Superconductivity in highly disordered dense carbon disulfide. (57/101)

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Bacterial CS2 hydrolases from Acidithiobacillus thiooxidans strains are homologous to the archaeal catenane CS2 hydrolase. (58/101)

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Diversity and ecophysiology of new isolates of extremely acidophilic CS2-converting Acidithiobacillus strains. (59/101)

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Carbon disulfide effects on the visual system. II. Retinogeniculate degeneration. (60/101)

We examined the morphological effects of carbon disulfide exposure on neurons and vasculature of the visual system of macaque monkeys. Five monkeys were exposed to 256 ppm carbon disulfide (CS2) by inhalation for 6 hr a day, 5 days a week. One monkey, sacrificed immediately after exposure, had numerous axonal swellings in the distal optic tract. Four other monkeys survived the exposure period for at least 1 year and were found to have suffered marked degeneration of central retinal ganglion cells, with little or no effect on other neurons in the retina. No evidence was found for arteriosclerotic or aneurysmal changes, suggesting that visual system injury in primates induced by carbon disulfide exposure is not dependent on the occurrence of structural changes in retinal blood vessels.  (+info)

Carbon disulfide effects on the visual system. I. Visual thresholds and ophthalmoscopy. (61/101)

The visual effects of carbon disulfide exposure were studied in macaque monkeys with measurements of visual thresholds, fluorescein angiography and fundus photography. Five monkeys were exposed by inhalation for 6 hr a day, 5 days a week to 256 ppm carbon disulfide (CS2). The motor dysfunction observed in these monkeys appeared to be entirely reversible. All five suffered severe reductions in visual acuity and contrast sensitivity although flicker resolution was not affected. Visual loss was found to be irreversible, with degeneration of substantial numbers of retinal ganglion cells (companion paper) in those monkeys permitted to survive after the termination of exposure. None of the monkeys developed retinal microaneurysms or hemorrhages, major accepted signs of visual toxicity in CS2 exposed humans; thus, permanent visual loss may result from carbon disulfide exposure even in the absence of retinal vascular effects.  (+info)

Exposure to carbon disulphide and ischaemic heart disease in a viscose rayon factory. (62/101)

The cohort of viscose rayon workers previously described by Tiller et al has been reconstructed and followed up to the end of 1982. The pattern of mortality at ages 45 to 64 for the extended period 1950-82 is similar to that described by Tiller et al for 1950-64. The spinners, the workers most heavily exposed to carbon disulphide, have a significantly higher mortality from all causes than the least exposed group. The excess mortality is largely accounted for by ischaemic heart disease (IHD) for which the spinners have an SMR of 172. When mortality is related to an exposure score in the same group, both all cause (p less than 0.01) and IHD (p less than 0.001) mortality increase with increasing exposure level. When this analysis is repeated covering all ages these trends become much less strong and only that for IHD remains significant (p less than 0.05). Over the age of 65 there is a tendency for mortality to decline with increasing exposure. This is contrary to expectation under the usual hypothesis that carbon disulphide promotes atherosclerosis. Instead it suggests that carbon disulphide has some type of reversible, direct cardiotoxic or thrombotic effect. This is supported by the findings that there is a strong trend (p less than 0.01) for IHD mortality to increase with increasing exposure in the previous two years. Further, both IHD (p less than 0.001) and total (p less than 0.01) mortality show highly significant trends with exposure among current workers but no such trends among workers who have left the industry.  (+info)

Carbon disulphide exposure affects the response of rat adrenal medulla to hypothermia and hypoglycaemia. (63/101)

The effects of hypothermia and hypoglycaemia on adrenal catecholamines and dopamine-beta-hydroxylase were compared in control and carbon disulphide (CS2) exposed rats 24 h after the last of ten daily 4 h inhalation exposures to CS2, 2 mg 1(-1) air. Animals were either kept in a cold room (0 degrees C) for 210 min with or without immobilization or were injected with insulin 100 u kg-1. Before these treatments CS2 exposed rats had more dopamine and less adrenaline in their adrenals than controls, and CS2 exposure also elevated the adrenal synthesis of catecholamines. Cold with immobilization or insulin treatment depressed the adrenal adrenaline content and increased the plasma concentrations of noradrenaline and adrenaline. There were no consistent differences between control and CS2 exposed rats. The adrenal dopamine content increased during cold exposure with immobilization or after insulin treatment both in CS2 exposed and control rats. The increase was smaller in CS2 exposed rats but the final dopamine values were nearly identical in the two groups. Exposure to cold (without immobilization) increased the adrenal dopamine content and the rate of catecholamine synthesis in control, but not in CS2 exposed rats. The increase in controls was less than the difference between the pre-cold exposure values of control and CS2 exposed rats. It is concluded that the elevation of adrenal dopamine content and catecholamine synthesis in CS2 exposed rats satisfy part of the demand placed on the adrenal medulla by hypothermia and hypoglycaemia. Consequently the changes induced by the latter treatments were smaller in CS2 exposed than in non-exposed rats. Moreover, when CS2 exposed rats were subjected to cold stress without immobilization their catecholamine synthesis was higher than the level measured in control rats after cold exposure.  (+info)

Organic solvent neurotoxicity. Facts and research needs. (64/101)

While many organic solvents are, in large doses, capable of inducing an acute, reversible narcotic state, few unequivocally induce chronic, long-lasting, or irreversible changes in nervous system structure and/or function. For organic solvents with proved neurotoxic properties, the type of neurological damage is closely related to the structure of the chemical agent, while the degree of impairment and the extent of reversibility are related to the potency, dose, and duration of exposure. Examples include solvents containing n-hexane or methyl n-butyl ketone, which have caused many cases of occupational neuropathy. Chronic inhalation abuse of pure toluene produces irreversible cerebellar, brainstem, and pyramidal-tract dysfunction, but comparable changes have not been found in solvent workers occupationally exposed to toluene. Ototoxicity is found in experimental animals exposed to toluene, xylene, or styrene. Impure trichloroethylene has a predilection for damaging the trigeminal nerve; dichloroacetylene, a breakdown product of trichloroethylene, is probably responsible for this neurotoxic property. Prolonged occupational exposure to mixed solvents, notably white spirit, has been reported to induce a mild, nonprogressive dementing illness with or without peripheral nerve dysfunction, but supporting data from neuropathological and experimental animal studies are lacking. Many other solvents have been reported to induce adverse effects in workers. The pivotal biological role of the nervous system and its vulnerability to selected organic solvents widely used in industry underline the urgent need for further clinical and experimental research on this problem.  (+info)