In this thesis, we draw attention to the problem of cross-service attacks, that is, attacks that exploit information collected about users from one service to launch an attack on the same users on another service. With the increased deployment and use of what fundamentally are integrated-services networks, such as 4G/LTE networks and now 5G, we expect that cross-service attacks will become easier to stage and therefore more prevalent. As running example to illustrate the effectiveness and the potential impact of cross-service attacks we will use the problem of account association in 4G/LTE networks. Account association attacks aim at determining whether a target mobile phone number is associated with a particular online account. In the case of 4G/LTE, the adversary launches the account association attacks by sending SMS messages to the target phone number and analyzing patterns in traffic related to the online account. We evaluate the proposed attacks in both a local 4G/LTE testbed and a major commercial 4G/LTE network. Our extensive experiments show that the proposed attacks can successfully identify account association with close-to-zero false negative and false positive rates. Our experiments also illustrate that the proposed attacks can be launched in a way that the victim receives no indication of being under attack.

Reactive oxygen species (ROS) are a group of small molecules that regulate tissue redox status and oxidative stress. Redox regulation is an important determinant for cell development, activities, and function. ROS and oxidative stress also have a significant impact on the regulation of stem cells including bone marrow stem cells (BMSCs) and bone marrow-derived endothelial progenitor cells (EPCs). Oxidized low density lipoprotein (ox-LDL), a key contributor to the development of atherosclerosis in hyperlipidemic state, produces a significant amount of ROS spontaneously in vitro at clinically relevant concentrations. The present project was designed to test the hypothesis that ox-LDL was generated from native LDL and altered the populations of stem cells and EPCs via (at least partially) ROS-mediated mechanism. A single dose of human native LDL (25 µg) was injected intravenously into male C57BL/6 mice with and without NAC treatment. Human ox-LDL levels in the blood were measured at different time after LDL injection using ELISA kit. Measurable serum level of human ox-LDL was detected 30 min after the injection, reached peak in 3 hours, started to decline afterwards, and became undetectable in 12 hours. NAC treatment significantly reduced serum ox-LDL level with no detectable ox-LDL in blood 6 hours after injection. No difference in ox-LDL clearance was observed in NAC-treated animals. There were significant increases in intracellular and extracellular ROS production in the animals treated with native LDL and ox-LDL and in hyperlipidemic LDL receptor knockout (LDLR-/-) mice that were completely prevented with NAC treatment. Treatment with ox-LDL significantly altered the populations of stem cells and EPCs in both BM and blood similar to chronic hyperlipidemia (with 4 months of HFD), although significant differences in the impact of ox-LDL and hyperlipidemia on stem/progenitors in vivo exist. Inhibition of ROS production with NAC treatment or expression of (open full item for complete abstract)

Type 2 diabetes mellitus is a major risk factor for ischemic stroke. Also diabetes is associated with poor outcome after stroke. Underlying mechanisms are however not fully understood. Alteration in the expression of the SDF-1a/CXCR4 axis, which is important for ischemic tissue repair, can be a probable cause. In this study, we have determined the expression of SDF-1a/CXCR4 in the brains of type II diabetic mice at basal and in response to ischemic stroke and have investigated a method for overexpression of SDF-1a in the brains of the diabetic mice. Adult male C57BLKS/J mice (db/db) of age 8 weeks were used as the murine model for type II diabetes and their age matched lean littermates served as controls (db/+). Microvascular density was first determined in the cerebral cortex of db/db diabetic mice by immunohistochemical analysis. Focal cerebral ischemia was induced by middle cerebral artery occlusion surgery (MCAO) in type 2 diabetic db/db mice and their controls. 48 hours after surgery, volume of ischemic damage was determined by TTC staining. The expression of SDF-1a and CXCR4 in the ischemic and non ischemic sides of brains of both the groups were determined using western blot and real time RT PCR. The db/db diabetic mice were injected with the vector, adeno associated virus 9 (AAV-SDF-1a) in the brain striatum and the overexpression of SDF-1a was determined by immunohistochemical analysis. Double immunohistochemistry was used to determine the localization of SDF-1a in brain after injection of the vector. The microvascular density in the cerebral cortex was reduced in db/db mice as compared with db/+ mice (p<0.05). Volume of ischemic damage was significantly increased in db/db mice after focal cerebral ischemia (p< 0.01). The levels of SDF-1a expression in both ischemic and non ischemic side of brain were reduced in db/db mice as compared with those in db/+ mice at mRNA (p< 0.01) and protein level (p< 0.01). The amount of CXCR4 expression was significantly redu (open full item for complete abstract)

This research focuses on the space-confined P123-silica hybrid self-assembly. Mesoporous silica nanowires with various diameters (10 – 400nm) were synthesized via sol-gel combined vapor-induced self-assembly in both AAO and EPC channels. Scanning transmission electron Microscope (STEM) was used to characterize the samples in terms of nanopore size, ordering, and orientation. The mesoporous structure of silica wires formed in EPC with diameter less than 400 nm are first reported. Substrate effect (EPC vs AAO) and processing condition effect on the morphology of the mesoporous structure of silica wires are present and discussed. The more ordered and uniform mesoporous structure is preferentially formed in narrower substrate channel confinement. A critical diameter (dc) of hard template channels is around 30-50 nm, below which the space confinement effect leads to more uniform nanostructured nanowires; above the dc, mixed mesostrcucture usually exist. The formation of various meso-structures of silica wires is sensitive to process conditions.

Viral hemorrhagic septicemia virus (VHSv), a member of the family Rhabdoviridae, is a highly contagious fish virus responsible for large-scale fish die-offs worldwide. A new strain of VHSv, designated IVb, has recently spread to the Great Lakes threatening the tourism, sports fishing and fishery industries of the region. Research on virus-host interactions in VHSv infected fish has been mostly limited to population and ecological based studies while the molecular basis of the disease remains widely uncharacterized. To study virus-host interactions on a molecular level, we cloned four of the six VHSv genes including the matrix (m), nucleocaspid (n), non-virion (nv), and phosphoprotein (p) genes. Of primary interest, the M protein encoded by VHSv seems to share similar characteristics with the matrix protein of a related rhabdovirus. Comparable to the well-studied rhabdovirus vesicular stomatitis virus (VSV) M protein, ectopically expressed VHSv M inhibits promoter activity of both an interferon stimulated response element containing promoter and a constitutively active simian vacuolating virus 40 (SV40) promoter in Epithelioma Papulosum Cyprini (EPC) cells. Interestingly, real-time PCR data suggest mRNA levels remain steady, while protein levels decrease. Together, these data may suggest a similar interaction found in VSV between the M protein and the RAE1-NUP98 complex preventing nuclear export of mRNA. Furthermore, as seen in related rhabdoviruses, we have cell rounding after ectopic expression of the M protein for greater than 48h. Annexin V staining suggests these morphological changes in the cells are due to the induction of apoptosis. Together, these observations suggest two novel functions for the VHSv M protein. Future work will focus on determining the mechanisms utilized by VHSvM to inhibit transcription and induce apoptosis. Additionally, we identified the VHSv phosphoprotein as an inhibitor of both IFN gene activation and IFN-mediated activation of ISGs. (open full item for complete abstract)

The development and analysis of quality control adjustment schemes for process regulation