Employer perspectives on ‘zero hours’ contracts in UK higher education

The use of casual and temporary labour in the UK labour market is not a new phenomenon, but an increase in the use of so-called ‘zero hours contracts’ has drawn considerable attention from pressure groups, the media and all three main political parties over the past 18 months. While official figures indicate that the majority of zero hours contracts are found in the retail, hospitality, and healthcare sectors, the use of these arrangements at higher education establishments has also attracted attention and has become an area of focus for HE trade unions. This paper begins with a review of the legal framework for these contracts and temporary work in the UK, the economic conditions that have prevailed, and the political responses to pressure from media and civil society to curb their use and, where this may be the case, abuse. The main body of the paper focuses on the use of these contracts in higher education based on research by the Universities and Colleges Employers Association (UCEA) and the paper concludes with reflections on the employment relations issues and tensions within the context of an increasingly competitive higher education landscape

Employer perspectives on ‘zero hours’ contracts in UK higher education

The use of casual and temporary labour in the UK labour market is not a new phenomenon, but an increase in the use of so-called ‘zero hours contracts’ has drawn considerable attention from pressure groups, the media and all three main political parties over the past 18 months. While official figures indicate that the majority of zero hours contracts are found in the retail, hospitality, and healthcare sectors, the use of these arrangements at higher education establishments has also attracted attention and has become an area of focus for HE trade unions. This paper begins with a review of the legal framework for these contracts and temporary work in the UK, the economic conditions that have prevailed, and the political responses to pressure from media and civil society to curb their use and, where this may be the case, abuse. The main body of the paper focuses on the use of these contracts in higher education based on research by the Universities and Colleges Employers Association (UCEA) and the paper concludes with reflections on the employment relations issues and tensions within the context of an increasingly competitive higher education landscape

On hepatic stem cells and their role in chronic liver disease and carcinogenesis

Hepatic stem cells are found in the liver at all stages of development, including adult, and have the potential to give rise to daughter cells of biliary, hepatocytic and pancreatic lineages. Hepatic stem cells contribute significantly to liver regeneration, but may be associated with development of primary liver cancer, and are being investigated as a cellular therapy for liver failure. This thesis describes the development of methods for the immunohistochemical quantification of hepatic stem cell activation, allowing assessment of the association between hepatic stem cell activation in needle biopsy tissue and subsequent development of HCC in a retrospectively identified cohort of cirrhotic patients. A murine dietary model of NASH and HCC was developed and characterised in detail demonstrating progressive hepatic stem cell activation with increasing injury severity. We then went on to describe and prospectively isolate a resident population of stromal stem/progenitor cells in adult, uninjured mouse liver with the potential to give rise to both myofibroblasts, and under selective conditions, epithelial stem/progenitor cells. Finally, we demonstrated the isolation of hepatic stem cell from explanted cirrhotic liver and normal common bile duct and assessed their utility as a source of hepatic stem cells for cellular or regenerative therapy

Speeding up Madgraph5 aMC@NLO through CPU vectorization and GPU offloading: towards a first alpha release

The matrix element (ME) calculation in any Monte Carlo physics event generator is an ideal fit for implementing data parallelism with lockstep processing on GPUs and vector CPUs. For complex physics processes where the ME calculation is the computational bottleneck of event generation workflows, this can lead to large overall speedups by efficiently exploiting these hardware architectures, which are now largely underutilized in HEP. In this paper, we present the status of our work on the reengineering of the Madgraph5_aMC@NLO event generator at the time of the ACAT2022 conference. The progress achieved since our previous publication in the ICHEP2022 proceedings is discussed, for our implementations of the ME calculations in vectorized C++, in CUDA and in the SYCL framework, as well as in their integration into the existing MadEvent framework. The outlook towards a first alpha release of the software supporting QCD LO processes usable by the LHC experiments is also discussed.Comment: 7 pages, 4 figures, 4 tables; submitted to ACAT 2022 proceedings in IO

Epigenomics and Metabolomics Reveal the Mechanism of the \u3cem\u3eAPOA2\u3c/em\u3e-Saturated Fat Intake Interaction Affecting Obesity

Background: The putative functional variant −265T \u3e C (rs5082) within the APOA2 promoter has shown consistent interactions with saturated fatty acid (SFA) intake to influence the risk of obesity. Objective: The aim of this study was to implement an integrative approach to characterize the molecular basis of this interaction. Design: We conducted an epigenome-wide scan on 80 participants carrying either the rs5082 CC or TT genotypes and consuming either a low-SFA (\u3c 22 g/d) or high-SFA diet (≥ 22 g/d), matched for age, sex, BMI, and diabetes status in the Boston Puerto Rican Health Study (BPRHS). We then validated the findings in selected participants in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) Study (n = 379) and the Framingham Heart Study (FHS) (n = 243). Transcription and metabolomics analyses were conducted to determine the relation between epigenetic status, APOA2 mRNA expression, and blood metabolites. Results: In the BPRHS, we identified methylation site cg04436964 as exhibiting significant differences between CC and TT participants consuming a high-SFA diet, but not among those consuming low-SFA. Similar results were observed in the GOLDN Study and the FHS. Additionally, in the FHS, cg04436964 methylation was negatively correlated with APOA2 expression in the blood of participants consuming a high-SFA diet. Furthermore, when consuming a high-SFA diet, CC carriers had lower APOA2 expression than those with the TT genotype. Lastly, metabolomic analysis identified 4 pathways as overrepresented by metabolite differences between CC and TT genotypes with high-SFA intake, including tryptophan and branched-chain amino acid (BCAA) pathways. Interestingly, these pathways were linked to rs5082-specific cg04436964 methylation differences in high-SFA consumers. Conclusions: The epigenetic status of the APOA2 regulatory region is associated with SFA intake and APOA2 -265T \u3e C genotype, promoting an APOA2 expression difference between APOA2 genotypes on a high-SFA diet, and modulating BCAA and tryptophan metabolic pathways. These findings identify potential mechanisms by which this highly reproducible gene-diet interaction influences obesity risk, and contribute new insights to ongoing investigations of the relation between SFA and human health. This study was registered at clinicaltrials.gov as NCT03452787

Epigenomics and metabolomics reveal the mechanism of the APOA2-saturated fat intake interaction affecting obesity

Background: The putative functional variant -265T\u3eC (rs5082) within the APOA2 promoter has shown consistent interactions with saturated fatty acid (SFA) intake to influence the risk of obesity. Objective: The aim of this study was to implement an integrative approach to characterize the molecular basis of this interaction. Design: We conducted an epigenome-wide scan on 80 participants carrying either the rs5082 CC or TT genotypes and consuming either a low-SFA (\u3c22 g/d) or high-SFA diet (≥22 g/d), matched for age, sex, BMI, and diabetes status in the Boston Puerto Rican Health Study (BPRHS). We then validated the findings in selected participants in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) Study (n = 379) and the Framingham Heart Study (FHS) (n = 243). Transcription and metabolomics analyses were conducted to determine the relation between epigenetic status, APOA2 mRNA expression, and blood metabolites. Results: In the BPRHS, we identified methylation site cg04436964 as exhibiting significant differences between CC and TT participants consuming a high-SFA diet, but not among those consuming low-SFA. Similar results were observed in the GOLDN Study and the FHS. Additionally, in the FHS, cg04436964 methylation was negatively correlated with APOA2 expression in the blood of participants consuming a high-SFA diet. Furthermore, when consuming a high-SFA diet, CC carriers had lower APOA2 expression than those with the TT genotype. Lastly, metabolomic analysis identified 4 pathways as overrepresented by metabolite differences between CC and TT genotypes with high-SFA intake, including tryptophan and branched-chain amino acid (BCAA) pathways. Interestingly, these pathways were linked to rs5082-specific cg04436964 methylation differences in high-SFA consumers. Conclusions: The epigenetic status of the APOA2 regulatory region is associated with SFA intake and APOA2 -265T\u3eC genotype, promoting an APOA2 expression difference between APOA2 genotypes on a high-SFA diet, and modulating BCAA and tryptophan metabolic pathways. These findings identify potential mechanisms by which this highly reproducible gene-diet interaction influences obesity risk, and contribute new insights to ongoing investigations of the relation between SFA and human health. This study was registered at clinicaltrials.gov as NCT03452787

Noninterventional statistical comparison of BTS and CHEST guidelines for size and severity in primary pneumothorax.

Hilar rather than apical interpleural distance more accurately predicts need for intercostal chest drain insertion http://ow.ly/JvKFYThe study was funded by the East Anglian Thoracic Society. M.Z. Nikolić is a Wellcome Trust PhD Programme for Clinicians Fellow at the University of Cambridge. S.J. Marciniak is a Medical Research Council Senior Clinical Fellow. J. Wason is funded by the Cambridge Biomedical Research Centre. Funding information for this article has been deposited with FundRef.This is the final version of the article. It first appeared from the European Respiratory Society via http://dx.doi.org/10.1183/09031936.0011861