Can a brain drain be good for growth?

This paper shows how a brain drain - the emigration of agents with a relatively high level of human capital in an economy - can paradoxically increase the productivity of an economy where productivity is a function of the average level of human capital. The model uses Galor and Tsiddon's model of income distribution, endogenous human capital formation and growth, to analyze the interaction between income distribution and migration. The paradoxical positive effect of a brain drain on productivity occurs when successful emigration is not a certainty and when the increase in human capital accumulation by people wishing to become eligible to emigrate, causes a change in the long run income distribution which outweighs the decrease in human capital caused by the brain drain itself.Economic Growth;Human Capital;Income Distribution;Productivity;Emigration;macroeconomics

Trade dynamics and endogenous growth: An overlapping generations model

Growth Models;International Trade

The brain drain and the world distribution of income and population

This paper models the evolution of the world distribution of income and shows that while the distribution of income per capita across economies in the world will be stable in the long run, the world distribution of population may be divergent. The paper then uses this model to analyze the impact of the current trend towards predominantly skilled emigration from poor to rich countries on fertility, human capital formation, and growth, in both the sending and receiving countries. It shows that in the long run, brain drain migration patterns may increase world inequality as relatively poor countries grow large in terms of population. In the short run however, it is possible for world inequality to fall due to rises in GDP per capita in large developing economies with low skilled emigration rates

Dendritic cells activated with products released by schistosome larvae drive Th2-type immune responses, which can be inhibited by manipulation of CD40 costimulation

The early immune events in response to infective larvae of the parasitic helminth Schistosoma mansoni are poorly understood, but here for the first time we report on the potential of products released by schistosome larvae (material released in the first 3 It after transformation [0-3hRP]) to stimulate the maturation of dendritic cells (DC) and alter their T-cell-polarizing function. This was performed in comparison with lipopolysaccharide (LPS) and zymosan A, which classically activate DC to prime for Th1- and Th2-type responses, respectively. In our study, immature bone marrow-derived DC stimulated in vitro with 0-3hRP exhibited up-regulated expression of major histocompatibility complex class II, CD40, and CD86 and increased production of interleukin 12p40 (IL-12p40) and IL-6, albeit at lower levels than in response to LPS or zymosan A. Using an in vitro ovalbumin peptide-restricted priming assay, DC matured with 0-3hRP exhibited a potent capacity to drive Th2 polarization of CD4(+) cells from DO11.10 transgenic mice. This was characterized by increased IL-4 production (but not gamma interferon) of a magnitude similar to that primed by DC matured with zymosan A. Inoculation of DO11.10 mice with 0-3hRP-activated DC pulsed with ovalbumin peptide also led to the development of a Th2-type polarized response in the skin-draining lymph nodes and spleen. However, ligation of CD40 on DC by anti-CD40 antibody treatment reversed the ability of 0-3hRP-activated DC to prime for Th2-type responses and instead caused the induction of a more Th1-type response

In the absence of CD154, administration of interleukin-12 restores Th1 responses but not protective immunity to Schistosoma mansoni

The cytokine interplay during the development of protective immunity to the radiation-attenuated (RA) schistosome vaccine has been extensively characterized over recent years, yet the role of costimulatory molecules in the development of cell-mediated immunity is much less well understood. Here we demonstrate the importance of CD40/CD154 in vaccine-induced immunity, as CD154(-/-) mice exposed to RA schistosomes develop no protection to challenge infection. We showed that vaccinated CD154(-/-) mice have defective Th1-associated immune responses in the skin-draining lymph nodes and the lungs, with reduced or absent levels of interleukin-12p40 (IL-12p40), gamma interferon, and nitric oxide, but elevated levels of lung IL-4 and IL-5. The expression of major histocompatibility complex II (MHC-II) on antigen-presenting cells recovered from the lungs of vaccinated CD154(-/-) mice was also severely compromised. The administration of anti-CD40 monoclonal antibody (MAb) to CD154(-/-) mice did not reconstitute sustained Th1 responses in the lymph nodes or the lungs, nor did the MAb restore anti-parasite immunoglobulin G production or protective immunity. On the other hand, the administration of recombinant IL-12 (rIL-12) to CD154(-/-) mice shortly after vaccination caused elevated and sustained levels of Th1-associated cytokines, rescued MHC-II expression by lung CD11c(+) cells, and restored the appearance of inflammatory effector foci in the lungs. However, the treatment of CD154(-/-) mice with rIL-12 did not restore protection. We conclude that protective immunity to the RA schistosome vaccine is CD154 dependent but is independent of IL-12-orchestrated cellular immune mechanisms in the lungs

Interleukin-12 p40 secretion by cutaneous CD11c(+) and F4/80(+) cells is a major feature of the innate immune response in mice that develop Th1-mediated protective immunity to Schistosoma mansoni

Radiation-attenuated (RA) schistosome larvae are potent stimulators of innate immune responses at the skin site of exposure (pinna) that are likely to be important factors in the development of Th1-mediated protective immunity. In addition to causing an influx of neutrophils, macrophages, and dendritic cells (DCs) into the dermis, RA larvae induced a cascade of chemokine and cytokine secretion following in vitro culture of pinna biopsy samples. While macrophage inflammatory protein 1alpha and interleukin-1beta (IL-1beta) were produced transiently within the first few days, the Th1-promoting cytokines IL-12 and IL-18 were secreted at high levels until at least day 14. Assay of C3H/HeJ mice confirmed that IL-12 secretion was not due to lipopolysaccharide contaminants binding Toll-like receptor 4. Significantly, IL-12 p40 secretion was sustained in pinnae from vaccinated mice but not in those from nonprotected infected mice. In contrast, IL-10 was produced from both vaccinated and infected mice. This cytokine regulates IL-12-associated dermal inflammation, since in vaccinated IL-10(-/-) mice, pinna thickness was greatly increased concurrent with elevated levels of IL-12 p40. A significant number of IL-12 p40(+) cells were detected as emigrants from in vitro-cultured pinnae, and most were within a population of rare large granular cells that were Ia(+), consistent with their being antigen-presenting cells. Labeling of IL-12(+) cells for CD11c, CD205, CD8alpha, CD11b, and F4/80 indicated that the majority were myeloid DCs, although a proportion were CD11c(-) F4/80(+), suggesting that macrophages were an additional source of IL-12 in the skin

Framing higher education: questions and responses in the British Social Attitudes survey, 1983-2010

This is the final version of the article. Available from Taylor & Francis (Routledge) via the DOI in this record.This article focuses on questions and attitudes towards higher education in the British Social Attitudes (BSA) survey series. First, we analyse the changing BSA questions (1983-2010) in the context of key policy reports. Our results show that changes in the framing of higher education questions correspond with changes in the macro-discourse of higher education policies. Second, we focus on the 2010 BSA survey responses to investigate how attitudes towards higher education are related to respondents' characteristics. Respondents' socio-economic position predicts attitudes towards higher education. Graduates and professionals are most likely to support a reduction in higher education opportunities, but those who have so far benefitted least from higher education are supportive of expansion. One interpretation - with potential implications for social mobility - is that those who have already benefited from higher education are most inclined to pull the ladder up behind them

Is contextualised admission the answer to the access challenge?

This is the final version of the article. Available from Taylor & Francis (Routledge) via the DOI in this record.This article reviews the idea of contextualising applicants to higher education in order to widen access. First, the meaning of contextualised admissions (CAs) is discussed before laying out the rationale for contextualising applicants and the beneficiaries of the policy. The final sections discuss key critiques of CA and conclude by arguing that CA does go some way to addressing the access challenge. To fully realise its potential as a policy intervention though, it is most helpfully part of integrated support for students throughout university and is mindful of the role of universities in wider society to create more equal progression trajectories for young people from a range of backgrounds.This work was supported by Supporting Professionalism in Admissions

Signaling via interleukin-4, receptor alpha chain is required for successful vaccination against schistosomiasis in BALB/c mice

Radiation-attenuated (RA) schistosome larvae are potent stimulators of innate immune responses at the skin site of exposure (pinna) that are likely to be important factors in the development of Th1-mediated protective immunity. In addition to causing an influx of neutrophils, macrophages, and dendritic cells (DCs) into the dermis, RA larvae induced a cascade of chemokine and cytokine secretion following in vitro culture of pinna biopsy samples. While macrophage inflammatory protein 1 and interleukin-1 (IL-1) were produced transiently within the first few days, the Th1-promoting cytokines IL-12 and IL-18 were secreted at high levels until at least day 14. Assay of C3H/HeJ mice confirmed that IL-12 secretion was not due to lipopolysaccharide contaminants binding Toll-like receptor 4. Significantly, IL-12 p40 secretion was sustained in pinnae from vaccinated mice but not in those from nonprotected infected mice. In contrast, IL-10 was produced from both vaccinated and infected mice. This cytokine regulates IL-12-associated dermal inflammation, since in vaccinated IL-10/ mice, pinna thickness was greatly increased concurrent with elevated levels of IL-12 p40. A significant number of IL-12 p40 cells were detected as emigrants from in vitro-cultured pinnae, and most were within a population of rare large granular cells that were Ia, consistent with their being antigen-presenting cells. Labeling of IL-12 cells for CD11c, CD205, CD8, CD11b, and F4/80 indicated that the majority were myeloid DCs, although a proportion were CD11c F4/80, suggesting that macrophages were an additional source of IL-12 in the skin