Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A multi-channel recorder has been employed for the simultaneous recording of various neuro-physiological parameters such as EEG, respiration, tremor, ECG, PGR, pulse-tracing and EMG. The present pilot study shows that of all parameters only EEG, pulse-form, PGR and EMG are of high diagnostic value. The importance of these records, in conjunction with neuro-clinical findings, in the differential diagnosis of ergotropic and trophotropic forms of attacks, as well as their differentiation from epileptic fits is pointed out. The pulse-form described in detail, particularly the characteristics of the "ergotropic pulse-form". The special advantage of the present method lies in its non-aggressive nature. Operational details are given in order to facilitate comparisons.
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PMID:[Polygraphic studies on ergotropic and trophotropic attacks (a contribution to the question of hyperactivity of the central sympathetic system) (author's transl)]. 89 27

The Jimpy mouse is an x-linked recessive mutation of the house mouse resulting a myelin deficiency in the central nervous system. It is of interest as an animal model of human leukodystrophy. Clinical symptoms include ataxia and tremor as initial signs, followed by tonic-clonic convulsions prefinally. The myelin deficiency is probably caused by a developmental disturbance of the oligodendrogial cell line. Clinical and pathological findings in the mouse mutant Jimpy show some remarkable similarities to Pelizaeus-Merzbacher disease.
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PMID:[The mouse mutant "Jimpy". Animal model of leukodystrophy]. 91 20

Central activity, antihypertensive action and antiulcerogenic actions of Neurotropin (NSP), an extract isolated from vaccinia virus-innoculated skin or tissues of rabbits were investigated herein. When actions of NSP were examined in isolated muscle preparations by the Magnus-method, peristalsis and ACh-induced contraction in the small intestine isolated from crayfish were not influenced, peristalsis and ACh-induced contraction in the small intestine from mice were slightly accelerated, but adrenaline-induced relaxation in the small intestine from mice was not affected. Histamine-induced contraction in the small intestine and tracheal muscles isolated from guinea pigs was antagonized slightly, or not at all by NSP in a high concentration. NSP had no direct action nor anti-ACh action on abdominal muscles from frogs. NSP had no influence on E1-mice-convulsions. Both spontaneous motor activities and exploratory movements in mice were depressed. Sleeping time induced by hexobarbital-Na was prolonged in mice. Tremorine-induced tremor in mice was inhibited by NSP, while perphenazine-induced catalepsy in rats was not. Normal blood pressure in Wistar rats was not influenced, but high blood pressure in SHR (spontaneously hypertensive rats) decreased close to normal levels after NSP. NSP had antiulcerogenic effects on Takagi's restraint-plus-water-immersing ulcers in rats and histamine-induced duodenal ulcers in guinea pigs, but no influence on Shay ulcers in Wistar rats. From the data obtained herein, it may be concluded that NSP has many central depressant-like activities.
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PMID:[Central activity, antihypertensive action and antiulcerogenic effects of neurotropin]. 103 90

The effects of 5-(4'-chlorobutyl)-picolinic acid (FD-008), a new dopamine beta-hydroxylase inhibitor of fusaric acid derivatives, on the central nervous system in mice and rats were investigated. FD-008 and fusaric acid did not show marked effects on spontaneous movement, convulsion, sleeping time, tremor and conditioned avoidance response but lowered the body temperature of rats at 100 mg/kg p.o. FD-008 potentiated the depressive action of ethanol on conditioned avoidance response in spite of the lack of aldehyde dehydrogenase inhibition. FD-008 markedly depressed the performance on a shuttle box and lowered the body temperature in rats after reserpine treatment at a dose at which FD-008 per se had no effect.
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PMID:Pharmacological action of FD-008, a new dopamine-beta-hydroxylase inhibitor. 117 34

During an experiment of shaking in El mice, a strain which was less susceptible to convulsion was found out. In this strain (ASK), the mortality to anaphylactic shock and susceptibility to audiogenic seizure were compared with five other strains of mice. Six strains of mice (ASK, EL, IDT, JCC-ICR, dd, C57BL/6J) were sensitized by two subcutaneous injections with 2 mg/head of crystalline egg albumin at five and six weeks of age, and then challenged by the intravenous injection of 0.125, 1, 8, 64, 512 and 4096 mug/head at seven weeks of age. In both sexes of ASK strain, the mortality was the maximum (75--95%) after the challenge of 8--4096 mug egg albumin. The mortality of the female El and IDT and the both sexes of JCL-ICR strains was middle (55--70%) after the challenge with 64 mug egg albumin, while that of other strains (dd and C57BL/6J) was very low (0--20%). The susceptibility of 3-weeks-old mice of ASK, El, IDT, JCL-ICR and dd strains was low (1.9--19.0%), whereas mice of DBA/2 strain showed a very high susceptibility (80%) to 110 phons.
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PMID:[A few characteristics of mouse having high sensibility to anaphylatic shock separated from El mouse (author's transl)]. 123 61

The effect of maprotiline (N-methyl-9, 10-ethanoanthracene-9 (10H)-propylamine) on animal behavior was investigated in mice and rats and compared with those of amitriptyline and imipramine. Maprotiline inhibited reserpine hypothermia in mice and tetrabenazine ptosis in rats, while it potentiated the effects of methamphetamine, L-DOPA and apomorphine in mice, in a similar manner to that of amitriptyline and imipramine. Maprotiline was more potent than anitriptyline and imipramine in antagonizing haloperidol-induced catalepsy as well as in suppressing muricide induced by either olfactory bulbectomy or delta-9-tetrahydrocannabinol in rats. Maprotiline potentiated anesthesia induced by thiopental or ether in mice to a lesser degree than did amitriptyline, and failed to counteract the lethal effect of physostigmine or oxotremorine tremor in mice, indicating that this drug has no central anti-cholinergic effect. Maprotiline markedly inhibited hyperemotionality of the rat with either septal lesions or olfactory bulb ablations, suggesting that it does have a tranquilizing effect. Inhibition of conditioned avoidance response of the rat in the shuttle box and reduction of methamphetamine group toxicity with maprotiline were similar to those with amitriptyline. Maprotiline exaggerated pentetrazol convulsion, decreased muscle tone and impaired coordinated motor activity in mice to a much lesser degree than amitriptyline and imipramine. LD50 of maprotiline was approximately twice that of imipramine and three times that of amitriptyline. These results indicate that maprotiline is a new type of antidepressant, has a low toxicity and shares both potent antidepressant and some tranquilizing effect, without possessing central anticholinergic action.
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PMID:[Behavior pharmacology of maprotiline, a new antidepressant]. 124 Aug 30

In mice, DMPS (250 mg/kg, i.v.) combined with diazepam (1.25 mg/kg, i.p.) could increase LD50 of p. o. SCD 5.3 times. DMPS (62.5 mg/kg, i.v.) antagonized completely the respiratory depression and neuromuscular blockade caused by SCD(7.5 mg/kg, i.v.) in rabbits. SCD (15 mg/kg, i.v.) caused tremor, tonic convulsion and the abnormal paroxysmal discharges in EEG in rabbits. DMPS (0.5 mg/kg, i.c.v) could not eliminate the abnormal paroxysmal discharges in EEG of rabbits. DMPS (62.5 mg/kg, i.v.) combined with diazepam (5 mg/kg, i.v.) completely and rapidly antagonize these toxic symptoms and the abnormal changes in EEG.
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PMID:[Antidotal effects of 2,3-dimercaptopropane-1-sulfonate sodium (DMPS) and combined with diazepam on acute poisoning caused by sodium ammonium dimethyl-2-propano-1,3-dithiosulfate monohydrate (SCD)]. 133 78

The mld mutation is a complex genetic lesion affecting the myelin basic protein (MBP) locus in the mouse. The mutation consists of a variety of DNA rearrangements including: tandem duplication of the MBP structural gene, partial inversion of the 3' end of the upstream gene copy, duplication of a region flanking the rearrangement junction in the upstream copy and insertion between the two gene copies of a segment of extraneous DNA not associated with the wild-type MBP locus. The net result of the mutation is a dysfunctional MBP locus. Homozygous mld/mld mice produce very little MBP and consequently very little myelin. They exhibit a clinical phenotype characteristic of hypomyelination (shaking, convulsions). We have discovered a revertant mld mouse which does not exhibit clinical symptoms of hypomyelination. Genetic analysis indicates that the reversion is allelic to mld. We have designated the revertant locus mldr. Restriction analysis of mldr genomic DNA indicates that there is a single intact MBP gene. Analysis of various junction regions using the polymerase chain reaction indicates that the single MBP gene in mldr is derived by recombination from the 5' end of the upstream gene and the 3' end of the downstream gene. Studies on MBP expression in mldr mice indicate that the developmental regulation, level of expression and pattern of post-transcriptional processing of MBP gene products in mldr are similar to wild type. These results indicate that the recombinant MBP gene in mldr is fully functional. From this we infer that the MBP-deficient phenotype of the original mld mutant is attributable to the complex rearrangements in the upstream gene copy which render the locus dysfunctional.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Molecular genetic analysis of the mldr mouse: a spontaneous revertant at the mld locus containing a recombinant myelin basic protein gene. 137 58

The purpose of the present study was to investigate physical dependence upon diazepam systematically in two inbred strains of rats, Lewis (LEW) and Fischer 344 (F344). Rats were chronically fed food containing diazepam on an escalating drug dosage schedule, from 1 and 2 to 12 mg/g of food, over a period of 30 days. During treatment, the growth curve in LEW and F344 rats was suppressed compared with the respective controls. Motor incoordination was evaluated by a rotarod performance test. The ranking of the motor incoordination during the final concentration of diazepam was as follows: F344 greater than LEW. After substitution of normal food for the diazepam-admixed food, various signs of diazepam withdrawal occurred 16-120 h later. These signs included vocalization, irritability, muscle rigidity, ear-twitching, Straub's tail, piloerection, fascicular twitch, tremor, convulsion, and death. The incidences of vocalization, ear-twitching, piloerection, and tremor in F344 were significantly higher than those in LEW rats. Furthermore, two of six F344 rats showed spontaneous convulsions and one rat died of convulsions. Overall withdrawal scores were significantly greater in F344 (16.0) than in LEW (6.3) rats. These results suggest that diazepam withdrawal severity is strongly influenced by genetic factors, and F344 rats are highly susceptible to dependence upon benzodiazepines.
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PMID:Genetic differences in the development of physical dependence upon diazepam in Lewis and Fischer 344 inbred rat strains. 143 78

The cause of the yearly death of an estimated 1,000 to 2,000 migrating dabbling ducks (Anas spp.) and 10 to 50 swans (Cygnus buccinator and C. columbianus) has remained a mystery for the last ten years in Eagle River Flats (ERF), a 1,000 ha estuarine salt marsh near Anchorage, Alaska, used for artillery training by the U.S. Army. We have gathered evidence that the cause of this mortality is the highly toxic, incendiary munition white phosphorus (P4). The symptoms of poisoning we observed in wild ducks included lethargy, repeated drinking, and head shaking and rolling. Death was preceded by convulsions. Farm-reared mallards dosed with white phosphorus showed nearly identical behavioral symptoms to those of wild ducks that became sick in ERF. White phosphorus does not occur in nature but was found in both the sediments where dabbling ducks and swans feed and in the gizzards of all carcasses collected in ERF. We hypothesize that feeding waterfowl are ingesting small particles of the highly toxic, incendiary munition P4 stored in the bottom anoxic sediments of shallow salt marsh ponds.
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PMID:White phosphorus poisoning of waterfowl in an Alaskan salt marsh. 147 72


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