Database anonymization and protections of sensitive attributes

The importance of database anonymization has become increasingly critical for organizations that publish their database to the public. Current security measures for anonymization poses different manner of drawbacks. k-anonymity is prone to many varieties of attack; !-diversity does not work well with categorical or numerical attributes; t-closeness erases too much information in the database. Moreover, some measures of information loss are designed for anonymization measure, such as k-anonymity, where sensitive attributes do not play a part in measuring database's security. Not measuring the re-distribution of sensitive attributes will result in an underestimate for information loss such as 1- diversity or t-closeness which intentionally tries removing the association between non-sensitive attributes and sensitive attributes for better protecting individuals from being indentified. This thesis provides a more generalized version of !-diversity that will better protect categorical attributes and numerical attributes and analyzes the effectiveness and complexity of our new security scheme. Another focus of this thesis is to design a better approach of measuring information loss and lay down a new standard for evaluating information loss on security measures such as 1- diversity and t-closeness and quantify actual information loss from deliberately hiding relations between non-sensitive attributes and sensitive attributes. This new standard of information loss measure should provide a better estimation of the data mining potential remained in a generalized database. This thesis also proves that unlike k-anonymity which can be solved in polynomial time when k=2. 1-diversity in fact remains NP-Hard in the special case where 1=2, and even when there are only 2 possible sensitive attributes in the alphabet

Exploring Strategies to Enhance the Presentation of Information in Print DTCA to Improve Consumers’ Recall of Information

This study examines how best to present information in an antidepressant print DTCA. The objectives of this study are to: (1) modify an antidepressant print advertisement to enhance consumers’ understanding of the presented information, (2) create a questionnaire to measure consumers’ recall of the information presented in an antidepressant print advertisement and (3) pilot test the study instruments by comparing consumers’ recall of the information in the antidepressant print advertisement between those who view the original advertisement and those who view the modified advertisement. Modifications of the advertisement were based on the Explanatory Structure Building Model, findings from previous studies, and literature pertaining to the enhancement of the readability and comprehension of written health information. Data collection was conducted in three stages using mixed methods. This study details potential techniques that can be used to enhance the presentation of information in print DTCA in order to improve consumers’ recall of the information. Furthermore, this study shows that strategies to improve the presentation of information in print DTCA exist and that the strategies are feasible to apply. Conflict of Interest This research study was supported by the University of Wisconsin-Madison Population Health Dissertation Grants sponsored by the Robert Wood Johnson Foundation and the Sonderegger Research Center Dissertation Research Grants.   Type: Original Researc

Developing Blue Ocean Strategy of Sustainable Product Design and Development for Business Opportunities of BOP Groups in Taiwan

This study expands the definition of the poor group and attempts to delve into and make known the phenomenon of poverty in Taiwan and aims to explore the goals and possibilities of the BOP consumer market. Through a questionnaire survey and expert interviews, this research adopts the concept of sustainability to discuss the lifestyle and consumption characteristics of the BOP group and establishes a design strategic norm of the sustainable products. The findings show that the BOP group in Taiwan is new poverty or working poor and high quality and common prices are the main requirements; these should be introduced into the development model of sustainable design

Molecular identification for epigallocatechin-3-gallate-mediated antioxidant intervention on the H2O2-induced oxidative stress in H9c2 rat cardiomyoblasts

Epigallocatechin-3-gallate (EGCG) has been documented for its beneficial effects protecting oxidative stress to cardiac cells. Previously, we have shown the EGCG-mediated cardiac protection by attenuating reactive oxygen species and cytosolic Ca2+ in cardiac cells during oxidative stress and myocardial ischemia. Here, we aimed to seek a deeper elucidation of the molecular anti-oxidative capabilities of EGCG in an H2O2-induced oxidative stress model of myocardial ischemia injury using H9c2 rat cardiomyoblasts

Gallic Acid Induces a Reactive Oxygen Species-Provoked c-Jun NH 2

Idiopathic pulmonary fibrosis is a chronic lung disorder characterized by fibroblasts proliferation and extracellular matrix accumulation. Induction of fibroblast apoptosis therefore plays a crucial role in the resolution of this disease. Gallic acid (3,4,5-trihydroxybenzoic acid), a common botanic phenolic compound, has been reported to induce apoptosis in tumor cell lines and renal fibroblasts. The present study was undertaken to examine the role of mitogen-activated protein kinases (MAPKs) in lung fibroblasts apoptosis induced by gallic acid. We found that treatment with gallic acid resulted in activation of c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and protein kinase B (PKB, Akt), but not p38MAPK, in mouse lung fibroblasts. Inhibition of JNK using pharmacologic inhibitor (SP600125) and genetic knockdown (JNK specific siRNA) significantly inhibited p53 accumulation, reduced PUMA and Fas expression, and abolished apoptosis induced by gallic acid. Moreover, treatment with antioxidants (vitamin C, N-acetyl cysteine, and catalase) effectively diminished gallic acid-induced hydrogen peroxide production, JNK and p53 activation, and cell death. These observations imply that gallic acid-mediated hydrogen peroxide formation acts as an initiator of JNK signaling pathways, leading to p53 activation and apoptosis in mouse lung fibroblasts

Negative magnetoresistance, negative electroresistance, and metallic behavior on the insulating side of the two-dimensional superconductor-insulator transition in granular Pb films

Granular Pb thin films on the insulating side of the two-dimensional superconductor-insulator transition are observed to exhibit a large negative magnetoresistance and electroresistance change in resistance with electric field at low temperatures. At high measurement voltages and low temperatures, the film resistances become temperature independent creating a metallic state. These phenomena are explained as manifestations of transport due to intergranular quasiparticle tunneling. This explanation might also provide insights into the similar behavior observed in other superconductors

Epigallocatechin-3-gallate-mediated cardioprotection by Akt/GSK-3β/caveolin signalling in H9c2 rat cardiomyoblasts

Background: Epigallocatechin-3-gallate (EGCg) with its potent anti-oxidative capabilities is known for its beneficialeffects ameliorating oxidative injury to cardiac cells. Although studies have provided convincing evidence tosupport the cardioprotective effects of EGCg, it remains unclear whether EGCg affect trans-membrane signalling incardiac cells. Here, we have demonstrated the potential mechanism for cardioprotection of EGCg againstH2O2-induced oxidative stress in H9c2 cardiomyoblasts.Results: Exposing H9c2 cells to H2O2 suppressed cell viability and altered the expression of adherens and gapjunction proteins with increased levels of intracellular reactive oxygen species and cytosolic Ca2+. These detrimentaleffects were attenuated by pre-treating cells with EGCg for 30 min. EGCg also attenuated H2O2-mediated cell cyclearrest at the G1-S phase through the glycogen synthase kinase-3β (GSK-3β)/β-catenin/cyclin D1 signalling pathway.To determine how EGCg targets H9c2 cells, enhanced green fluorescence protein (EGFP) was ectopically expressedin these cells. EGFP-emission fluorescence spectroscopy revealed that EGCg induced dose-dependent fluorescencechanges in EGFP expressing cells, suggesting that EGCg signalling events might trigger proximity changes of EGFPexpressed in these cells.Proteomics studies showed that EGFP formed complexes with the 67 kD laminin receptor, caveolin-1 and -3,β-actin, myosin 9, vimentin in EGFP expressing cells. Using in vitro oxidative stress and in vivo myocardial ischemiamodels, we also demonstrated the involvement of caveolin in EGCg-mediated cardioprotection. In addition,EGCg-mediated caveolin-1 activation was found to be modulated by Akt/GSK-3β signalling in H2O2-induced H9c2cell injury.Conclusions: Our data suggest that caveolin serves as a membrane raft that may help mediate cardioprotectiveEGCg transmembrane signalling

Molecular population genetics and gene expression analysis of duplicated CBF genes of Arabidopsis thaliana

<p>Abstract</p> <p>Background</p> <p><it>CBF/DREB </it>duplicate genes are widely distributed in higher plants and encode transcriptional factors, or CBFs, which bind a DNA regulatory element and impart responsiveness to low temperatures and dehydration.</p> <p>Results</p> <p>We explored patterns of genetic variations of <it>CBF1, -2</it>, and -<it>3 </it>from 34 accessions of <it>Arabidopsis thaliana</it>. Molecular population genetic analyses of these genes indicated that <it>CBF2 </it>has much reduced nucleotide diversity in the transcriptional unit and promoter, suggesting that <it>CBF2 </it>has been subjected to a recent adaptive sweep, which agrees with reports of a regulatory protein of <it>CBF2</it>. Investigating the ratios of K_a/K_sbetween all paired <it>CBF </it>paralogus genes, high conservation of the AP2 domain was observed, and the major divergence of proteins was the result of relaxation in two regions within the transcriptional activation domain which was under positive selection after <it>CBF </it>duplication. With respect to the level of <it>CBF </it>gene expression, several mutated nucleotides in the promoters of <it>CBF3 </it>and <it>-1 </it>of specific ecotypes might be responsible for its consistently low expression.</p> <p>Conclusion</p> <p>We concluded from our data that important evolutionary changes in <it>CBF1, -2</it>, and -<it>3 </it>may have primarily occurred at the level of gene regulation as well as in protein function.</p