In Search of Community: Historic Preservation and the Quest to Recover Fort Gatlin

In a city dominated by large numbers of transplant residents, very few citizens of Orlando know or care about the area\u27s rich and colorful history or its historical figures. Local history is not taught in the Orange County schools unless a teacher has a particular interest in the subject and makes a special effort. 1 Recently, efforts have been made to curb this trend. In 1997, a small organization known as the Fort Gatlin Historical Group sought to trace Orlando\u27s origins through a community-wide effort to preserve the presumed site of Fort Gatlin, a United States Army fort of the Second Seminole War. In doing so, the group promoted a sense of community by uniting Orlandoans with their history and sparking general interest not only in Orlando\u27s past but in its present and, more importantly, its future

Complex Relationships: Public Policy and Law Solutions to Rebalance the Confrontation Clause, Evidence-Based Intimate-Partner Violence Prosecution, and Public and Private Violence After the Resurrection of Roberts

Following the Supreme Court’s 2004 decision in Crawford v. Washington, tensions between the Sixth Amendment Confrontation Clause and evidence-based prosecution of intimate-partner violence increased. In consequence, the Court forged a path of Constitutional jurisprudence which has weakened the power of the Confrontation Clause, reverted to a disguised reliability test reminiscent of Ohio v. Roberts, and diminished the rights of the accused. Simultaneously, these rulings have created a hierarchy where the severity of private, domestic violence is regarded as a lower level of emergency than public violence. Consequently, the Supreme Court’s primary purpose test for testimonial statements should be replaced with a two-part test which analyzes both the purpose and function of out-of-court statements, and evidence-based prosecutions should be supported by policy solutions adopted at local and state levels

Periaqueductal Gray Glia Modulate Morphine Tolerance Development via Soluble Tumor Necrosis Factor Signaling

Each year, over 50 million Americans suffer from persistent pain, including debilitating headaches, joint pain, and severe back pain. Although morphine is amongst the most effective analgesics available for the management of severe pain, prolonged morphine treatment results in decreased analgesic efficacy (i.e., tolerance). Despite significant headway in the field, the mechanisms underlying the development of morphine tolerance are not well understood. The midbrain ventrolateral periaqueductal gray (vlPAG) is a primary neural substrate for the analgesic effects of morphine, as well as for the development of morphine tolerance. A growing body of literature indicates that activated glia (i.e., microglia and astrocytes) facilitate pain transmission and oppose morphine analgesia, making these cells important potential targets in the treatment of chronic pain. Morphine affects glia by binding to the innate immune receptor toll-like receptor 4 (TLR4), leading to the release of proinflammatory cytokines and opposition of morphine analgesia. Despite the established role of the vlPAG as an integral locus for the development of morphine tolerance, to date, no studies have examined the role of glia activation within this region. Additionally, the role of TLR4 in the development of tolerance has not been elucidated. This dissertation seeks to address the lack of knowledge regarding the role of vlPAG glia and TLR4 in the development of morphine tolerance by (1) Characterizing the effects of chronic morphine and peripheral inflammatory pain on vlPAG glial cell activity; (2) Investigating the role of glia activation within the vlPAG in the development of morphine tolerance; (3) Characterizing the role of the glial receptor TLR4 within the vlPAG in the development of morphine tolerance; and (4) Characterizing the glia to neuron signaling mechanisms involved in the development of morphine tolerance. These experiments, together, provide novel information about the mechanism by which central nervous system glia regulate morphine tolerance, and identify a potential therapeutic target for the enhancement of analgesic efficacy in the clinical treatment of chronic pain