Soil carbon stock in the tropical rangelands of Australia: Effects of soil type and grazing pressure, and determination of sampling requirement

On-going, high-profile public debate about climate change has focussed attention on how to monitor the soil organic carbon stock (C) of rangelands (savannas). Unfortunately, optimal sampling of the rangelands for baseline C - the critical first step towards efficient monitoring - has received relatively little attention to date. Moreover, in the rangelands of tropical Australia relatively little is known about how C is influenced by the practice of cattle grazing. To address these issues we used linear mixed models to: (i) unravel how grazing pressure (over a 12-year period) and soil type have affected C and the stable carbon isotope ratio of soil organic carbon (δC) (a measure of the relative contributions of C and C vegetation to C); (ii) examine the spatial covariation of C and δC; and, (iii) explore the amount of soil sampling required to adequately determine baseline C. Modelling was done in the context of the material coordinate system for the soil profile, therefore the depths reported, while conventional, are only nominal.Linear mixed models revealed that soil type and grazing pressure interacted to influence C to a depth of 0.3m in the profile. At a depth of 0.5m there was no effect of grazing on C, but the soil type effect on C was significant. Soil type influenced δC to a soil depth of 0.5m but there was no effect of grazing at any depth examined. The linear mixed model also revealed the strong negative correlation of C with δC, particularly to a depth of 0.1m in the soil profile. This suggested that increased C at the study site was associated with increased input of C from C trees and shrubs relative to the C perennial grasses; as the latter form the bulk of the cattle diet, we contend that C sequestration may be negatively correlated with forage production. Our baseline C sampling recommendation for cattle-grazing properties of the tropical rangelands of Australia is to: (i) divide the property into units of apparently uniform soil type and grazing management; (ii) use stratified simple random sampling to spread at least 25 soil sampling locations about each unit, with at least two samples collected per stratum. This will be adequate to accurately estimate baseline mean C to within 20% of the true mean, to a nominal depth of 0.3m in the profile

Cytogenetics of basal cell carcinoma and squamous cell carcinomas

Cytogenetic analysis is a powerful tool that allows analysis of chromosomal aberrations associated with diseased states. In particular, a combination of cytogenetic techniques has allowed the identification of aberrations associated with cancer development, including cancers of the skin. This chapter provides a comprehensive overview of cytogenetic alterations in basal and squamous cell carcinomas of the skin. These two distinct lesions have altered karyotypes that are consistent with their malignant potential. Basal cell carcinomas, although relatively stable lesions, are highly associated with recurrent aberrations of chromosomes 6, 7, 9 and X, as detected by a number of cytogenetic techniques. Squamous cell carcinomas, on the other hand are associated with a much higher degree of instability, involving aberrations of chromosomes 3, 7, 8, 11, 13, 17 and 18, as detected using a number of cytogenetic techniques. Overall, the numbers and types of aberrations associated with basal and squamous cell carcinoma, define the characteristic behaviour associated with these lesions and identification of these aberrations may aid in the understanding of malignant potential, prognosis and treatment of these skin cancers

The clonal origin and clonal evolution of epithelial tumours

While the origin of tumours, whether from one cell or many, has been a source of fascination for experimental oncologists for some time, in recent years there has been a veritable explosion of information about the clonal architecture of tumours and their antecedents, stimulated, in the main, by the ready accessibility of new molecular techniques. While most of these new results have apparently confirmed the monoclonal origin of human epithelial (and other) tumours, there are a significant number of studies in which this conclusion just cannot be made. Moreover, analysis of many articles show that the potential impact of such considerations as patch size and clonal evolution on determinations of clonality have largely been ignored, with the result that a number of these studies are confounded. However, the clonal architecture of preneoplastic lesions provide some interesting insights — many lesions which might have been hitherto regarded as hyperplasias are apparently clonal in derivation. If this is indeed true, it calls into some question our hopeful corollary that a monoclonal origin presages a neoplastic habitus. Finally, it is clear, for many reasons, that methods of analysis which involve the disaggregation of tissues, albeit microdissected, are far from ideal and we should be putting more effort into techniques where the clonal architecture of normal tissues, preneoplastic and preinvasive lesions and their derivative tumours can be directly visualized in situ