Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A term of 'disproportionately large, communicating fourth ventricle' (DLCFV) was first proposed by in Harwood-Nash in 1980. It is somewhat different from the well known clinical entity of 'isolated or trapped fourth ventricle', because of apparent patency of aqueductal canal. Two cases of typical DLCFV encountered in our clinic were described. First patient was a 24 year old man in whom this condition developed following operations for lumber disc and second patient was 22 year old woman in whom the disease developed after subarachnoid hemorrhage. In both cases, main symptoms were attributable to hydrocephalus but three posterior fossa symptoms, nystagmus, Parinaud' sign and truncal ataxia were also characteristic. On the CT scan, the fourth ventricle was extraordinarily enlarged. Patency of the aqueductal canal was demonstrated by air study or Conray and Metrizamide ventriculography. On the other hand, occlusion was demonstrated or highly suspected in or near the foramina Magendie and Luschka. After a routine ventriculo-peritoneal shunt operation, the fourth ventricle decreased in size and the symptoms were immediately relieved. Plausible explanation for mechanism involved in occurrence of DLCFV were (1) occlusion process in or near the fourth ventricle outlets seems to be crucial in this pathologic condition. Collision of CSF pulse waves against the obstruction may yield a water hammer effect on the fourth ventricle. (2) abnormal weakness of the brain stem parenchyma around the fourth ventricle to CSF pressure may be another contributory factor.
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PMID:[Disproportionately large communicating fourth ventricle--report of 2 cases]. 660 22

The silver salt of 2-metanilamido-5-chloropyrimidine (AgMCP) and the sodium, amminosilver and trimethylphosphite-silver salts of 3',5'-dichlorobenzenesulfonanilide (NaDBS, AgNH3DBS and AgP(OCH3)3DBS were synthesized as possible antibiotic of antiparasitic drugs. All the organosilver compounds were extremely water-insoluble. For animal studies these, and other reference compounds, were given as fine suspensions in an Emulphor-safflower oil mixture. The ip LD50's in mice in mmol/kg were: 1.67 for NaDBS, 0.22 for silver acetate (AgAc), 0.15 for AgP(OCH3)3DBS, 0.13 for AgMCP and 0.10 for AgNH3DBS. When given by mouth, 15 mmol AgAc/kg produced a high mortality, but none of the organosilver compounds caused death in maximal doses (1.9 to 2.6 mmol/kg) that could be given based on considerations of total volume and stability of the suspension. All the silver compounds, including AgAc, produced a similar toxic syndrome with initial hyperexcitability, ataxia, central nervous depression, labored breathing, loss of righting reflex and death. Most deaths occurred between 12 and 24 hours after dosing. In contrast, animals given NaDBS often died within 3 hours although the major signs were very similar to those produced by the silver compounds. When given ip as a single dose 30 minutes after AgAc, D-penicillamine was effective in reducing mortality, but it had no effect on the mortality of the organosilver compounds. Histological studies revealed similar patterns of silver deposition, especially in the liver and kidneys, at 6, 18 and 24 hours after the organosilver compounds and after AgAc. We conclude that the presence of silver contributes significantly to the acute toxicity of these sulfonamides although they may dissociate free silver less readily than does AgAc.
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PMID:Acute toxicity of some silver salts of sulfonamides in mice and the efficacy of penicillamine in silver. 662 59

Recent reports have demonstrated that organolead and -tin compounds can alter behavioral reactivity to noxious stimuli. To further define the dose response and temporal characteristics of these neurobehavioral effects, male Fischer 344 rats were injected sc with either one-fourth, one-half, or three-fourths the acute LD50 of triethyl lead (TEL), triethyl tin (TET), trimethyl lead (TML), trimethyl tin (TMT), or distilled water and tested on a 57.5 degrees C hot plate 1, 7, 14, 21, and 28 days after dosing. All four organometals altered hot plate latencies, but the magnitude and time course of these effects differed among the compounds. TEL produced a dose-related increase in latencies which was maximal 1 and 7 days postdosing and had dissipated by 28 days. In contrast, the group administered TML (3/4 LD50) exhibited a late developing antinocioception which became evident 14 days after dosing and persisted throughout the period of testing. The intermediate dose of TMT (1/2 LD50) also produced a delayed increase in response times which was observed 21 and 28 days post-treatment. The 3/4 LD50 dose of TMT produced increased hot plate latencies on all post-treatment test days except Day 14. TET (1/2 LD50) produced increased hot plate latencies 1, 7, 14, and 21 days postdosing and also induced a reversible ataxia and akinesia. Higher doses of TET proved lethal to 80% of the animals and lower doses failed to alter response times in the hot plate. These data demonstrate that trialkyl lead and tin compounds can produce time- and dose-related increases in hot plate latencies.
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PMID:Organometal-induced antinociception: a time- and dose-response comparison of triethyl and trimethyl lead and tin. 671 May 29

Three monkeys self-administered orally-delivered phencyclidine, 1-(1-phencyclohexyl) piperidine (PCP), N-ethyl-1-phencyclohexylamine (PCE), and 1-[1-(2-thienyl)cyclohexyl]piperidine (TCP) over a wide range of concentrations (0.0156, 0.0312, 0.0625, 0.125, 0.25, and 0.5 mg/ml). Water was also available under a concurrent fixed-ratio (FR) 16 schedule. Drug deliveries were substantially higher than concurrent water deliveries at all concentrations, indicating that the three compounds functioned as effective reinforcers. Maximum liquid deliveries occurred at concentrations of 0.0625 (PCP and TCP) and 0.125 mg/ml (PCE). TCP was much shorter-acting (10-15 min) than PCP (4-6h) based on observations of severe ataxia at high concentrations. To investigate the conditioned reinforcing effects of taste, a quinine solution (0.088 mg/ml) was substituted for PCP (0.25 mg/ml) in five monkeys. Four monkeys responded for quinine in excess of water for a range of seven to over 30 sessions, while one monkey (M-R) did not show any substantial responding for quinine. With the same five monkeys (treatment order mixed), the effect of visual stimuli was tested by substituting water for PCP while retaining the visual stimuli indicating drug availability. Four monkeys showed increased responding on the side signaling drug for only 0-4 sessions, while one monkey (M-R) showed persistent responding for water on the side with drug stimuli for 29 sessions. These results indicated that taste functioned as an effective conditioned reinforcer, while visual stimuli appeared to be less effective in the oral drug self-administration paradigm.
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PMID:Oral self-administration of phencyclidine analogs by rhesus monkeys: conditioned taste and visual reinforcers. 681 65

Etomidate (Hypnomidate; Janssen) 1,25% in sterile water was given rectally on 100 occasions to 50 male Long-Evans rats in doses ranging from 4 mg/kg to 12 mg/kg. The onset and duration of ataxia and hypnosis (i.e. loss of righting ability) were recorded. Ataxia was observed in all rats, even at the lowest dose levels. The lowest hypnotic dose was 6 mg/kg, when 2 out of 5 rats lost their righting ability. In all 50 rats given 8 mg/kg or more hypnosis occurred within 4 minutes (range 2-4 minutes, average 3,3 minutes), from which they recovered within an average of 10,4 minutes. The duration of hypnosis and time to full recovery from ataxia were dose-dependent. The rectal hypnotic dose of etomidate in rats has been found to be approximately ten times the documented intravenous dose. No mortality was recorded despite the rectal administration of ten times the intravenous lethal dose (LD50) for rats. Histological examination of the rectal and colonic mucosa showed that etomidate 1,25% in sterile water (pH 3,5) caused no significant mucosal change, but undiluted etomidate 12,5% (pH 1,8) caused haemorrhagic necrosis. We conclude that rectal etomidate 1,25% in sterile water is an efficient, predictable, evanescent and safe method of inducing anaesthesia in rats and warrants further investigation in clinical anaesthesia in children.
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PMID:Etomidate as a rectal induction agent. Part I. A preliminary study in rats. 687 87

The toxic effects of PR toxin were observed in mice, rats, anesthetized cats and isolated rat auricle preparations. In mice and rats the toxic effects included abdominal writhing, decrease of motor activity and respiratory rate, weakness of hindleg and ataxia. In mice, the i.p. LD50 was 5.8 mg/kg. In mice, rats and cats PR toxin given i.p. caused ascites fluid an edema in the scrotum and lungs, and i.v. injection caused edema in the lungs, giving rise to a large volume of pleural and pericardial fluid. In rats, at the LD50 dose level (11.6 mg/kg, i.p. and 8.2 mg/kg, i.v.), the water content in the lungs was increased, but in the skin it was decreased. Blood K+, hematocrit, red blood cell, white blood cell, hemoglobin, uric acid, cholesterol, blood urea nitrogen and alkaline phosphatase concentrations were all increased, while the total protein and albumin contents were decreased after i.p. injection of PR toxin. High content of protein was found in the pleural fluid and fluid due to ascites. In anesthetized cats the blood pressure and respiratory rate were progressively decreased and the heart rate was reflexly increased after i.p. injection. The i.v. injection produced a multiple response on the arterial blood pressure, but with a progressively decreasing heart rate. Arrhythmias were observed in the late shock stage in the case of i.p. or i.v. injection. In the isolated rat auricle preparations contractile force was more affected that heart rate. We conclude that PR toxin produced acute toxic effects in animals via an increase of capillary permeability and a direct damage to the lungs, heart, liver and kidney.
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PMID:Acute toxicity of PR toxin, a mycotoxin from Penicillium roqueforti. 708 52

Undiluted 2-ethoxyethanol or water (control) was applied to the skin of pregnant Sprague-Dawley rats on days 7--16 of gestation (sperm = day 1). Applications were made 4 times daily in volumes of 0.25 or 0.50 ml 2-ethoxyethanol. Females exhibited ataxia following treatment of the high-dose group, and weight gain was significantly (p less than u. 0.001) reduced in the last half of gestation. Litters were collected by caesarian section on day 21 of gestation, and fetuses were examined for external defects. Half of the fetuses were cleared and stained in alizarin red S for skeletal examinations, and half were examined for visceral defects by the Wilson technique. Intrauterine death was 100% in the high-dose group. In the lower dosage group, there was a significant increase in the number of pregnant females with 100% dead implants (p less than 0.001), a significant reduction in the number of live fetuses per litter (p less than 0.001), a significant reduction in fetal body weight (p less than 0.001), and a significant increase in the incidence of skeletal variations (p less than 0.05) and cardiovascular malformations (p less than 0.05).
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PMID:Teratogenicity of 2-ethoxyethanol by dermal application. 715 21

Lead, cadmium, mercury and arsenic are widely dispersed in the environment. Adults are primarily exposed to these contaminants in the workplace. Children may be exposed to toxic metals from numerous sources, including contaminated air, water, soil and food. The chronic toxic effects of lead include anemia, neuropathy, chronic renal disease and reproductive impairment. Lead is a carcinogen in three animal species. Cadmium causes emphysema, chronic renal disease, cancer of the prostate and possibly of the lung. Inorganic mercury causes gingivitis, stomatitis, neurologic impairment and nephrosis, while organic mercurials cause sensory neuropathy, ataxia, dysarthria and blindness. Arsenic causes dermatitis, skin cancer, sensory neuropathy, cirrhosis, angiosarcoma of the liver, lung cancer and possibly lymphatic cancer.
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PMID:Occupational and community exposures to toxic metals: lead, cadmium, mercury and arsenic. 716 33

Rats were fed on diets containing methyl mercury dicyandiamide (MMD) at concentrations of 1.5, 7.5 or 75 ppm, and observations made of their social and exploratory behaviour and of gross neurotoxicity (ataxia). Mercury concentration in the blood was monitored. MMD at 75 ppm (50 ppm Hg) for 24 days caused ataxia with a sudden onset at 21-27 days. Social behaviour was reduced at 16-17 days. In two experiments at 7.5 ppm MMD, activity was increased in observations of social behaviour after 2 to 17 days, and treated rats found water in an unfamiliar cage sooner than controls. No difference from controls was apparent from then until increased activity re-appeared after 9 mon of the diet (exp. 1) or after 7 days recovery from 31 or 45 days diet (exp. 2). Ataxia was not observed after 7.5 ppm MMD for up to 47 weeks or in 14 weeks recovery. No consistent effect was observed at 1.5 ppm MMD for 31-45 days. MMD, therefore, had a behavioural effect in rats, independent of gross neurotoxicity; its details were consistent with a hyperresponsiveness to stimuli. Tolerance occurred to this effect at a time when blood-mercury concentration was still rising, but the tolerance appeared to be subject to overload.
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PMID:Early change and adaptation in the social behaviour or rats given methyl mercury in the diet. 719 56

Dosages of 95% ethanol (0, .5, or 1 ml) with variable quantities of water were administered to mixed sex chicks (263 g initial weight) on each of 7 consecutive days. The 1 ml dosage of ethanol significantly reduced body weight gains and feed consumption and increased liver weight per 100 g of body weight. Gross crop lesions (accumulation of exudates and hemorrhage) were observed for both the .5 and 1 ml dosage level of ethanol. For birds given the .5 ml ethanol dosage, dilution with water tended to reduce the severity of crop lesions but not for birds given 1 ml ethanol. All levels of ethanol produced mild ataxia within 5 to 10 min of dosage. Mild or moderate hepatocellular fatty change was present in livers from 5 to 6 birds given 1 ml ethanol. Crop exudates were composed of necrotic cells, fibrin and bacteria. Crop walls of birds given 1 ml of undiluted ethanol were ulcerated and inflamed. Areas within the crop wall were hemorrhagic, edematous, and infiltrated by heterophils and mononuclear cells.
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PMID:Toxic effects of repeated ethanol intubations to chicks. 726 48


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