Developing New Tourism Services: Dinosaurs a New Drive Tourism Resource for Remote Areas

This paper examines issues encountered when developing new tourism services generally, and specific aspects relating to the development of remote area dinosaur fossil fields for tourism. It studies two sites, one in the USA and one in Australia. Access to both sites is by minor roads, and both sites are characterised by long drives separating the sites from small communities that offer limited infrastructure and few other attractions for visitors. In both areas, however, tourism is seen as one of the few possible ways to sustain existing communities in the face of declining primary-industry-based employment. In general, tourists visiting these areas are on touring holidays of two weeks’ duration or more where the attraction is the general attributes of the region as well as to a lesser extent their interest in dinosaur fossils. These provide a potential resource for remote-region economic development through commodification as a new tourism attraction. Development of dinosaur fossil finds as a tourism resource is conceptualised here as new service development. Developing new tourism services, especially in remote regions, is challenging and has not been well examined in the tourism literature. The new service development process used in this case study first examines the characteristics of the existing tourists travelling through the region. The characteristics of a number of potential market segments currently interested in dinosaur fossils were then examined and contrasted with the existing market. This is conceptualised on a specialist-generalist spectrum of interest in fossils. A study of the tourist service features associated with dinosaur fossil tourism in remote regions of the USA was conducted, leading to the identification of a number of possible incremental development opportunities. The paper then takes a strategic approach to examining potential new tourism service development related to dinosaur fossils in remote regions of Queensland, Australia. In particular, it describes use of information about existing services in similar regions as the basis for ideas about development as well as comparison between existing and potential markets.

Neoplastic progression occurs through mutator pathways in hyperplastic polyposis of the colorectum

Aim-Colorectal cancer has been described in association with hyperplastic polyposis but the mechanism underlying this observation is unknown. The aim of this study was to characterise foci of dysplasia developing in the polyps of subjects with hyperplastic polyposis on the basis of DNA microsatellite status and expression of the DNA mismatch repair proteins hMLH1, hMSH2, and hMSH6. Materials and methods-The material was derived from four patients with hyperplastic polyposis and between one and six synchronous colorectal cancers. Normal (four), hyperplastic (13), dysplastic (13), and malignant (11) samples were microdissected and a PCR based approach was used to identify mutations at 10 microsatellite loci, TGF beta IIR, IGF2R, BAX, MSH3, and MSH6. Microsatellite instability-high (MSI-H) was diagnosed when 40% or more of the microsatellite loci showed mutational bandshifts. Serial sections were stained for hMLH1, hMSH2, and hMSH6. Result-DNA microsatellite instability was found in 1/13 (8%) hyperplastic samples, in 7/13 (54%) dysplastic foci, and in 8/11 (73%) cancers. None of the MSI-low (MSI-L) samples (one hyperplastic, three dysplastic, two cancers) showed loss of hMLH1 expression. All four MSI-H dysplastic foci and six MSI-H cancers showed loss of hMLH1 expression. Loss of hMLH1 in MSI-H but not in MSI-L lesions showing dysplasia or cancer was significant (p< 0.001, Fisher's exact test). Loss of hMSH6 occurred in one MSI-H cancer and one MSS focus of dysplasia which also showed loss of hMLH1 staining. Conclusion-Neoplastic changes in hyperplastic polyposis may occur within a hyperplastic polyp. Neoplasia may be driven by DNA instability that is present to a low (MSI-L) or high (MSI-H) degree. MSI-H but not MSI-L dysplastic foci are associated with loss of hMLH1 expression. At least two mutator pathways drive neoplasia in hyperplastic polyposis. The role of the hyperplastic polyp in the histogenesis of sporadic DNA microsatellite unstable colorectal cancer should be examined.