A lithic analysis of the Jackson site (DiMe-17) in southwestern Manitoba

The Jackson site (DiMe-17) is a Late Precontact site located in the Lauder Sand Hills of southwestern Manitoba. Primarily a bison kill and processing locale for Vickers focus people, this winter occupation has a calibrated radiocarbon date range between A.D. 1427 and A.D. 1683. Although a small Blackduck component was evident in the southwest corner of the site, the Vickers focus occupation was the dominant presence at this site and is the focus of this thesis. Archaeological investigations between 1994 and 1997 yielded a sample from 36 one square metres excavation units and 67 shovel tests pits. As part of an extensive investigation of Plains Woodland occupation of the region over the past 1200 years, excavation of the site served to provide additional information about Vickers focus occupation within the Makotchi-Ded Dontipi locale. This study offers a lithic analysis that encompasses the debitage and tools with an emphasis on the spatial distribution of the lithic materials. This seeks to assess the validity of the proposed activity areas at the Jackson site. The lithic analysis verified the presence of habitation and kill areas. Lithics from the east-central part of the site indicated processing activities as opposed to a large midden area associated with faunal processing as initially proposed in earlier studies. Late Side-notched projectile point types dominate the assemblage from the site. Plains and Prairie Side-notched point styles are affiliated with the Mortlach phase, Central Plains Tradition, Mississippian Tradition, and Middle Missouri Tradition. The Vickers focus people may have interacted and exchanged lithic materials with these groups. The Vickers focus people utilized exotic (Knife River flint, Tongue River silicified sediment, obsidian) as well as local materials (chalcedony, chert) to manufacture their tools

Foot-and-mouth disease: past, present and future

Foot-and-mouth disease (FMD) is a highly contagious disease of cloven-hoofed animals including cattle, pigs, sheep and many wildlife species. It can cause enormous economic losses when incursions occur into countries which are normally disease free. In addition, it has long-term effects within countries where the disease is endemic due to reduced animal productivity and the restrictions on international trade in animal products. The disease is caused by infection with foot-and-mouth disease virus (FMDV), a picornavirus. Seven different serotypes (and numerous variants) of FMDV have been identified. Some serotypes have a restricted geographical distribution, e.g. Asia-1, whereas others, notably serotype O, occur in many different regions. There is no cross-protection between serotypes and sometimes protection conferred by vaccines even of the same serotype can be limited. Thus it is important to characterize the viruses that are circulating if vaccination is being used for disease control. This review describes current methods for the detection and characterization of FMDVs. Sequence information is increasingly being used for identifying the source of outbreaks. In addition such information can be used to understand antigenic change within virus strains. The challenges and opportunities for improving the control of the disease within endemic settings, with a focus on Eurasia, are discussed, including the role of the FAO/EuFMD/OIE Progressive Control Pathway. Better control of the disease in endemic areas reduces the risk of incursions into disease-free regions

Identification of key residues that regulate the interaction of kinesins with microtubule ends

Kinesins are molecular motors that use energy derived from ATP turnover to walk along microtubules, or when at the microtubule end, regulate growth or shrinkage. All kinesins that regulate microtubule dynamics have long residence times at microtubule ends, whereas those that only walk have short end‐residence times. Here, we identify key amino acids involved in end binding by showing that when critical residues from Kinesin‐13, which depolymerises microtubules, are introduced into Kinesin‐1, a walking kinesin with no effect on microtubule dynamics, the end‐residence time is increased up to several‐fold. This indicates that the interface between the kinesin motor domain and the microtubule is malleable and can be tuned to favour either lattice or end binding