Thesis (Ph.D.) - University of Queensland, 2003. / Includes bibliography.

Thesis (Ph. D.)--University of Wisconsin, Madison, 1974. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (M.A.) -- Central Connecticut State University, 2006. / Thesis advisor: Damon Mitchell. "... in partial fulfillment of the requirements for the degree of Master of Arts in Criminology." Includes bibliographical references (leaves 28-31). Also available via the World Wide Web.

Thesis (Ph. D.)--University of California, San Diego and San Diego State University, 2006. / Includes facsimiles of articles previously published (leaves 37-79). Includes bibliographical references.

Thesis (M.S.)--University of Delaware, 2007. / Principal faculty advisor: Karl E. Wommack, Dept. of Plant & Soil Sciences. Includes bibliographical references.

Thesis (Ph. D.)--University of Missouri-Columbia, 2007. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on October 18, 2007) Vita. Includes bibliographical references.

Thesis (Ph.D.)(Botany)--University of Pretoria, 2006. / Includes summary. Includes bibliographical references. Available on the Internet via the World Wide Web.

No description available.

In this thesis, we consider the problem of decontaminating networks from black viruses (BVs) with a team of mobile agents, using parallel strategies. The BV is a harmful process whose initial location is unknown a priori. It destroys any agent arriving at the network site where it resides and, once triggered, it spreads to all the neighboring sites, creating copies of itself, thus increasing its presence in the network. To eliminate a virus present in a node, an agent has to move on that node; however, once the disinfection is performed, the agent is destroyed (i.e., it becomes inactive and cannot operate anymore). Existing literature has proposed sequential strategies that minimize the spread of the virus, such techniques are however quite inefficient in terms of time complexity. Instead of exploring the network sequentially, we propose to employ a group of agents that cooperate to follow a collective protocol to explore the network simultaneously. In this way, we dramatically reduce the decontamination time, still keeping the spread (and the number of agents loss) asymptotically optimal. In the thesis, various protocols are proposed in meshes, tori, and chordal rings following the monotonicity principle (i.e., once a node is disinfected we prevent it from being recontaminated). Finally, a solution is proposed also for the general case of the arbitrary topology. We analyze theoretically the cost of all our solutions for special topologies showing the advantages of our strategies with respect to the existing ones. In the case of the arbitrary topology, we conduct experimental analysis to assess the performance of our solution, confirming its efficiency. In all cases, our strategies significantly improve time while maintaining asymptotically optimal spread and agent losses.

A continuous line of fetal rhesus monkey kidney cells, FRhK-4, has been used for the propagation of hepatitis A virus (HAV) to prepare diagnostic antigen. While studying the fine structure of HAV grown in these cells, I discovered an unsuspected polyomavirus in both HAV-inoculated and control, uninoculated cultures. The virus, designated FRKV, was also detected in low pass FRhK-4 cultures and in FRhK-6, a cell line used in the development of a live, attenuated hepatitis A vaccine. The presence of an adventitious polyomavirus in FRhK-6 cultures poses questions about the suitability of these cells for vaccine preparation. I have used immunoelectron microscopy (IEM) to identify FRKV, which is not antigenically related to the primate polyomaviruses SV40, SA12, BKV or JCV, but reacts with antibodies that are present in fetal, newborn and adult bovine sera. By IEM the virus is indistinguishable from WRSV, a polyomavirus isolated from calf kidney. FRKV is antigenically similar to recently isolated calf kidney polyomaviruses. I have demonstrated that a commercial pool of fetal bovine serum contains infectious virus and its antibody. FRKV is therefore almost certainly a bovine polyomavirus. IEM has also shown that FRKV is indistinguishable from STMV and CMKV, the polyomaviruses isolated from cultures of stump-tailed and cynomolgus macaque kidney, and is antigenically similar to a polyomavirus from another monkey kidney cell line, LLC-MK2. By implication FRKV is similar to HD, the STMV-like polyomavirus from Vero cells. It thus appears that various monkey kidney cultures from several laboratories have been contaminated with a bovine polyomavirus. It follows that highly sensitive techniques are required for screening bovine sera used in culture media, especially those used in vaccine production. I have explored the use of antibody-coated grids to increase the sensitivity of EM but conclude that the greater sensitivity of DNA amplification techniques might be more appropriate for this purpose.