A Common-Factor Approach for Multivariate Data Cleaning with an Application to Mars Phoenix Mission Data

Data quality is fundamentally important to ensure the reliability of data for stakeholders to make decisions. In real world applications, such as scientific exploration of extreme environments, it is unrealistic to require raw data collected to be perfect. As data miners, when it is infeasible to physically know the why and the how in order to clean up the data, we propose to seek the intrinsic structure of the signal to identify the common factors of multivariate data. Using our new data driven learning method, the common-factor data cleaning approach, we address an interdisciplinary challenge on multivariate data cleaning when complex external impacts appear to interfere with multiple data measurements. Existing data analyses typically process one signal measurement at a time without considering the associations among all signals. We analyze all signal measurements simultaneously to find the hidden common factors that drive all measurements to vary together, but not as a result of the true data measurements. We use common factors to reduce the variations in the data without changing the base mean level of the data to avoid altering the physical meaning.Comment: 12 pages, 10 figures, 1 tabl

Multiparameter Stochastic Dynamics of Ecological Tourism System with Continuous Visitor Education Interventions

Management of ecological tourism in protected areas faces many challenges, with visitation-related resource degradations and cultural impacts being two of them. To address those issues, several strategies including regulations, site managements, and visitor education programs have been commonly used in China and other countries. This paper presents a multiparameter stochastic differential equation model of an Ecological Tourism System to study how the populations of stakeholders vary in a finite time. The solution of Ordinary Differential Equation of Ecological Tourism System reveals that the system collapses when there is a lack of visitor educational intervention. Hence, the Stochastic Dynamic of Ecological Tourism System is introduced to suppress the explosion of the system. But the simulation results of the Stochastic Dynamic of Ecological Tourism System show that the system is still unstable and chaos in some small time interval. The Multiparameters Stochastic Dynamics of Ecological Tourism System is proposed to improve the performance in this paper. The Multiparameters Stochastic Dynamics of Ecological Tourism System not only suppresses the explosion of the system in a finite time, but also keeps the populations of stakeholders in an acceptable level. In conclusion, the Ecological Tourism System develops steadily and sustainably when land managers employ effective visitor education intervention programs to deal with recreation impacts

Invited - Droplets driving and sensing pixel circuits for thin film transistor-based digital microfluidics

Thin film transistor-based active-matrix digital microfluidics (AM-DMF) is an emerging and promising technology for large-scale parallel biological sample handling. With electrowetting-on-dielectric (EWOD) method, DMF chip can realize accurately controlling discrete droplets, thus it has great application prospects in biology, chemistry, and drug discovery. With the rapid development of micro-analysis and detection requirements, the precise control of droplets in DMF chips is increasingly required, so it is necessary to conduct the real-time sensing of droplet position. Figure 1 shows the designed droplet position detection unit circuit. The circuit consists of six thin film transistors, T1-T6. The input signals mainly include the enable signal Ven, the reverse enable signal Venb, the discharge signal Vdischarge, the detection signal Vdetect, and the ground signal Vgnd. The signal Vdrive is the driving voltage applied for driving electrode. Cpixel is the equivalent capacitance between the two plates of a pixel electrode in a microfluidic chip. Vout is the output voltage signal. Please click Download on the upper right corner to see the full abstract

Radiosensitization of Cancer Cells by Inactivation of Cullin-RING E3 Ubiquitin Ligases

Although radiotherapy represents one of the most effective treatment modalities for patients with cancer, inherent and/or acquired resistance of cancer cells to radiotherapy is often an impediment to effective treatment. Diverse strategies have been developed to improve the efficacy of radiotherapy. The ubiquitin-proteasome system (UPS) operates in numerous vital biologic processes by controlling the protein turnover in cells. Ubiquitination is central to the UPS pathway, and it relies on the E3 ubiquitin ligases to catalyze the covalent attachment of ubiquitin to its protein substrates. Cullin-based RING ligases (CRLs) are the largest family of E3 ligases that are responsible for the ubiquitination and destruction of numerous cancer-relevant proteins. Its deregulation has been linked to many human cancers, making it an attractive target for therapeutic intervention. This review discusses how targeting the ubiquitin-proteasome system, particularly CRLs, is an exciting new strategy for radiosensitization in cancer and, specifically, focuses on MLN4924, a recently discovered small-molecule inhibitor of the NEDD8-activating enzyme, which is being characterized as a novel radiosensitizing agent against cancer cells by inactivating CRL E3 ubiquitin ligases

Targeting Mcl-1 for Radiosensitization of Pancreatic Cancers

AbstractIn order to identify targets whose inhibition may enhance the efficacy of chemoradiation in pancreatic cancer, we previously conducted an RNAi library screen of 8,800 genes. We identified Mcl-1 (myeloid cell leukemia-1), an anti-apoptotic member of the Bcl-2 family, as a target for sensitizing pancreatic cancer cells to chemoradiation. In the present study we investigated Mcl-1 inhibition by either genetic or pharmacological approaches as a radiosensitizing strategy in pancreatic cancer cells. Mcl-1 depletion by siRNA produced significant radiosensitization in BxPC-3 and Panc-1 cells in association with Caspase-3 activation and PARP cleavage, but only minimal radiosensitization in MiaPaCa-2 cells. We next tested the ability of the recently identified, selective, small molecule inhibitor of Mcl-1, UMI77, to radiosensitize in pancreatic cancer cells. UMI77 caused dissociation of Mcl-1 from the pro-apoptotic protein Bak and produced significant radiosensitization in BxPC-3 and Panc-1 cells, but minimal radiosensitization in MiaPaCa-2 cells. Radiosensitization by UMI77 was associated with Caspase-3 activation and PARP cleavage. Importantly, UMI77 did not radiosensitize normal small intestinal cells. In contrast, ABT-737, an established inhibitor of Bcl-2, Bcl-XL, and Bcl-w, failed to radiosensitize pancreatic cancer cells suggesting the unique importance of Mcl-1 relative to other Bcl-2 family members to radiation survival in pancreatic cancer cells. Taken together, these results validate Mcl-1 as a target for radiosensitization of pancreatic cancer cells and demonstrate the ability of small molecules which bind the canonical BH3 groove of Mcl-1, causing displacement of Mcl-1 from Bak, to selectively radiosensitize pancreatic cancer cells

PTEN Regulates PDGF Ligand Switch for β-PDGFR Signaling in Prostate Cancer

Platelet-derived growth factor (PDGF) family members are potent growth factors that regulate cell proliferation, migration, and transformation. Clinical studies have shown that both PDGF receptor β (β-PDGFR) and its ligand PDGF D are up-regulated in primary prostate cancers and bone metastases, whereas PDGF B, a classic ligand for β-PDGFR, is not frequently detected in clinical samples. In this study, we examined the role of the tumor suppressor phosphatase and tensin homologue deleted on chromosome 10 (PTEN) in the regulation of PDGF expression levels using both a prostate-specific, conditional PTEN-knockout mouse model and mouse prostate epithelial cell lines established from these mice. We found an increase in PDGF D and β-PDGFR expression levels in PTEN-null tumor cells, accompanied by a decrease in PDGF B expression. Among Akt isoforms, increased Akt3 expression was most prominent in mouse PTEN-null cells, and phosphatidylinositol 3-kinase/Akt activity was essential for the maintenance of increased PDGF D and β-PDGFR expression. In vitro deletion of PTEN resulted in a PDGF ligand switch from PDGF B to PDGF D in normal mouse prostate epithelial cells, further demonstrating that PTEN regulates this ligand switch. Similar associations between PTEN status and PDGF isoforms were noted in human prostate cancer cell lines. Taken together, these results suggest a mechanism by which loss of PTEN may promote prostate cancer progression via PDGF D/β-PDGFR signal transduction