancement effect can be regulated by controlling the pressure to modulating the Schottky barrier height at the interface. Overall, the Pt NPs-modified V 2 O 5 nanobelts photodetector exhibits a broad response spectrum (visible to near infrared), fast rise/fall response time (less than 6.12/6.15 ms), high responsivity (5.6 A/W), and high specific detectivity (6.9 × 108 Jones). This study demonstrates the feasibility of building a Schottky barrier to enhance the photodetection performance, which provides a general and effective strategy towards the construction and its practical application of supersensitive and fast-response nanosensors. [ABSTRACT FROM AUTHOR]

The phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway plays an important role in the development of papillary thyroid cancer. While rapamycin has been shown to exhibit anti-tumor effects, it may also activate AKT, resulting in increased cell survival and drug resistance, thereby limiting its anti-tumor effects. Resveratrol can also inhibit tumor growth by regulating the PI3K/AKT/mTOR signaling pathway. The present study investigated the anti-tumor effects of the combined use of rapamycin and resveratrol in papillary thyroid cancer. We first treated two human papillary thyroid cancer cell lines (KTC-1 and TPC-1) with single or combined administration, and examined the effects on proliferation, the cell cycle, apoptosis, and invasion/migration of papillary thyroid cancer cells. A mouse xenograft model was induced with KTC-1 and TPC-1 cells followed by treatment with single or combined administration. Body weight and tumor size were monitored to assess the toxicity of each compound. The phosphorylation of AKT and the mTORC1 target p70S6 kinase (p70S6K) in tumors was also examined. Both rapamycin and resveratrol inhibited proliferation, altered the cell cycle, and induced apoptosis of papillary thyroid cancer cells. Invasion and migration were also reduced, as was the tumor growth rate in the xenograft model. Co-administration significantly enhanced the anti-tumor effects than use of any one drug, and significantly reduced the phosphorylation of AKT and p70S6K compared to treatment with rapamycin alone. Overall, compared to single use of rapamycin or resveratrol, co-administration had a synergistic effect in inhibiting proliferation and invasion/migration of papillary thyroid cancer cells and inducing apoptosis. Resveratrol is sensitizing the anti-tumor effects of rapamycin and the PI3K/AKT/mTOR signaling is involved. Although further animal and clinical studies are needed to clarify the mechanism and assess drug safety, the present study suggests that the combination of rapamycin and resveratrol may be a promising strategy for the treatment of papillary thyroid cancer. [ABSTRACT FROM AUTHOR]

Skin photoaging refers to the phenomenon of skin aging or accelerated aging as a result of long-term UV exposure. Ultraviolet radiation can lead to DNA damage, cell apoptosis, cell growth inhibition and carcinogenic effects. Evidence suggests that hsp27 can protect cells from apoptosis induced by various stimuli in vivo and in vitro. However, modulation in hsp27 expression toward skin protection against UVB treatment has not been investigated clearly. In this study, we aimed to investigate the effects of hsp27 against UVB-induced photoaging in rat skin and to explore the underlying mechanisms. In the present study, we identified that the level of hsp27 increased after UVB irradiation induced chronic photoaging rat model. In order to investigate the function of hsp27 in UVB-induced skin photoaging, we used adeno-associated virus (AAV) to specificity reduce the expression of hsp27 in rat skin. In contrast to UVB group, we found that collagen fibers were disorganized and elastic fibers were thickened and twisted in UVB-AAV group. In the UVB-AAV group, reduced hsp27 enhanced the oxidative stress. Aging markers (SA-β-Gal staining and the protein levels of p16, p53, p21) were significantly changed in the hsp27 decreased group. However, in hsp27 deletion group, the expression of antiapoptotic factor bcl-2 was decreased, while the apoptosis factor bax was increased after UVB irradiation. These findings suggested that hsp27 was involved in oxidative stress, aging and apoptosis of skin after UV exposure. Management the expression of hsp27 can be used as a potential intervention method to alleviate UVB-induced skin damage. • Down-regulating hsp27 enhanced UVB-induced cell damage. • Hsp27 plays a protective role in skin by regulating the innate antioxidant activities. • The level of hsp27 is strongly associated with cell senescence. • Down-regulating hsp27 increased the expression of cell senescence associated proteins such as p16 and p53. • Hsp27 inhibited UVB-induced apoptosis through regulating bax and bcl-2 expression. [ABSTRACT FROM AUTHOR]

Graphical abstract Abstract Constructing novel graphic carbon nitride (g-C 3 N 4)-based nanohybrids via a facile method for high-performance polymeric materials which exhibit enhanced fire safety properties are highly desirable. Here, the g-C 3 N 4 /carbon sphere/Cu (denoted as CSACS-C) nanohybrid was prepared by metal ions-induced gel reaction using sodium alginate as a green template, and thereafter introduced into thermoplastic polyurethane (TPU) matrix to prepare nanocomposites. Microstructure analyses indicated the successful synthesis of the ternary nanohybrid, where both the g-C 3 N 4 nanosheets and Cu nanoparticles were well-dispersed in the carbon material. Moreover, the ternary nanohybrid showed good distribution in TPU matrices, and exhibited strong interfacial adhesion with the polymeric host. It is worth noting that addition of these nanohybrids led to significantly improved fire safety. Particularly, remarkably reduced pyrolysis gaseous products generation and peak of heat release rate were achieved for TPU/CSACS-C system. This enhanced fire safety was due to the interpretations that the SACS and g-C 3 N 4 nanosheets retarded the heat and mass propagation, while the incorporation of Cu nanoparticles induced earlier thermal decomposition into more char residues and less pyrolysis gaseous products. The work provides a new, simple strategy to prepare nanohybrids for polymeric materials with enhanced fire safety. [ABSTRACT FROM AUTHOR]

Highlights • A novel architecture of software-defined optical network (SDON) which is secured by quantum key distribution (QKD) is proposed to ensure the secure communication. • A flexible key-updating method (Flex-KUM) and a key-updating algorithm based on Flex-KUM and fixed method are proposed with different update periods to enhance the security. • Simulation results show Flex-KUM can realize a better security of key services (MNSK) compared with fixed update method, and a trade-off between enhanced security and resource utilization exists when considering key update. Abstract Security threat is a challenging issue for data transmission in optical networks. Quantum key distribution (QKD) is a promising security solution to optical networks to provide secure keys. Meanwhile, key update is of importance to enhance the security of key in the networks. The previous update method is to provide a fixed key-updating period which has a strong regularity to be easily found. To enhance the security of data services, we proposed a quantum key-updating process by introducing the architecture of SDON secured by QKD. Then, a flexible quantum key-updating method (Flex-KUM) and a quantum key-updating algorithm based on Flex-KUM are designed in the comparison with the fixed method with different update periods. The results show that a higher level of security requires more updating keys, which leads to an increase in the blocking probability. Therefore, there is a trade-off between the enhanced security and resources. [ABSTRACT FROM AUTHOR]

Abstract ISO 4387 Standard determines the main aerosol constituents (total particulate matter, water, nicotine, and nicotine-free-dry-particulate matter, referred to as "tar") in cigarette mainstream smoke (ISO, 2000). Heated Tobacco Products (also called Tobacco Heating Products or Heat-not-Burn Products) are designed to form aerosol by heating tobacco rather than burning like in combustible cigarettes. In this study we have evaluated the suitability of ISO 4387 Standard to be adapted for quantifying main aerosol constituents for HTP aerosol. HTP emissions have much higher levels of water and humectants (e.g., glycerol) in dynamic equilibria between gaseous and particulate phases. Several modifications to ISO 4387 Standard on aerosol collection were tested to improve the accuracy and reliability of aerosol capturing, with minimal deviation to the standard method. The proposed modifications are readily adoptable by laboratories already practicing the Standard for cigarette smoke analyses. Taking collectively with other available aerosol chemistry and biological results on HTPs in the literature, they show a fundamentally different aerosol in HTPs and call for category-specific product standards and terminology. Highlights • Heated tobacco products (HTPs) are an emerging category for regulatory consideration. • HTP emissions differ fundamentally to smoke in its aerosol constituents, e.g., water. • The differences are considered and measures are tested to improve ISO 4387 Standard for HTP testing. • Satisfactory assessment of nicotine-free-dry-particulate-matter for HTPs based on improved method is presented. • The results add to the body of evidence demonstrating different physiochemical properties of HTP aerosol. [ABSTRACT FROM AUTHOR]

Abstract Background/Aim Nasopharyngeal cancer (NPC) has a high local recurrence rate due to its resistance to ionizing radiation (IR). Replication protein A1 (RPA1) is one of the main elements in the homologous repair (HR) pathway, which is closely associated with the repair of DNA double strand breaks (DDBs). Studies on the relationship between RPA1 and the radiosensitivity of NPC are substantially limited. It was hypothesized that RPA1 plays a crucial role in predicting the radiosensitivity of NPC. Methods The protein expression of RPA1 in 182 patients with NPC in the complete response (CR) and non-complete response (nCR) groups was evaluated using immunohistochemistry. Then, univariate and multivariate analysis were performed using SPSS software vision 22 to determine the relationship between the expression of RPA1 and the clinicopathological features. In addition, the mRNA expression of RPA1 was tested in 24 fresh samples using qRT-PCR. RPA1 was silenced in CNE-2R cell lines combined with IR to measure the radiosensitivity, proliferation, DNA damage repair and cell cycle of CNE-2R cells. Xenograft models in nude mice were used to determine the effect of RPA1 on tumor growth after IR. Immunoblotting and immunofluorescence staining were performed to identify proteins that interacted with RPA1. All statistical tests were two-sided. Results RPA1 protein was overexpressed in NPC patients with nCR (65.31%), and was an independent predictor of radiosensitivity (HR: 3.755, 95% CI: 1.990–7.085), in addition to Epstein-Barr virus (EBV; HR: 3.984; 95% CI: 1.524–10.410). The silencing of RPA1 increased the radiosensitivity of CNE-2R cells, blocked the repair of DNA, impaired cell proliferation, and contributed to G2/M cell cycle arrest. Furthermore, the xenograft models in nude mice revealed that silencing RPA1 combined with irradiation significantly retarded the growth of tumors. Moreover, the knockdown of RPA1 decreased Rad51 collection to the damage site and prolonged the time of DNA repair. Conclusion RPA1 protein is frequently overexpressed in NPC patients with nCR. The silencing of RPA1 enhanced the radiosensitivity of CNE-2R cells. These present findings reveal that RPA1 is a potential biomarker for predicting the radiosensitivity in NPC. Highlights • RPA1 is highly expressed in NPC patients with radioresistance. • RPA1 can be used as a predictor of radiosensitivity in NPC. • RPA1 silencing reduces the recruitment of RAD51 at the site of the DNA lesion and inhibits the repair of DSBs. [ABSTRACT FROM AUTHOR]

The skin is the outermost protective barrier between the internal and external environment in humans. Chronic exposure to ultraviolet (UV) radiation is a major cause of photoaging. Evidence suggests that resveratrol suppresses UVB-induced photoaging. In this study, we aimed to investigate the protective effects of resveratrol against UVB-induced photoaging in HaCaT cells and to determine the underlying mechanisms. Apoptosis of normal or HSP27-overexpressing HaCaT cells in the presence of UVB was analyzed by flow cytometry. The mRNA and protein expression levels were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting. Resveratrol inhibited UVB-induced apoptosis by upregulating the expression of HSP27, reducing the production of proapoptotic proteins such as p65, Bax, and cleaved caspase-3, and promoting the expression of anti-apoptotic protein Bcl-2. However, UVB irradiation on HaCaT cells pretreated with resveratrol led to the upregulation of Bax, downregulation of Bcl-2, and promotion of p65 and caspase-3 activation after silencing of HSP27 gene. These findings suggest that the inhibition of HSP27 expression can partially reverse the anti-apoptotic effect of resveratrol and confirm that resveratrol can regulate HSP27 and thus control p65 and caspase-3 activation. In summary, resveratrol plays a role in photoprotection by upregulating HSP27 expression, increasing Bcl-2/Bax ratio, and inhibiting caspase-3 activity and p65 expression. [ABSTRACT FROM AUTHOR]

For a tobacco heating product (THP), which heats rather than burns tobacco, the emissions of toxicants in the aerosol were compared with those in cigarette smoke under a machine-puffing regimen of puff volume 55 ml, puff duration 2 s and puff interval 30 s. The list of toxicants included those proposed by Health Canada, the World Health Organization Study Group on Tobacco Product Regulation (TobReg), the US Food and Drug Administration and possible thermal breakdown products. In comparison to the University of Kentucky 3R4F reference cigarette the toxicant levels in the THP1.0 emissions were significantly reduced across all chemical classes. For the nine toxicants proposed by TobReg for mandated reduction in cigarette emissions, the mean reductions in THP1.0 aerosol were 90.6–99.9% per consumable with an overall average reduction of 97.1%. For the abbreviated list of harmful and potentially harmful constituents of smoke specified by the US Food and Drug Administration Tobacco Products Scientific Advisory Committee for reporting in cigarette smoke (excluding nicotine), reductions in the aerosol of THP1.0 were 84.6–99.9% per consumable with an overall average reduction of 97.5%. [ABSTRACT FROM AUTHOR]

A novel tobacco heating product, THP1.0, that heats tobacco below 245 °C is described. It was designed to eliminate tobacco combustion, while heating tobacco to release nicotine, tobacco volatiles and glycerol to form its aerosol. The stewardship assessment approach behind the THP 1.0 design was based on established toxicological principles. Thermophysical studies were conducted to examine the extent of tobacco thermal conversion during operation. Thermogravimetric analysis of the tobacco material revealed the major thermal behaviour in air and nitrogen up to 900 °C. This, combined with the heating temperature profiling of the heater and tobacco rod, verified that the tobacco was not subject to combustion. The levels of tobacco combustion markers (CO, CO 2 , NO and NO x ) in the aerosol of THP1.0 were significantly lower than the levels if there were any significant pyrolysis or combustion. Quantification of other tobacco thermal decomposition and evaporative transfer markers showed that these levels were, on average, reduced by more than 90% in THP1.0 aerosol as compared with cigarette smoke. The physical integrity of the tobacco consumable rod showed no ashing. Taken together, these data establish that the aerosol generated by THP1.0 is produced mainly by evaporation and distillation, and not by combustion or pyrolysis. [ABSTRACT FROM AUTHOR]

Cigarette smoking causes many human diseases including cardiovascular disease, lung disease and cancer. Novel tobacco products with reduced yields of toxicants compared to cigarettes, such as tobacco-heating products, snus and electronic cigarettes, hold great potential for reducing the harms associated with tobacco use. In the UK several public health agencies have advocated a potential role for novel products in tobacco harm reduction. Public Health England has stated that “The current best estimate is that e-cigarettes are around 95% less harmful than smoking” and the Royal College of Physicians has urged public health to “Promote e-cigarettes widely as substitute for smoking”. Health related claims on novel products such as ‘reduced exposure’ and ‘reduced risk’ should be substantiated using a weight of evidence approach based on a comprehensive scientific assessment. The US FDA, has provided draft guidance outlining a framework to assess novel products as Modified Risk Tobacco Products (MRTP). Based on this, we now propose a framework comprising pre-clinical, clinical, and population studies to assess the risk profile of novel tobacco products. Additionally, the utility of this framework is assessed through the pre-clinical and part of the clinical comparison of a commercial e-cigarette (Vype ePen) with a scientific reference cigarette (3R4F) and the results of these studies suggest that ePen has the potential to be a reduced risk product. [ABSTRACT FROM AUTHOR]

With the capacity increasing in optical networks enabled by spatial division multiplexing (SDM) technology, spatial division multiplexing elastic optical networks (SDM-EONs) attract much attention from both academic and industry. Super-channel is an important type of service provisioning in SDM-EONs. This paper focuses on the issue of super-channel construction in SDM-EONs. Mixed super-channel oriented routing, spectrum and core assignment (MS-RSCA) algorithm is proposed in SDM-EONs considering inter-core crosstalk. Simulation results show that MS-RSCA can improve spectrum resource utilization and reduce blocking probability significantly compared with the baseline RSCA algorithms. [ABSTRACT FROM AUTHOR]

Chromatin folding and dynamics are critically dependent on nucleosome–nucleosome interactions with important contributions from internucleosome binding of the histone H4 N-terminal tail K16-R23 domain to the surface of the H2A/H2B dimer. The H4 Lys16 plays a pivotal role in this regard. Using in vitro reconstituted 12-mer nucleosome arrays, we have investigated the mechanism of the H4 N-terminal tail in maintaining nucleosome–nucleosome stacking and mediating intra- and inter-array chromatin compaction, with emphasis on the role of K16 and the positive charge region, R17-R23. Analytical ultracentrifugation sedimentation velocity experiments and precipitation assays were employed to analyze effects on chromatin folding and self-association, respectively. Effects on chromatin folding caused by various mutations and modifications at position K16 in the H4 histone were studied. Additionally, using charge-quenching mutations, we characterized the importance of the interaction of the residues within the H4 positive charge region R17-R23 with the H2A acidic patch of the adjacent nucleosome. Furthermore, crosslinking experiments were conducted to establish the proximity of the basic tail region to the acidic patch. Our data indicate that the positive charge and length of the side chain of H4 K16 are important for its access to the adjacent nucleosome in the process of nucleosome–nucleosome stacking and array folding. The location and orientation of the H4 R17-R23 domain on the H2A/H2B dimer surface of the neighboring nucleosome core particle (NCP) in the compacted chromatin fiber were established. The dominance of electrostatic interactions in maintaining intra-array interaction was demonstrated. [ABSTRACT FROM AUTHOR]

This study sought to explore the effect of staphylococcal lipoteichoic acid (LTA) on autophagy in mouse mesenchymal stem cells (MSCs), and then influence osteogenesis through the change of autophagy. C3H10T1/2 cells were induced by osteogenic medium with the treatment of LTA at different concentrations (1, 5, 10 μg/mL); 3-methyladenine (3-MA) were used as the autophagy inhibitor, and rapamycin (rapamycin, Rap) were used to activate autophagy; the effects on osteogenesis were detected by alkaline phosphatase staining, alizarin red staining, real-time quantitative PCR, and western blotting; autophagic activity was investigated by the expression of LC3-Ⅱand p62 proteins. Compared with control group, the expression of osteogenesis markers was significantly up-regulated with the LTA treatment on the mRNA and protein level; the positive rate of alkaline phosphatase was enhanced in the LTA groups; and the formation of calcium nodules was increased simultaneously. The expression of LC3-Ⅱ protein was increased in LTA groups, while the expression of p62 protein was decreased. Inhibition of autophagy significantly reduced the effect of LTA on osteogenesis of MSCs; the promotion of LTA on osteogenic differentiation was further enhanced when adding rapamycin to activate autophagic activity. It provides new insight of prevention and treatment for bone infection. [ABSTRACT FROM AUTHOR]

Cigarettes with reduced circumference are increasingly popular in some countries, hence it is important to understand the effects of circumference reduction on their burning behaviour, smoke chemistry and bioactivity. Reducing circumference reduces tobacco mass burn rate, puff count and static burn time, and increases draw resistance and rod length burned during puff and smoulder periods. Smoulder temperature increases with decreasing circumference, but with no discernible effect on cigarette ignition propensity during a standard test. At constant packing density, mainstream (MS) and sidestream (SS) tar and nicotine yields decrease approximately linearly with decreasing circumference, as do the majority of smoke toxicants. However, volatile aldehydes, particularly formaldehyde, show a distinctly non-linear relationship with circumference and increases in the ratios of aldehydes to tar and nicotine have been observed as the circumference decreases. Mutagenic, cytotoxic and tumorigenic specific activities of smoke condensates (i.e. per unit weight of condensate) decrease as circumference decreases. Recent studies suggest that there is no statistical difference in mouth-level exposure to tar and nicotine among smokers of cigarettes with different circumferences. Commercially available slim cigarettes usually have changes in other cigarette design features compared with cigarettes with standard circumference, so it is difficult to isolate the effect of circumference on the properties of commercial products. However, available data shows that changes in cigarette circumference offer no discernible change to the harm associated with smoking. [ABSTRACT FROM AUTHOR]

With application of nano-sized nickel-containing particles (Nano-Ni) expanding, the health concerns about their adverse effects on the pulmonary system are increasing. However, the mechanisms for the pulmonary toxicity of these materials remain unclear. In the present study, we focused on the impacts of NiO nanoparticles (NiONPs) on sirtuin1 (SIRT1), a NAD-dependent deacetylase, and investigated whether SIRT1 was involved in NiONPs-induced apoptosis. Although the NiONPs tended to agglomerate in fluid medium, they still entered into the human bronchial epithelial cells (BEAS-2B) and released Ni 2 + inside the cells. NiONPs at doses of 5, 10, and 20 μg/cm 2 inhibited the cell viability. NiONPs' produced cytotoxicity was demonstrated through an apoptotic process, indicated by increased numbers of Annexin V positive cells and caspase-3 activation. The expression of SIRT1 was markedly down-regulated by the NiONPs, accompanied by the hyperacetylation of p53 (tumor protein 53) and overexpression of Bax (Bcl-2-associated X protein). However, overexpression of SIRT1 through resveratrol treatment or transfection clearly attenuated the NiONPs-induced apoptosis and activation of p53 and Bax. Our results suggest that the repression of SIRT1 may underlie the NiONPs-induced apoptosis via p53 hyperacetylation and subsequent Bax activation. Because SIRT1 participates in multiple biologic processes by deacetylation of dozens of substrates, this knowledge of the impact of NiONPs on SIRT1 may lead to an improved understanding of the toxic mechanisms of Nano-Ni and provide a molecular target to antagonize Nano-Ni toxicity. [ABSTRACT FROM AUTHOR]

Abstract: Nucleosome–nucleosome interaction plays a fundamental role in chromatin folding and self-association. The cation-induced condensation of nucleosome core particles (NCPs) displays properties similar to those of chromatin fibers, with important contributions from the N-terminal histone tails. We study the self-association induced by addition of cations [Mg2+, Ca2+, cobalt(III)hexammine3+, spermidine3+ and spermine4 +] for NCPs reconstituted with wild-type unmodified histones and with globular tailless histones and for NCPs with the H4 histone tail having lysine (K) acetylations or lysine-to-glutamine mutations at positions K5, K8, K12 and K16. In addition, the histone construct with the single H4K16 acetylation was investigated. Acetylated histones were prepared by a semisynthetic native chemical ligation method. The aggregation behavior of NCPs shows a general cation-dependent behavior similar to that of the self-association of nucleosome arrays. Unlike nucleosome array self-association, NCP aggregation is sensitive to position and nature of the H4 tail modification. The tetra-acetylation in the H4 tail significantly weakens the nucleosome–nucleosome interaction, while the H4 K→Q tetra-mutation displays a more modest effect. The single H4K16 acetylation also weakens the self-association of NCPs, which reflects the specific role of H4K16 in the nucleosome–nucleosome stacking. Tailless NCPs can aggregate in the presence of oligocations, which indicates that attraction also occurs by tail-independent nucleosome–nucleosome stacking and DNA–DNA attraction in the presence of cations. The experimental data were compared with the results of coarse-grained computer modeling for NCP solutions with explicit presence of mobile ions. [Copyright &y& Elsevier]

Abstract: Ikaros is an important transcription factor involved in the development and differentiation of hematopoietic cells. In this work, we found that chemotherapeutic drugs or ultraviolet radiation (UV) treatment could reduce the expression of full-length Ikaros (IK1) protein in less than 3h in leukemic NB4, Kasumi-1 and Jurkat cells, prior to the activation of caspase-3. Etoposide treatment could not alter the mRNA level of IK1 but it could shorten the half-life of IK1. Co-treatment with the proteasome inhibitor MG132 or epoxomicin but not calpain inhibitor calpeptin inhibited etoposide-induced Ikaros downregulation. Overexpression of IK1 could accelerate etoposide-induced apoptosis in NB4 cells, as evidenced by the increase of Annexin V positive cells and the more early activation of caspase 3. To our knowledge, this is the first report to show that upon chemotherapy drugs or UV treatment, IK1 could be degraded via the proteasome system in the early phase of apoptosis induction. These data might shed new insight on the role of IK1 in apoptosis and the post-translational regulation of IK1. [Copyright &y& Elsevier]

Abstract: Dendritic cells (DC), as professional antigen presenting cells, play the central role in the process of body initiating the anti-tumor immunity, and the study on DC anti-tumor vaccine has become heated in recent years. In this study, we used polyethylene glycol (PEG) to induce renal cell carcinoma (RCC) 786-O cell line fused with peripheral blood DC of healthy volunteers, and discuss the biological characteristics of fusion vaccine and its anti-tumor effects in vitro and in human immune reconstituted SCID mice model of RCC. The study found that PEG could effectively induce cell fusion, and the expressions of CD86 and HLA-DR in fusion vaccine group were significantly up-regulated compared with the DC control group; the secretion of IL-12 was much higher and longer than that of the control; the functions of dendritic cell-tumor fusion vaccine to stimulate the proliferation of allogenic T lymphocytes and to kill RCC786-O cells in vitro were significantly higher than those of the control group, and after the killing, apoptosis body was observed in the target cells; after the injection of fusion vaccine into human immune reconstituted SCID mice model of RCC786-O via vena caudalis, the volume of mice tumor was reduced significantly, proliferation index of tumor cells decreased obviously compared with that of the control group, and more hemorrhage and putrescence focuses presented, accompanying large quantity of lymphocytes soakage. The results of this experimental study shows that fusion vaccine of RCC786-O cell line and DC can significantly stimulate the proliferation of allogenic T cells and specifically inhibit and kill RCC cells in vitro and in vivo, which makes the DC–RCC786-O fusion vaccine a possible new way of effective RCC immunotherapy. [Copyright &y& Elsevier]

Abstract: We reported previously that NSC606985, a camptothecin analogue, induces apoptosis of acute myeloid leukemia (AML) cells through proteolytic activation of protein kinase C delta (ΔPKC-δ). By subcellular proteome analysis, heterogeneous nuclear ribonucleoprotein K (hnRNP K) was identified as being significantly down-regulated in NSC606985-treated leukemic NB4 cells. HnRNP K, a docking protein for DNA, RNA, and transcriptional or translational molecules, is implicated in a host of processes involving the regulation of gene expression. However, the molecular mechanisms of hnRNP K reduction and its roles during apoptosis are still not understood. In the present study, we found that, following the appearance of the ΔPKC-δ, hnRNP K protein was significantly down-regulated in NSC606985, doxorubicin, arsenic trioxide and ultraviolet–induced apoptosis. We further provided evidence that ΔPKC-δ mediated the down-regulation of hnRNP K protein during apoptosis: PKC-δ inhibitor could rescue the reduction of hnRNP K; hnRNP K failed to be decreased in PKC-δ-deficient apoptotic KG1a cells; conditional induction of ΔPKC-δ in U937T cells directly down-regulated hnRNP K protein. Moreover, the proteasome inhibitor also inhibited the down-regulation of hnRNP K protein by apoptosis inducer and the conditional expression of ΔPKC-δ. More intriguingly, the suppression of hnRNP K with siRNA transfection significantly induced apoptosis. To our knowledge, this is the first demonstration that proteolytically activated PKC-δ down-regulates hnRNP K protein in a proteasome-dependent manner, which plays an important role in apoptosis induction. [Copyright &y& Elsevier]

• A signal can be decomposed and reconstructed by group filters by DCWT in time domain. • The decomposition filters of DCWT can be chosen freely in time domain. • The reconstruction filters group can be obtained by RC equation in frequency domain. • By correlation analysis, optimized filters are solved to get main features of signal. • Decomposition and reconstruction based on convolution method is easier to implement. • The computation cost of FMPA is very low. Thus, FMPA can be used in large-scale data. This paper introduces a new kind of signal decomposition and reconstruction method called Discrete Convolution Wavelet Transform (DCWT), and it is used to analyze the accident pattern data of battery electric vehicles (BEV). Normally, some feature signals directly related to accidents can be obtained from the BEV daily monitoring system, but how can we match pursuit those similar feature signals when BEV is running? The DCWT method is proposed from the Frequency Slice Wavelet Transform (FSWT) defined in frequency-domain, but DCWT is defined in time-domain by convolution filters. Though the original signal can be easily decomposed and reconstructed by FSWT, it is difficult to use in large-scale and real-time computation. At first, a simple signal Decomposition & Reconstruction Technical Framework (DRTF) is presented. In order to reconstruct the original signal completely, it is important to discuss the reconstruction condition (RC) of DCWT and the filter selection methods. By means of the correlation analysis, an filter optimization algorithm is designed to obtain the main features of pattern signals. Finally, a feature matching pursuit algorithm based on DCWT is proposed to find the accident feature in a real BEV accident data. Summarily, this paper presents a new convolution wavelet transform method, in which the original signal can be decomposed and reconstructed by two groups of filters. The decomposition filters can be designed as need and the reconstruction filters can also be obtained by RC equation, and both of them can be easily optimized in practice. By comparing analysis, DCWT method can fast decompose signal to obtain its feature signals. Some conclusions are drawn that the DCWT method is practical and will become a new idea of signal decomposing and signal identifying. [ABSTRACT FROM AUTHOR]