Small linear wind tunnel saltation experiments: Some experiences

Since the wind tunnels proposed to be used for the Space Station Planetology Experiments are of a rather limited size, some experience and techniques used for saltation experiments in a small linear wind tunnel may be of interest. Three experiments will be presented. The first concerns a length effect of saltation mass flux in which the size of the wind tunnel exaggerates the physical process taking place. The second experiment concerns a nonoptical technique that does not interfere with flow and by which momentum flux to the floor may be measured. The technique may also be used to calculate saltation flux (using appropriate assumptions). The third experiment concerns the use of the momentum equation to estimate momentum fluxes by difference

High efficiency compound semiconductor concentrator photovoltaics

Special emphasis was given to the high yield pilot production of packaged AlGaAs/GaAs concentrator solar cells, using organometallic VPE for materials growth, the demonstration of a concentrator module using 12 of these cells which achieved 16.4 percent conversion efficiency at 50 C coolant inlet temperature, and the demonstration of a spectral splitting converter module that achieved in excess of 20 percent efficiency. This converter employed ten silicon and ten AlGaAs cells with a dichroic filter functioning as the beam splitter. A monolithic array of AlGaAs/GaAs solar cells is described

Productivity, Factor Accumulation and Social Networks: Theory and Evidence

The paper analyzes how social barriers to communication affect economy-wide productivity and factor accumulation. Using a dynamic model of an economy that includes a reproducible capital stock (physical or human) and effective labor, a negative relationship is shown to exist between social barriers to communication and total factor productivity (TFP), per capita consumption and reproducible capital. Robust estimates obtained from cross-country data are consistent with the model’s predictions. The theory and empirical results help explain cross-country differences in TFP, the high productivity performance of leading industrialized countries and how productivity ‘catch up’ may be initiated.productivity, dynamic model, barriers to communication

Migrant workers in the East Midlands labour market 2010

This report is an update of previous intelligence (Migrant Workers in the East Midlands Labour Market 2007) on the profile and economic impact of migrant labour in the East Midlands economy

Productivity, Factor Accumulation and Social Networks: Theory and Evidence

The paper analyses how barriers to communication across social groups affect economy-wide productivity and factor accumulation. Using a dynamic model of an economy that includes a reproducible capital stock (physical or human) and effective labour, social barriers to communication are shown to have a negative effect on total factor productivity (TFP), per capita consumption and the accumulation of reproducible capital. Propositions from the model are tested using cross-country data from over a 100 countries. The results obtained from OLS and instrumental variables estimation, and with an exhaustive set of robustness tests, support the hypothesis that social barriers to communication, as measured by linguistic diversity, reduce TFP. Some evidence is also found to support the idea that the effects of social barriers to communication may be mitigated by improvements in mass communications. In addition, changes in the stocks of human and physical capital are found to be negatively related to social barriers to communication, after controlling for the initial levels of income and human or physical capital. The theory and empirical results together help explain the persistence of cross-country differences in TFP and provide insights as to how economies may initiate productivity 'catch up'.productivity, social networks, economic growth

Multiscale modelling of tumour growth and therapy: the influence of vessel normalisation on chemotherapy

Following the poor clinical results of antiangiogenic drugs, particularly when applied in isolation, tumour biologists and clinicians are now turning to combinations of therapies in order to obtain better results. One of these involves vessel normalisation strategies. In this paper, we investigate the effects on tumour growth of combinations of antiangiogenic and standard cytotoxic drugs, taking into account vessel normalisation. An existing multiscale framework is extended to include new elements such as tumour-induced vessel dematuration. Detailed simulations of our multiscale framework allow us to suggest one possible mechanism for the observed vessel normalisation-induced improvement in the efficacy of cytotoxic drugs: vessel dematuration produces extensive regions occupied by quiescent (oxygen-starved) cells which the cytotoxic drug fails to kill. Vessel normalisation reduces the size of these regions, thereby allowing the chemotherapeutic agent to act on a greater number of cells

The impact of cell crowding and active cell movement on vascular tumour growth

A multiscale model for vascular tumour growth is presented which includes systems of ordinary differential equations for the cell cycle and regulation of apoptosis in individual cells, coupled to partial differential equations for the spatio-temporal dynamics of nutrient and key signalling chemicals. Furthermore, these subcellular and tissue layers are incorporated into a cellular automaton framework for cancerous and normal tissue with an embedded vascular network. The model is the extension of previous work and includes novel features such as cell movement and contact inhibition. We presented a detailed simulation study of the effects of these additions on the invasive behaviour of tumour cells and the tumour's response to chemotherapy. In particular, we find that cell movement alone increases the rate of tumour growth and expansion, but that increasing the tumour cell carrying capacity leads to the formation of less invasive dense hypoxic tumours containing fewer tumour cells. However, when an increased carrying capacity is combined with significant tumour cell movement, the tumour grows and spreads more rapidly, accompanied by large spatio-temporal fluctuations in hypoxia, and hence in the number of quiescent cells. Since, in the model, hypoxic/quiescent cells produce VEGF which stimulates vascular adaptation, such fluctuations can dramatically affect drug delivery and the degree of success of chemotherapy

Oscillatory dynamics in a model of vascular tumour growth -- implications for chemotherapy

Background\ud \ud Investigations of solid tumours suggest that vessel occlusion may occur when increased pressure from the tumour mass is exerted on the vessel walls. Since immature vessels are frequently found in tumours and may be particularly sensitive, such occlusion may impair tumour blood flow and have a negative impact on therapeutic outcome. In order to study the effects that occlusion may have on tumour growth patterns and therapeutic response, in this paper we develop and investigate a continuum model of vascular tumour growth.\ud Results\ud \ud By analysing a spatially uniform submodel, we identify regions of parameter space in which the combination of tumour cell proliferation and vessel occlusion give rise to sustained temporal oscillations in the tumour cell population and in the vessel density. Alternatively, if the vessels are assumed to be less prone to collapse, stable steady state solutions are observed. When spatial effects are considered, the pattern of tumour invasion depends on the dynamics of the spatially uniform submodel. If the submodel predicts a stable steady state, then steady travelling waves are observed in the full model, and the system evolves to the same stable steady state behind the invading front. When the submodel yields oscillatory behaviour, the full model produces periodic travelling waves. The stability of the waves (which can be predicted by approximating the system as one of λ-ω type) dictates whether the waves develop into regular or irregular spatio-temporal oscillations. Simulations of chemotherapy reveal that treatment outcome depends crucially on the underlying tumour growth dynamics. In particular, if the dynamics are oscillatory, then therapeutic efficacy is difficult to assess since the fluctuations in the size of the tumour cell population are enhanced, compared to untreated controls.\ud Conclusions\ud \ud We have developed a mathematical model of vascular tumour growth formulated as a system of partial differential equations (PDEs). Employing a combination of numerical and analytical techniques, we demonstrate how the spatio-temporal dynamics of the untreated tumour may influence its response to chemotherapy.\ud Reviewers\ud \ud This manuscript was reviewed by Professor Zvia Agur and Professor Marek Kimmel

Modelling the response of vascular tumours to chemotherapy: A multiscale approach

An existing multiscale model is extended to study the response of a vascularised tumour to treatment with chemotherapeutic drugs which target proliferating cells. The underlying hybrid cellular automaton model couples tissue-level processes (e.g. blood flow, vascular adaptation, oxygen and drug transport) with cellular and subcellular phenomena (e.g. competition for space, progress through the cell cycle, natural cell death and drug-induced cell kill and the expression of angiogenic factors). New simulations suggest that, in the absence of therapy, vascular adaptation induced by angiogenic factors can stimulate spatio-temporal oscillations in the tumour's composition.\ud \ud Numerical simulations are presented and show that, depending on the choice of model parameters, when a drug which kills proliferating cells is continuously infused through the vasculature, three cases may arise: the tumour is eliminated by the drug; the tumour continues to expand into the normal tissue; or, the tumour undergoes spatio-temporal oscillations, with regions of high vascular and tumour cell density alternating with regions of low vascular and tumour cell density. The implications of these results and possible directions for future research are also discussed

Responsible research and innovation: A manifesto for empirical ethics?

In 2013 the Nuffield Council on Bioethics launched their report Novel Neurotechnologies: Intervening in the Brain. The report, which adopts the European Commission's notion of Responsible Research and Innovation, puts forward a set of priorities to guide ethical research into, and the development of, new therapeutic neurotechnologies. In this paper, we critically engage with these priorities. We argue that the Nuffield Council's priorities, and the Responsible Research and Innovation initiative as a whole, are laudable and should guide research and innovation in all areas of healthcare. However, we argue that operationalising Responsible Research and Innovation requires an in-depth understanding of the research and clinical contexts. Providing such an understanding is an important task for empirical ethics. Drawing on examples from sociology, science and technology studies, and related disciplines, we propose four avenues of social science research which can provide such an understanding. We suggest that these avenues can provide a manifesto for empirical ethics.The paper derives from a project that was funded by Wellcome Trust (Wellcome Trust Biomedical Strategic Award 086034)