Greenbury Report (UK)

The Greenbury Report on Directors Remuneration (1995) (hereafter called the Greenbury Report) was one of the first comprehensive governance codes directly addressing executive and director remuneration. The Greenbury Report was commissioned by the Confederation of British Industry in response to public concerns over recently privatized public utilities and the salaries and bonuses earned by executives, while they implemented job cuts, and service price increases. The Greenbury Report recommended an independent remuneration committee, linking executive pay to corporate financial and operational performance measures, and increased the requirements for disclosure and transparency on directors’ remuneration. However, the credibility of the Greenbury Report was challenged due to the composition of the group; it was not deemed to be independent of the sector it was to investigate, and it was argued that its recommendations did not go far enough. The financial crisis of 2008 highlighted the failure of the Greenbury Report’s recommendations for limiting excessive executive pay. In particular, the Walker Review of the Banking Sector found that performance-based bonus schemes in banking corporations that are supposed to align executive objectives with shareholder objectives increased corporate risk in the period leading up to the financial crisis. In addition, during the crisis, executive pay in large publicly listed corporations (PLCs) continued to increase, while workers’ wages stagnated. Therefore, despite Greenbury’s recommendations, executive pay continued, and still continues, to be a concern for the public and policymakers alike. Nonetheless, improved transparency on remuneration and a greater linking of pay to performance followed from the Greenbury Report and most corporations now include operational measures linked to performance and sustainability

The impact of migration on tuberculosis epidemiology and control in high-income countries: a review.

Tuberculosis (TB) causes significant morbidity and mortality in high-income countries with foreign-born individuals bearing a disproportionate burden of the overall TB case burden in these countries. In this review of tuberculosis and migration we discuss the impact of migration on the epidemiology of TB in low burden countries, describe the various screening strategies to address this issue, review the yield and cost-effectiveness of these programs and describe the gaps in knowledge as well as possible future solutions.The reasons for the TB burden in the migrant population are likely to be the reactivation of remotely-acquired latent tuberculosis infection (LTBI) following migration from low/intermediate-income high TB burden settings to high-income, low TB burden countries.TB control in high-income countries has historically focused on the early identification and treatment of active TB with accompanying contact-tracing. In the face of the TB case-load in migrant populations, however, there is ongoing discussion about how best to identify TB in migrant populations. In general, countries have generally focused on two methods: identification of active TB (either at/post-arrival or increasingly pre-arrival in countries of origin) and secondly, conditionally supported by WHO guidance, through identifying LTBI in migrants from high TB burden countries. Although health-economic analyses have shown that TB control in high income settings would benefit from providing targeted LTBI screening and treatment to certain migrants from high TB burden countries, implementation issues and barriers such as sub-optimal treatment completion will need to be addressed to ensure program efficacy

Classification of polyhedral shapes from individual anisotropically resolved cryo-electron tomography reconstructions

Background Cryo-electron tomography (cryo-ET) enables 3D imaging of macromolecular structures. Reconstructed cryo-ET images have a “missing wedge” of data loss due to limitations in rotation of the mounting stage. Most current approaches for structure determination improve cryo-ET resolution either by some form of sub-tomogram averaging or template matching, respectively precluding detection of shapes that vary across objects or are a priori unknown. Various macromolecular structures possess polyhedral structure. We propose a classification method for polyhedral shapes from incomplete individual cryo-ET reconstructions, based on topological features of an extracted polyhedral graph (PG). Results We outline a pipeline for extracting PG from 3-D cryo-ET reconstructions. For classification, we construct a reference library of regular polyhedra. Using geometric simulation, we construct a non-parametric estimate of the distribution of possible incomplete PGs. In studies with simulated data, a Bayes classifier constructed using these distributions has an average test set misclassification error of?<?5 % with upto 30 % of the object missing, suggesting accurate polyhedral shape classification is possible from individual incomplete cryo-ET reconstructions. We also demonstrate how the method can be made robust to mis-specification of the PG using an SVM based classifier. The methodology is applied to cryo-ET reconstructions of 30 micro-compartments isolated from E. coli bacteria. Conclusions The predicted shapes aren’t unique, but all belong to the non-symmetric Johnson solid family, illustrating the potential of this approach to study variation in polyhedral macromolecular structures

Structural basis for cisplatin DNA damage tolerance by human polymerase η during cancer chemotherapy

A major clinical problem in the use of cisplatin to treat cancers is tumor resistance. DNA polymerase η (Pol-η) is a crucial polymerase that allows cancer cells to cope with the cisplatin–DNA adducts that are formed during chemotherapy. We present here a structure of human Pol-η inserting deoxycytidine triphosphate (dCTP) opposite a cisplatin intrastrand cross-link (PtGpG). We show that the specificity of human Pol-η for PtGpG derives from an active site that is open to permit Watson-Crick geometry of the nascent PtGpG-dCTP base pair and to accommodate the lesion without steric hindrance. This specificity is augmented by the residues Gln38 and Ser62, which interact with PtGpG, and Arg61, which interacts with the incoming dCTP. Collectively, the structure provides a basis for understanding how Pol-η in human cells can tolerate the DNA damage caused by cisplatin chemotherapy and offers a framework for the design of inhibitors in cancer therapy