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Deployment of Dynamic Differential Logics (DDL) appears to be a promising choice for providing resistance against leakage of side channel information. However, the resistance provided by these logics is too costly for widespread area-constrained applications. Implementation of a secure DDL-based countermeasure also requires a complex layout methodology for balancing the load at the differential outputs. This thesis, unlike previous logic level approaches, presents a novel exploitation of static and single-ended logic for designing the side channel countermeasure. The proposed technique is used in the implementation of a protected crypto core consisting of the AES ???AddRoundKey??? and ???SubByte??? transformation. The test chip including the protected and unprotected crypto cores is fabricated in 180nm CMOS technology. A correlation analysis on the unprotected core results in revealing the key at the output of the combinational networks and the registers. The quality of the measurements is further improved by introducing an enhanced data capturing method that inserts a minimum power consuming input as a reference vector. In comparison, no key-related information is leaked from the protected core even with an order of magnitude increase in the number of averaged traces. For the first time, fabricated chip results are used to validate a new logic level side channel countermeasure that offers lower area and reduced circuit design complexity compared to the DDL-based countermeasures. This thesis also provides insight into the side channel vulnerability of cryptosystems in sub-90nm CMOS technology nodes. In particular, data dependency of leakage power is analyzed. The number of traces to disclose the key is seen to decrease by 35% from 90nm to 45nm CMOS technology nodes. Analysis shows that the temperature dependency of the subthreshold leakage has an important role in increasing the ability to attack future nanoscale crypto cores. For the first time, the effectiveness of a circuit-based leakage reduction technique is examined for side channel security. This investigation demonstrates that high threshold voltage transistor assignment improves resistance against information leakage. The analysis initiated in this thesis is crucial for rolling out the guidelines of side channel security for the next generation of Cryptosystem.

With the limited wireless spectrum and the ever-increasing demand for wireless services, two issues are pressing and difficult: efficient spectrum utilization and heterogeneous traffic management. Throughput and utility maximization problems are proposed to quantify these two issues. To exploit the wireless spatial multiplex gain, concurrent transmissions, if controlled appropriately, can lead to overall higher network throughput as well as utility. The optimal scheduling and power control for concurrent transmissions in rate-adaptive wireless networks is a very challenging NPhard problem. In the thesis, we propose efficient power allocation and scheduling algorithms for concurrent transmissions which can improve network throughput and utility with fairness consideration. We first formulate the optimal power allocation and scheduling problem for network throughput and utility maximization individually, and convert the original non-convex problems into a series of convex problems using a two-phase approximation. Then, we propose power and channel allocation with fairness for network throughput maximization (PCAF-NTM) and for network utility maximization (PCAF-NUM) algorithms to solve the converted problems. Extensive simulation results show the substantial improvement in terms of both network throughput and utility, comparing to the previous scheduling algorithms. / Graduate

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The present research is focused on the topic of inflammation-drug interaction. Inflammation complicates many human diseases and conditions ranging from obesity to cancer. Therefore, the study of the effect of inflammation on drug pharmacokinetics and pharmacodynamics is pivotal. First, we tested the hypothesis that controlling inflammation using valsartan can restore the previously reported altered verapamil pharmacokinetics and pharmacodynamics. Such an effect is expected due to the anti-inflammatory properties of angiotensin II inhibition. Inflammation resulted in L-type calcium channel target protein (Cav1.2) downregulation and reduced verapamil potency in pre-adjuvant arthritis rat model. Valsartan treatment reversed the observed downregulation of L-type calcium channels thereby enhancing verapamil potency. This beneficial interaction, once proven in humans, may be of value in cardiac patients with superimposing inflammatory diseases. Second, we investigated whether the response to verapamil is reduced in experimentally induced acute myocardial injury (AMI) in rats. AMI caused a 75% reduction in verapamil potency and Cav1.2 target protein downregulation. If extrapolated to humans, our observations may suggest that L-type calcium channel downregulation can contribute, at least in part, to the poor outcome in myocardial infarction patients treated with calcium channel blockers (CCBs). Third, we studied the effect of obesity on the pharmacological response of CCBs in children with renal disease. Our data indicated that obese children are less responsive to CCBs than non-obese ones. Therefore, obesity should be considered when initiating antihypertensive drug therapy in children. Last, we were interested in finding out if the expression of other target genes is also altered by inflammation. We used real time polymerase chain reaction, after determination of the best housekeeping gene to be used as an internal control. Inflammation resulted in significant alterations of several molecular targets and transporters affecting the pharmacokinetics and pharmacodynamics of drugs. These findings may provide an insight into the effect of inflammation on drug targets and modulators of disease pathogenesis. In conclusion, inflammation is a missed ring in the chain of therapy. The research presented in this thesis will add to the inflammation-drug interaction field important findings that will help understanding the role of inflammation in pharmacotherapy outcomes. / pharmaceutical sciences

Voltage clamp fluorometry (VCF) was first developed in the mid 1990s by Isacoff and his colleagues. In this approach fluorophores are attached to substituted cysteine residues that are engineered by site-directed mutagenesis. Changes in the dielectric environment of the fluorophore report local transitions that are associated with electrically-related and electrically-silent transitions. VCF provides a powerful technique to observe real time reports of ion channel gating conformations. It has proven to be a useful technique because it adds insight that is not available using other techniques. X-ray crystallography studies give a predominantly static picture of the channel, while patch clamping of channels gives information only about residues that effect ionic current flow. Similarly, gating current provides insight only about residues that are charged and move across the membrane electric field. In this thesis we examined the structural rearrangements of the Shaker channel and the effect of 4-AP on channel gating. We also examined for the first time the structural rearrangements of the Kv1.5 gating and the how the channel responds to depolarization pulses. This work is instrumental in the examination of the potassium channel gating.

Thesis(M.S.)--Auburn University, 2005. / Abstract. Vita. Includes bibliographic references.