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

A leucoencephalomyelitis in 6 goat kids 2 to 5 months old is described. The disease was characterised by fever, ataxia, posterior paresis, circling and hyperaesthesia progressing to prostration. The neural lesion was confined to the white matter of the cerebellum and posterior brain stem in 4 kids, but in 2 others the cervical spinal cord was the main site affected. The lesion was characterised microscopically by dense perivascular cuffing with mononuclear cells, infiltration of the parenchyma with macrophages and a proliferation of glial cells and by a marked primary demyelination. In more advanced lesions, areas of the neurophil were replaced by a loose glial scar. There were associated pulmonary lesions of interstitial pneumonitis and hyperplasia of the peribronchiolar lymphoid tissue. Attempts to isolate an aetiological agent and to transmit the disease to young goat kids and lambs were unsuccessful. The disease has not been reported before in Australia but has distinct similarities to an infectious leucoencephalomyelitis of young goats which has been described in North America.
 ...
PMID:Leucoencephalomyelitis of goat kids. 74 45

The comparative acute, oral toxicity of ochratoxin A for three day-old avian species is presented. The seven-day LD50 value for White Leghorns was calculated to be 3.4 +/-0.19 mgm./kg., for turkeys to be 5.9 +/- 0.72 mgm./kg., and for Japanese quail to be 16.5 +/- 0.56 mgm./kg., body weight. The dose-response curves are linear and parallel through one standard deviation on either side of the LD50 when log-dose is plotted against probit for survivors. It is suggested that the mechanism of action of ochratoxin A is similar in the three species, though the potency differs. The reduction in weight gain of Leghorn survivors was proportional to dose, and was observed in two separate traials over an overall dosage range from 0.2 mgm./kg. to 5 mgm./kg. The turkeys showed only a slight reduction in weight gain at doses less than 4mgm./kg., a more marked reduction being observed at higher dose levels. The quail did not show reduction of weight gain at dose levels below 10.9 mgm./kg., though the reduction was proportional to dose at higher levels. All birds dying of acute ochratoxicosis revealed a progression of symptoms from listlessness, huddling, occassionally diarrhoea, ataxia, prostration and death. Viscereal gout was observed at necropsy of the Leghorns.
 ...
PMID:Acute oral ochratoxicosis in day-old White Leghorns, turkeys and Japanese Quail. 93 32

Elephantopus scaber has been used in Brazil as a traditional remedy to cause diuresis, antipyresis and to eliminate bladder stones. In the current study, aqueous and hydroalcoholic extracts of whole plants were tested for acute toxicity, analgesic, antipyretic, antiinflammatory, cardiovascular, diuretic and constipating activities. Both extracts (0.3-6 g/kg i.p.) induced writhing, loss of muscle tone, ataxia, prostration and death in mice. No analgesic effects of these extracts were detected using mouse hot-plate and acetic acid-induced writhing tests. Both extracts failed to modify diuresis or carrageenan-induced rat paw edema. In contrast, given intraperitoneally, both reduced brewer's yeast-induced hyperthermia in rats, but when given orally did not affect it. Moreover, the aqueous extract decreased the intestinal transit time in mice while the hydroalcoholic extract increased it. Finally, these extracts, given intravenously, reduced blood pressure and heart rate in rats; these effects could be blocked by atropine but not by co-administration of pyrilamine and cimetidine.
 ...
PMID:Preliminary pharmacologic evaluation of crude whole plant extracts of Elephantopus scaber. Part I: In vivo studies. 145 4

Arginine vasopressin (AVP) induces motor effects when administered into the cerebral ventricles, the ventral septal area (VSA), or the vestibular cerebellum of the rat brain. Because AVP-like immunoreactivity and AVP-binding sites exist in the central medial amygdala (cmeA), and because the amygdala can be kindled to produce motor effects, we hypothesized that the amygdala might play a role in AVP-induced motor effects. This hypothesis was tested by observing motor behavior in response to injection of AVP into the central medial region of the amygdala. Our results demonstrate that an initial injection of AVP into the cmeA caused minor motor effects, including immobility, prostration and ataxia, whereas a similar injection, given 24 h later, caused severe motor effects including barrel rotations and myoclonic/myotonic-like convulsive behavior. A potential receptor basis for the AVP-induced motor and sensitization effects in the cmeA was investigated using AVP analogues. A V1 antagonist, d(CH2)5Tyr(Me)AVP, blocked both the motor and sensitization effects produced by cmeA AVP injection. A V2 receptor agonist, DDAVP, did not affect motor activity upon cmeA injection, but did, however, sensitize animals to subsequent cmeA AVP injection. These results suggest that the cmeA is a sensitive site for AVP-induced motor effects and that these motor effects are sensitized by prior exposure to AVP. While the motor effects observed after cmeA AVP injection are mediated via AVP receptors that resemble the V1 type, the sensitization effect may be mediated via multiple receptor systems.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Vasopressin-induced motor effects: localization of a sensitive site in the amygdala. 146 3

The insect repellent DEET and the structurally related herbicide diphenamid both cause ataxia associated with a spongiform myelinopathy largely confined to the cerebellar roof nuclei. This local myelinopathy was accompanied by the formation of neuronal cytoplasmic clefts and was produced by a single dose of 1 to 3 g/kg N,N-diethyl-m-toluamide (DEET). These dose levels also produced a severe and often fatal prostration and clear electrophysiological signs of prolonged suppressed seizure activity. Diphenamid produced an identical myelinopathy after doses of 0.8 to 1.5 g/kg but without the severe prostration, suppressed seizures, or neuronal clefts. The effects of diphenamid were shown to be reversible over 3 to 7 days by neuropathological, motor, and auditory evoked response indices. Both compounds caused characteristic changes in auditory evoked response which may be useful in clinical diagnosis. Six other alkyl amides, two of which produce signs of CNS excitation, failed to produce myelinopathy at the maximum tolerated doses. Our findings show close parallels with a number of human cases of DEET poisoning and indicate that other amides, like diphenamid, also pose a potential hazard.
 ...
PMID:A comparison of the acute toxicity, neuropathology, and electrophysiology of N,N-diethyl-m-toluamide and N,N-dimethyl-2,2-diphenylacetamide in rats. 160 Dec 13

Natural pyrethrin and synthetic pyrethroid insecticides have been considered among the safest classes of insecticides available. Pyrethrins and pyrethroids are classified on the basis of their chemical structures and their toxicologic, neurophysiologic and pharmacologic effects. Cellular effects of pyrethrin and pyrethroid insecticides have been postulated to involve interactions with sodium channels, receptor-ionophore complexes, neurotransmitters, and ATPases. Toxicity is a function of chemical structure, metabolism, route of exposure, and the presence or absence of synergists. Pyrethroid insecticides are neurotoxic, and the development and severity of clinical signs is proportional to the nervous tissue pyrethroid concentration. Type I pyrethroid poisoning in mice and rats produces a syndrome characterized by tremors, prostration and altered startle reflexes. Type II pyrethroid poisoning in mice and rats causes ataxia, convulsions, hyperactivity, choreoathetosis and profuse salivation. A presumptive diagnosis of pyrethrin/pyrethroid poisoning is based upon history of exposure, development of appropriate clinical signs, and chemical analysis for insecticide residues. Treatment of pyrethrin and pyrethroid toxicosis involves basic life support, seizure control when needed, and the prevention of further insecticide absorption.
 ...
PMID:Neurotoxicology of pyrethrin and the pyrethroid insecticides. 171 67

Three piperidine alkaloid containing plants, Conium maculatum (poison-hemlock), Nicotiana glauca (tree tobacco) and Lupinus formosus (lunara lupine), induced multiple congenital contractures (MCC) and palatoschisis in goat kids when their dams were gavaged with the plant during gestation days 30-60. The skeletal abnormalities included fixed extension or flexure of the carpal, tarsal, and fetlock joints, scoliosis, lordosis, torticollis and rib cage abnormalities. Clinical signs of toxicity included those reported in sheep, cattle and pigs--ataxia, incoordination, muscular weakness, prostration and death. One quinolizidine alkaloid containing plant, Lupinus caudatus (tailcup lupine), on the other hand, which is also known to cause MCC in cows, caused only slight signs of toxicity in pregnant goats and no teratogenic effects in their offspring.
 ...
PMID:Congenital skeletal malformations and cleft palate induced in goats by ingestion of Lupinus, Conium and Nicotiana species. 208 36

Selenium poisoning occurs worldwide in nearly all domestic animals. Acute selenium poisoning is associated with feeding high levels or injecting excessive amounts of selenium and is usually fatal. The acute poisoning may cause gastrointestinal disturbance, muscle weakness, depression of the central nervous system, prostration and death (1-2). Chronic selenium poisoning in cattle, sheep and horses may result from the consumption of seleniferous plants over an extended period of time. Chronic selenium results in ataxia, incoordination, partial blindness, paralysis, loss of hair or wool, abnormal hoof growth and possibly abnormal changes in behavior (1). There is little information regarding the clinical signs and pathology of selenium toxicosis in marine mammals. Likewise, there is little information regarding normal tissue levels or toxicologically significant levels of selenium in these species. The results of these investigations in sea lions, based on clinical signs, pathologic findings and tissue levels of selenium, suggest subacute or chronic selenium poisoning was most likely from dietary fish high in selenium.
 ...
PMID:Selenium toxicosis in three California sea lions (Zalophus californianus). 261 40

Acute and 1-month toxicity studies with SCH 31846, a nonsulfhydryl anti-hypertensive agent which acts by inhibiting angiotensin-converting enzyme, were initiated to evaluate its toxicity. The oral LD50s in mice and rats were approximately 1.8 and 2.5 g/kg, respectively, while the iv LD50 was approximately 450 mg/kg in mice and 150 mg/kg in rats. Signs of acute toxicity in rats and mice included salivation, hypoactivity, ataxia, prostration, and convulsions. In a 1-month dog study at oral doses of 25, 75, or 150 mg/kg, there was a dose-related increase in emesis between 1 and 2 hr after dosing. Absorption studies showed peak blood concentrations occurring in dogs between 0.3 and 1 hr after dosing. No other noteworthy antemortem changes were observed. In a 1-month rat study at oral doses of 30, 180, or 600 mg/kg, the hematocrit and hemoglobin values of the 600 mg/kg-dosed female rats were slightly but significantly (p less than 0.05) decreased and the blood urea nitrogen was slightly but significantly (p less than 0.05) increased in all SCH 31846-dosed male rats and the 600 mg/kg-dosed female rats. Absorption studies in male rats at doses of 30, 180, and 600 mg/kg indicate that SCH 31846 is well absorbed in rats. The 150 mg/kg-dosed dogs and the 180- and 600 mg/kg-dosed rats had a slight increase in the number of renin-containing granules in the renal juxtaglomerular cells. No other compound-related microscopic changes were observed. These data are similar to data reported for Captopril and suggest that in the dog and rat the toxicity of ACE inhibitors is not dependent upon the presence or absence of a sulfhydryl group.
 ...
PMID:Acute and subchronic toxicity of a nonsulfhydryl angiotensin-converting enzyme inhibitor. 300 64

Two incidents of toxin-type food poisoning in N.E. Scotland associated with the consumption of red whelks (Neptunea antiqua) are described. Four patients developed symptoms within 1 h of consuming whole whelks. These included visual disturbances--double vision and difficulty in focusing--tingling of the fingers, prostration and in one subject nausea, vomiting, diarrhoea and ataxia. In all cases recovery was complete in 24 h. Using a newly developed analytical technique the concentration of the causative toxin, tetramine, in the salivary glands of the whelks consumed was estimated at 0.07%, equivalent to a content of 3.75 mg/100 g of the shellfish.
 ...
PMID:Food poisoning due to the consumption of red whelks (Neptunea antiqua). 318 22


1 2 3 4 Next >>