Executive remuneration consultancy in the UK: exploring a professional project through the lens of institutional work

This article responds to recent calls to examine the development of professionalism through the lens of institutional theory. We investigate the development of the new professional service of executive remuneration consultancy (ERC) in the UK through the lens of institutional work. Specifically, drawing upon Lawrence and Suddaby (2006) and Suddaby and Viale (2011), we explore the relationship between macro-scale occupational/organizational and micro-scale individual-level dynamics of the ERC professional project and situate its development in relation to the broader field of executive remuneration practices. We show that the institutional work of creating the new professional project is contested and that the ERC development may be better understood as part of broader efforts to create and maintain the institution of executive pay-setting practices. We argue that the institutional work lens has the potential to produce a more nuanced understanding of the internal dynamics of the ERC professionalization process and its role in reconfiguring broader institutional arrangements. By exploring the analytical purchase of the concept of institutional work, the article contributes to the emerging body of empirical evidence outlining the potential of (neo-) institutional approaches to offer a more productive understanding of contemporary professionalis

Muscle 4EBP1 activation modifies the structure and function of the neuromuscular junction in mice

Dysregulation of mTOR complex 1 (mTORC1) activity drives neuromuscular junction (NMJ) structural instability during aging; however, downstream targets mediating this effect have not been elucidated. Here, we investigate the roles of two mTORC1 phosphorylation targets for mRNA translation, ribosome protein S6 kinase 1 (S6K1) and eukaryotic translation initiation factor 4E-binding protein 1 (4EBP1), in regulating NMJ structural instability induced by aging and sustained mTORC1 activation. While myofiber-specific deletion of S6k1 has no effect on NMJ structural integrity, 4EBP1 activation in murine muscle induces drastic morphological remodeling of the NMJ with enhancement of synaptic transmission. Mechanistically, structural modification of the NMJ is attributed to increased satellite cell activation and enhanced post-synaptic acetylcholine receptor (AChR) turnover upon 4EBP1 activation. Considering that loss of post-synaptic myonuclei and reduced NMJ turnover are features of aging, targeting 4EBP1 activation could induce NMJ renewal by expanding the pool of post-synaptic myonuclei as an alternative intervention to mitigate sarcopenia

PARP-1 dependent recruitment of the amyotrophic lateral sclerosis-associated protein FUS/TLS to sites of oxidative DNA damage

Amyotrophic lateral sclerosis (ALS) is associated with progressive degeneration of motor neurons. Several of the genes associated with this disease encode proteins involved in RNA processing, including fused-in-sarcoma/translocated-in-sarcoma (FUS/TLS). FUS is a member of the heterogeneous nuclear ribonucleoprotein (hnRNP) family of proteins that bind thousands of pre-mRNAs and can regulate their splicing. Here, we have examined the possibility that FUS is also a component of the cellular response to DNA damage. We show that both GFP-tagged and endogenous FUS re-localize to sites of oxidative DNA damage induced by UVA laser, and that FUS recruitment is greatly reduced or ablated by an inhibitor of poly (ADP-ribose) polymerase activity. Consistent with this, we show that recombinant FUS binds directly to poly (ADP-ribose) in vitro, and that both GFP-tagged and endogenous FUS fail to accumulate at sites of UVA laser induced damage in cells lacking poly (ADP-ribose) polymerase-1. Finally, we show that GFP-FUS(R521G), harbouring a mutation that is associated with ALS, exhibits reduced ability to accumulate at sites of UVA laser-induced DNA damage. Together, these data suggest that FUS is a component of the cellular response to DNA damage, and that defects in this response may contribute to ALS

Phylogeography of the Mekong mud snake (Enhydris subtaeniata): the biogeographic importance of dynamic river drainages and fluctuating sea levels for semiaquatic taxa in Indochina

During the Cenozoic, Southeast Asia was profoundly affected by plate tectonic events, dynamic river systems, fluctuating sea levels, shifting coastlines, and climatic variation, which have influenced the ecological and evolutionary trajectories of the Southeast Asian flora and fauna. We examined the role of these paleogeographic factors on shaping phylogeographic patterns focusing on a species of semiaquatic snake, Enhydris subtaeniata (Serpentes: Homalopsidae) using sequence data from three mitochondrial fragments (cytochrome b, ND4, and ATPase—2785 bp). We sampled E. subtaeniata from seven locations in three river drainage basins that encompassed most of this species’ range. Genetic diversities were typically low within locations but high across locations. Moreover, each location had a unique suite of haplotypes not shared among locations, and pairwise φST values (0.713–0.998) were highly significant between all location pairs. Relationships among phylogroups were well resolved and analysis of molecular variance (AMOVA) revealed strong geographical partitioning of genetic variance among the three river drainage basins surveyed. The genetic differences observed among the populations of E. subtaeniata were likely shaped by the Quaternary landscapes of Indochina and the Sunda Shelf. Historically, the middle and lower Mekong consisted of strongly dissected river valleys separated by low mountain ranges and much of the Sunda Shelf consisted of lowland river valleys that served to connect faunas associated with major regional rivers. It is thus likely that the contemporary genetic patterns observed among populations of E. subtaeniata are the result of their histories in a complex terrain that created abundant opportunities for genetic isolation and divergence yet also provided lowland connections across now drowned river valleys

Activation of eIF4E-binding-protein-1 rescues mTORC1-induced sarcopenia by expanding lysosomal degradation capacity

Background: Chronic mTORC1 activation in skeletal muscle is linked with age-associated loss of muscle mass and strength, known as sarcopenia. Genetic activation of mTORC1 by conditionally ablating mTORC1 upstream inhibitor TSC1 in skeletal muscle accelerates sarcopenia development in adult mice. Conversely, genetic suppression of mTORC1 downstream effectors of protein synthesis delays sarcopenia in natural aging mice. mTORC1 promotes protein synthesis by activating ribosomal protein S6 kinases (S6Ks) and inhibiting eIF4E-binding proteins (4EBPs). Whole-body knockout of S6K1 or muscle-specific over-expression of a 4EBP1 mutant transgene (4EBP1mt), which is resistant to mTORC1-mediated inhibition, ameliorates muscle loss with age and preserves muscle function by enhancing mitochondria activities, despite both transgenic mice showing retarded muscle growth at a young age. Why repression of mTORC1-mediated protein synthesis can mitigate progressive muscle atrophy and dysfunction with age remains unclear. Methods: Mice with myofiber-specific knockout of TSC1 (TSC1mKO), in which mTORC1 is hyperactivated in fully differentiated myofibers, were used as a mouse model of sarcopenia. To elucidate the role of mTORC1-mediated protein synthesis in regulating muscle mass and physiology, we bred the 4EBP1mt transgene or S6k1 floxed mice into the TSC1mKO mouse background to generate 4EBP1mt-TSC1mKO or S6K1-TSC1mKO mice, respectively. Functional and molecular analyses were performed to assess their role in sarcopenia development. Results: Here, we show that 4EBP1mt-TSC1mKO, but not S6K1-TSC1mKO, preserved muscle mass (36.7% increase compared with TSC1mKO, P < 0.001) and strength (36.8% increase compared with TSC1mKO, P < 0.01) at the level of control mice. Mechanistically, 4EBP1 activation suppressed aberrant protein synthesis (two-fold reduction compared with TSC1mKO, P < 0.05) and restored autophagy flux without relieving mTORC1-mediated inhibition of ULK1, an upstream activator of autophagosome initiation. We discovered a previously unidentified phenotype of lysosomal failure in TSC1mKO mouse muscle, in which the lysosomal defect was also conserved in the naturally aged mouse muscle, whereas 4EBP1 activation enhanced lysosomal protease activities to compensate for impaired autophagy induced by mTORC1 hyperactivity. Consequently, 4EBP1 activation relieved oxidative stress to prevent toxic aggregate accumulation (0.5-fold reduction compared with TSC1mKO, P < 0.05) in muscle and restored mitochondrial homeostasis and function. Conclusions: We identify 4EBP1 as a communication hub coordinating protein synthesis and degradation to protect proteostasis, revealing therapeutic potential for activating lysosomal degradation to mitigate sarcopenia

The impact of plug-in fragrance diffusers on residential indoor VOC concentrations

Plug-in fragrance diffusers are one of myriad volatile organic compound-containing consumer products that are commonly found in homes. The perturbing effects of using a commercial diffuser indoors were evaluated using a study group of 60 homes in Ashford, UK. Air samples were taken over 3 day periods with the diffuser switched on and in a parallel set of control homes where it was off. At least four measurements were taken in each home using vacuum-release into 6 L silica-coated canisters and with >40 VOCs quantified using gas chromatography with FID and MS (GC-FID-QMS). Occupants self-reported their use of other VOC-containing products. The variability between homes was very high with the 72 hour sum of all measured VOCs ranging between 30 and >5000 μg m−3, dominated by n/i-butane, propane, and ethanol. For those homes in the lowest quartile of air exchange rate (identified using CO2 and TVOC sensors as proxies) the use of a diffuser led to a statistically significant increase (p-value < 0.02) in the summed concentration of detectable fragrance VOCs and some individual species, e.g. alpha pinene rising from a median of 9 μg m−3 to 15 μg m−3 (p-value < 0.02). The observed increments were broadly in line with model-calculated estimates based on fragrance weight loss, room sizes and air exchange rates

Interplay between Vacuum-Grown Monolayers of Alkylphosphonic Acids and the Performance of Organic Transistors Based on Dinaphtho[2,3-b:2?,3?-f]thieno[3,2-b]thiophene

Monolayers of six alkylphosphonic acids ranging from C8 to C18 were prepared by vacuum evaporation and incorporated into low-voltage organic field-effect transistors based on dinaphtho[2,3-b:2?,3?-f ]thieno[3,2-b]thiophene (DNTT). Similar to solution-assembled monolayers, the molecular order for vacuum-deposited monolayers improved with increasing length of the aliphatic tail. At the same time, Fourier transform infrared (FTIR) measurements suggested lower molecular coverage for longer phosphonic acids. The comparison of FTIR and vibration frequencies calculated by density functional theory indicated that monodentate bonding does not occur for any phosphonic acid. All monolayers exhibited low surface energy of ?17.5 mJ/m2 with a dominating Lifshitz?van der Waals component. Their surface roughness was comparable, while the nanomechanical properties were varied but not correlated to the length of the molecule. However, large improvement in transistor performance was observed with increasing length of the aliphatic tail. Upon going from C8 to C18, the mean threshold voltage decreased from ?1.37 to ?1.24 V, the field-effect mobility increased from 0.03 to 0.33 cm2/(V·s), the off-current decreased from ?8 × 10?13 to ?3 × 10?13 A, and for transistors with L = 30 ?m the on-current increased from ?3 × 10?8 to ?2 × 10?6 A, and the on/off-current ratio increased from ?3 × 104 to ?4 × 106. Similarly, transistors with longer phosphonic acids exhibited much better air and bias-stress stability. The achieved transistor performance opens up a completely “dry” fabrication route for ultrathin dielectrics and low-voltage organic transistors

Post-postfeminism? New feminist visibilities in postfeminist times

This article contributes to debates about the value and utility of the notion of postfeminism for a seemingly “new” moment marked by a resurgence of interest in feminism in the media and among young women. The paper reviews current understandings of postfeminism and criticisms of the term’s failure to speak to or connect with contemporary feminism. It offers a defence of the continued importance of a critical notion of postfeminism, used as an analytical category to capture a distinctive contradictory-but-patterned sensibility intimately connected to neoliberalism. The paper raises questions about the meaning of the apparent new visibility of feminism and highlights the multiplicity of different feminisms currently circulating in mainstream media culture – which exist in tension with each other. I argue for the importance of being able to “think together” the rise of popular feminism alongside and in tandem with intensified misogyny. I further show how a postfeminist sensibility informs even those media productions that ostensibly celebrate the new feminism. Ultimately, the paper argues that claims that we have moved “beyond” postfeminism are (sadly) premature, and the notion still has much to offer feminist cultural critics

Coronary artery perforations: Glasgow Natural History Study of Covered Stent Coronary Interventions (GNOCCI) Study

Background: The objective of the GNOCCI (Glasgow Natural History Study of Covered Stent Coronary Interventions) Study was to report the incidence and outcomes of coronary artery perforations over an 18‐year period at a single, high‐volume percutaneous coronary intervention center. We considered both the temporal trends and long‐term outcomes of covered stent deployment. Methods and Results: We evaluated procedural and long‐term clinical outcomes following coronary perforation in a cohort of 43,343 consecutive percutaneous coronary intervention procedures. Procedural major adverse cardiac events were defined as a composite of death, myocardial infarction, stroke, target vessel revascularization, or cardiac surgery within 24 hours. A total of 161 (0.37%) procedures were complicated by coronary perforation of which 57 (35%) were Ellis grade III. Incidence increased with time over the study period (r=0.73; P&lt;0.001). Perforation severity was linearly associated with procedural mortality (median 2.9‐year follow‐up): Ellis I (0%), Ellis II (1.7%), Ellis III/IIIB (21%), P&lt;0.001. Procedural major adverse cardiac events occurred in 47% of patients with Ellis III/IIIB versus 13.5% of those with Ellis I/II perforations (odds ratio, 5.8; 95% CI, 2.7–12.5; P&lt;0.001). Covered stents were associated with an increased risk of stent thrombosis at 2.9‐year follow‐up (Academic Research Consortium definite or probable; 9.1% versus 0.9%; risk ratio, 10.5; 95% CI, 1.1–97; P=0.04). Conclusions: The incidence of coronary perforation increased between 2001 and 2019. Severe perforation was associated with higher procedural major adverse cardiac events and was an independent predictor of long‐term mortality. Although covered stents are a potentially lifesaving treatment, the generation of devices used during the study period was limited by their efficacy and high risk of stent thrombosis. Registration Information: Clinicaltrials.gov. Identifier: NCT03862352