Pay or conditions? The role of workplace characteristics in nurses’ labor supply

Acknowledgments We are grateful for the thoughtful comments of two referees. We would also like to thank conference participants at the Scottish Economic Society Conference and seminar participants at Newcastle University. Receipt of financial support from the ESRC is gratefully acknowledged (RES-000-23-1240). The Health Economics Research Unit is funded by the Chief Scientist Office of the Scottish Government Health and Social Care Directorates. The views expressed in this article are solely those of the authors.Peer reviewedPostprin

Denoising Scanning Tunneling Microscopy Images of Graphene with Supervised Machine Learning

Machine learning (ML) methods are extraordinarily successful at denoising photographic images. The application of such denoising methods to scientific images is, however, often complicated by the difficulty in experimentally obtaining a suitable expected result as an input to training the ML network. Here, we propose and demonstrate a simulation-based approach to address this challenge for denoising atomic-scale scanning tunneling microscopy (STM) images, which consists of training a convolutional neural network on STM images simulated based on a tight-binding electronic structure model. As model materials, we consider graphite and its mono- and few-layer counterpart, graphene. With the goal of applying it to any experimental STM image obtained on graphitic systems, the network was trained on a set of simulated images with varying characteristics such as tip height, sample bias, atomic-scale defects, and non-linear background. Denoising of both simulated and experimental images with this approach is compared to that of commonly-used filters, revealing a superior outcome of the ML method in the removal of noise as well as scanning artifacts - including on features not simulated in the training set. An extension to larger STM images is further discussed, along with intrinsic limitations arising from training set biases that discourage application to fundamentally unknown surface features. The approach demonstrated here provides an effective way to remove noise and artifacts from typical STM images, yielding the basis for further feature discernment and automated processing.Comment: Includes S

The Pathology of EMT in Mouse Mammary Tumorigenesis

Epithelial-mesenchymal-transition (EMT) tumorigenesis in the mouse was first described over 100 years ago using various terms such as carcinosarcoma and without any comprehension of the underlying mechanisms. Such tumors have been considered artifacts of transplantation and of tissue culture. Recently, EMT tumors have been recognized in mammary glands of genetically engineered mice. This review provides a historical perspective leading to the current status in the context of some of the key molecular biology. The biology of mouse mammary EMT tumorigenesis is discussed with comparisons to human breast cancer

DNA methylome analysis in Burkitt and follicular lymphomas identifies differentially methylated regions linked to somatic mutation and transcriptional control

Although Burkitt lymphomas and follicular lymphomas both have features of germinal center B cells, they are biologically and clinically quite distinct. Here we performed whole-genome bisulfite, genome and transcriptome sequencing in 13 IG-MYC translocation-positive Burkitt lymphoma, nine BCL2 translocation-positive follicular lymphoma and four normal germinal center B cell samples. Comparison of Burkitt and follicular lymphoma samples showed differential methylation of intragenic regions that strongly correlated with expression of associated genes, for example, genes active in germinal center dark-zone and light-zone B cells. Integrative pathway analyses of regions differentially methylated in Burkitt and follicular lymphomas implicated DNA methylation as cooperating with somatic mutation of sphingosine phosphate signaling, as well as the TCF3-ID3 and SWI/SNF complexes, in a large fraction of Burkitt lymphomas. Taken together, our results demonstrate a tight connection between somatic mutation, DNA methylation and transcriptional control in key B cell pathways deregulated differentially in Burkitt lymphoma and other germinal center B cell lymphomas

Genomic and transcriptomic changes complement each other in the pathogenesis of sporadic Burkitt lymphoma

Burkitt lymphoma (BL) is the most common B-cell lymphoma in children. Within the International Cancer Genome Consortium (ICGC), we performed whole genome and transcriptome sequencing of 39 sporadic BL. Here, we unravel interaction of structural, mutational, and transcriptional changes, which contribute to MYC oncogene dysregulation together with the pathognomonic IG-MYC translocation. Moreover, by mapping IGH translocation breakpoints, we provide evidence that the precursor of at least a subset of BL is a B-cell poised to express IGHA. We describe the landscape of mutations, structural variants, and mutational processes, and identified a series of driver genes in the pathogenesis of BL, which can be targeted by various mechanisms, including IG-non MYC translocations, germline and somatic mutations, fusion transcripts, and alternative splicing

Escalation provisions in DoD procurement: a review of the problem and a framework for analysis.

This study reviewed the opinions and concerns expressed by various government and private industry sources with regard to the use and structure of escalation (i.e., economic price adjustment) provisions in government procurement contracting. There was found to be little general agreement among these sources on many of the aspects of escalation provisions, including the "proper" objectives of such clauses. After this review a framework was designed to facilitate the analysis of the relationship of escalation provisions and price level uncertainty. The specific model employed examined interacting objectives of the government and a firm in a sole-source contract negotiation scenario. A method was developed to approximate the increase in contract price required by the firm as compensation for accepting the risk of uncertain price levels. A criterion was established for the employment of the escalation provision in the modeled scenario.http://archive.org/details/escalationprovis00eberLieutenant, United States NavyApproved for public release; distribution is unlimited

Team 3: Total Life Cycle Management: Automated Model Development

from Scythe : Proceedings and Bulletin of the International Data Farming Community, Issue 6 Workshop 18Total Life Cycle Management (TLCM) is the process which enables program managers to make life-cycle decisions across all phases of the acquisitions process. Life-cycle sustainment, operational performance issues and requirements are system dependant. Relevant issues arise from early in the process during the Material Solutions Analysis Phase, all the way through Operations and Support. Adaptive and modular modeling and simulation tools have been developed to address these complex issues throughout the life-cycle the Marine Corps weapons systems

The impact of flow-induced forces on the morphogenesis of the outflow tract

One percent of infants are born with congenital heart disease (CHD), which commonly involves outflow tract (OFT) defects. These infants often require complex surgeries, which are associated with long term adverse remodeling effects, and receive replacement valves with limited strength, biocompatibility, and growth capability. To address these problematic issues, researchers have carried out investigations in valve development and valve mechanics. A longstanding hypothesis is that flow-induced forces regulate fibrous valve development, however, the specific mechanisms behind this mechanotransduction remain unclear. The purpose of this study was to implement an in vitro system of outflow tract development to test the response of embryonic OFT tissues to fluid flow. A dynamic, three-dimensional bioreactor system was used to culture embryonic OFT tissue under different levels of flow as well as the absence of flow. In the absence of flow, OFT tissues took on a more primitive phenotype that is characteristic of early OFT cushion development where widely dispersed mesenchymal cells are surrounded by a sparse, disorganized extracellular matrix (ECM). Whereas OFT tissues subjected to physiologically matched flow formed compact mounds of cells, initated,fibrous ECM development, while prolonged supraphysiological flow resulted in abnormal tissue remodeling. This study indicates that both the timing and magnitude of flow alter cellular processes that determine if OFT precursor tissue undergoes normal or pathological development. Specifically, these experiments showed that flow-generated forces regulate the deposition and localization of fibrous ECM proteins, indicating that mechanosensitive signaling pathways are capable of driving pathological OFT development if flows are not ideal

Transforming Growth Factor Beta3 is Required for Cardiovascular Development

Transforming growth factor beta3 (TGFB3) gene mutations in patients of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD1) and Loeys-Dietz syndrome-5 (LDS5)/Rienhoff syndrome are associated with cardiomyopathy, cardiac arrhythmia, cardiac fibrosis, cleft palate, aortic aneurysms, and valvular heart disease. Although the developing heart of embryos express Tgfb3, its overarching role remains unclear in cardiovascular development and disease. We used histological, immunohistochemical, and molecular analyses of Tgfb3−/− fetuses and compared them to wildtype littermate controls. The cardiovascular phenotypes were diverse with approximately two thirds of the Tgfb3−/− fetuses having one or more cardiovascular malformations, including abnormal ventricular myocardium (particularly of the right ventricle), outflow tract septal and alignment defects, abnormal aortic and pulmonary trunk walls, and thickening of semilunar and/or atrioventricular valves. Ventricular septal defects (VSD) including the perimembranous VSDs were observed in Tgfb3−/− fetuses with myocardial defects often accompanied by the muscular type VSD. In vitro studies using TGFβ3-deficient fibroblasts in 3-D collagen lattice formation assays indicated that TGFβ3 was required for collagen matrix reorganization. Biochemical studies indicated the ‘paradoxically’ increased activation of canonical (SMAD-dependent) and noncanonical (MAP kinase-dependent) pathways. TGFβ3 is required for cardiovascular development to maintain a balance of canonical and noncanonical TGFβ signaling pathways