Almost sure consensus for multi-agent systems with two level switching

In most literatures on the consensus of multi-agent systems (MASs), the agents considered are time-invariant. However in many cases, for example in airplane formation, the agents have switching dynamics and the connections between them are also changing. This is called two-level switching in this paper. We study almost sure (AS) consensus for a class of two-level switching systems. At the low level of agent dynamics, switching is determin- istic and controllable. The upper level topology switching is random and follows a Markov chain. The transition probability of the Markov chain is not fixed, but varies when low level dynamics changes. For this class of MASs, a sufficient condition for AS consensus is developed in this paper

Interferon Consensus Sequence-Binding Protein 8, a Tumor Suppressor, Suppresses Tumor Growth and Invasion of Non-Small Cell Lung Cancer by Interacting with the Wnt/β-Catenin Pathway

Background/Aims: Interferon consensus sequence-binding protein 8 (IRF8) belongs to a family of interferon (IFN) regulatory factors that modulates various important physiological processes including carcinogenesis. As reported by others and our group, IRF8 expression is silenced by DNA methylation in both human solid tumors and hematological malignancies. However, the role of IRF8 in lung carcinoma remains elusive. In this study, we determined IRF8 epigenetic regulation, biological functions, and the signaling pathway involved in non-small cell lung cancer (NSCLC). Methods: IRF8 expression were determined by Q- PCR. MSP and A+T determined promotor methylation. MTS, clonogenic, Transwell assay, Flow cytometry, three-dimensional culture and AO/EB stain verified cell function. In vivo tumorigenesis examed the in vivo effects. By Chip-QPCR, RT-PCR, Western blot and Immunofluorescence staining, the mechanisms were studied. Results: IRF8 was significantly downregulated in lung tumor tissues compared with adjacent non-cancerous tissues. Furthermore, methylation-specific PCR analyses revealed that IRF8 methylation in NSCLC was a common event, and demethylation reagent treatment proved that downregulation of IRF8 was due to its promoter CpG hypermethylation. Clinical data showed that the IRF8 methylation was associated with tumor stage, lymph node metastasis status, patient outcome, and tumor histology. Exogenous expression of IRF8 in the silenced or downregulated lung cancer cell lines A549 and H1299 at least partially restored the sensitivity of lung cancer cells to apoptosis, and arrested cells at the G0/G1 phase. Cell viability, clonogenicity, and cell migration and invasive abilities were strongly inhibited by restored expression of IRF8. A three-dimensional culture system demonstrated that IRF8 changed the cells to a more spherical phenotype. Moreover, ectopic expression of IRF8 enhanced NSCLC chemosensitivity to cisplatin. Furthermore, as verified by Chip-qPCR, immunofluorescence staining, and western blotting, IRF8 bound to the T-cell factor/lymphoid enhancer factor (TCF /LEF) promoter, thus repressing β-catenin nuclear translocation and its activation. IRF8 significantly disrupted the effects of Wnt agonist, bml284, further suggesting its involvement in the Wnt/β-catenin pathway. Conclusion: IRF8 acted as a tumor suppressor gene through the transcriptional repression of β-catenin-TCF/LEF in NSCLC. IRF8 methylation may serve as a potential biomarker in NSCLC prognosis

New skin depth plasma interaction by ps-TW laser pulses and consequences for fusion energy

A new type of MeV ion generation at laser-plasma interaction has been measured based on the observation [1] that ps neodymium glass laser pulses of about TW and higher power do not produce the relativistic self-focusing based very high ion energies but more than 50 times lower energies. On top the strange observation was reported [1] that the number of the emitted fast ions did not change at variation of the laser focus intensity by a factor of 30. This can be explained by the effect that without an irradiating prepulse, a pure plane geometric skin layer interaction mechanismoccurs [2]. Neither relativistic self-focusing is possible nor the process of thermalization of quiver energy by quantum modified collisions. Following our conclusions about the difficulties for the fast ignitor concept of laser fusion [3], we can explain how these mechanisms can be used for studying the self-sustained fusion combustion waves [4] as known from the spark ignition at laser fusion. We further expect an improvement of the conditions for the experiments [5] with the highest laser fusion gains ever reported where even no pre-compression of the fusion plasma was necessary

Epigenetic identification of mitogen-activated protein kinase 10 as a functional tumor suppressor and clinical significance for hepatocellular carcinoma

Background Mitogen-activated protein kinase 10 (Mapk10) is a member of the c-jun N-terminal kinases (jnk) subgroup in the MAPK superfamily, and was proposed as a tumor suppressor inactivated epigenetically. Its role in hepatocellular carcinoma (HCC) has not yet been illustrated. We aimed to investigate the expression and epigenetic regulation of mapk10 as well as its clinical significance in HCC. Results Mapk10 was expressed in almost all the normal tissues including liver, while we found that the protein expression of MAPK10 was significantly downregulated in clinical samples of HCC patients compared with these levels in adjacent normal tissues (29/46, P < 0.0001). Clinical significance of MAPK10 expression was then assessed in a cohort of 59 HCC cases, which indicated its negative expression was significantly correlated with advanced tumor stage (P = 0.001), more microsatellite nodules (P = 0.025), higher serum AFP (P = 0.001) and shorter overall survival time of HCC patients. Methylation was further detected in 58% of the HCC cell lines we tested and in 66% of primary HCC tissues by methylation-specific PCR (MSP), which was proved to be correlated with the silenced or downregulated expression of mapk10. To get the mechanisms more clear, the transcriptional silencing of mapk10 was reversed by pharmacological demethylation, and ectopic expression of mapk10 in silenced HCC cell lines significantly inhibited the colony formation ability, induced apoptosis, or enhanced the chemosensitivity of HCC cells to 5-fluorouracil. Conclusion Mapk10 appears to be a functional tumor suppressor gene frequently methylated in HCC, which could be a valuable biomarker or a new diagnosis and therapy target in a clinical setting

Multi objective reactive power and voltage optimization of distribution network based on adaptive genetic annealing algorithm

In this paper, a multi-objective reactive power optimization model of distribution network is established, which takes the minimum of line loss, reactive compensation capacitor switching loss and node voltage deviation as objective, considering the constraints of node voltage, reactive power of wind turbine, capacitor switching times. The improved adaptive genetic annealing algorithm is used to solve the model. IEEE33 system is taken as an example to verify the effectiveness of the reactive power optimization model. When the shunt capacitor and wind turbine are in the optimal reactive power compensation, the line loss of the distribution network can be minimized

The effectiveness of a self-efficacy-enhancing intervention for Chinese patients with colorectal cancer: a randomized controlled trial with 6-month follow up

Background: Colorectal cancer is a major public health problem. There is growing support for colorectal cancer survivors who are experiencing problems after cancer treatment to engage in self-management programs to reduce symptom distress. However, there is inconclusive evidence as to the effectiveness of such program especially in Asian region.Objectives: This study tested the effects of a six-month nurse-led self-efficacy-enhancing intervention for patients with colorectal cancer, compared with routine care over a six-month follow up.Design: A randomized controlled trial with repeated measures, two-group design.Setting: Three teaching hospitals in Guangzhou, China.Participants: One hundred and fifty-two Chinese adult patients with a diagnosis of colorectal cancer were recruited. The intervention group (n = 76) received self-efficacy-enhancing intervention and the control group (n = 76) received standard care.Method: The participants were randomized into either intervention or control group after baseline measures. The outcomes of the study (self-efficacy, symptom distress, anxiety, depression and quality of life) were compared at baseline, three and six months after the intervention.Results: Sixty-eight participants in the intervention group and 53 in the control group completed the study. Their mean age was 53 (SD = 11.3). Repeated measure MANOVA found that the patients in the intervention group had significant improvement in their self-efficacy (F = 7.26, p = 0.003) and a reduction of symptom severity (F = 5.30, p = 0.01), symptom interference (F = 4.06, p = 0.025), anxiety (F = 6.04, p = 0.006) and depression (F = 6.96, p = 0.003) at three and six months, compared with the control group. However, no statistically significant main effect was observed in quality of life perception between the two groups.Conclusions: The nurse-led self-efficacy enhancing intervention was effective in promoting self-efficacy and psychological well-being in patients with colorectal cancer, compared with standard care. The intervention can be incorporated into routine care. Future empirical work is required to determine the longer term effects of the intervention. (C) 2014 Elsevier Ltd. All rights reserved

ADAMTS9 is Silenced by Epigenetic Disruption in Colorectal Cancer and Inhibits Cell Growth and Metastasis by Regulating Akt/p53 Signaling

Background/Aims: ADAMTS (disintegrin-like and metalloproteinase with thrombospondin motifs) proteins are extracellular zinc metalloproteinases that play an important role in extracellular matrix assembly and degradation, connective tissue structuring, angiogenesis, and cell migration. Multiple studies suggest that ADAMTS proteins (e.g. ADAMTS9) can act as tumor suppressors. In gastric, esophageal, and nasopharyngeal carcinomas ADAMTS9 is frequently down-regulated by promoter methylation. Whether ADAMTS9 can function as a tumor suppressor gene (TSG) in colorectal cancer is still unclear. Methods: We performed immunohistochemistry, RT-PCR, and qRT-PCR, to examine the expression of ADAMTS9 in colorectal cancer cell lines and primary colorectal cancer tissues. Methylation-specific PCR was also carried out to investigate the promoter methylation status of ADAMTS9. We also explored the functions of ADAMTS9 in colorectal cancer cell lines through in vitro experiments. Results: ADAMTS9 expression was down-requlated or silenced in 83.3% (5/6) of colorectal cancer cell lines, and frequently repressed in 65.6% (21/32) of colorectal cancer tissues. Down-regulation of ADAMTS9 was partially due to promoter methylation. Exogenous expression of ADAMTS9 in colorectal cancer cell lines inhibited cell proliferation and migration through the regulation of cell cycle and apoptosis. In addition, ADAMTS9 prevented the activation of Akt, and its downstream targets in colorectal cancer cell lines. Conclusion: Our findings suggest ADAMTS9 is a TSG in colorectal cancer

Physical and psychological predictors of quality of life in Chinese colorectal cancer patients during chemotherapy

Background: Maintaining quality of life (QOL) during chemotherapy is a critical aspect of cancer treatment. Instruments have been developed to assess symptom distress, self-efficacy, anxiety, depression, and other factors impacting QOL during cancer treatment, but Chinese versions have become available only recently.Objective: The aim of this study was to identify factors predictive of QOL during chemotherapy in Chinese colorectal cancer (CRC) patients.Methods: Patients completed Chinese versions of the Hospital Anxiety and Depression Scale, MD Anderson Symptom Inventory (a measure of symptom distress), Stanford Inventory of Cancer Patient Adjustment (a measure of self-efficacy), and Functional Assessment of Cancer Treatment-General (a measure of QOL) before and after 3 and 6 months of chemotherapy.Results: Of 152 consecutive CRC patients (men/women, 98/54; mean age, 53.3 11.3 years, 25-75 years; stage II/III, 59/93), 121 completed all questionnaires (79.6%). Self-efficacy dimensions communication, activity management, personal management, and affective management improved progressively over 6 months (all P < .05). Fatigue, nausea, lack of appetite, disturbed sleep, and vomiting peaked at 3 months and declined thereafter (P < .05). Patients who are younger than 60 years, are male, and with stage II CRC exhibited higher 3- and 6-month QOL scores (all P < .05). Multiple regression identified self-efficacy, anxiety, and symptom distress as independent predictors of QOL at 6 months.Conclusions: Enhanced self-efficacy, reduced symptom distress, and lower general anxiety would improve QOL during chemotherapy for CRC patients. Implications for Practice: These instruments can help identify CRC patients at risk of low QOL for additional psychotherapy or specific treatment modifications

The epigenetically downregulated factor CYGB suppresses breast cancer through inhibition of glucose metabolism

Abstract Background Recent studies suggested the globin family member cytoglobin (CYGB) as a potential tumor suppressor; however, the mechanism by which CYGB suppresses cancer is elusive. We investigated the role and mechanism of CYGB in suppressing breast cancer. Methods CYGB expression was examined by reverse transcription PCR, quantitative reverse transcription PCR and open database analysis. Promoter methylation was examined by methylation-specific PCR. Metabolomics and proteomics were analyzed by gas chromatography-mass spectrometry and isobaric tags for relative and absolute quantitation, respectively. The effects and mechanisms of ectopic CYGB expression in breast cancer cells were assessed with molecular biological and cellular approaches in vitro and with a xenograft tumor model in nude mice. Results CYGB expression was downregulated in breast cancer tissues and cell lines, which was associated with promoter methylation. Ectopic CYGB expression suppressed proliferation, migration, invasion and induced apoptosis in breast cancer cell lines MCF7 (p53WT) and MB231 (p53mt) in vitro, and inhibited xenograft tumor growth in vivo. By proteomics and metabolomics analysis, glucose metabolism was found to be one of the main pathways suppressed by CYGB. The CYGB-expressing cells had lower ATP and compromised glycolysis. Additionally, CYGB suppressed key glucose metabolism factors including GLUT1 and HXK2 in p53-dependent and -independent manners. Restoration of GLUT1 or HXK2 expression attenuated CYGB-mediated proliferation suppression and apoptosis induction. Conclusions CYGB is a potential tumor suppressor in breast cancer that is epigenetically suppressed. The results for the first time suggest that CYGB suppresses breast cancer through inhibiting glucose metabolism, which could be exploited for breast cancer prevention and therapy