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)

Beta1-Fetoprotein (Fbeta1) and fetal hemoglobin (HbF) were compared with the help of immunodiffusion methods. They were shown to be non-identical although Fbeta1, as well as HbF, is stained by benzidine. Antisera against Fbeta1 do not form the line of precipitation with HbF. Besides, we succeeded to differentiate Fbeta1 from Fbeta2 (they are separated under chromatography on sephadex G-200). Fbeta1 differs from Fbeta2 by benzidine staining: Fbeta1 is benzidine-positive and Fbeta2 is benzidine-negative. The constant parallelism in the appearance of Fbeta2 and a monomeric subunit IgMs of the immunoglobulin molecule IgM. Both the proteins, Fbeta1 and Fbeta2, are present in the serum of a newborn, as well as of a patient with ataxia-teleangiectasia. At the same time erythrocytes of the latter do not contain HbF, as was shown by electrophoresis in polyacrylamide gel.
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PMID:[The place of beta-fetoproteins among other fetal proteins]. 81 62

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.
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PMID:Acute and subchronic toxicity of a nonsulfhydryl angiotensin-converting enzyme inhibitor. 300 64

Effects of a single IM injection of selenium-vitamin E (Se-E; 5 mg of Se + 68 IU of alpha-tocopherol/60 kg of body weight) as a pretreatment 14 days before an oral dose of aflatoxin B1 (1.0 mg/kg) were studied in 24 dairy calves. Treatment groups were designated as follows: group 1 = no Se-E or aflatoxin B1 (control); group 2 = Se-E supplementation only; group 3 = aflatoxin B1 dose only; and group 4 = Se-E supplementation before aflatoxin B1 dose. Clinical signs of toxicosis in aflatoxin B1-treated calves included anorexia, ataxia, rough haircoats, increased respiration rates, dyspnea, dehydration, and nasal discharge. Packed-cell volume, RBC, WBC, and hemoglobin were increased in aflatoxin-treated calves. Significant increases in serum aspartate aminotransferase (P less than 0.05) and gamma-glutamyl-transferase (P less than 0.001) activities and prothrombin times (P less than 0.001) were observed in aflatoxin-treated calves, indicating that there was hepatic involvement. Although aflatoxin exposure caused a significant decrease in body weight (P less than 0.01) and feed intake (P less than 0.001) in treatment groups 3 and 4, Se was demonstrated to interact significantly (P less than 0.001) with aflatoxin B1 for feed intake, causing an improved feed intake in treatment group 4 calves.
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PMID:Aflatoxin B1 toxicosis in dairy calves pretreated with selenium-vitamin E. 308 Sep 29

Eleven alcoholics with cerebellar degeneration (eight with computerized tomography confirmation of cerebellar atrophy) were matched with nonataxic alcoholics and nonalcoholics. There were no laboratory or physiological markers for ataxia, including hemoglobin A1a + b, red blood cell transketolase, liver function enzymes, and measures of reaction time and hand-eye coordination. Acetaldehyde-modified hemoglobin levels (as hemoglobin A1a + b) did not, as previously reported, distinguish between alcoholics and nonalcoholics. There was 24% less annual alcohol consumption in ataxic alcoholics compared with nonataxic alcoholics, 9% less lifetime consumption in ataxic alcoholics, and 33% less maximal daily intake. The finding that ataxic alcoholics do not have higher alcohol consumption than nonataxic alcoholics suggests that alcoholic cerebellar degeneration is not a dose-dependent phenomenon, and that alcoholics with cerebellar degeneration may have an idiosyncratic sensitivity to the neuronal effects of alcohol.
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PMID:Alcoholic cerebellar degeneration is not a dose-dependent phenomenon. 330 8

The effects produced by the administration of aqueous suspensions of the green or dried leaves of Azadirachta indica, a common tropical plant, were investigated in goats and guinea pigs. At doses of 50 or 200 mg/kg given orally over a period of up to eight weeks, the plant produced a progressive decrease in body weight, weakness, inappetence, and loss of condition. There were also decreases in heart, pulse and respiratory rates. Diarrhea was observed in animals given the fresh leaves. In goats, the higher doses of the plant leaves produced tremors and ataxia during the last few days of treatment. No statistically significant hematological changes were observed after dosing the animals with A indica leaves, although there was a tendency towards lowered erythrocyte counts, packed cell volume and hemoglobin concentration. The treatments caused significant rises in the plasma activity of aspartate transferase, sorbitol dehydrogenase, and concentrations of cholesterol, urea, creatinine and potassium. No significant changes in the plasma concentration of sodium, chloride or bilirubin were detected. On necropsy of treated goats there were areas of hemorrhagic erosions. The hearts appeared flappy and in some animals there were hydropericarium. Histopathologically, there was evidence of various degrees of hemorrhage, congestion, and degeneration in the liver, kidney, lung, duodenum and brain. Degeneration of the seminiferous tubules was also seen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The toxicity of Azadirachta indica leaves in goats and guinea pigs. 382 69

Early administration of vitamin E to low birth weight (less than 1500 g) infants results in alleviation of the symptoms of retinopathy of prematurity and a lowered incidence of intraventricular hemorrhage. If vitamin E is given to children with cholestatic liver disease (orally or parenterally) before 3 years of age, neurological symptoms such as areflexia, ataxia, and sensory neuropathy are prevented or reversed. Restitution of neurological function is more limited in children ages 5-17 years even after prolonged therapy. Vitamin E is also useful in prevention of neuropathy and retinopathy associated with abetalipoproteinemia and cystic fibrosis. Blood levels of tocopherol are often low in subjects with hemolytic anemias. Administration of vitamin E to G-6-P-D-deficient subjects increased hemoglobin levels, and decreased the number of irreversibly sickled cells in sickle-cell anemia subjects. Most trials have indicated that administration of vitamin E for 6 months or more to subjects with intermittent claudication results in longer walking distance and improved blood flow. Vitamin E reduces platelet aggregation, platelet adhesion to collagen, and platelet thromboxane production. Prostacyclin production is generally enhanced. The significance of these effects to thrombotic diseases. Epidemiological studies have indicated that subjects with higher blood levels of vitamin E have lower risk of death from ischemic heart disease and cancer, a lower risk of breast cancer, and a lower incidence of infections.
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PMID:Clinical uses of vitamin E. 391 44

Two subchronic studies were conducted to assess the potential toxicity of N-D-ornithyl amphotericin B methyl ester (OAME). In both studies the comparative control substance was amphotericin B (AMB). Dogs (5/sex/group) were given OAME (82% pure, based on high-pressure liquid chromatographic (HPLC) analysis) at 0.6, 2.5, and 10 mg/kg or AMB at 0.6 mg/kg intravenously once daily for 3 months. Two dogs per sex per group were retained for a 7-week postdose observation period. Rats (15/sex/group) were given daily doses of OAME at 4, 12, 24, and 36 mg/kg or AMB at 5 and 12 mg/kg intraperitoneally for 3 months. The principal organs of toxicity in both species were the liver, kidneys, and circulating erythrocytes. Hepatic changes in dogs consisted of periportal and centrilobular inflammation in animals of all dosed groups and were equivalent in dogs given 0.6 mg/kg OAME or AMB. In rats, acute hepatic necrosis with periportal, centrilobular, or panlobular distribution in animals of all OAME (except 4 mg/kg) and AMB-dosed groups was observed. These changes were equivalent in the 36-mg/kg OAME- and 12-mg/kg AMB-dosed animals. Renal changes, evidenced by increases in serum urea nitrogen water consumption, urine volume, decreased urine osmolality, and renal tubular changes (ranging from degeneration and regeneration to necrosis), were observed in both species. In dogs, these changes in the OAME-dosed animals were less severe at all doses than those observed in the AMB-dosed dogs. Renal changes in rats, which were mild in comparison to the dogs, were equivalent at doses of 5 and 12 mg/kg AMB and 36 mg/kg OAME. Decreased erythrocyte counts, hematocrit, and hemoglobin values were observed in both species. Unique to the dog study, however, were irreversible behavioral (somnolence, ataxia, tremors, and compulsive searching) and/or morphologic brain changes (gliosis with astrocytic hypertrophy and hyperplasia) at doses of 2.5 and 10 mg/kg OAME. Similar changes were observed in two dogs given 10 mg/kg OAME (100% pure, based on HPLC analysis) in a 6-week pilot study, indicating that the neurological changes were induced by OAME rather than by an impurity. These changes appear related to prolonged exposure to high plasma concentrations of OAME.
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PMID:Subchronic toxicity studies of N-D-ornithyl amphotericin B methyl ester in dogs and rats. 404 96

Lead subacetate (0.5g) and 1000 units of vitamin D were given three times a week to four newly-weaned rhesus monkeys. In addition, two animals received only the vitamin D. The poisoned animals had an increase in the urinary excretion of delta-aminolevulinic acid, an elevated content of lead in the blood, and a fall in hemoglobin concentration. Between 6 and 18 weeks the animals suddenly developed ataxia, nystagmus, generalized weakness, and convulsions. At this time the animals were killed by perfusion of fixative and the brain prepared for light and electron microscopic studies. Definite morphological evidence of disease was confined to the central nervous system, except for one animal which showed the characteristic renal inclusions of lead poisoning. All animals showed PAS-positive globules associated with blood vessels and an exudative edema involving the white matter of the cerebral hemispheres and cerebellum. Ultra-structurally, this appeared as a granular precipitate within an expanded extracellular space. Alterations of nerve fibers were not seen in the white matter but axonal swelling was observed in the cerebral cortex. The perikaryon and neuropil appeared normal. The control animals showed no significant cerebral changes.
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PMID:Experimental acute lead encephalopathy in the juvenile rhesus monkey. 420 57

The clinical and clinicopathologic effects of excess oral pyridoxine hydrochloride (150 mg/kg body weight/day) and clioquinol (200 mg/kg body weight/day) alone and in combination were evaluated in adult Beagle dogs over an experimental period of approximately 100 days. Anorexia and loss of body weight occurred in the first weeks of the trial period in each treatment group, but was most severe in dogs given both compounds. Dogs in each treatment group (10 of 10 pyridoxine-treated dogs, 6 of 13 clioquinol-treated dogs and 12 of 13 pyridoxine plus clioquinol-treated dogs) developed neurologic disease, manifested principally by ataxia. Pyridoxine-treated dogs had proprioceptive loss involving both fore- and hindquarters, characterized by stiff, spastic, dysmetric leg movements. In clioquinol-treated dogs, dysmetric leg movements were accompanied by failure to support body weight in the hindquarters, but similar forelimb involvement occurred in severely affected dogs. The neurologic disease in dogs given both compounds varied; signs in some dogs resembled those of affected dogs of the pyridoxine-treated group, and in others, those in clioquinol-treated group. Erythrocyte counts, hemoglobin concentrations and packed cell volumes were reduced in dogs in each treatment group and were lowest in dogs given both compounds. Plasma protein was mildly reduced in dogs given pyridoxine or pyridoxine plus clioquinol. Few or no differences were present in the leukocyte counts, blood urea nitrogen concentrations, in activities of serum alanine aminotransferase and aspartate aminotransferase, and in concentrations of sodium, chloride or potassium in treated dogs as compared to control dogs.
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PMID:The subacute neurotoxicity of excess pyridoxine HCl and clioquinol (5-chloro-7-iodo-8-hydroxyquinoline) in beagle dogs. I. Clinical disease. 645 37

Groups of six male and six female Beagle dogs were fed diets containing 0, 250, 500, or 1000 ppm fenvalerate for a period of 6 months. Prominent in-life observations related to treatment were emesis, head shaking, biting of the extremities, ataxia, and tremors. One high-dose male dog was sacrificed in extremis during the study period. Mean body weights of 1000-ppm female dogs were significantly lower than those of controls. Red blood cell counts and hematocrit and hemoglobin values in high-dose male and female dogs were significantly lower than those of controls at most sampling intervals. Serum cholesterol and alkaline phosphatase levels were also increased primarily in the high-dose group. Ophthalmic examination revealed changes in retinal vessel tortuosity in some mid- and high-dose dogs. Hepatic multifocal microgranulomata were observed in control and treated dogs microscopically. These changes increased in incidence and severity with dose and were considered to be related to treatment. Histiocytic cell infiltrate in mesenteric lymph nodes in some 500- and 1000-ppm female and 1000-ppm male dogs was the only other treatment-related microscopic effect.
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PMID:Six-month feeding study of fenvalerate in dogs. 647 3


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