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This study proposes a multi-consensus formation control algorithm by artificial potential field (APF) method based on velocity threshold. The algorithm improves the multi-consensus technique. This algorithm can split a group of agents into multiple agent groups. Note that the algorithm can easily complete the queue transformation as long as the entire proxy group is connected initially and no specific edges need to be removed. Furthermore, collision avoidance and maintenance of existing communication connectivity should be considered during the movement of all agents. Therefore, we design a new swarm motion potential function. The stability of multi-consensus formation control has proven to be effective in avoiding collisions, maintaining connectivity, and generating formations. The final numerical simulation results show the role of the controller we designed. [ABSTRACT FROM AUTHOR]

Paleogene depositional systems in the south of Lufeng sag have complex spatial distribution, which are influenced by pre-depositional paleogeomorphology and multiperiod tectonic activities. In this paper, to clarify the controlling effect of tectonicpaleogeomorphology on sedimentary facies distribution and effectively guide oil and gas exploration, the Paleogene paleogeomorphic pattern in the south of Lufeng sag is reconstructed by the impression method, and the temporal and spatial evolution laws of the main faults are clarified. The results show that braided river deltas developed stably in the long-axis gentle slope belt of the lake basin, while the short-axis sedimentary system changed from fan deltas to braided river deltas in response to the change of active strength of dominant faults from strong to weak. It is found that the scale of the sedimentary fan is closely related to the activity of the main fault, the area of the catchment, and the vertical elevation difference. The steep cliff is controlled by the boundary fault with large fault throw and steep section, and there are wedge-shaped sand bodies near the steep cliff. The multi-level fault-step zone provides the driving force for the advancement of the sedimentary system, and the sand body extends for a long distance. It is established that the supply capacity of the source area and the accommodated space of the lake basin are coupled to control the deposition scale. Moreover, the slope controlled by the combination of paleogeomorphic assemblage and the activity of the main fault determines the sedimentary type, and the structural slope-break zone defines the spreading pattern of the sands. [ABSTRACT FROM AUTHOR]

The human cysteine dioxygenase 1 (CDO1) gene is a non-heme structured, iron-containing metalloenzyme involved in the conversion of cysteine to cysteine sulfinate, and plays a key role in taurine biosynthesis. In our search for novel methylated gene promoters, we have analyzed differential RNA expression profiles of colorectal cancer (CRC) cell lines with or without treatment of 5-aza-2'-deoxycytidine. Among the genes identified, the CDO1 promoter was found to be differentially methylated in primary CRC tissues with high frequency compared to normal colon tissues. In addition, a statistically significant difference in the frequency of CDO1 promoter methylation was observed between primary normal and tumor tissues derived from breast, esophagus, lung, bladder and stomach. Downregulation of CDO1 mRNA and protein levels were observed in cancer cell lines and tumors derived from these tissue types. Expression of CDO1 was tightly controlled by promoter methylation, suggesting that promoter methylation and silencing of CDO1 may be a common event in human carcinogenesis. Moreover, forced expression of full-length CDO1 in human cancer cells markedly decreased the tumor cell growth in an in vitro cell culture and/or an in vivo mouse model, whereas knockdown of CDO1 increased cell growth in culture. Our data implicate CDO1 as a novel tumor suppressor gene and a potentially valuable molecular marker for human cancer. [ABSTRACT FROM AUTHOR]

Background: The major established etiologic risk factor for bladder cancer is cigarette smoking and one of the major antineoplastic agents used for the treatment of advanced bladder cancer is cisplatin. A number of reports have suggested that cancer patients who smoke while receiving treatment have lower rates of response and decreased efficacy of cancer therapies. Methodology/Principal Findings: In this study, we investigated the effect of cigarette smoke condensate (CSC) vapor on cisplatin toxicity in urothelial cell lines SV-HUC-1 and SCaBER cells. We showed that chronic exposure to CSC vapor induced cisplatin resistance in both cell lines. In addition, we found that the expression of mitochondrial-resident protein adenylate kinase-3 (AK3) is decreased by CSC vapor. We further observed that chronic CSC vapor-exposed cells displayed decreased cellular sensitivity to cisplatin, decreased mitochondrial membrane potential (&Dgr;&PSgr;m) and increased basal cellular ROS levels compared to unexposed cells. Re-expression of AK3 in CSC vapor-exposed cells restored cellular sensitivity to cisplatin. Finally, CSC vapor increased the growth of the tumors and also curtail the response of tumor cells to cisplatin chemotherapy in vivo. Conclusions/Significance: The current study provides evidence that chronic CSC vapor exposure affects AK3 expression and renders the cells resistant to cisplatin. [ABSTRACT FROM AUTHOR]

The article presents a research study that aimed to identify the molecular changes during cigarette smoke-induced esophageal squamous cell carcinoma (ESCC). A background on ESCC is provided together with the material and methods used in the study such as the establishment of cigarette smoke extract (CSE)-resistant cells, bisulfite sequencing, and western blot analyses. Results are discussed which indicate that cigarette smoking causes sequence-specific single-stranded deoxyribonucleic acid (DNA)-binding protein 2 (SSBP2) promoter methylation.

Aerobic glycolysis and mitochondrial dysfunction are common features of aggressive cancer growth. We observed promoter methylation and loss of expression in neurofilament heavy polypeptide (NEFH) in a significant proportion of primary esophageal squamous cell carcinoma (ESCC) samples that were of a high tumor grade and advanced stage. RNA interference-mediated knockdown of NEFH accelerated ESCC cell growth in culture and increased tumorigenicity in vivo, whereas forced expression of NEFH significantly inhibited cell growth and colony formation. Loss of NEFH caused upregulation of pyruvate kinase-M2 type and down-regulation of pyruvate dehydrogenase, via activation of the Akt/β-catenin pathway, resulting in enhanced aerobic glycolysis and mitochondrial dysfunction. The acceleration of glycolysis and mitochondrial dysfunction in NEFH-knockdown cells was suppressed in the absence of β-catenin expression, and was decreased by the treatment of 2-Deoxyglucose, a glycolytic inhibitor, or API-2, an Akt inhibitor. Loss of NEFH activates the Akt/β-catenin pathway and increases glycolysis and mitochondrial dysfunction. Cancer cells with methylated NEFH can be targeted for destruction with specific inhibitors of deregulated downstream pathways. [ABSTRACT FROM AUTHOR]

Studies have linked the consumption of broccoli and other cruciferous vegetables to a reduced risk of breast cancer. The phytochemical indole-3-carbinol (I3C), present in cruciferous vegetables, and its major acid-catalyzed reaction product 3,3'-diindolylmethane (DIM) have bioactivities relevant to the inhibition of carcinogenesis. In this study, the effect of DIM on angiogenesis and tumorigenesis in a rodent model was investigated. We found that DIM produced a concentration-dependent decrease in proliferation, migration, invasion and capillary tube formation of cultured human umbilical vein endothelial cells (HUVECs). Consistent with its antiproliferative effect, which was significant at only 5 M DIM, this indole caused a G1 cell cycle arrest in actively proliferating HUVECs. Furthermore, DIM downregulated the expression of cyclin-dependent kinases 2 and 6 (CDK2, CDK6), and upregulated the expression of CDK inhibitor, p27Kip1, in HUVECs. We observed further in a complementary in vivo Matrigel plug angiogenesis assay that, compared with vehicle control, neovascularization was inhibited up to 76% following the administration of 5 mg/kg DIM to female C57BL/6 mice. Finally, this dose of DIM also inhibited the growth of human MCF-7 cell tumor xenografts by up to 64% in female athymic (nu/nu) mice, compared with the vehicle control. This is the first study to show that DIM can strongly inhibit the development of human breast tumor in a xenograft model and to provide evidence for the antiangiogenic properties of this dietary indole. [ABSTRACT FROM AUTHOR]