Export Restrictions, Tax Incentives and the National Artistic Patrimony

This paper analyses the main forms of government intervention used in the UK to protect the national artistic patrimony. It examines the two most common policy measures used in the art market: export regulation and tax incentives and reports their use over an 8 year period from 1990 to 1998. It also reviews the UK's collective obligations to patrimony internationally and specifically as a member of the European Union.

'Protecting' the National Artistic Patrimony; An Economics Perspective

This paper analyses the rationale for restricting the international trade in art, namely protection of the national artistic patrimony. The meaning of national patrimony is analysed and rationales for state ownership and interventions in the art market analysed in light of the non-private benefits that this category of art produces. Distributional concerns in the international movement of art are considered along with the 'endowment effect' that can arise when dealing with potential transactions of patrimony art. Finally the paper provides a taxonomy of restrictions used to prevent art objects leaving a nation namely export restrictions, import regulations, and tax policies and incentives.

Interrogating ‘excellence’: Implicit bias in academic promotion decisions perpetuates gender inequality.

The ostensibly objective criteria outlined in many Key Performance Indicators of excellence can become highly subjective and gendered when applied in practice. Pat O’Connor and Clare O’Hagan share the findings of a cross-national project concerned with women’s underrepresentation at senior levels in STEM disciplines. Structural aspects, including the bureaucratisation of the promotion process and the composition of the boards, were seen as inhibiting and implicit bias facilitated the perpetuation of gender inequality and undermined the assessments of ‘excellence’. Making gender privilege visible is essential if universities are serious about addressing the under-representation of women

Early life disadvantage strengthens flight performance trade-offs in European starlings, Sturnus vulgaris

Developmental stress has been shown to affect adult flight performance in birds, with both negative and positive effects reported in the literature. Previous studies have used developmental manipulations that had substantial effects on patterns of growth. They have also examined mean levels of flight performance per individual, rather than investigating how developmental stress might alter trade-offs between different components of flight performance. We recorded multiple components of escape flight performance in 20 adult European starlings previously subjected to a manipulation likely to have altered levels of developmental stress. Siblings had been cross-fostered to nests where they were either slightly larger (advantaged treatment) or slightly smaller (disadvantaged treatment) than their competitors. The manipulation had no detectable effect on growth. However, developmental treatment affected performance in escape flights a year later by strengthening the trade-offs between different flight parameters. Disadvantaged birds faced a steeper trade-off between take-off speed and take-off angle, and a steeper trade-off between take-off angle and total time in flight, than advantaged birds. The results suggest that even subtle early life adversity that has no obvious effect on growth or size can leave a lasting legacy in the form of constraints on locomotor performance later in life

Early life adversity increases foraging and information gathering in European starlings, Sturnus vulgaris

Animals can insure themselves against the risk of starvation associated with unpredictable food availability by storing energy reserves or gathering information about alternative food sources. The former strategy carries costs in terms of mass-dependent predation risk, while the latter trades off against foraging for food; both trade-offs may be influenced by an individual's developmental history. Here, we consider a possible role of early developmental experience in inducing different mass regulation and foraging strategies in European starlings. We measured the body mass, body condition, foraging effort, food consumption and contrafreeloading (foraging for food hidden in sand when equivalent food is freely available) of adult birds (!10 months old) that had previously undergone a subtle early life manipulation of food competition (cross-fostering into the highest or lowest ranks in the brood size hierarchy when 2 e12 days of age). We found that developmentally disadvantaged birds were fatter in adulthood and differed in foraging behaviour compared with their advantaged siblings. Disadvantaged birds were hy-perphagic compared with advantaged birds, but only following a period of food deprivation, and also spent more time contrafreeloading. Advantaged birds experienced a trade-off between foraging success and time spent contrafreeloading, whereas disadvantaged birds faced no such trade-off, owing to their greater foraging efficiency. Thus, developmentally disadvantaged birds appeared to retain a phenotypic memory of increased nestling food competition, employing both energy storage and information-gathering insurance strategies to a greater extent than their advantaged siblings. Our results suggest that subtle early life disadvantage in the form of psychosocial stress and/or food insecurity can leave a lasting legacy on foraging behaviour and mass regulation even in the absence of food insufficiency during development or adulthood

Search for single production of a heavy vector-like T quark decaying to a Higgs boson and a top quark with a lepton and jets in the final state

Peer reviewe

CSF1R inhibitor JNJ-40346527 attenuates microglial proliferation and neurodegeneration in P301S mice

Neuroinflammation and microglial activation are significant processes in Alzheimer’s disease pathology. Recent genome-wide association studies have highlighted multiple immune-related genes in association with Alzheimer’s disease, and experimental data have demonstrated microglial proliferation as a significant component of the neuropathology. In this study, we tested the efficacy of the selective CSF1R inhibitor JNJ-40346527 (JNJ-527) in the P301S mouse tauopathy model. We first demonstrated the anti-proliferative effects of JNJ-527 on microglia in the ME7 prion model, and its impact on the inflammatory profile, and provided potential CNS biomarkers for clinical investigation with the compound, including pharmacokinetic/pharmacodynamics and efficacy assessment by TSPO autoradiography and CSF proteomics. Then, we showed for the first time that blockade of microglial proliferation and modification of microglial phenotype leads to an attenuation of tau-induced neurodegeneration and results in functional improvement in P301S mice. Overall, this work strongly supports the potential for inhibition of CSF1R as a target for the treatment of Alzheimer’s disease and other tau-mediated neurodegenerative diseases

Inflammatory biomarkers in Alzheimer's disease plasma

Introduction:Plasma biomarkers for Alzheimer’s disease (AD) diagnosis/stratification are a“Holy Grail” of AD research and intensively sought; however, there are no well-established plasmamarkers.Methods:A hypothesis-led plasma biomarker search was conducted in the context of internationalmulticenter studies. The discovery phase measured 53 inflammatory proteins in elderly control (CTL;259), mild cognitive impairment (MCI; 199), and AD (262) subjects from AddNeuroMed.Results:Ten analytes showed significant intergroup differences. Logistic regression identified five(FB, FH, sCR1, MCP-1, eotaxin-1) that, age/APOε4 adjusted, optimally differentiated AD andCTL (AUC: 0.79), and three (sCR1, MCP-1, eotaxin-1) that optimally differentiated AD and MCI(AUC: 0.74). These models replicated in an independent cohort (EMIF; AUC 0.81 and 0.67). Twoanalytes (FB, FH) plus age predicted MCI progression to AD (AUC: 0.71).Discussion:Plasma markers of inflammation and complement dysregulation support diagnosis andoutcome prediction in AD and MCI. Further replication is needed before clinical translatio