National Security in the Information Age: Are We Heading Toward Big Brother?

Symposium Welcome: Alexander McDaniel, Symposium Editor, University of Richmond Law Review, and Wendy C. Perdue, Dean of the University of Richmond School of Law. (9:00 a.m. - 9:15 a.m.) “How Does the Government Collect Data Through Surveillance?” Panel Discussion: William C. Banks, Distinguished Professor of Law at Syracuse University College of Law and Founding Director of the Institute for National Security and Counterterrorism, and Jake Laperruque, Privacy Fellow with The Constitution Project. Professor Paul D. Crane, Associate Professor at the University of Richmond School of Law, served as moderator. (9:15 a.m. - 10:30 a.m.) “How Does the Government Retain and Destroy Data?” lecture: Douglas Cox, Associate Professor at CUNY School of Law. (10:45 a.m. - 11:45 a.m.) “How Does Data Impact the Courtroom?” Panel: Lt. Colonel Jeffrey Addicott (U.S. Army, ret.), Professor of Law and Director of the Center for Terrorism Law at St. Mary’s University School of Law, and Paul Gill, Assistant Federal Public Defender for the Federal Public Defender, Eastern District of Virginia. Douglas A. Ramseur, Capital Defender with the Office of the Capital Defender in Central Virginia, served as moderator. (1:00 p.m.- 2:15 p.m.) Keynote Address: Thomas J. Ridge, former Pennsylvania Governor and the first U.S. Secretary of Homeland Security. (2:30 p.m. – 3:30 p.m.

Methane Capture: Options for Greenhouse Gas Emission Reduction

This report discusses legislative alternatives for addressing methane capture, sources of methane, opportunities and challenges for methane capture, and current federal programs that support methane recovery

Assistive technology and consulting services for DRS

Issued as final repor

Inhibition of murine leukemia virus production in chronically infected akr cells. A novel effect of interferon.

Treatment of AKR cells that had spontaneously become procedures of a murine leukemia virus with a partially purified mouse interferon (> 5 × 10(7) international mouse reference units per mg of protein) inhibited endogenous virus production. This inhibitory effect decreased over a 72-hr period in a manner similar to interferon-induced antiviral activity directed against vesicular stomatitis virus in AKR cells. Despite the inhibitory effect of interferon on infectious murine leukemia virus and viral reverse transcriptase (RNA-dependent DNA polymerase) titers in the culture fluids, intracellular levels of viral groups-specific antigens were significantly increased. These results suggest that interferon treatment in AKR cells inhibited the assembly or release of the virus

Methane Capture: Options for Greenhouse Gas Emission Reduction

This report discusses alternatives for addressing methane capture, sources of methane, opportunities and challenges for methane capture, and current federal programs that support methane recovery

Interferon-directed inhibition of chronic murine leukemia virus production in cell cultures: lack of effect on intracellular viral markers.

Extracellular murine leukemia virus (MLV) reverse transcriptase activity was decreased by interferon treatment in four interferon-sensitive mouse cell lines which were chronic MLV producers. In three cell lines which were relatively insensitive to interferon, extracellular enzyme activity remained unchanged by interferon treatment. The concentrations of interferon used had no effect on DNA synthesis or cell replication of AKR,C+ cells which were chronic producers of AKR-MLV. In AKR,C+ cultures interferon treatment also had no effect on the level of intracellular viral reverse transcriptase activity in spite of an inhibition of extracellular enzyme activity. Treatment of AKRC+ cultures with interferon for 9 days inhibited extracellular viral reverse transcriptase levels throughout the period of treatment; however, the intracellular enzyme activity remained unchanged, and concentrations of viral p30 (gs) antigen were increased in the interferon-treated cells. When the cells were washed to remove interferon, however, virus production rapidly rose and intracellular p30 antigen fell to the levels of untreated AKR,C+ cells. These and previously reported results suggested that in interferon-treated AKR,C+ cells virus production is inhibited at a late step in the MLV replication cycle, either directly or through the inhibition of the production of a protein required for virus assembly