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PACLIC 23 / City University of Hong Kong / 3-5 December 200

Blackboard System Generator (BSG): An Alternative Distributed Problem-Solving Paradigm

The classical blackboard model employs a number of relaxations of team decision theory that are commonly organized into three panels of AI heuristics, including: 1) a shared information panel that offers a capability for ensuring agent knowledge sharing, 2) a contract formalism for the agent and event scheduling, coordinating, and control panel, and 3) a blackboard panel for metalevel planning and guidance that offers whole situation recognition, top down reasoning, and adaptive learning. The nature and implications of these relaxations are explained in terms of the blackboard system generator (BSG) and via comparisons to what is done in other blackboard shells. Particular attention is paid to theoretical relaxations inherent in the classical blackboard model and to research opportunities arising as a result. Progress made to date to counteract adverse effects of some of these relaxations is described in terms of a project management/work breakdown paradigm adopted in BSG that: 1) alleviates the knowledge engineering bottlenecks of traditional blackboards and that provides BSG with a semantic rather than just syntactic understanding of blackboard control and scheduling; 2) allows a distributed problem-solving capability for connecting agents at virtual addresses on a logical network and that permits concurrent processing on any machine available on the network; 3) establishes an open architecture that includes techniques for integrating preexisting agent methods (e.g., expert systems, procedures, or data bases) while laying the foundation for assessing the impact of “black boxes” on the global and local objective functions; and 4) utilizes project management techniques for team agents planning as well as an analogical reasoner subsystem for BSG metaplanning and generic controlled learning. This latter item is supported by a connectionist scheme for its associative memory. The techniques of each of the three panels and of the four sets of paradigm-related advances are described along with selected results from classroom teaching experiments and from three applications using BSG to date

Chronic CSE Treatment Induces the Growth of Normal Oral Keratinocytes via PDK2 Upregulation, Increased Glycolysis and HIF1α Stabilization

Exposure to cigarette smoke is a major risk factor for head and neck squamous cell carcinoma (HNSCC). We have previously established a chronic cigarette smoke extract (CSE)-treated human oral normal keratinocyte model, demonstrating an elevated frequency of mitochondrial mutations in CSE treated cells. Using this model we further characterized the mechanism by which chronic CSE treatment induces increased cellular proliferation.We demonstrate that chronic CSE treatment upregulates PDK2 expression, decreases PDH activity and thereby increases the glycolytic metabolites pyruvate and lactate. We also found that the chronic CSE treatment enhanced HIF1α accumulation through increased pyruvate and lactate production in a manner selectively reversible by ascorbate. Use of a HIF1α small molecule inhibitor blocked the growth induced by chronic CSE treatment in OKF6 cells. Furthermore, chronic CSE treatment was found to increase ROS (reactive oxygen species) production, and application of the ROS scavengers N-acetylcysteine abrogated the expression of PDK2 and HIF1α. Notably, treatment with dichloroacetate, a PDK2 inhibitor, also decreased the HIF1α expression as well as cell proliferation in chronic CSE treated OKF6 cells.Our findings suggest that chronic CSE treatment contribute to cell growth via increased ROS production through mitochondrial mutations, upregulation of PDK2, attenuating PDH activity thereby increasing glycolytic metabolites, resulting in HIF1α stabilization. This study suggests a role for chronic tobacco exposure in the development of aerobic glycolysis and normoxic HIFα activation as a part of HNSCC initiation. These data may provide insights into development of chemopreventive strategies for smoking related cancers

Widespread recombination, reassortment, and transmission of unbalanced compound viral genotypes in natural arenavirus infections.

Arenaviruses are one of the largest families of human hemorrhagic fever viruses and are known to infect both mammals and snakes. Arenaviruses package a large (L) and small (S) genome segment in their virions. For segmented RNA viruses like these, novel genotypes can be generated through mutation, recombination, and reassortment. Although it is believed that an ancient recombination event led to the emergence of a new lineage of mammalian arenaviruses, neither recombination nor reassortment has been definitively documented in natural arenavirus infections. Here, we used metagenomic sequencing to survey the viral diversity present in captive arenavirus-infected snakes. From 48 infected animals, we determined the complete or near complete sequence of 210 genome segments that grouped into 23 L and 11 S genotypes. The majority of snakes were multiply infected, with up to 4 distinct S and 11 distinct L segment genotypes in individual animals. This S/L imbalance was typical: in all cases intrahost L segment genotypes outnumbered S genotypes, and a particular S segment genotype dominated in individual animals and at a population level. We corroborated sequencing results by qRT-PCR and virus isolation, and isolates replicated as ensembles in culture. Numerous instances of recombination and reassortment were detected, including recombinant segments with unusual organizations featuring 2 intergenic regions and superfluous content, which were capable of stable replication and transmission despite their atypical structures. Overall, this represents intrahost diversity of an extent and form that goes well beyond what has been observed for arenaviruses or for viruses in general. This diversity can be plausibly attributed to the captive intermingling of sub-clinically infected wild-caught snakes. Thus, beyond providing a unique opportunity to study arenavirus evolution and adaptation, these findings allow the investigation of unintended anthropogenic impacts on viral ecology, diversity, and disease potential