Impact of Government Intervention on Employment Change and Plant Closure in Northern Ireland, 1983-97

Harris R. and Trainor M. (2007) Impact of government intervention on employment change and plant closure in Northern Ireland, 1983-97, Regional Studies 41, 51-63. Financial assistance to manufacturing industry is an important element of the industrial development policy in Northern Ireland. This paper uses the individual plant-level records of the Annual Respondents Database (ARD) for the Northern Ireland manufacturing sector (1983-97) matched to the plant-level details of financial support provided by the Industrial Development Board to examine the effect of selective financial assistance (SFA) on employment change and plant closure. It is found that SFA concentrated on protecting existing, rather than new, enterprises in terms of employment change. Using a hazard model, it is found that the receipt of SFA significantly reduced the probability of plant closure by, on average, between 15 and 24%.

Self-cooling of a micro-mirror by radiation pressure

Cooling of mechanical resonators is currently a popular topic in many fields of physics including ultra-high precision measurements, detection of gravitational waves and the study of the transition between classical and quantum behaviour of a mechanical system. Here we report the observation of self-cooling of a micromirror by radiation pressure inside a high-finesse optical cavity. In essence, changes in intensity in a detuned cavity, as caused by the thermal vibration of the mirror, provide the mechanism for entropy flow from the mirror's oscillatory motion to the low-entropy cavity field. The crucial coupling between radiation and mechanical motion was made possible by producing free-standing micromirrors of low mass (m approximately 400 ng), high reflectance (more than 99.6%) and high mechanical quality (Q approximately 10,000). We observe cooling of the mechanical oscillator by a factor of more than 30; that is, from room temperature to below 10 K. In addition to purely photothermal effects we identify radiation pressure as a relevant mechanism responsible for the cooling. In contrast with earlier experiments, our technique does not need any active feedback. We expect that improvements of our method will permit cooling ratios beyond 1,000 and will thus possibly enable cooling all the way down to the quantum mechanical ground state of the micromirror.

Differential effects of an anti-oxidant intervention on cardiomyocyte expression of adrenomedullin and intermedin and their receptor components in chronic nitric oxide deficiency

Background: Chronic inhibition of nitric oxide (NO) synthesis is associated with hypertension, myocardial oxidative stress and hypertrophic remodeling. Up-regulation of the cardiomyocyte adrenomedullin (AM) / intermedin (IMD) receptor signaling cascade is also apparent in NO-deficient cardiomyocytes: augmented expression of AM and receptor activity modifying proteins RAMP2 and RAMP3 is prevented by blood pressure normalization while that of RAMP1 and intermedin (IMD) is not, indicating that the latter is regulated by a pressure-independent mechanism. Aims: to verify the ability of an anti-oxidant intervention to normalize cardiomyocyte oxidant status and to investigate the influence of such an intervention on expression of AM, IMD and their receptor components in NO-deficient cardiomyocytes. Methods: NO synthesis inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 35mg/kg/day) was given to rats for 8 weeks, with/without con-current administration of antioxidants (Vitamin C (25mg/kg/day) and Tempol (25mg/kg/day)). Results: In left ventricular cardiomyocytes isolated from L-NAME treated rats, increased oxidative stress was indicated by augmented (3.6 fold) membrane protein oxidation, enhanced expression of catalytic and regulatory subunits of pro-oxidant NADPH oxidases (NOX1, NOX2) and compensatory increases in expression of anti-oxidant glutathione peroxidase and Cu/Zn superoxide dismutases (SOD1, SOD3). Vitamin C plus Tempol did not reduce systolic blood pressure but normalized augmented plasma levels of IMD, but not of AM, and in cardiomyocytes: (i) abolished increased membrane protein oxidation; (ii) normalized augmented expression of prepro-IMD and RAMP1, but not prepro-AM, RAMP2 and RAMP3; (iii) attenuated (by 42%) increased width and normalized expression of hypertrophic markers, skeletal-�-actin and prepro-endothelin-1 similarly to blood pressure normalization but in contrast to blood pressure normalization did not attenuate augmented brain natriuretic peptide (BNP) expression. Conclusion: normalization specifically of augmented IMD/RAMP1 expression in NO-deficient cardiomyocytes by antioxidant intervention in the absence of blood pressure reduction indicates that these genes are likely to be induced directly by myocardial oxidative stress. Although oxidative stress contributed to cardiomyocyte hypertrophy, induction of IMD and RAMP1 is unlikely to be secondary to cardiomyocyte hypertrophy.