Purpose
– This paper aims to adopt a conservation of resources (COR) theoretical approach to examine the process of value co-destruction (VCD) emanating from the misuse of customer resources by ...organisations.
Design/methodology/approach
– A critical incidents approach was adopted where 120 customers recounted their negative experiences. The analysis identified both the nature of resources and processes involved.
Findings
– From a customer perspective, the VCD process is triggered by a failure of the resource integration process to co-create expected value (resources). This involves customers in unexpected primary, and often secondary, resource loss. Loss “cycles” or “spirals” develop impacting negatively on well-being. Customers' attempts to restore their resources through coping strategies typically involve loss of well-being for the organisation.
Research limitations/implications
– The research is limited to a relatively small sample of UK customers involving diverse contexts. However, COR theory provides a framework for a better understanding of customer perceived value, the value co-creation and co-destruction process.
Practical implications
– The findings offer a new perspective to practitioners for understanding customer expectations and behaviour. There is a need to re-evaluate and re-design value propositions in line with organisational capabilities and customers' resource needs.
Social implications
– Organisations' misuse of customers' resources negatively impacts on “well-being”: a phenomenon of increasing interest at the societal level.
Originality/value
– This study is the first to empirically examine the concept of VCD, as perceived and experienced by customers, from a resource ecology perspective. It contributes to the growing body of work deriving from the service-dominant logic approach to value co-creation.
Purpose: We advanced a multifactorial, dynamic account of the complex, nonlinear interactions of motor, linguistic, and emotional factors contributing to the development of stuttering. Our purpose ...here is to update our account as the multifactorial dynamic pathways theory. Method: We review evidence related to how stuttering develops, including genetic/epigenetic factors; motor, linguistic, and emotional features; and advances in neuroimaging studies. We update evidence for our earlier claim: Although stuttering ultimately reflects impairment in speech sensorimotor processes, its course over the life span is strongly conditioned by linguistic and emotional factors. Results: Our current account places primary emphasis on the dynamic developmental context in which stuttering emerges and follows its course during the preschool years. Rapid changes in many neurobehavioral systems are ongoing, and critical interactions among these systems likely play a major role in determining persistence of or recovery from stuttering. Conclusion: Stuttering, or childhood onset fluency disorder ("Diagnostic and Statistical Manual of Mental Disorders," 5th edition; American Psychiatric Association APA, 2013), is a neurodevelopmental disorder that begins when neural networks supporting speech, language, and emotional functions are rapidly developing. The multifactorial dynamic pathways theory motivates experimental and clinical work to determine the specific factors that contribute to each child's pathway to the diagnosis of stuttering and those most likely to promote recovery.
The emerging awareness of the contribution of epigenetic processes to genome function in health and disease is underpinned by decades of research in model systems. In particular, many principles of ...the epigenetic control of genome function have been uncovered by studies of genomic imprinting. The phenomenon of genomic imprinting, which results in some genes being expressed in a parental--origin-specific manner, is essential for normal mammalian growth and development and exemplifies the regulatory influences of DNA methylation, chromatin structure and non-coding RNA. Setting seminal discoveries in this field alongside recent progress and remaining questions shows how the study of imprinting continues to enhance our understanding of the epigenetic control of genome function in other contexts.
Heritability has traditionally been thought to be a characteristic feature of the genetic material of an organism—notably, its DNA. However, it is now clear that inheritance not based on DNA sequence ...exists in multiple organisms, with examples found in microbes, plants, and invertebrate and vertebrate animals. In mammals, the molecular mechanisms have been challenging to elucidate, in part due to difficulties in designing robust models and approaches. Here we review some of the evidence, concepts, and potential mechanisms of non-DNA sequence-based transgenerational inheritance. We highlight model systems and discuss whether phenotypes are replicated or reconstructed over successive generations, as well as whether mechanisms operate at transcriptional and/or posttranscriptional levels. Finally, we explore the short- and long-term implications of non-DNA sequence-based inheritance. Understanding the effects of non-DNA sequence-based mechanisms is key to a full appreciation of heritability in health and disease.
Both human and animal studies indicate that environmental exposures experienced during early life can robustly influence risk for adult disease. Moreover, environmental exposures experienced by ...parents during either intrauterine or postnatal life can also influence the health of their offspring, thus initiating a cycle of disease risk across generations. In this Perspective, we focus on epigenetic mechanisms in germ cells, including DNA methylation, histone modification, and non-coding RNAs, which collectively may provide a non-genetic molecular legacy of prior environmental exposures and influence transcriptional regulation, developmental trajectories, and adult disease risk in offspring.
Sales et al. provide perspective on how environmental exposures, particularly those experienced during intrauterine life, can influence metabolic disease risk in adulthood. Moreover, both early-life exposures and metabolic disease in adult parents can modulate epigenetic regulation in germ cells, thus providing a non-genetic molecular legacy to influence the health of subsequent generations.
The importance of maternal folate consumption for normal development is well established, yet the molecular mechanism linking folate metabolism to development remains poorly understood. The enzyme ...methionine synthase reductase (Mtrr) is necessary for utilization of methyl groups from the folate cycle. We found that a hypomorphic mutation of the mouse Mtrr gene results in intrauterine growth restriction, developmental delay, and congenital malformations, including neural tube, heart, and placental defects. Importantly, these defects were dependent upon the Mtrr genotypes of the maternal grandparents. Furthermore, we observed widespread epigenetic instability associated with altered gene expression in the placentas of wild-type grandprogeny of Mtrr-deficient maternal grandparents. Embryo transfer experiments revealed that Mtrr deficiency in mice lead to two distinct, separable phenotypes: adverse effects on their wild-type daughters’ uterine environment, leading to growth defects in wild-type grandprogeny, and the appearance of congenital malformations independent of maternal environment that persist for five generations, likely through transgenerational epigenetic inheritance.
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•Mutation in the Mtrr gene causes abnormal folate metabolism in mice•Mtrr genotype of maternal grandparent affects development of wild-type grandprogeny•Placentas of wild-type grandprogeny display widespread epigenetic instability•Mtrr mutation impacts both the in utero environment and epigenetic inheritance
A genetic deficiency in folate metabolism in maternal grandparents affects development of their wild-type grandprogeny, even if the mothers are also wild-type. A restricted growth phenotype is due to uterine environment, but congenital malformations are not and are associated with altered DNA methylation.
An important question when setting appropriate air quality standards for fine particulate matter (PM2.5) is whether there exists a "threshold" in the concentration-response (C-R) function, such that ...PM2.5 levels below this threshold are not expected to produce adverse health effects. We hypothesize that measurement error may affect the recognition of a threshold in long-term cohort epidemiological studies. This study conducts what is, to the best of our knowledge, the first simulation of the effects of measurement error on the statistical models commonly employed in long-term cohort studies. We test the degree to which classical-type measurement error, such as differences between the true population-weighted exposure level to a pollutant and the observed measures of that pollutant, affects the ability to statistically detect a C-R threshold. The results demonstrate that measurement error can obscure the existence of a threshold in a cohort study's C-R function for health risks from chronic exposures. With increased measurement error the ability to statistically detect a C-R threshold decreases, and both the estimated location of the C-R threshold and the estimated hazard ratio associated with PM2.5 are attenuated. This result has clear implications for determining appropriate air quality standards for pollutants.
Differential mRNA expression studies implicitly assume that changes in mRNA expression have biological meaning, most likely mediated by corresponding changes in protein levels. Yet studies into ...mRNA-protein correspondence have shown notoriously poor correlation between mRNA and protein expression levels, creating concern for inferences from only mRNA expression data. However, none of these studies have examined in particular differentially expressed mRNA. Here, we examined this question in an ovarian cancer xenograft model. We measured protein and mRNA expression for twenty-nine genes in four drug-treatment conditions and in untreated controls. We identified mRNAs differentially expressed between drug-treated xenografts and controls, then analysed mRNA-protein expression correlation across a five-point time-course within each of the four experimental conditions. We evaluated correlations between mRNAs and their protein products for mRNAs differentially expressed within an experimental condition compared to those that are not. We found that differentially expressed mRNAs correlate significantly better with their protein product than non-differentially expressed mRNAs. This result increases confidence for the use of differential mRNA expression for biological discovery in this system, as well as providing optimism for the usefulness of inferences from mRNA expression in general.
Occupational sedentary behaviour is an important contributor to overall sedentary risk. There is limited evidence for effective workplace interventions to reduce occupational sedentary time and ...increase light activity during work hours. The purpose of the study was to determine if participatory workplace interventions could reduce total sedentary time, sustained sedentary time (bouts >30 minutes), increase the frequency of breaks in sedentary time and promote light intensity activity and moderate/vigorous activity (MVPA) during work hours.
A randomised controlled trial (ANZCTR NUMBER: ACTN12612000743864) was conducted using clerical, call centre and data processing workers (n = 62, aged 25-59 years) in 3 large government organisations in Perth, Australia. Three groups developed interventions with a participatory approach: 'Active office' (n = 19), 'Active Workstation' and promotion of incidental office activity; 'Traditional physical activity' (n = 14), pedometer challenge to increase activity between productive work time and 'Office ergonomics' (n = 29), computer workstation design and breaking up computer tasks. Accelerometer (ActiGraph GT3X, 7 days) determined sedentary time, sustained sedentary time, breaks in sedentary time, light intensity activity and MVPA on work days and during work hours were measured before and following a 12 week intervention period.
For all participants there was a significant reduction in sedentary time on work days (-1.6%, p = 0.006) and during work hours (-1.7%, p = 0.014) and a significant increase in number of breaks/sedentary hour on work days (0.64, p = 0.005) and during work hours (0.72, p = 0.015); there was a concurrent significant increase in light activity during work hours (1.5%, p = 0.012) and MVPA on work days (0.6%, p = 0.012).
This study explored novel ways to modify work practices to reduce occupational sedentary behaviour. Participatory workplace interventions can reduce sedentary time, increase the frequency of breaks and improve light activity and MVPA of office workers by using a variety of interventions.
Australian New Zealand Clinical Trials Registry ACTN12612000743864.
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