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Structure toxicity relationship analysis was conducted using principal component analysis (PCA) for a panel of nanoparticles that included dry powders of oxides of titanium, zinc, cerium and silicon, dry powders of silvers, suspensions of polystyrene latex beads and dry particles of carbon black, nanotubes and fullerene, as well as diesel exhaust particles. Acute in vitro toxicity was assessed by different measures of cell viability, apoptosis and necrosis, haemolytic effects and the impact on cell morphology, while structural properties were characterised by particle size and size distribution, surface area, morphology, metal content, reactivity, free radical generation and zeta potential. Different acute toxicity measures were processed using PCA that classified the particles and identified four materials with an acute toxicity profile: zinc oxide, polystyrene latex amine, nanotubes and nickel oxide. PCA and contribution plot analysis then focused on identifying the structural properties that could determine the acute cytotoxicity of these four materials. It was found that metal content was an explanatory variable for acute toxicity associated with zinc oxide and nickel oxide, while high aspect ratio appeared the most important feature in nanotubes. Particle charge was considered as a determinant for high toxicity of polystyrene latex amine.

It is unknown whether respiratory motor output is constrained during exhaustive exercise in healthy adults. We hypothesised that neural inhibition did occur; to test this hypothesis we measured diaphragm EMG from a maximal inspiratory capacity maneuver (EMG(di)-IC) at rest and during exercise. EMG(di)-IC was measured before and after the amplitude of the diaphragm EMG entered a plateau phase in eleven healthy adults undertaking exercise at 60% and 80% of maximal workload achieved from incremental exercise. The mean EMG(di)-IC at rest was 65 ± 16% of the maximum that could be obtained from a battery of inspiratory tasks. Before and after the plateau phase of diaphragm EMG, EMG(di)-IC was 68 ± 13% and 72 ± 12% (p > 0.05) during 60% of the maximum workload, and was 70 ± 13% and 78 ± 13% (p > 0.05) during 80% of the maximum workload achieved on an incremental test. A further sub-study in which 5 participants exercised at 90% of the maximum workload also showed that EMG(di)-IC was not diminished during exercise. Our data show that exercise condition does not reduce the magnitude of EMG(di)-IC. This argues against neural inhibition as feature of submaximal exercise in healthy adults., (Copyright © 2013 Elsevier B.V. All rights reserved.)

We examined the effects of dead space loading (DSL) on ventilation (V˙E), neural respiratory drive (EMGdi%max, diaphragm EMG expressed as a % of maximal EMGdi), contractile respiratory muscle effort (Pes,tidal%P(Imax), tidal esophageal pressure swing expressed as a % of maximal inspiratory Pes) and exertional dyspnea intensity ratings in 11 healthy adults with normal spirometry. Subjects completed, in random order, symptom-limited incremental cycle exercise tests under control (CTRL) and DSL (500 ml) conditions. Compared with CTRL, DSL decreased exercise tolerance by 20-25%; increased exertional dyspnea intensity ratings in direct proportion to concurrent increases in EMGdi%max, Pes,tidal%P(Imax) and V˙E; and had little/no effect on the inter-relationships between EMGdi%max, Pes,tidal%P(Imax) and V˙E during exercise. In conclusion, DSL was associated with an earlier onset of intolerable dyspnea; however, neuro-muscular and neuro-ventilatory coupling of the respiratory system remained relatively preserved during exercise in the presence of an increased external dead space. Under these circumstances, DSL-induced increases in exertional dyspnea intensity ratings reflected, at least in part, the awareness of increased neural respiratory drive, contractile respiratory muscle effort and ventilatory output., (Copyright © 2011 Elsevier B.V. All rights reserved.)