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Biomedical subjects

T R Clark

Publications and source records attributed to T R Clark.

10 recordsLinked to original sources

Biogenic production of cyanide and its application to gold recovery.

Chromobacterium violaceum is a cyanogenic (cyanide-producing) microorganism. Cyanide is used on an industrial scale to complex and recover gold from ores or concentrates of ores bearing the precious metal. A potentially useful approach in gold mining operations could be to produce cyanide biologically in relatively small quantities at the ore surface. In this study, C. violaceum grown in nutrient broth formed a biofilm and could complex and solubilize 100% of the gold on glass test slides within 4-7 days. Approximately 50% of the cyanide- recoverable gold could be mobilized from a biooxidized sulfidic-ore concentrate. Complexation of cyanide in solution by gold appeared to have a beneficial effect on cell growth--viable cell counts were nearly two orders of magnitude greater in the presence of gold-coated slides or biooxidized ore substrates than in their absence. C. violaceum was cyanogenic when grown in alternative feedstocks. When grown in a mineral salt solution supplemented with 13.3% v/v swine fecal material (SFM), cells exhibited pigmentation and suspended cell concentrations comparable to cultures grown in nutrient broth. Glycine supplements stimulated production of cyanide in 13.3% v/v SFM. In contrast, glycine was inhibitory when added at the time of inoculation in the more concentrated SFM, decreasing cell numbers and reducing ultimate bulk-solution cyanide concentrations. However, aeration and addition of glycine to stationary phase cells grown on 13.3% v/v SFM anaerobically resulted in rapid production and high concentrations (up to 38 mg l(-1)) of cyanide. This indicates that biogenesis of cyanide may be supported in remote areas using locally produced and inexpensive agricultural feedstocks in place of commercial media.

Animals↗

Neural lesions in the rat and their relationship to EEG delta activity following seizures induced by the nerve agent soman.

This study describes the neural structures damaged following exposure to the nerve agent soman, shows there are time-dependent differences in the extent of damage in certain structures, and relates seizure-induced increases in delta band (0-3.5 Hz) electroencephalographic (EEG) activity with severity of subsequent neuropathology. Rats, instrumented to record cortical EEG activity, were pretreated with the oxime HI-6 (125 mg/kg, i.p.) and then challenged with soman (180 ug/kg, s.c.). All animals developed continuous epileptiform seizures that lasted in excess of 4 hr. Groups of animals were perfused 1, 3, 10 or 30 days following exposure. Paraffin-embedded brains were stained with hematoxylin and eosin; thirty-four neural structures were examined and scored for neural damage. All cortical areas sustained damage, with piriform and perirhinal cortices exhibiting the most severe. Subcortical limbic areas (amygdala, amygdala-piriform transition zone, hippocampus, claustrum) and various thalamic nuclei were most consistently and severely damaged in all animals regardless of survival time. Brainstem structures, cerebellum, spinal cord, and other motor output nuclei were never damaged. It was found that some structures were rated as more severely damaged when evaluated at shorter survival times. Severity of neural damage was related to high levels of EEG delta power recorded 24 hr after exposure; power during the acute seizure or 24 hr body weight loss did not predict lesion severity. Sections between AP -0.8 to -4.8 contain cortical and subcortical structures that can be readily and reproducibly evaluated for brain damage.

Animals↗