Injuries associated with continuous miners, shuttle cars, load-haul-dump and personnel transport in New South Wales underground coal mines

In the three years to June 2005, 959 injuries associated with continuous miners (CMs), shuttle cars (SCs), load–haul–dump and personnel transport (PT) were reported by NSW underground coal mines, comprising 23% of all injuries reported. The present paper reports an analysis of the narrative field accompanying these reports to determine opportunities for controlling injury risks. The most common combinations of activity and mechanism were: strain while handling CM cable (96 injuries); caught between or struck by moving parts while bolting on a CM (86 injuries); strains while bolting on CM (54 injuries); and slipping off a CM during access, egress or other activity (60 injuries). For the other equipment considered, the common injury mechanism was the vehicle running over a pothole or other roadway abnormality causing the driver or passengers to be injured (169 injuries). Potential control measures include: monorails for CM services; hydraulic cable reelers; handrails on CM platforms; redesign of CM platforms and bolting rigs to reduce reach distances during drilling and bolting; improvements to guarding of bolting controls; standardisation and shape coding of bolting controls; two handed fast feed; improvements in underground roadway maintenance, vehicle suspension, visibility and seating; and pedestrian proximity warning devices.

Computer animation of hot spot development in bulk coal as an aid for training coal miners

The processes that take place during the development of a heating are difficult to visualise. Bulk coal self-heating tests at The University of Queensland (UQ) using a two-metre column are providing graphic evidence of the stages that occur during a heating. Data obtained from these tests, both temperature and corresponding off-gas evolution can be transformed into what is effectively a video-replay of the heating event. This is achieved by loading both sets of data into a newly developed animation package called Hotspot. The resulting animation is ideal for spontaneous combustion training purposes as the viewer can readily identify the different hot spot stages and corresponding off-gas signatures. Colour coding of the coal temperature, as the hot spot forms, highlights its location in the coal pile and shows its ability to migrate upwind. An added benefit of the package is that once a mine has been tested in the UQ two-metre column, there is a permanent record of that particular coals performance for mine personnel to view.

An evaluation of potential mechanism-based inactivation of human drug metabolizing cytochromes P450 by monoamine oxidase inhibitors, including isoniazid

To characterize potential mechanism-based inactivation (MBI) of major human drug-metabolizing cytochromes P450 (CYP) by monoamine oxidase (MAO) inhibitors, including the antitubercular drug isoniazid. Human liver microsomal CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A activities were investigated following co- and preincubation with MAO inhibitors. Inactivation kinetic constants (K-I and k(inact)) were determined where a significant preincubation effect was observed. Spectral studies were conducted to elucidate the mechanisms of inactivation. Hydrazine MAO inhibitors generally exhibited greater inhibition of CYP following preincubation, whereas this was less frequent for the propargylamines, and tranylcypromine and moclobemide. Phenelzine and isoniazid inactivated all CYP but were most potent toward CYP3A and CYP2C19. Respective inactivation kinetic constants (K-I and k(inact)) for isoniazid were 48.6 mu M and 0.042 min(-1) and 79.3 mu M and 0.039 min(-1). Clorgyline was a selective inactivator of CYP1A2 (6.8 mu M and 0.15 min(-1)). Inactivation of CYP was irreversible, consistent with metabolite-intermediate complexation for isoniazid and clorgyline, and haeme destruction for phenelzine. With the exception of phenelzine-mediated CYP3A inactivation, glutathione and superoxide dismutase failed to protect CYP from inactivation by isoniazid and phenelzine. Glutathione partially slowed (17%) the inactivation of CYP1A2 by clorgyline. Alternate substrates or inhibitors generally protected against CYP inactivation. These data are consistent with mechanism-based inactivation of human drug-metabolizing CYP enzymes and suggest that impaired metabolic clearance may contribute to clinical drug-drug interactions with some MAO inhibitors.

In vitro characterization of lamotrigine N2-glucuronidation and the lamotrigine-valproic acid interaction

Studies were performed to investigate the UDP-glucuronosyltransferase enzyme( s) responsible for the human liver microsomal N2-glucuronidation of the anticonvulsant drug lamotrigine ( LTG) and the mechanistic basis for the LTG-valproic acid ( VPA) interaction in vivo. LTG N2-glucuronidation by microsomes from five livers exhibited atypical kinetics, best described by a model comprising the expressions for the Hill ( 1869 +/- 1286 mu M, n = 0.65 +/- 0.16) and Michaelis-Menten ( Km 2234 +/- 774 mu M) equations. The UGT1A4 inhibitor hecogenin abolished the Michaelis-Menten component, without affecting the Hill component. LTG N2-glucuronidation by recombinant UGT1A4 exhibited Michaelis-Menten kinetics, with a K-m of 1558 mu M. Although recombinant UGT2B7 exhibited only low activity toward LTG, inhibition by zidovudine and fluconazole and activation by bovine serum albumin ( BSA) ( 2%) strongly suggested that this enzyme was responsible for the Hill component of microsomal LTG N2-glucuronidation. VPA ( 10 mM) abolished the Hill component of microsomal LTG N2-glucuronidation, without affecting the Michaelis-Menten component or UGT1A4-catalyzed LTG metabolism. K-i values for inhibition of the Hill component of LTG N2-glucuronidation by VPA were 2465 +/- 370 mu M and 387 +/- 12 mu M in the absence and presence, respectively, of BSA ( 2%). Consistent with published data for the effect of fluconazole on zidovudine glucuronidation by human liver microsomal UGT2B7, the Ki value generated in the presence of BSA predicted the magnitude of the LTG-VPA interaction reported in vivo. These data indicate that UGT2B7 and UGT1A4 are responsible for the Hill and Michaelis-Menten components, respectively, of microsomal LTG N2-glucuronidation, and the LTG-VPA interaction in vivo arises from inhibition of UGT2B7.