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)

We investigated the effects of a turf application of the insecticide diazinon AG500 on Canada geese (Branta canadensis) on a golf course in coastal Washington (USA). On both 19 and 26 March 1987, 1 ha of turf on a golf course located in Birch Bay, Washington was treated with diazinon AG500 at a target application rate of 2.2 kg active ingredient per hectare (AI/ha). Treated areas were then irrigated with 6 mm water. Grass and water samples were collected from three different sites one day before and 1, 3, 7 and 14 days after each application. Diazinon residues > or = 20 ppm were found in golf course grasses for one week after each application. Diazinon residues in study area ponds and creeks were > or = 17 ppb. Samples from two irrigation puddles one day post-application had 1.00 and 0.20 ppm of diazinon, respectively. Numbers of geese present declined following diazinon application; however, no goose mortality was observed. Geese spent 422 and 538 min feeding on the treated areas after the first and second diazinon applications, respectively. One goose feeding in treated areas demonstrated signs of poisoning (lethargy, ataxia) for several hours. Two other geese feeding in the treated areas may have been slightly intoxicated. During carcass searches, three American wigeon (Anas americana) carcasses were found. Based on brain cholinesterase (ChE) levels and gastrointestinal (GI) tract residues of diazinon present, we concluded that these wigeon died from diazinon poisoning. Numerous songbirds (Passeriformes) also fed on the treated turf but no apparent response to the insecticide was observed.
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PMID:Response of Canada geese to a turf application of diazinon AG500. 835 49

The effect of benidipine on experimental cerebral ischemia was investigated in rats subjected to occlusion of the bilateral common carotid arteries. Benidipine (30 micrograms/kg, i.p.) improved neurological symptoms such as ataxia, convulsion and loss of righting reflex, and prolonged survival time after occlusion of the bilateral common carotid arteries. In the nicardipine (100 micrograms/kg, i.p.)-treated group, a similar effect was observed, whereas nifedipine (100, 300 micrograms/kg, i.p.) and verapamil (300 micrograms/kg, i.p.) did not show any beneficial effect in this model. Furthermore, pretreatment with benidipine (30 micrograms/kg, i.p.) suppressed the increase in cerebral water content 3 h after the occlusion. Nicardipine (100 micrograms/kg, i.p.) showed a tendency to reduce the increase in cerebral water content, though the effect was not statistically significant. Nifedipine (100 micrograms/kg, i.p.) produced no improvement. After occlusion of the bilateral common carotid arteries, depletion of adenosine triphosphate (ATP) and phosphocreatine (CP) and an accumulation of lactate occurred in a time-dependent manner. Prophylactic administration of benidipine (30 micrograms/kg, i.p.), 20 min before occlusion, attenuated the depletion of ATP and CP and the accumulation of lactate 3h after the occlusion. Furthermore, post-treatment with benidipine 30 min after occlusion also suppressed these metabolic disorders. In conclusion, the beneficial effects of benidipine in this severe cerebral ischemia model show that the compound has advantages over nicardipine, nifedipine and verapamil. Thus, these results suggest that benidipine may be useful in the treatment of acute ischemic cerebral damage.
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PMID:Effect of benidipine hydrochloride (KW-3049), on cerebral ischemia induced by bilateral occlusion of the common carotid arteries in rats. 836 94

The pig has been proposed as a potential animal model for methanol-induced neuro-ocular toxicosis in humans because of its low liver tetrahydrofolate levels and slower rate of formate metabolism compared to those of humans. To examine the validity of this animal model, 12 4-month-old female minipigs (minipig YU) were given a single oral dose of water or methanol at 1.0, 2.5, or 5.0 g/kg body wt by gavage (n = 3 pigs/dose). Dose-dependent signs of acute methanol intoxication, which included mild CNS depression, tremors, ataxia, and recumbency, developed within 0.5 to 2.0 hr, and resolved by 52 hr. Average maximum methanol concentrations in plasma, of 3100 +/- 700 (SD), 6200 +/- 2300, and 15,200 +/- 900 micrograms/ml were reached within 0.5 to 4 hr following methanol administration in animals given 1.0, 2.5, or 5.0 g methanol/kg, respectively. The mean initial elimination half-lives of methanol were 9.0 +/- 1.6, 22.4 +/- 6.1, and 18.9 +/- 4.3 hr, for 1, 2.5, and 5.0 g/kg doses, respectively. In 3 minipigs, a transient increase in plasma formate concentration (1.74-3.40 mEq/liter vs control = 0.5 +/- 0.3 mEq/liter) occurred 4 to 30 hr following methanol administration. Methanol- and formate-dosed pigs did not develop optic nerve lesions, toxicologically significant formate accumulation, or metabolic acidosis. Based on results following a single dose, female minipigs do not appear to be overtly sensitive to methanol and thus may not be a suitable animal model for acute methanol-induced neuro-ocular toxicosis.
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PMID:Acute methanol toxicity in minipigs. 850 8

Twenty-one normal adults were the subjects of this study. They were instructed to step in the same position with eyes closed for a total of 50 steps under two conditions: i) Immediately after simultaneous irrigation of the right and left auditory canals for 10 s with 30 degrees C water and 44 degrees C water, respectively, and ii) following irrigation of the right auditory canal with 30 degrees C water. The two conditions simulate two different types of imbalance of labyrinthine function: The former physiological and the latter non-physiological. Under the first condition, 33% of the subjects tended to fall to the right side during stepping. Under the second conditions, 86% showed ataxia. The difference was statistically highly significant, p < 0.01. The results indicate that physiological imbalance does not always cause ataxia. A physiological imbalance occurs during active turning. The motion brings about an ampullopetal lymphatic flow in the ipsilateral horizontal semicircular canal and an ampullofugal flow in the contralateral canal, as under the second condition. The former increases the function of the labyrinth, while the latter decreases it. This results in imbalance but no ataxia.
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PMID:Factors contributing to labyrinthine ataxia. 851 23

Fosphenytoin is a water-soluble disodium phosphate ester of phenytoin that is converted in plasma to phenytoin. Fosphenytoin is compatible with most common i.v. solutions and can be administered safely through the i.m.route. An additional safety factor is the absence of propylene glycol in the fosphenytoin formulation. Propylene glycol is used as a vehicle in the i.v. phenytoin preparation and by itself may produce serious cardiovascular complications. Studies of the pharmacokinetics, safety, and tolerance of i.v. fosphenytoin have demonstrated that fosphenytoin produces phenytoin plasma concentrations similar to those achieved with oral and i.v. phenytoin, but without significant cardiovascular effects and only minimal discomfort at the injection site. Aside from local reactions, the most common adverse events associated with fosphenytoin have been pruritus and reactions typical of phenytoin (e.g., dizziness, somnolence, and ataxia). Fosphenytoin represents a significant advance in the treatment of patients with seizures who require parenteral therapy.
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PMID:Intravenous administration of fosphenytoin: options for the management of seizures. 864 9

Substantial evidence links alcohol drinking and serotonin (5-HT) functioning in animals. Lowered central 5-HT neurotransmission has been found in a subgroup of alcoholics, possibly those with more aggressive, assaultive tendencies. Several rodent studies have also suggested that intact 5-HT systems are important determinants of sensitivity and/or tolerance to ethanol-induced ataxia and hypothermia. Null mutant mice lacking the 5-HT1B receptor gene (5-HT1B-/-) have been developed that display enhanced aggression and altered 5-HT release in slice preparations from some, but not all, brain areas. We characterized these mice for sensitivity to several effects of ethanol. Mutant mice drank twice as much ethanol as wild-type mice, and voluntarily ingested solutions containing up to 20% ethanol in water. Their intake of food and water, and of sucrose, saccharin and quinine solutions, was normal. Mutants were less sensitive than wild-types on a test of ethanol-induced ataxia and, with repeated drug administration, tended to develop tolerance more slowly. In tests of ethanol withdrawal and metabolism, mutants and wild-type mice showed equivalent responses. Our results suggest that the 5-HT1B receptor participates in the regulation of ethanol drinking, and demonstrate that serotonergic manipulations lead to reduced responsiveness to certain ataxic effects of ethanol without affecting dependence.
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PMID:Elevated alcohol consumption in null mutant mice lacking 5-HT1B serotonin receptors. 878 28

An 11-month-old female Vietnamese pot-bellied pig was examined for severe dehydration and neurologic signs including disorientation, ataxia, blindness, and involuntary twitching of the muscles of the neck and head. Biochemical analyses of serum revealed hypernatremia, hyperchloremia, hyperkalemia, azotemia, hyperphosphatemia, hyperalbuminemia, and high activities of aspartate transaminase and creatine kinase. A diagnosis of salt toxicosis/water deprivation was made. Medical management consisted of intravenous administration of a high-sodium crystalloid solution, anti-inflammatory drugs, and other supportive care. Sodium concentration of fluids administered intravenously was adjusted to be slightly less than the pig's serum sodium concentration so that the serum sodium concentration was reduced gradually over 48 hours. Resolution of clinical signs was rapid and the pig was discharged after 8 days of hospitalization. Fourteen days after the initial examination, the pig appeared healthy except for visual deficits. Historically, prognosis with conventional treatment of salt toxicosis/water deprivation is poor; however, this alternative approach to treating this condition appears promising.
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PMID:High-sodium crystalloid solution for treatment of hypernatremia in a Vietnamese pot-bellied pig. 883 48

Strategies for developing selective water diuretic agents have involved development of kappa opioid receptor agonists and vasopressin V2 receptor antagonists; however, these two classes of compounds have not been compared directly. We have investigated the activity of three kappa receptor agonists and one nonpeptide vasopressin receptor antagonist in conscious dogs. SB 215520, SB 215519 and niravoline are selective kappa agonists with variable abilities to cause a water diuresis and ataxia in rats. When administered to conscious hydropenic dogs, the kappa agonists resulted in an increase in free water clearance; however, these effects were associated with an antinatriuresis, an increase in heart rate and, at the higher doses, central nervous system side effects. Conversely, the vasopressin receptor antagonist, OPC 31260, resulted in a significant water diuresis without any accompanying changes in sodium excretion and heart rate, and with no apparent central nervous system effects. These studies suggest that, at least in dogs, a vasopressin receptor antagonist is a more selective water diuretic than a kappa receptor agonist.
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PMID:Comparison of the water diuretic activity of kappa receptor agonists and a vasopressin receptor antagonist in dogs. 906 1

Aquaporin-4 is a mammalian water channel protein that is predominately expressed in brain, where it is believed to mediate water homeostasis. Here we report the isolation and characterization of the cDNA for mouse Aqp4 and map the gene to the proximal region of mouse chromosome 18. This region contains the neurological mutation ataxia, but further analysis reveals that Aqp4 is not responsible for the ataxia phenotype.
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PMID:Cloning and chromosomal localization of mouse aquaporin 4: exclusion of a candidate mutant phenotype, ataxia. 914 4

Diazepam has been reported to impair spatial learning in the water maze. This experiment reexamined this topic using control groups that had first been non-spatially pretrained to familiarize them with the general behavioral strategies required in the water maze task. Naive rats given diazepam (0.5, 3.0, 6.0 mg/kg, IP) displayed dose-related maze acquisition impairments and sensorimotor disturbances (swimming in the periphery of the pool, deflecting off or swimming over the hidden platform, jumping off the platform when placed there after a trial, ataxia on a narrow wooden beam). The sensorimotor disturbances interfered with the acquisition of information about the spatial location of the platform, occurred in the absence of impairments in a subsequent visible platform task or swim speed, and correlated strongly with measures of acquisition. In contrast, the non-spatially pretrained groups did not exhibit sensorimotor disturbances in the water maze and acquired the maze task as rapidly under diazepam as control rats. The non-spatially pretrained groups continued to display diazepam-induced sensorimotor disturbances (ataxia) in a novel beam walking task. CGS8216 (10.0 or 20.0 mg/kg), a benzodiazepine receptor antagonist, attenuated the effect of 3.0 or 6.0 mg/kg diazepam in naive rats, suggesting that the effects of diazepam were mediated by benzodiazepine receptors. Occupancy of benzodiazepine receptors by diazepam does not prevent robust spatial learning in the water maze.
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PMID:Prior non-spatial pretraining eliminates sensorimotor disturbances and impairments in water maze learning caused by diazepam. 916 Aug 46


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