Enabling Multi-level Trust in Privacy Preserving Data Mining

Privacy Preserving Data Mining (PPDM) addresses the problem of developing accurate models about aggregated data without access to precise information in individual data record. A widely studied \emph{perturbation-based PPDM} approach introduces random perturbation to individual values to preserve privacy before data is published. Previous solutions of this approach are limited in their tacit assumption of single-level trust on data miners. In this work, we relax this assumption and expand the scope of perturbation-based PPDM to Multi-Level Trust (MLT-PPDM). In our setting, the more trusted a data miner is, the less perturbed copy of the data it can access. Under this setting, a malicious data miner may have access to differently perturbed copies of the same data through various means, and may combine these diverse copies to jointly infer additional information about the original data that the data owner does not intend to release. Preventing such \emph{diversity attacks} is the key challenge of providing MLT-PPDM services. We address this challenge by properly correlating perturbation across copies at different trust levels. We prove that our solution is robust against diversity attacks with respect to our privacy goal. That is, for data miners who have access to an arbitrary collection of the perturbed copies, our solution prevent them from jointly reconstructing the original data more accurately than the best effort using any individual copy in the collection. Our solution allows a data owner to generate perturbed copies of its data for arbitrary trust levels on-demand. This feature offers data owners maximum flexibility.Comment: 20 pages, 5 figures. Accepted for publication in IEEE Transactions on Knowledge and Data Engineerin

Family structure, the State Children\u27s Health Insurance Program (SCHIP) and child outcomes

This dissertation consists of three separate but interrelated essays that investigate how family structure and public policy are linked to health and developmental child outcomes. Each essay employs two or three waves of the National Survey of America\u27s Families (NSAF) as the primary data source. The first essay broadly investigates how family structure, including the less typical non-traditional families such as single father and grandparent households, are related to a wide of array of child outcomes with a focus on the interplay of parent-child gender. The results from this study show that children in single father families have better health status than children living in all other non-traditional families. Adding economic resources and inputs appears to mitigate the adverse effect of poverty associated with non-traditional families, but does not eliminate such negative impact. The second essay investigates how the State Children\u27s Health Insurance Programs (SCHIP), which are designed to provide coverage for uninsured children with family income too high to qualify for Medicaid but not high enough to secure private insurance, affect coverage, medical care utilization and child health outcomes. I find strong and consistent evidence that the number of publicly insured children increases; however, the number of privately insured children also declines suggesting significant crowd-out. As a result, there are no consistent findings that SCHIP increased the overall number of insured children. The results also indicate that SCHIP programs encourage medical care utilization such as well-child care visits and doctor visits. Nevertheless, there is little evidence on the effectiveness of SCHIP with respect to improving children\u27s health outcomes. The third essay contributes to the sparse existing literature on two different fronts. First, it empirically investigates the impact of welfare reform on the formation of grandparent-headed households, while at the same time taking into account the interplay of other contemporary public programs such as state kinship care policies and SCHIP. Second, this essay explores the motivations underlying grandparent caregiving behaviors and offers insights to such behaviors from an economist\u27s perspective. I do not find evidence that welfare reform encourage grandparent household formation. However, there is strong evidence that kinship care policies encourage grandparent caregiving behaviors

Restriction of human immunodeficiency virus by T-cell immunoglobulin and mucin domain-family proteins and antagonism by nuclear export signal

Includes vita.Dr. Shan-Lu Liu, Dissertation Supervisor.|Includes vita.Includes bibliographical references (142-168 pages)

Signaling Transduction Network Mediated by Tumor Suppressor/Susceptibility Genes in NPC

Nasopharyngeal carcinoma (NPC) is a polygenetic disease. SPLUNC1, UBAP1, BRD7, NAG7, NOR1, NGX6 and LTF genes were found to be tumor suppressor/susceptibility genes in different stages of NPC. SPLUNC1, an early warning molecular diagnosis marker, inhibits the bacteria clone formation, and is an innated immune molecule. SPLUNC1 can negatively regulate the ERK/MAPK signaling transduction pathway to inhibit NPC cell proliferation and induce apoptosis. BRD7, a transcript regulation factor, interacts with BRD2, and promotes apoptosis induced by BRD2. Its promoter is regulated by c-Myc and SP1. BRD7 inhibits NPC cell cycle progression, preventing passage through G0/G1 by suppressing ras/MEK/ERK, Rb/E2F and Wnt signaling pathways. Abnormal activation of BRD7 is crucial to cell cycle turbulence in NPC. NGX6, a metastasis-associated protein, can negative-regulate the EGF/Ras/MAPK signaling transduction pathway, and interacts with ezrin protein to inhibit NPC cell invasion and metastasis. LTF, also a metastasis-associated protein, can negatively regulate MAPK signal transduction pathways, such as JNK2 and ERK, to inhibit NPC cell proliferation and growth. Taken together, it was found that these tumor suppressor/susceptibility genes can regulate key molecules involved in cell signal pathways such as ras/MEK/ERK, Rb/E2F and EGFR ras/MEK/MAPK, and can regulate the expression of some adhesion molecules such as ezrin, nm23 and α-catenin. According to functional genomics and signaling transduction pathways, we have described a signaling cross-talk network between the tumor suppressor/susceptibility genes involved in NPC. These tumor suppressor/susceptibility genes may be potential treatment targets for NPC in the future