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Tracking and detection have brought great challenges to network security. Therefore, this paper proposes a monitoring method of stealthy complex network attacks considering security situation awareness. By constructing a tracking model of invisible complex network attacks, public monitoring nodes are selected for monitoring. The cost of a single monitoring node is calculated by the algorithm, and the monitoring node is determined by the monitoring node algorithm, so as to reduce the resource occupancy rate of the monitoring node and improve the monitoring accuracy. The simulation results show that this method is stable in the range of 1000 to 4000 nodes, and can effectively monitor the complex network attacks of stealing secrets.

The use of rotations is an effective strategy to control crop diseases and improve plant health. The soil bacterial communities in the rhizosphere are highly important for maintaining soil productivity. However, the composition and structure of soil bacterial communities in the rotations of vegetable crops remain unclear. In this study, we explored the bacterial diversity and community structure of the tomato rhizosphere, including enzyme activities, yield, and fruit quality, under three different cropping systems: tomato-tomato (Solanum lycopersicum) continuous cropping (TY1), eggplant (Solanum melongena)-tomato rotation (TY2) and arrowhead (Sagittaria trifolia)-tomato rotation (TY3). The composition and diversity of the rhizosphere bacterial communities differed significantly. The diversity was more in the TY2 and TY3 treatments than those in the TY1 treatment. Chujaibacter and Rhodanobacter were two predominant and unique strains detected only in TY1, while the relative abundances of Curvibacter and Luteimonas were the highest in TY2 and TY3, respectively. Moreover, Lysobacter was a relatively abundant type of biocontrol bacterium found only in the TY3 treatment, which could contribute to alleviating the obstacle of tomato continuous cropping. Compared with the TY1 treatment, the activities of catalase were significantly higher in the TY2 and TY3 treatments. In addition, compared with TY1, the TY2 and TY3 plots increased the following parameters: tomato yields by 24–46%, total soluble solids by 37-93%, total organic acid by 10-15.7% and soluble protein by 10-21%, while the content of nitrate was significantly reduced by 23%. Altogether, compared with the tomato monoculture, the rotations of tomato with eggplant and arrowhead shifted the rhizosphere bacterial communities and improved the yield and quality of the tomato. Moreover, a tomato rotation, particularly with arrowhead, was an effective way to alleviate the obstacles of continuous cropping.

β-lapachone (β-lap), anNad(p)hquinone oxidoreductase 1 (NQO1) targeting antitumor drug candidate in phase II clinical trials, is metabolically eliminated via NQO1 mediated quinone reduction and subsequent UDP-glucuronosyltransferases (UGTs) catalyzed glucuronidation. This study intends to explore the inner link between the cellular glucuronidation and pharmacokinetics of β-lap and its apoptotic effect in human colon cancer cells. HT29 cells S9 fractions exhibited high glucuronidation activity towards β-lap, which can be inhibited by UGT1A9 competitive inhibitor propofol. UGT1A siRNA treated HT29 cells S9 fractions displayed an apparent low glucuronidation activity. Intracellular accumulation of β-lap in HCT116 cells was much higher than that in HT29 cells, correlated with the absence of UGT1A in HCT116 cells. The cytotoxic and apoptotic effect of β-lap in HT29 cells were much lower than that in HCT116 cells; moreover, β-lap triggered activation of SIRT1-FOXO1 apoptotic pathway was observed in HCT116 cells but not in HT29 cells. Pretreatment of HT29 cells with UGT1A siRNA or propofol significantly decreased β-lap's cytotoxic and apoptotic effects, due to the repression of glucuronidation and the resultant intracellular accumulation. In conclusion, UGT1A is an important determinant, via switching NQO1-triggered redox cycle to metabolic elimination, in the intracellular accumulation of β-lap and thereafter its cytotoxicity in human colon cancer cells. Together with our previous works, we propose that UGTs determined cellular pharmacokinetics is an important determinant in the apoptotic effects of NQO1 targeting substrates serving as chemotherapeutic drugs.

BACKGROUND: Asialoglycoprotein receptor (ASGPR)-ligand-based separation combined with identification with Hep Par 1 or pan-cytokeratin (P-CK) antibody have been demonstrated to detect circulating tumor cells (CTCs) in hepatocellular carcinoma (HCC). The aim of this study was to develop an improved enrichment and identification system that allows the detection of all types of HCC CTCs. METHODS: The specificity of the prepared anti-ASGPR monoclonal antibody was characterized. HCC cells were bound by ASGPR antibody and subsequently magnetically isolated by second antibody-coated magnetic beads. Isolated HCC cells were identified by immunofluorescence staining using a combination of anti-P-CK and anti-carbamoyl phosphate synthetase 1 (CPS1) antibodies. Blood samples spiked with HepG2 cells were used to determine recovery and sensitivity. CTCs were detected in blood samples from HCC patients and other patients. RESULTS: ASGPR was exclusively expressed in human hepatoma cell line, normal hepatocytes and HCC cells in tissue specimens detected by the ASGPR antibody staining. More HCC cells could be identified by the antibody cocktail for CPS1 and P-CK compared with a single antibody. The current approach obtained a higher recovery rate of HepG2 cells and more CTC detection from HCC patients than the previous method. Using the current method CTCs were detected in 89% of HCC patients and no CTCs were found in the other test subjects. CONCLUSIONS: Our anti-ASGPR antibody could be used for specific and efficient HCC CTC enrichment, and anti-P-CK combined with anti-CPS1 antibodies is superior to identification with one antibody alone in the sensitivity for HCC CTC detection.

To provide a basis for using indigenous bacteria for bioremediation of heavy metal contaminated soil, the heavy metal resistance and plant growth-promoting activity of 136 isolates from V-Ti magnetite mine tailing soil were systematically analyzed. Among the 13 identified bacterial genera, the most abundant genus was Bacillus (79 isolates) out of which 32 represented B. subtilis and 14 B. pumilus, followed by Rhizobium sp. (29 isolates) and Ochrobactrum intermedium (13 isolates). Altogether 93 isolates tolerated the highest concentration (1000 mg kg(-1)) of at least one of the six tested heavy metals. Five strains were tolerant against all the tested heavy metals, 71 strains tolerated 1,000 mg kg(-1) cadmium whereas only one strain tolerated 1,000 mg kg(-1) cobalt. Altogether 67% of the bacteria produced indoleacetic acid (IAA), a plant growth-promoting phytohormone. The concentration of IAA produced by 53 isolates was higher than 20 µg ml(-1). In total 21% of the bacteria produced siderophore (5.50-167.67 µg ml(-1)) with two Bacillus sp. producing more than 100 µg ml(-1). Eighteen isolates produced both IAA and siderophore. The results suggested that the indigenous bacteria in the soil have beneficial characteristics for remediating the contaminated mine tailing soil.

NQO1 is an emerging and promising therapeutic target in cancer therapy. This study was to determine whether the anti-tumor effect of tanshinone IIA (TSA) is NQO1 dependent and to elucidate the underlying apoptotic cell death pathways. NQO1(+) A549 cells and isogenically matched NQO1 transfected and negative H596 cells were used to test the properties and mechanisms of TSA induced cell death. The in vivo anti-tumor efficacy and the tissue distribution properties of TSA were tested in tumor xenografted nude mice. We observed that TSA induced an excessive generation of ROS, DNA damage, and dramatic apoptotic cell death in NQO1(+) A549 cells and H596-NQO1 cells, but not in NQO1(-) H596 cells. Inhibition or silence of NQO1 as well as the antioxidant NAC markedly reversed TSA induced apoptotic effects. TSA treatment significantly retarded the tumor growth of A549 tumor xenografts, which was significantly antagonized by dicoumarol co-treatment in spite of the increased and prolonged TSA accumulations in tumor tissues. TSA activated a ROS triggered, p53 independent and caspase dependent mitochondria apoptotic cell death pathway that is characterized with increased ratio of Bax to Bcl-xl, mitochondrial membrane potential disruption, cytochrome c release, and subsequent caspase activation and PARP-1 cleavage. The results of these findings suggest that TSA is a highly specific NQO1 target agent and is promising in developing as an effective drug in the therapy of NQO1 positive NSCLC.