Small laminar diffusion flames (flame height ≃2–3 mm) established by a fuel jet issuing into a quiescent medium are investigated. It was found that for these flames buoyancy effects disappeared as the flame size decreased (Fr≫1), and diffusive transport of the fuel was comparable to the convective transport of the fuel. The effect of buoyancy on these flames was studied by examining the flame shape for horizontally oriented burners. A phenomenological model was developed (based on experimentally determined flame shapes) to compare diffusion and convection transport effects. Finally, the flame shapes were theoretically determined by solving the conservation equations using similarity methods. It was seen that when the axial diffusion (in momentum and species equations) terms are included in the conservation equations, the calculated flame shape is in better agreement (as compared to without the axial diffusion term) with the experimentally measured flame shape.
Organophosphate poisoning in the context of self-harm is a common medical emergency in Asia. Prolonged muscle weakness is an important but poorly understood cause of morbidity and mortality of the poisoning. This study examined mitochondrial function and its modulation by nitric oxide in muscle weakness of rats exposed to an acute, oral (0.8LD50) dose of monocrotophos. Muscle mitochondrial ATP synthase activity was inhibited in the rat in acute exposure to monocrotophos while respiration per se was not affected. This was accompanied by decreased mitochondrial uptake of calcium and increased levels of nitric oxide. Reactive cysteine groups of ATP synthase subunits were reduced in number, which may contribute to decreased enzyme activity. The decrease in ATP synthase activity and reactive cysteine groups of ATP synthase subunits was prevented by treatment of animals with the nitric oxide synthase inhibitor, L-NG Nitroarginine methyl ester, at 12 mg/kg body weight for 9 days in drinking water, prior to monocrotophos exposure. This indicated a role for nitric oxide in the process. The alterations in mitochondrial calcium uptake may influence cytosolic calcium levels and contribute to muscle weakness of acute organophosphate exposure.
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