In our common interest: Liability and redress for damage caused to the natural environment during armed conflict

Although not generally accorded primary consideration during armed conflict, a vast number of provisions aimed at protecting the natural environment in times of war exist under international law. This article critically and comprehensively examines the challenges presented in terms of liability and redress for damage caused to the natural environment during armed conflict. In particular, the effectiveness of the various principles and rules that grant general, specific and indirect protection to the natural environment during warfare, coupled with the liability regimes established under the applicable international instruments, are scrutinised critically. The article argues that most international instruments dealing specifically with the means and methods of warfare, reveal serious inadequacies, and that some establish no liability regime whatsoever. Those instruments that do, however, contain a liability regime, reveal serious flaws to the degree that not all categories of armed conflict are attended to and only criminal sanctions (with no civil liability) are envisaged, coupled with the significant failure to extend liability to States Parties. Some international instruments fail to provide adequate mechanisms for legal redress or in instances where redress is provided, the mechanisms are flawed. The problem is exacerbated by the fact that customary international law has not yet developed to the degree that both adequate and comprehensive protection is available to protect the natural environment during armed conflict, irrespective of the nature of the conflict. This article therefore considers critically the adoption of an entirely new convention expressly intended to address all instances of environmental damage during (or as a consequence of) armed conflict, and concludes that such a step is preferred to the mere amendment of existing provisions or possibly even the drafting of yet another protocol to the four Geneva Conventions

ABC implementation in the Nelson Mandela Bay Metropole: How far should manufacturing organisations go?

Activity-based costing (ABC) success factors have been studied in past research, mostly by using commonly  known success factors. In this qualitative study, a literature review and interviews were used to establish what factors are responsible for the successful implementation of ABC. The number of semi-structured  interviews was limited to 13 ABC adopters in the Nelson Mandela Bay Metropole. The fi ndings suggested that ABC can be enhanced with the use of activity-based budgeting (ABB) and activity-based management (ABM). In addition, the use of ABC in conjunction with capital investment decisions may ensure that correct decisions are made when critical long-term projects are considered. Extensive identifi cation of cost drivers is benefi cial to the extent where the product loses its relationship with the overhead cost. It is evident from this research that considering fi xed indirect overheads in ABC is not always benefi cial for a manufacturing organisation  unless there is a clear link to the end-product.Key words: activity-based costing (ABC), budgeting, implementation, success factors, metropole, capital investments, competitio

The DAG1 transcription factor negatively regulates the seed-to-seedling transition in Arabidopsis acting on ABA and GA levels

BACKGROUND: In seeds, the transition from dormancy to germination is regulated by abscisic acid (ABA) and gibberellins (GAs), and involves chromatin remodelling. Particularly, the repressive mark H3K27 trimethylation (H3K27me3) has been shown to target many master regulators of this transition. DAG1 (DOF AFFECTING GERMINATION1), is a negative regulator of seed germination in Arabidopsis, and directly represses the GA biosynthetic gene GA3ox1 (gibberellin 3-β-dioxygenase 1). We set to investigate the role of DAG1 in seed dormancy and maturation with respect to epigenetic and hormonal control. RESULTS: We show that DAG1 expression is controlled at the epigenetic level through the H3K27me3 mark during the seed-to-seedling transition, and that DAG1 directly represses also the ABA catabolic gene CYP707A2; consistently, the ABA level is lower while the GA level is higher in dag1 mutant seeds. Furthermore, both DAG1 expression and protein stability are controlled by GAs. CONCLUSIONS: Our results point to DAG1 as a key player in the control of the developmental switch between seed dormancy and germination

A Comparison of Time-Memory Trade-Off Attacks on Stream Ciphers

Contains fulltext : 117176.pdf (preprint version ) (Open Access

DNA repair capacity as a possible biomarker of breast cancer risk in female BRCA1 mutation carriers

The BRCA1 gene product helps to maintain genomic integrity through its participation in the cellular response to DNA damage: specifically, the repair of double-stranded DNA breaks. An impaired cellular response to DNA damage is a plausible mechanism whereby BRCA1 mutation carriers are at increased risk of breast cancer. Hence, an individual's capacity to repair DNA may serve as a useful biomarker of breast cancer risk. The overall aim of the current study was to identify a biomarker of DNA repair capacity that could distinguish between BRCA1 mutation carriers and non-carriers. DNA repair capacity was assessed using three validated assays: the single-cell alkaline gel electrophoresis (comet) assay, the micronucleus test, and the enumeration of γ-H2AX nuclear foci. DNA repair capacity of peripheral blood lymphocytes from 25 cancer-free female heterozygous BRCA1 mutation carriers and 25 non-carrier controls was assessed at baseline and following cell exposure to γ – irradiation (2 Gy). We found no significant differences in the mean tail moment, in the number of micronuclei or in the number of γ-H2AX nuclear foci between the carriers and non-carriers at baseline, and following γ-irradiation. These data suggest that these assays are not likely to be useful in the identification of women at a high risk for breast cancer