Tensile Strength of Geological Discontinuities Including Incipient Bedding, Rock Joints and Mineral Veins

Geological discontinuities have a controlling influence for many rock-engineering projects in terms of strength, deformability and permeability, but their characterisation is often very difficult. Whilst discontinuities are often modelled as lacking any strength, in many rock masses visible rock discontinuities are only incipient and have tensile strength that may approach and can even exceed that of the parent rock. This fact is of high importance for realistic rock mass characterisation but is generally ignored. It is argued that current ISRM and other standards for rock mass characterisation, as well as rock mass classification schemes such as RMR and Q, do not allow adequately for the incipient nature of many rock fractures or their geological variability and need to be revised, at least conceptually. This paper addresses the issue of the tensile strength of incipient discontinuities in rock and presents results from a laboratory test programme to quantify this parameter. Rock samples containing visible, natural incipient discontinuities including joints, bedding, and mineral veins have been tested in direct tension. It has been confirmed that such discontinuities can have high tensile strength, approaching that of the parent rock. Others are, of course, far weaker. The tested geological discontinuities all exhibited brittle failure at axial strain less than 0.5 % under direct tension conditions. Three factors contributing to the tensile strength of incipient rock discontinuities have been investigated and characterised. A distinction is made between sections of discontinuity that are only partially developed, sections of discontinuity that have been locally weathered leaving localised residual rock bridges and sections that have been ‘healed’ through secondary cementation. Tests on bedding surfaces within sandstone showed that tensile strength of adjacent incipient bedding can vary considerably. In this particular series of tests, values of tensile strength for bedding planes ranged from 32 to 88 % of the parent rock strength (intact without visible discontinuities), and this variability could be attributed to geological factors. Tests on incipient mineral veins also showed considerable scatter, the strength depending upon the geological nature of vein development as well as the presence of rock bridges. As might be anticipated, tensile strength of incipient rock joints decreases with degree of weathering as expressed in colour changes adjacent to rock bridges. Tensile strengths of rock bridges (lacking marked discolouration) were found to be similar to that of the parent rock. It is concluded that the degree of incipiency of rock discontinuities needs to be differentiated in the process of rock mass classification and engineering design and that this can best be done with reference to the tensile strength relative to that of the parent rock. It is argued that the science of rock mass characterisation may be advanced through better appreciation of geological history at a site thereby improving the process of prediction and extrapolating properties

Evolutionary Determinants of Genetic Variation in Susceptibility to Infectious Diseases in Humans

Although genetic variation among humans in their susceptibility to infectious diseases has long been appreciated, little focus has been devoted to identifying patterns in levels of variation in susceptibility to different diseases. Levels of genetic variation in susceptibility associated with 40 human infectious diseases were assessed by a survey of studies on both pedigree-based quantitative variation, as well as studies on different classes of marker alleles. These estimates were correlated with pathogen traits, epidemiological characteristics, and effectiveness of the human immune response. The strongest predictors of levels of genetic variation in susceptibility were disease characteristics negatively associated with immune effectiveness. High levels of genetic variation were associated with diseases with long infectious periods and for which vaccine development attempts have been unsuccessful. These findings are consistent with predictions based on theoretical models incorporating fitness costs associated with the different types of resistance mechanisms. An appreciation of these observed patterns will be a valuable tool in directing future research given that genetic variation in disease susceptibility has large implications for vaccine development and epidemiology

Pan-cancer analysis of whole genomes

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale(1-3). Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter(4); identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation(5,6); analyses timings and patterns of tumour evolution(7); describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity(8,9); and evaluates a range of more-specialized features of cancer genomes(8,10-18).Peer reviewe