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This paper reviews the monitoring, reporting and verification of greenhouse-gas emissions needed for carbon-pricing and management mechanisms. The monitoring, reporting and verification (MRV) of greenhouse-gas emissions is the cornerstone of carbon pricing and management mechanisms. Here we consider peer-reviewed articles and 'grey literature' related to existing MRV requirements and their costs. A substantial part of the literature is the regulatory texts of the 15 most important carbon pricing and management mechanisms currently implemented. Based on a comparison of key criteria such as the scope, cost, uncertainty and flexibility of procedures, we conclude that conventional wisdom on MRV is not often promoted in existing carbon pricing mechanisms. Quantification of emissions uncertainty and incentives to reduce this uncertainty are usually only partially applied, if at all. Further, the time and resources spent on small sources of emissions would be expected to be limited. Although provisions aiming at an effort proportionate to the amount of emissions at stake — 'materiality' — are widespread, they are largely outweighed by economies of scale: in all schemes, MRV costs per tonne are primarily driven by the size of the source.

Nature Clim. Change 5, 319–328 (2015); published online 25 March 2015; corrected after print 8 September 2015 In the version of this Review Article originally published, the following affiliation should have been included for Igor Shishlov: CIRED (Centre International de Recherche sur l'Environnement et le Développement), 94736 Nogent-sur-Marne, France.

A critical management decision, which has a direct effect on project success, is the prequalification of contractors for bidding purposes. A substantial amount of data is generated during contractor prequalification, which must be compiled, processed, analyzed and stored, for the proper selection of contractors, who will successfully complete the contracted work if awarded to them. This research thesis examines the prequalification process with a case study emphasis on minority contractors, identifies areas that can be streamlined and provide construction managers with valuable information to assist with their final selection, through the development and implementation of a construction management information system (CMIS) conceptual model and framework. The following areas: prequalification, minority contractor procurement and information systems are explored and formulate the basis on which the CMIS is developed. The final output of this study is the development of implementation scheme for the proposed CMIS for contractor prequalification and a prototype in Microsoft Access.

In the 9 years since the publication of our 2011 review of targeted treatment of thyroid cancer with multikinase inhibitors, much has changed in the landscape of this heterogeneous disease. New multikinase and selective inhibitor treatments for medullary thyroid cancer, radioiodine-refractory thyroid cancer and anaplastic thyroid cancer have completed trials and improved progression-free survival. Many physicians are concerned by dose-limiting adverse effects of these drugs and are wary to begin treatment in patients who are systemically well but have marked disease burden, which makes the timing of treatment initiation challenging. Published mechanistic data on tyrosine kinase inhibitors (TKIs) have helped guide our understanding of how to dose effectively with these drugs. A major goal in TKI therapy is to optimize inhibition of oncogenic kinase drivers while maintaining patient quality of life. Real-world data have now been published on how TKIs have fared outside the clinical trial environment. In this Review, we provide a summary of published data on the efficacy of TKIs in clinical practice, to provide clinicians with a more realistic view of how their patients will manage and respond to TKI therapy. Furthermore, we review the data on mechanisms of inhibition, outcomes and adverse effects of TKIs and provide an update on targeted treatment of thyroid cancer, focusing on optimizing the timing of treatment initiation.This Review summarizes the evidence from clinical trials for the efficacy of tyrosine kinase inhibitors in the treatment of thyroid cancer. The data from the experience with these drugs in clinical practice are also discussed, and factors that can help clinicians decide when to start or whether to continue tyrosine kinase inhibitor therapy are considered.

Remote therapeutic (RTM) and remote physiological monitoring (RPM) in chronic pain management are new Current Procedural Terminology (CPT) codes introduced in the last decade in an effort to capture continuous patient data in the outpatient setting. RTM and RPM facilitate steady patient engagement and real-time data collection, offering a comprehensive overview into potentially both subjective patient experiences and outcomes and objective physiological measures. This review delves into the benefits of these technologies, including improved patient outcomes, and addresses challenges such as data security and technological literacy. Furthermore, examples from other specialties in medicine are given to draw possible conclusions of how it may be used in chronic pain. The potential of RTM and RPM to enhance chronic pain management is contingent upon careful consideration of ethical and regulatory issues and has the potential to provide the objective data that the field of pain may need.

The incidence of thyroid cancer is rapidly increasing, mostly due to the overdiagnosis and overtreatment of differentiated thyroid cancer (TC). The increasing use of potent preclinical models, high throughput molecular technologies, and gene expression microarrays have provided a deeper understanding of molecular characteristics in cancer. Hence, molecular markers have become a potent tool also in TC management to distinguish benign from malignant lesions, predict aggressive biology, prognosis, recurrence, as well as for identification of novel therapeutic targets. In differentiated TC, molecular markers are mainly used as an adjunct to guide management of indeterminate nodules on fine needle aspiration biopsies. In contrast, in advanced thyroid cancer, molecular markers enable targeted treatments of affected signalling pathways. Identification of the driver mutation of targetable kinases in advanced TC can select treatment with mutation targeted tyrosine kinase inhibitors (TKI) to slow growth and reverse adverse effects of the mutations, when traditional treatments fail. This review will outline the molecular landscape and discuss the impact of molecular markers on diagnosis, surveillance and treatment of differentiated, poorly differentiated and anaplastic follicular TC.

Cardiac hypertrophic growth in response to pathological cues is associated with reexpression of fetal genes and decreased cardiac function and is often a precursor to heart failure. In contrast, physiologically induced hypertrophy is adaptive, resulting in improved cardiac function. The processes that selectively induce these hypertrophic states are poorly understood. Here, we have profiled 2 repressive epigenetic marks, H3K9me2 and H3K27me3, which are involved in stable cellular differentiation, specifically in cardiomyocytes from physiologically and pathologically hypertrophied rat hearts, and correlated these marks with their associated transcriptomes. This analysis revealed the pervasive loss of euchromatic H3K9me2 as a conserved feature of pathological hypertrophy that was associated with reexpression of fetal genes. In hypertrophy, H3K9me2 was reduced following a miR-217-mediated decrease in expression of the H3K9 dimethyltransferases EHMT1 and EHMT2 (EHMT1/2). miR-217-mediated, genetic, or pharmacological inactivation of EHMT1/2 was sufficient to promote pathological hypertrophy and fetal gene reexpression, while suppression of this pathway protected against pathological hypertrophy both in vitro and in mice. Thus, we have established a conserved mechanism involving a departure of the cardiomyocyte epigenome from its adult cellular identity to a reprogrammed state that is accompanied by reexpression of fetal genes and pathological hypertrophy. These results suggest that targeting miR-217 and EHMT1/2 to prevent H3K9 methylation loss is a viable therapeutic approach for the treatment of heart disease.