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To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.jss.2008.06.042 Byline: Xingwei Wang (a), Lei Guo (a)(b), Xuetao Wei (c), Lan Pang (a), Tengfei Wu (a), Juan Du (a), Xuekui Wang (a) Keywords: Survivable networks; Multicast; Heuristic algorithm; Segment protection; Load balancing Abstract: In this paper, we investigate the problem of failure tolerated multicast requests in survivable networks and propose a new heuristic algorithm called segment protection with load balancing (SPLB) to address the single-link failure. In order to obtain better performances, in SPLB first we consider the techniques of cross-sharing and self-sharing to improve the resource utilization ratio, second we propose a segment protection routing algorithm to overcome the trap problem, and third we design a load balancing method to reduce the blocking probability. Compared with conventional algorithm, SPLB performs better performances. Simulation results meet our expectation. Author Affiliation: (a) College of Information Science and Engineering, Northeastern University, Shenyang 110004, China (b) Key Laboratory of Broadband Optical Fiber Transmission and Communication Networks, University of Electronic Science and Technology of China, Chengdu 610054, China (c) Department of Computer Science and Engineering, University of California, Riverside, CA 92521, USA Article History: Received 13 March 2008; Revised 29 June 2008; Accepted 29 June 2008 Article Note: (footnote) [star] The preliminary work of this paper was presented at the International Conference on Advanced Communication Technology (ICACT) 2008. This work was supported in part by the National Natural Science Foundation of China (Nos. 60673159, 70671020), the National High-Tech Research and Development Plan of China (No. 2006AA01Z214), the Key Project of Chinese Ministry of Education (No. 108040), the Specialized Research Fund for the Doctoral Program of Higher Education (Nos. 20070145096, 20070145017, 20060145012), the Program for New Century Excellent Talents in University, and the Open Foundation of Key Laboratory of Broadband Optical Fiber Transmission and Communication Networks, Ministry of Education (UESTC), China.

Docosahexaenoic acid [22:6(n-3), DHA] plays an important role in human physiology including gut health. This research aimed to investigate the impact of positional distribution of DHA in dietary triacylglycerols (TAG) on gut metabolomic profile and microbiota. In the 4-week feeding trial, the Sprague-Dawley rats were fed on an n-3 deficient feed supplemented with TAG containing DHA at the sn -1, 2, or 3 position and palmitic acid at the remaining positions. Three groups receiving standard n-3 adequate feed, n-3 deficient feed, or n-3 deficient feed supplemented with tripalmitin were included as controls. The gut metabolome was studied using LC–MS-based non-targeted metabolomics, and microbiota profiles were investigated by 16S rRNA sequencing. Compared to the n-3 adequate diet, four-week feeding on the n-3 deficient diet affected the fecal pyrimidine metabolism, steroid biosynthesis, and arginine and proline metabolism. Feeding with DHA-containing TAGs, especially TAG with DHA at sn -3 position, increased the level of N5-Carboxy aminoimidazole ribonucleotide related to purine biosynthesis and dimethylbenzimidazole involved in vitamin B2 biosynthesis. N-3 deficient diet lowered the abundance of the genus Alistipes and the species Bacteroides massiliensis in the gut microbiota. Compared to the n-3 deficient groups, feeding with DHA-containing TAGs decreased the abundance of species Prevotella sp. CAG: 1031, and feeding with sn -2 DHA resulted in an increase in the abundance of Bacteroides fragilis and a decrease in the abundance of Faecalibacterium sp. CAP 74. This is the first study showing that dietary DHA from different positions of TAG may affect gut metabolites and microbiota differently. [ABSTRACT FROM AUTHOR]

Black carbon (BC) can combine with organic matter and form secondary pollutants known as aged BC. BC and aged BC can cause respiratory system inflammation and induce lesions at relevant sites, but the underlying mechanism has remained unknown. To gain insight into the potential mechanisms, we focused on macrophages and transforming growth factor β-activated kinase 1 (TAK1) which are a crucial factor in inflammation. Our research aims to determine the role of TAK1 in macrophages in pulmonary inflammation induced by particulate matter. In this study, BC and 1,4-naphthoquinone were mixed to model aged BC (1,4NQ-BC) in atmosphere. BC induced mice lung inflammation model, lung macrophage knock-down TAK1 animal model and primary macrophage knock-down TAK1 model were used to explore whether TAK1 in macrophage is a critical role in the process of inflammation. The results showed that the expressions of inflammatory cytokines (IL-1β, IL-6, IL-33) mRNA were significantly increased and the phosphorylation of MAPK and NF-κB signaling pathway related proteins were enhanced in RAW 264.7 cell lines. In vivo studies revealed that the indicators of pulmonary inflammation (pathology, inflammatory cell numbers) and related cytokines (IL-1β, IL-6, IL-33) mRNA expressions in CD11c-Map3k7−/− animals were significantly lower than wild-type animals after mice were instilled particles. In mice primary macrophages, the expressions of IL-6, IL-33 mRNA were inhibited after TAK1 gene was knock-down. These results unequivocally demonstrated that TAK1 plays a crucial role in BC induced lung inflammation in mice, and we can infer that BC and 1,4NQ-BC cause these inflammatory responses by stimulating pulmonary macrophages. • BC has different physico-chemical properties compared with 1,4NQ-BC. • TAK1 knock-down in macrophages could alleviate mice lung inflammation induced by BC and 1,4NQ-BC. • TAK1 plays a key role in the production of IL-33 by macrophages. [ABSTRACT FROM AUTHOR]

Highlights • The skyline query is very useful in data analysis, but is has the largesize problem. • Approximate skylining finds an informative and concise set of skylinefor usability. • A linear-time algorithm is presented for approximate skylining in intwo dimensions. • Greedy solutions with indexing techniques are presented for higher dimensions. Abstract Querying databases to search for "best" objects matching users' preferences is a fundamental problem of intelligent systems and applications. The skyline query is an important tool for solving such a best-matching problem from the concept of multi-criteria optimization. However, it has the size problem as the size of the results of a skyline query grows superlinearly with the number of criteria. Here, we propose to find both the informative and concise set of skyline, a refined skyline set without similar objects. The informativeness requires the reduced set to cover the skyline, i.e., for every skyline point in the original dataset, there exists a close point in the reduced set, which help users to understand the skyline in more detail and make a better decision. The conciseness requires the size of the reduced set that can cover the skyline is as smaller as possible, which help users to make a quick decision. Finding both the informative and concise set of skyline will boost the usability of intelligent systems. More specifically, we propose two new skyline queries to find the informative and concise set of skyline: minimum skyline query, and extended minimum skyline query. The main idea is to return the minimum number of approximation objects, in which there is an object within a predefined distance threshold for each skyline object. The difference of the two query types is that the former one selects approximation objects only from skyline set, while the latter one selects from the whole dataset. We present an exact solution which computes minimum skyline in linear time for a 2 d -space. As both minimum skyline and extended minimum skyline problems are NP-hard for dimensionality at least three, we present greedy solutions that obtain a 1 + ln R approximation of the optimums. A comprehensive performance evaluation demonstrates that the size of skyline set can be effectively reduced by using the proposed (extended) minimum skyline queries and our proposed algorithms have promising results. [ABSTRACT FROM AUTHOR]

The impacts of environmental PM 2.5 on public health have become a major concern all over the world. Many studies have shown that PM 2.5 still poses a threat to public health even at very low levels. Physical or chemical reactions occur between primary particles and other components in the environment, which changes the properties of primary particles. Such newly formed particles with changed properties are called secondary particles. Ozone-oxidized black carbon (oBC) is a key part of PM 2.5 and a representative secondary particle. Macrophages extracellular traps (METs) is a means for macrophages to capture and destroy invading pathogens, thereby exercising innate immunity. Necroptosis is a kind of programmed cell death, which is accompanied by the destruction of membrane integrity, thus inducing inflammatory reaction. However, there is no research on the crosstalk mechanism between necroptosis and MET after oBC exposure. In our study, AO/EB staining, SYTOX Green staining, fluorescent probe, qPCR, Western blot, and immunofluorescence were applied. This experiment found that under normal physiological conditions, when macrophages receive external stimuli (such as pathogens; in our experiment: phorbol 12-myristate 13-acetate (PMA)), they will form METs, capture and kill pathogens, thus exerting innate immune function. However, exposure to oBC can cause necroptosis in macrophages, accompanied by increased levels of reactive oxygen species (ROS) and cytosolic calcium ions, as well as the expression disorder of inflammatory factors and chemokines, and prevent the formation of METs, lose the function of capturing and killing pathogens, and weaken the innate immune function. Notably, inhibition of necroptosis restored the formation of METs, indicating that necroptosis inhibited the formation of METs. This study was the first to explore the crosstalk mechanism between necroptosis and METs after oBC exposure. [Display omitted] • Ozone-oxidized black carbon (oBC) is a form of simulating the aging of BC in nature. • oBC can cause necroptosis in macrophages. • oBC can prevent the formation of macrophage extracellular traps (METs). • Necroptosis inhibited the formation of METs, and the two can interconvert. • Crosstalk mechanism between necroptosis and METs was explore for the first time after oBC exposure. [ABSTRACT FROM AUTHOR]

Outdoor air pollution has been classified as carcinogenic to humans (Group 1) for lung cancer, but the underlying mechanism and key toxic components remain incompletely understood. Since DNA damage and metabolite alterations are associated with cancer progression, exploring potential mechanisms linking air pollution and cancer might be meaningful. In this study, a real-time ambient air exposure system was established to simulate the real-world environment of adult male SD rats in Beijing from June 13th, 2018, to October 8th, 2018. 8-OHdG in the urine, γ-H2AX in the lungs and mtDNA copy number in the peripheral blood were analyzed to explore DNA damage at different levels. Serum non-targeted metabolomics analysis was performed. Pair-wise spearman was used to explore the correlation between DNA damage biomarkers and serum differential metabolites. Carcinogenic risks of heavy metals and PAHs via inhalation were assessed according to US EPA guidelines. Results showed that PM 2.5 and O 3 were the major air pollutants in the exposure group and not detected in the control group. Compared with control group, higher levels of 8-OHdG, mtDNA copy number, γ-H2AX and PCNA-positive nuclei cells were observed in the exposure group. Histopathological evaluation suggested ambient air induced alveolar wall thickening and inflammatory cell infiltration in lungs. Perturbed metabolic pathways identified included glycolysis/gluconeogenesis metabolism, purine and pyrimidine metabolism, etc. γ-H2AX was positively correlated with serum ADP, 3-phospho-D-glyceroyl phosphate and N-acetyl-D-glucosamine. The BaPeq was 0.120 ng/m3. Risks of Cr(VI), As, V, BaP, BaA and BbF were above 1 × 10−6. We concluded that low-level air pollution was associated with DNA damage and serum metabolomic alterations in rats. Cr(VI) and BaP were identified as key carcinogenic components in PM 2.5. Our results provided experimental evidence for hazard identification and risk assessment of low-level air pollution. [Display omitted] • Low-level air pollution could induce genetic damage and lung injury. • Low-level PM 2.5 and O 3 remarkably altered the serum metabolome profile. • Low-level air pollutants may still increase carcinogenic risk. • Cr(VI) and BaP was identified as key carcinogenic components in atmospheric PM 2.5. [ABSTRACT FROM AUTHOR]

[Display omitted] • Dysbiosis of gut microbiota and metabolites in diabetic rat were observed. • Anthocyanins were extracted from purple potato and bilberry. • Acylated and nonacylated anthocyanins increased cecal sugars. • Acylated anthocyanins modulated gut oxidative phosphorylation and purine metabolism. • 50 mg/kg acylated anthocyanins increased cecal short-chain fatty acids. Anthocyanins have been shown to have prebiotic properties. This study investigated the impact of nonacylated anthocyanins and acylated anthocyanins on fecal and cecal metabolites and colonic gut microbiota in diabetic state using 1H nuclear magnetic resonance (NMR) metabolomics and metagenomic sequencing. Zucker diabetic fatty rats fed with high-fat diet were gavaged with nonacylated anthocyanins extracted from bilberries (NAAB) or acylated anthocyanins extracted from purple potatoes (AAPP) at daily doses of 25 and 50 mg/kg body weight for 8 weeks. Lean Zucker rats fed with normal diet (ND) and high-fat diet (Con) were used as healthy controls groups. Binned NMR spectra and sequenced gene abundance were used for data analysis. Dysbiosis of colonic microbiota and gut metabolites in the diabetic rats were observed compared to the lean Zucker rats. Both anthocyanin extracts increased cecal sugar levels and the abundance of Peptostreptococcaceae sp. and decreased the abundance of Parabacteroides spp. in colon. In addition to the increased fecal short-chain fatty acids, AAPP decreased colonic Ruminococcus torques and Lachnospiraceae bacterium 4_1_37FAA abundances and increased oxidative phosphorylation. The anthocyanin extracts modulated the gut metabolism and microbiota in diabetes, with AAPP showing more regulatory and beneficial effects on diabetes. [ABSTRACT FROM AUTHOR]

Abstract: Bisphenol A (BPA) is an environmental estrogen that exhibits non-genotoxic carcinogenicity, causing concern globally. The aim was to investigate the effects of BPA on the proliferation and cell cycle of human normal breast cells HBL-100. An improved E-Screen assay was used to study cell proliferation, and flow cytometry was used to study cell cycle phases. Western blot analysis was utilized to detect cell cycle proteins and estrogen receptor α (ERα) expression. The results showed that the highest cell proliferation rate induced by BPA was at 1.0×10−6 mol/L. At 1.0×10−10, 1.0×10−8, and 1.0×10−6 mol/L, BPA promoted more cells to enter into G2/M phase and caused an increase in the expression of cyclinD1 and CDK4. After adding ICI182780 into the system, the promoting effects of BPA on cell proliferation and cell cycle change decreased, but these promoting effects were still significantly greater compared with the solvent control (P <0.05). Regardless of ICI182780 exposure, BPA did not have significant effect on ERα expression. BPA has estrogen-like activity and can stimulate HBL-100 proliferation and cell division through the estrogen receptor pathway. BPA may have other pathways through which it can exert stimulating effects and exhibit non-genotoxic carcinogenicity. [Copyright &y& Elsevier]

Black carbon (BC) reacts with different substances to form secondary pollutants called aged black carbon, which causes inflammation and lung damage. BC and aged BC may enhance IL-33 in vivo, which may be derived from macrophages. The pro-inflammatory effect of IL-33 makes it essential to determine the source of IL-33, so it guides us to explore how to alleviate lung injury. In this study, a human bronchial epithelial cell line of 16HBE cells was selected, and aged BC (1,4-NQ coated BC and ozone oxidized BC) was used. We found that both BC and aged BC were able to up-regulate the mRNA expression of IL-1β, IL-6, and IL-8 except IL-33. However, the Mitogen-activated protein kinases (MAPKs) and Phosphatidylinositol 3-kinase (PI3K)/Protein kinase B (AKTs) pathways remained inactive. After pretreatment with Lipopolysaccharide (LPS), IL-33 mRNA expression was significantly increased in 16HBE cells and MAPKs and PI3K/AKT were activated. These results suggested that MAPKs and PI3K/AKT pathways were involved in the elevation of IL-33. Furthermore, epithelial cells are unlikely to be the source of lung inflammation caused by elevated IL-33 in BC and aged BC. Image 1 • Black carbon and aged black carbon induce inflammatory effects in human bronchial epithelial cells. • BC and aged BC-induced IL-33 in HBE cells might only be up-regulated following stimuli, like LPS challenge. • MAPKs and PI3K/AKTs get involved in the elevation of IL-33 in LPS-pretreated HBE cells. • BC and aged BC increase IL-1β, IL-6 and IL-33 not via MAPKs or PI3K/AKTs. • Epithelial cells may not be the source of IL-33 elevated in BC and aged BC-induced inflammation. [ABSTRACT FROM AUTHOR]

Black carbon (BC) is a product of incomplete combustion of fossil fuels and vegetation. The compelling evidence has demonstrated that it has a close relationship with several respiratory and cardiovascular diseases. BC provides the reactive sites and surfaces to absorb various chemicals, such as polycyclic aromatic hydrocarbons (PAH). Naphthoquinone is a typical PAHs which was found in particulate matter (PM) and 1,4NQ-BC owned high oxidative potential and cytotoxicity. IL-33 is an alarmin which increases innate immunity through Th2 responses. It was reported that IL-33 was a potent inducer of pro-inflammatory cytokines, like IL-6. In our previous study, it was revealed that 1,4NQ-BC instilled intratracheally to mice could trigger the lung inflammation and stimulate the secretion of IL-33 in lung tissue. We found that IL-33 could induce inflammation in lung itself. When the macrophages were eliminated, the secretion of IL-33 was reduced and the pathological damage in the lung was relieved after exposure to 1,4NQ-BC. Both MAPK and PI3K/AKT signal pathways were involved in the process of IL-33 secretion and the lung inflammation induced by 1,4NQ-BC. The findings herein support the notion that after exposure to 1,4NQ-BC, the increased secretion of IL-33 was mainly derived from macrophages through both MAPK and PI3K/AKT signal pathways. Image 1 • IL-33 can induce lung inflammation itself. • IL-33 plays a key role in the progress which 1,4NQ-BC triggered lung inflammation. • IL-33 may derive from macrophages after 1,4NQ-BC treatment. • MAPK and PI3K/AKT pathways are involved in the lung inflammation not only mediated by IL-33, but also 1,4NQ-BC. [ABSTRACT FROM AUTHOR]

Exploiting spatial–temporal correlations has long been regarded as the cornerstone of traffic state prediction. Among existing techniques, temporal graph neural networks (TGNNs) have recently emerged as a prominent solution for modeling complex spatial–temporal traffic data correlations. Existing studies on TGNNs mainly focus on developing new building blocks to embed hidden correlations into a unified latent representation, which is mapped to predictions of distinct horizons. However, mapping the same latent features to distinct scalar predictions makes the gradient computation challenging for updating model parameters in the relevant directions. Besides, TGNNs are biased towards the shared temporal patterns while neglecting the complex dependencies within each data series, which can be captured to enrich latent features. To handle these problems jointly, we propose a novel feature projection scheme for the traffic prediction framework of TGNNs. The proposed projection scheme is based on spatial convolutions that first generate horizon-specific feature maps and then transform them into scalar predictions of the corresponding horizons. These horizon-specific feature maps establish interactions between the unified latent representation and the corresponding output values to bring the predictions closer to the true values. Besides, the proposed scheme also serves as a pattern modeling phase that enhances the expressivity of TGNNs by enriching latent features with data source-wise patterns of distinct time steps. Comprehensive experiments on two real-world traffic datasets demonstrate that the proposed scheme enhances the predictive performance and reduces the model parameters of TGNNs. • A feature projection scheme is designed to enhance performance of traffic predictors. • The proposed scheme is parameter-efficient and enhances model robustness. • Experimental results show significant reduction in predictive errors on two datasets. [ABSTRACT FROM AUTHOR]

Best objects finding is a fundamental operation in decision support systems and applications. When numerical values of objects cannot be obtained from existing computer systems or in a machine learning manner, crowdsourcing proves a viable approach via harnessing human intelligence for data gathering. Most of existing studies ask crowds to submit pairwise preferences where a large number of crowdsourced questions are produced, thereby incurring huge monetary cost and long latency. To address this issue, we propose a framework for efficient best objects computation by leveraging crowdsourcing to provide object values. The framework employs three query operators (i.e., top- k , k nn, and skyline queries) to compute best objects, and minimizes the number of crowdsourced objects by eagerly pruning non-result objects via superiority probability based ordering. We first propose the concept of superiority probability, which describes the probability that an object is better than or equal to another object from the perspective of statistics. We then explore properties for objects pruning, and propose sequential and parallel ordering techniques for objects crowdsourcing based on the concept of superiority probability. Extensive experimental results show that the proposed framework achieves the promising efficiency in reducing the number of crowdsourced objects and latency. • Leveraging crowdsourcing to obtain object values for best objects finding problem. • Reducing both monetary cost and latency using the filtering-verification framework. • An object of a high superiority probability is likely to be a best object. • The ordering techniques facilitate the pruning of non-result objects. [ABSTRACT FROM AUTHOR]

Analyzing customers’ information for marketing insights is critical for the company to remain invincible in increasingly fierce market competition. Rank-based and dominance-based customer selections are widely used for the market analysis to find prospective customers. However, rank-based solutions required companies to define weight vectors, which is not practical in real applications. Dominance-based approaches (e.g., reverse skyline queries) had problems of a high overhead and the poor progressiveness. In this paper, we propose a cost-efficient framework to find prospective customers for a target product. We first target on the most prospective customers for whom no better product exists compared with the target product. We formulate the problem based on reverse skyline queries, and propose a new algorithm that significantly reduces the query cost by pruning unqualified customers without any false positive and identifies reverse skyline points as early as possible based on decision region and effect region. We then further target on arbitrary k prospective customers and formulate the problem as top- k reverse skyline (top- k RS) queries. We extend the notion of reverse skyline to reverse skyline order in order to support arbitrary k and group-based promotions. We evaluate our framework with extensive experiments, and our results demonstrate that our framework has the promising results for reverse skyline queries, and can efficiently support top- k RS queries. [ABSTRACT FROM AUTHOR]

Accurate and timely prediction of power system states is one of the most important challenging tasks in modern power systems. Considering the integration of renewable energy sources, recent deep learning-based models have been well studied and found to have benefits in exploiting spatial–temporal relationships in power system data. However, the complexity of different power system topology structures is not substantially captured since the existing models did not fully consider the graph-based information retrieved from power networks. To resolve the problem, a spatial–temporal attention graph-based network (ST-AGNet), an adaptive power system state prediction approach that utilizes graph-based information data to account various typologies of complex power systems, is proposed. Initially, the power flow model is used for generating historical system state data. With the graph-based topology information, the input dataset with the spatial and temporal features is fed into the proposed network for the training and validating process. Meanwhile, the connectivity of the time-varying graph-based information are accounted in the proposed model. Case studies demonstrate the superiority of the ST-AGNet model over the existing baselines under four different scales of complex systems, which can significantly support dynamic power system analysis and operational tasks. • We design a generalized spatio-temporal model ST-AGNet for power system states prediction. • The proposed model incorporates an adaptive graph for a dynamic power system and considers RES. • The model uses self-attention mechanism to fuse the spatial and temporal dependencies across scales. • Case studies are conducted to analyze the outstanding performance of ST-AGNet on different dataset. [ABSTRACT FROM AUTHOR]

Abstract: An unreliable wireless communication environment and limited energy resources have a severe impact on the Quality of Service (QoS) of Mobile Ad Hoc Networks (MANETs). To improve network performance, an Energy-balanced Cooperative Media Access Control (EC-MAC) protocol in MANETs is proposed in this paper. It adopts the best partnership selection algorithm based on opportunistic relaying to select the cooperative node with the best channel conditions, highest transmission rate and most balanced energy consumption. The simulation results of EC-MAC, Cooperative MAC (CoopMAC) and IEEE 802.11 Distributed Coordination Function (DCF) protocols show that EC-MAC outperforms the other two protocols in terms of the packet delivery ratio, network throughput and network lifetime under two distinct channel noise levels, especially under the bad channel condition. Meanwhile, the EC-MAC protocol does not increase the average end-to-end delay compared with IEEE 802.11 DCF. [Copyright &y& Elsevier]

Abstract: With the growing greenhouse effect and energy crisis, energy saving has become the focus of global concern. From the perspective of networks, greening the network for building an energy-efficient network has been presented in recent years. However, in previous works, once a lightpath is established, it cannot be changed until it is released due to its holding time expiration, even though this lightpath may not be reasonably configured to current traffic. To overcome the shortcoming of previous works, this paper considers the optical bypass reconfiguration for existing lightpaths, and proposes a new power-efficient grooming algorithm (PEGA) based on the improved grooming graph model (IGGM) to reduce the average energy consumption for each demand. PEGA takes into account the energy consumptions of various components, such as core routers, transceivers, optical amplifiers, and so on. By using the optical bypass reconfiguration method based on the bypass-cascading conversion link (BCCL) in IGGM, PEGA can properly split an existing lightpath into two new lightpaths to achieve better resource utilization. Simulation results show that, compared to previous algorithm, PEGA can effectively reduce both the average energy consumption for each demand (AEED) and the blocking rate (BR). [Copyright &y& Elsevier]

Abstract: Some studies show that Cd2+ and Hg2+ may induce cell proliferation and apoptosis via biphasic dose-response relationship in human cells. However, mechanisms underlying this phenomenon are still in puzzle. In this study, we aim at detecting the biphasic effects of Cd2+ and Hg2+ on proliferation and apoptosis of human embryonic kidney 293 (HEK293) cells, analyzing the change of the mitogen-activated protein kinase (MAPK) pathways, and discussing the relationship between them. The results demonstrate that Cd2+ and Hg2+ can stimulate cell proliferation at lower concentrations (0.05 and 0.5μM) but inhibit it at higher concentrations (50 and 500μM). Apoptosis increases at higher concentrations (50 and 500μM) of Cd2+ and Hg2+. While 0.5μM Cd2+ and Hg2+ decrease the JNK phosphorylation, 50μM Cd2+ and Hg2+ increase the JNK and P38 phosphorylation. When HEK293 cells are treated with 20μM JNK inhibitor or 100μM ERK1/2 inhibitor, the cell proliferation do not increase significantly at low concentrations (0.05 and 0.5μM), but still decrease at high concentrations (50 and 500μM). When HEK293 cells are treated with 20μM P38 inhibitor, the tendency of cell proliferation is not affected. Data in our study suggests that activation of MAPK pathway may be involved in the biphasic effect induced by Cd2+ and Hg2+. [Copyright &y& Elsevier]

Light pollution is now associated with an increased incidence of mental disorders in humans, and the unfixed light pattern (ULP) is a common light pollution that occurs in such as rotating shift work. However, how much contribution the ULP has to depression and its potential mechanism are yet unknown. Our study aimed to investigate the effect of the ULP on depressive-like behaviors in mice and to explore the links to the circadian-orexinergic system. Male C57BL/6 J mice were exposed to the ULP by subjecting them to an alternating light pattern every 6 days for 54 days. The tail suspension test (TST) and forced swimming test (FST) were conducted to assess depressive-like behaviors. The rhythm of locomotor activity and the circadian expression of cFOS in the suprachiasmatic nucleus (SCN), clock genes in the liver, and corticosterone (CORT) in serum were detected to observe changes in the circadian system. The circadian expression of orexin-A (OX-A) in the lateral hypothalamus area (LHA) and dorsal raphe nucleus (DRN) and serotonin (5-HT) in the DRN were measured to determine alterations in the orexinergic system. The results showed that mice exposed to the ULP exhibited increased immobility time in the TST and FST. The ULP significantly disrupted the circadian rhythm of locomotor activity, clock genes in the liver, and CORT in the serum. Importantly, when exposed to the ULP, cFOS expression in the SCN showed decreased amplitude. Its projection area, the LHA, had a lower mesor of OX-A expression. OX-A projection to the DRN and 5-HT expression in the DRN were reduced in mesor. Our research suggests that the ULP contributes to depressive-like behaviors in mice, which might be related to the reduced amplitude of circadian oscillation in the SCN and hypoactivity of the orexinergic system. These findings may provide novel insights into rotating shift work-related depression. [Display omitted] • The unfixed light pattern in shift work lead to depressive-like behaviors in mice. • Reduced amplitude in SCN is linked to depression caused by the unfixed light pattern. • Reduced levels of OX-A are linked to depression caused by the unfixed light pattern. • Reduced levels of 5-HT are linked to depression caused by the unfixed light pattern. [ABSTRACT FROM AUTHOR]

As an alternative to octabromodiphenyl ether (octa-BDE), 1, 2-bis (2,4, 6-tribromophenoxy) ethane (BTBPE) has been widely used in a variety of combustible materials, such as plastics, textiles and furniture. Previous studies have demonstrated the thyroid toxicity of traditional brominated flame retardants for example octa-BDE clearly. Nevertheless, little is known about the thyroid toxicity of alternative novel brominated flame retardants BTBPE. In this study, it was demonstrated that BTBPE in vivo exposure induced FT4 reduction in 2.5, 25 and 250 mg/kg bw treated group and TT4 reduction in 25 mg/kg bw treated group. TG, TPO and NIS are key proteins of thyroid hormone synthesis. The results of Western blot and RT-PCR from thyroid tissue showed decreased protein levels and gene expression levels of TG, TPO and NIS as well as regulatory proteins PAX8 and TTF2. To investigate whether the effect also occurred in humans, anthropogenic Nthy-ori 3–1 cells were selected. Similar results were seen in vitro condition. 2.5 mg/L BTBPE reduced the protein levels of PAX8, TTF1 and TTF2, which in turn inhibited the protein levels of TG and NIS. The results in vitro experiment were consistent with that in vivo , suggesting possible thyrotoxic effects of BTBPE on humans. It was indicated that BTBPE had the potential interference of T4 generation and the study provided more evidence of the effects on endocrine disorders. [Display omitted] [ABSTRACT FROM AUTHOR]

Abstract Black carbon (BC) is a key component of atmospheric particles which has adverse effects on human health. Oxidation could lead to chemical property and toxicity potency changes of BC. The key cytokines participating in lung damage in mice induced by BC and ozone-oxidized BC (oBC) particles have been investigated in this study. It was concluded that oBC has stronger potency of inducing lung damage in mice comparing to BC. IL-6 and IL-33 were hypothesized to play important roles in this damage. Accordingly, IL-6 and IL-33 neutralizing antibodies were used to explore which cytokine might play a key role in lung inflammation induced by BC and oBC. As a result, IL-6 neutralizing antibody did not alleviate the lung damage induced by BC and oBC. However, IL-33 neutralizing antibody prevented BC and oBC induced lung damage. Furthermore, IL-33 neutralizing antibody treatment reduced IL-6 mRNA expression. It is hypothesized that MAPK and PI3K-AKT pathways might be involved in the oBC particles caused lung damage. It was concluded that IL-33 plays a key role in BC and oBC induced lung damage in mice. Graphical abstract Unlabelled Image Highlights • oBC has stronger potency in inducing lung inflammation in mice than BC. • IL-33 neutralizing antibody prevented BC and oBC induced lung damage. • IL-33 neutralizing antibody prevented BC and oBC induced lung damage through MAPK and PI3K/AKT pathways. [ABSTRACT FROM AUTHOR]

β-Phellandrene, a plant extract, can be used as natural pesticides and synthetic materials. As a factor that human may be exposed to, the toxicity information about β-phellandrene is scared at present. This study focused on the genetic toxicity of β-phellandrene. The genetic toxicity of β-phellandrene was evaluated by micronucleus test, comet assay, Ames test, and chromosomal aberration test. In this study, 2850, 1425, 712.5 mg/kg β-phellandrene were used in vivo experiments (comet assay and micronucleus test). For Ames test, pure β-phellandrene and different concentrations were used in the experiment. According to the results of cell viability assay (MTT test), the concentration of chromosomal aberration test was formulated. The result of comet assay showed that β-phellandrene can significantly induce DNA damage at the dosage of 1425 and 2850 mg/kg. While the results of Micronucleus test and chromosome aberration test showed that β-phellandrene does not lead to apparently genetic toxicity on chromosome level. Ames tests suggest that β-phellandrene had the ability to increase gene mutation with or without S9 mixture. So, it could be drawn that β-phellandrene would have certain genetic toxicity, and the toxicity is reflected as DNA strand breaks and mutation. This study filled the lack of genetic toxicity study of β-phellandrene, and enriched information for risk assessment for β-phellandrene. [ABSTRACT FROM AUTHOR]

Black carbon (BC) is a key component of atmospheric particles and has a significant effect on human health. BC can provide reactive sites and surfaces thus absorb quinones which were primarily generated from fossil fuel combustion and/or atmospheric photochemical conversions of PAHs. Oxidation could change the characteristics of BC and increase its toxicity. The comparison of lung damage in mice exposed to BC and 1,4-NQ-coated BC (1,4NQ-BC) particles is investigated in this study. Mice which were intratracheally instilled with particles have a higher expression of IL-1β, IL-6 and IL-33 in bronchoalveolar lavage fluid (BALF). Also, the IL-6, IL-33 mRNA expression in the lung tissue of mice instilled with 1,4NQ-BC were higher than that of mice instilled with BC. The pathology results showed that the lung tissue of mice instilled with 1,4NQ-BC particles have much more inflammatory cells infiltration than that of mice treated with BC. It is believed that the MAPK and PI3K-AKT pathway might be involved in the 1,4NQ-BC particles caused lung damage. Results indicated that 1,4NQ-BC particles in the atmosphere may cause more damage to health. [ABSTRACT FROM AUTHOR]

Ethephon can liberate ethylene which could interfere the plant growth process. The aim of the present study was to determine the effect of ethephon on developing immune system of male offspring. Ethephon could enhance NK cell activity in male mice. For 4-week-old male mice, lymphocytes of peripheral blood increased while the hemolytic plaque number decreased. Delayed type hypersensitivity(DTH) was inhibited in all groups. The expression of protein Bcl11b and p-p38 in thymus of treatment groups were lower than control group. Our results indicated that cellular immunity of male offspring is more sensitive to ethephon when exposed in pregnancy and lactation period. It should be emphasized that exposure to ethephon during the in utero stage and lactation stage still could damage the immune function of animal in the period before fully mature even in the dosage that could not influence the immune function of adult animal. [ABSTRACT FROM AUTHOR]

Black carbon (BC) is a key component of atmospheric particles and has a significant effect on human health. Oxidation could change the characteristics of BC and increase its toxicity. The comparison of lung damage in mice exposed to BC and ozone-oxidized BC (oBC) particles is investigated in this study. Mice which were intratracheally instilled with particles have a higher expression of IL-1β, IL-6 and IL-33 in bronchoalveolar lavage fluid (BALF). Also, the IL-6, IL-33 mRNA expression in the lung tissue of mice instilled with oBC was higher than that of mice instilled with BC. The expression of CD3 in the lung tissue of mice intratracheally instilled with oBC was higher than the mice distilled with BC. The pathology results showed that the lung tissue of mice instilled with oBC particles have much more inflammatory cells infiltration than that of mice treated with BC. It is believed that the PI3K-AKT pathway might be involved in the oBC particles caused lung damage. Results indicated that oBC particles in the atmosphere may cause more damage to health. [ABSTRACT FROM AUTHOR]

[Display omitted] • The mode of DNA damage action was dependent on the exposed modes. • DNA damage caused by high-level short-term PM 2.5 can be alleviated by natural repair. • RAD51 hypermethylation caused by PM 2.5 might be the epigenetic mechanism for DSBs. • MiRNAs could regulate the expression level of repair genes in lungs. Ambient air pollution was classified as carcinogenic to humans (Group 1) for lung cancer. DNA damage was an important first step in the process of carcinogenesis, and could also be induced by air pollution. In this study, intratracheal instillation and real-time air exposure system were combined to establish SHP (short-term high-level PM 2.5) and LLPO (long-term low-level PM 2.5 and O 3) exposure patterns, respectively. Hierarchical levels of genetic biomarkers were analyzed to explore DNA damage effects in rats. Representative DNA repair genes from different repair pathways were selected to explore the relative expression levels. The methylation level of differentially expressed repair genes were also determined. Besides, miRNA sequencing and non-targeted metabolomic analysis were performed in rat lungs. KEGG and multi-omics analysis were used to explore the potential mechanism of genetic damage under different air pollution patterns. We found that LLPO exposure induced DSBs and chromosome damage. SHP exposure could induce DSBs and DNA oxidative damage, and the effects of genetic damage under this pollution pattern could be repaired by natural repair. Repair genes involved in two pattern were different. SHP exposure could induce higher methylation levels of RAD51, which might be a potential epigenetic mechanism for high-level PM 2.5 induced down-regulated expression of RAD51 and DSBs. Besides, 29 overlapped alterations in metabolic pathways were identified by metabolomic and miRNA sequencing, including purine metabolism and pyrimidine metabolism after LLPO exposure. Differential miRNAs expression in lung tissue were associated with apoptosis, DNA damage and damage repair. We concluded that under different air pollution patterns, DNA damage biomarkers and activated targets of DNA damage repair network were both different. The genetic damage effects caused by high-level short-term PM 2.5 can be alleviated by natural repair. We provided possible mechanisms by multi-omics which could explain the increased carcinogenic risk caused by air pollution. [ABSTRACT FROM AUTHOR]

As the main composition of combustion, black carbon (BC) is becoming more and more noticeable at home and abroad. Ozone-oxidized black carbon (oBC) was produced through aging of ozone, one of the near-surface pollutants, to black carbon. And oBC was found to be more oxidation and cell toxicity when compared with BC. Besides, as a key cell of immunity, whether CD4 + T cell would involve in lung inflammation induced by particular matter is still unclear. This study aims to observe the effect of oBC on lung damage in mice and discuss how the functional MAP4K4 defect CD4 + T cells (conditional knockout of MAP4K4) presents its role in this process. In our study, MAP4K4 deletion in CD4 + T cells (MAP4K4 cKO) could increase cell number of macrophages, lymphocytes and neutrophils in bronchoalveolar lavage fluid (BALF) exposed to oBC. MAP4K4 deletion in CD4 + T cell also affected CD4 + T cell differentiation in mediastinal lymph nodes after oBC stimulation. The number of CD4 + IL17 + T cell increased obviously. The levels of IL-6 mRNA of lung in MAP4K4 cKO mice was higher than that in wild type mice after exposed to oBC, while the level of IL-6 in BALF had the same trend. Histological examination showed that MAP4K4 deletion in CD4 + T cells affected lung inflammation induced by oBC. Results indicated that MAP4K4 cKO in CD4 + T cells upgraded the level of inflammation in lung when exposed to oBC, which may be connected to the CD4 + T cell differentiation and JNK, ERK and P38 pathways. [ABSTRACT FROM AUTHOR]

Grape-seed proanthocyanidins (GSPs) have been shown to function as an anti-oxidant and anti-inflammatory agent with little toxicity in vivo and in vitro. However, little is known about their anti-inflammatory properties and mechanisms of action. The specific focus being its effects on the MAP kinases and nuclear factor-kappaB (NF-κB) signal transduction pathways in lipopolysaccharide (LPS) -stimulated RAW264.7 cells. GSPs extract has been found to suppress the mRNA expression of pro-inflammatory cytokines like tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and inflammatory molecule of cyclooxygenase-2 (COX-2) while mRNA level of IL-10 was greatly promoted. Furthermore, GSPs extract inhibited the expression of phosphorylated ERK, JNK and P38, as well as phosphorylated IKKα/β and NF-κB p65 subunit. In conclusion, our results show that GSPs extract showed its anti-inflammatory and immunomodulatory properties by suppressing the activation of MAP kinases and NF-κB signal transduction pathways. [ABSTRACT FROM AUTHOR]

Highlights: [•] Bisphenol A and genistein were classified as weakly and strongly embryotoxic respectively in embryonic stem cell test. [•] The combined exposure effects of BPA and GEN were evaluated using a 4×4 full factorial design. [•] BPA and GEN have a synergistic effect on embryonic stem cells differentiation at lower dosages. [ABSTRACT FROM AUTHOR]

Abstract: Contact hypersensitivity (CHS) is a delayed-type hypersensitivity reaction which is mediated by hapten-specific T cells. Strong haptens, such as 2, 4-dinitrofluorobenzene (DNFB) can induce it. Grape seed proanthocyanidins extract (GSPs), which is an antioxidant derived from grape seeds, has been reported to possess a variety of potent properties. However, few reports demonstrated the effects of GSPs on contact hypersensitivity. Therefore, the present study was devised to describe the role of GSPs on a mouse model of experimental CHS induced by DNFB and try to explore the possible underlying mechanisms. We observed that, GSPs when orally administrated into the CHS mice, inhibited the aggravation of inflammation. After administration of GSPs, there was obvious fewer inflammatory cell infiltration in the inflamed ears. Ear swelling after challenge was significantly reduced. In addition, we investigated the effects of GSPs on T cells in vitro, which play critical role during the progress of CHS. It was found that GSPs inhibited proliferative activity of T cells by blocking the activation of mitogen-activated protein kinases (MAPK) and NF-кB signaling pathways. Collectively, these results showed that GSPs has protective effect on CHS induced by DNFB and it also could inhibit the proliferation ability of T cells in vitro, suggesting the potential of GSPs as new and effective compound for the treatment of T-cell mediated inflammatory diseases. [Copyright &y& Elsevier]