The centrality dependence of transverse momentum distributions and yields for ± , K ± , p, and p in Au + Au collisions at ͱ s NN = 200 GeV at midrapidity are measured by the PHENIX experiment at the Relativistic Heavy Ion Collider. We observe a clear particle mass dependence of the shapes of transverse momentum spectra in central collisions below ϳ2 GeV/ c in p T. Both mean transverse momenta and particle yields per participant pair increase from peripheral to midcentral and saturate at the most central collisions for all particle species. We also measure particle ratios of − / + , K − / K + , p / p, K / , p / , and p / as a function of p T and collision centrality. The ratios of equal mass particle yields are independent of p T and centrality within the experimental uncertainties. In central collisions at intermediate transverse momenta ϳ1.5-4.5 GeV/ c, proton and antiproton yields constitute a significant fraction of the charged hadron production and show a scaling behavior different from that of pions.

Abstract. We investigate the roles of climate forcings and chaos (unforced variability) in climate change via ensembles of climate simulations in which we add forcings one by one. The experiments suggest that most interannual climate variability in the period 1979-1996 at middle and high latitudes is chaotic. But observed SST anomalies, which themselves are partly forced and partly chaotic, account for much of the climate variability at low latitudes and a small portion of the variability at high latitudes. Both a natural radiative forcing (volcanic aerosols) and an anthropogenic forcing (ozone depletion) leave clear signatures in the simulated climate change that are identified in observations. Pinatubo aerosols warm the stratosphere and cool the surface globally, causing a tendency for regional surface cooling. Ozone depletion cools the lower stratosphere, troposphere and surface, steepening the temperature lapse rate in the troposphere. Solar irradiance effects are small, but our model is inadequate to fully explore this forcing.

We investigated pulmonary mechanics in 25 patients, 9 to 55 years of age, with a variety of generalised neuromuscular diseases and variable degrees of respiratory muscle weakness. The average degree of inspiratory muscle force was 39 2 % (range 8-83 %) of predicted. The lung volume restriction far exceeded that expected for the degree of muscle weakness: the observed decrement in respiratory muscle force should, theoretically, decrease vital capacity to 78 % of its control value, while the mean VC in our patients was only 500% of predicted. Analysis of lung pressure-volume curves indicated that the two principal causes of the disproportionate loss of lung volume were a reduction in lung distensibility probably caused by widespread microatelectasis, and a decrease in the outward pull of the chest wall. Because it reflects both direct (loss of distending pressure) and secondary (alterations in the elastic properties of the lungs and chest wall) effects of respiratory muscle weakness on lung function, we conclude that, in these patients, the vital capacity remains the most useful measurement to follow evolution of the disease process or response to treatment.