Work-life, diversity and intersectionality: a critical review and research agenda

Work-life issues have important implications at both organizational and individual levels. This paper provides a critical review of the work-life literature from 1990 onwards through the lens of diversity, with particular focus on disparities of power induced by methodological and conceptual framings of work and life. Our review seeks to answer the following questions: What are the gaps and omissions in the work-life research? How may they be overcome? To answer these questions we scrutinize blind spots in treatment of life, diversity and power in work-life research both in positivist and critical scholarship. In order to transcend the blind spots in positivist and critical work-life research, we argue the case for an intersectional approach, which captures the changing realities of family and workforce through the lens of diversity and intersectionality. Our theoretical contribution is three fold: First, our review demonstrates that contemporary framing of life in the work-life literature should be expanded to cover aspects of life beyond domestic life. Second, our review explains why and how other strands of diversity than gender also manifest as salient causes of difference in experiences of the work-life interface. Third, our review reveals that social and historical context has more explanatory power on work-life dynamics than micro-individual level of explanations. Work-life literature should capture the dynamism in these contexts. We also provide a set of useful recommendations to capture and operationalize methodological and theoretical changes required in the work-life literature

The effect of breaches of the psychological contract on the job satisfaction and wellbeing of doctors in Ireland: a quantitative study

Medicine is one of the most popular college degrees at both undergraduate and postgraduate level. Despite this, morale and wellbeing in doctors at all levels internationally is reportedly low. Long hours and stressful working environments have been implicated as the cause of this. The psychological contract is the implicit expectations and mutual obligations held between an employee and employer. Breaches in this contract can lead to strong negative emotional responses. This study will examine the psychological contract of non-consultant doctors and gain further insight into their job satisfaction and wellbeing. It aims to ascertain the effect of breaches of the psychological contract on their job satisfaction and wellbeing

Strategies for successful telework: how effective employees manage work/home boundaries

Purpose: This paper aims to 1) identify strategies used by successful teleworkers to create and maintain boundaries between work and home, and 2) determine how these strategies relate to employee preferences for segmentation or integration of work and home. Design/methodology/approach: Forty in-depth, face-to-face interviews were conducted with employees working from home either occasionally (occasional teleworkers), between 20-50% of the workweek (partial teleworkers), or the majority of the time (full teleworkers). Findings: Teleworkers use physical, temporal, behavioural and communicative strategies to recreate boundaries similar to those found in office environments. While teleworkers can generally develop strategies that align boundaries to their preferences for segmentation or integration, employees with greater job autonomy and control are better able to do so. Research limitations: A limitation of this research is its potential lack of generalizability to teleworkers in organizations with “always-on” cultures, who may experience greater pressure to allow work to permeate the home boundary. Practical implications: These findings can encourage organizations to proactively assess employee preferences for boundary permeability before entering a teleworking arrangement. The boundary management tactics identified can be used to provide teleworkers struggling to establish comfortable boundaries with tangible ideas to regulate interactions between home and work. Originality/value: This research makes a significant contribution to practitioner literature by applying a boundary management framework to the practice of teleworking, which is being adopted by organizations with increasing frequency

Effects of imperfections for Shor's factorization algorithm

We study effects of imperfections induced by residual couplings between qubits on the accuracy of Shor's algorithm using numerical simulations of realistic quantum computations with up to 30 qubits. The factoring of numbers up to N=943 show that the width of peaks, which frequencies allow to determine the factors, grow exponentially with the number of qubits. However, the algorithm remains operational up to a critical coupling strength $\epsilon_c$ which drops only polynomially with $\log_2 N$. The numerical dependence of $\epsilon_c$ on $\log_2 N$ is explained by analytical estimates that allows to obtain the scaling for functionality of Shor's algorithm on realistic quantum computers with a large number of qubits.Comment: 10 pages, 10 figures, 1 table. Added references and new data. Erratum added as appendix. 1 Figure and 1 Table added. Research is available at http://www.quantware.ups-tlse.fr

Implementing Shor's algorithm on Josephson Charge Qubits

We investigate the physical implementation of Shor's factorization algorithm on a Josephson charge qubit register. While we pursue a universal method to factor a composite integer of any size, the scheme is demonstrated for the number 21. We consider both the physical and algorithmic requirements for an optimal implementation when only a small number of qubits is available. These aspects of quantum computation are usually the topics of separate research communities; we present a unifying discussion of both of these fundamental features bridging Shor's algorithm to its physical realization using Josephson junction qubits. In order to meet the stringent requirements set by a short decoherence time, we accelerate the algorithm by decomposing the quantum circuit into tailored two- and three-qubit gates and we find their physical realizations through numerical optimization.Comment: 12 pages, submitted to Phys. Rev.

The lesson of causal discovery algorithms for quantum correlations: Causal explanations of Bell-inequality violations require fine-tuning

An active area of research in the fields of machine learning and statistics is the development of causal discovery algorithms, the purpose of which is to infer the causal relations that hold among a set of variables from the correlations that these exhibit. We apply some of these algorithms to the correlations that arise for entangled quantum systems. We show that they cannot distinguish correlations that satisfy Bell inequalities from correlations that violate Bell inequalities, and consequently that they cannot do justice to the challenges of explaining certain quantum correlations causally. Nonetheless, by adapting the conceptual tools of causal inference, we can show that any attempt to provide a causal explanation of nonsignalling correlations that violate a Bell inequality must contradict a core principle of these algorithms, namely, that an observed statistical independence between variables should not be explained by fine-tuning of the causal parameters. In particular, we demonstrate the need for such fine-tuning for most of the causal mechanisms that have been proposed to underlie Bell correlations, including superluminal causal influences, superdeterminism (that is, a denial of freedom of choice of settings), and retrocausal influences which do not introduce causal cycles.Comment: 29 pages, 28 figs. New in v2: a section presenting in detail our characterization of Bell's theorem as a contradiction arising from (i) the framework of causal models, (ii) the principle of no fine-tuning, and (iii) certain operational features of quantum theory; a section explaining why a denial of hidden variables affords even fewer opportunities for causal explanations of quantum correlation

Aspirin and some other nonsteroidal anti-inflammatory drugs inhibit cystic fibrosis transmembrane conductance regulator protein gene expression in T-84 cells.

Cystic fibrosis (CF) is caused by mutations in the CF gene, which encodes CF transmembrane conductance regulator protein (CFTR), a transmembrane protein that acts as a cAMP-regulated chloride channel The disease is characterized by inflammation but the relationship between inflammation, abnormal transepithelial ion transport, and the clinical manifestations of CF are uncertain. The present study was undertaken to determine whether three nonsteroidal anti-inflammatory drugs (NSAIDs) (aspirin, ibuprofen, and indomethacin) modulate CFTR gene expression in T-84 cells. Treatment with NSAIDs reduced CFTR transcripts, and decreased cAMP-stimulated anion fluxes, an index of CFTR function. However, the two phenomena occurred at different concentrations of both drugs. The results indicate that NSAIDs can regulate both CFTR gene expression and the function of CFTR-related chloride transport, and suggest that NSAIDs act via multiple transduction pathways

Targeting Impaired Antimicrobial Immunity in the Brain for the Treatment of Alzheimer’s Disease

Alzheimer’s disease (AD) is the most common form of dementia and aging is the most common risk factor for developing the disease. The etiology of AD is not known but AD may be considered as a clinical syndrome with multiple causal pathways contributing to it. The amyloid cascade hypothesis, claiming that excess production or reduced clearance of amyloid-beta (Aβ) and its aggregation into amyloid plaques, was accepted for a long time as the main cause of AD. However, many studies showed that Aβ is a frequent consequence of many challenges/pathologic processes occurring in the brain for decades. A key factor, sustained by experimental data, is that low-grade infection leading to production and deposition of Aβ, which has antimicrobial activity, precedes the development of clinically apparent AD. This infection is chronic, low grade, largely clinically silent for decades because of a nearly efficient antimicrobial immune response in the brain. A chronic inflammatory state is induced that results in neurodegeneration. Interventions that appear to prevent, retard or mitigate the devel- opment of AD also appear to modify the disease. In this review, we conceptualize further that the changes in the brain antimicrobial immune response during aging and especially in AD sufferers serve as a foundation that could lead to improved treatment strategies for preventing or decreasing the progression of AD in a disease-modifying treatment