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)

Sheets of mucosal epithelial cells were released from guinea pig small intestine after incubation with ethylenediaminetetraacetate. Cells in sheets retained their columnar shape for 24 hr at room temperature, and exclusion of nigrosine suggested they had intact plasma membranes. When sheets were disaggregated individual cells had normal morphology for at least 4 hr. During isolation 16% of the total protein and 24% of the total lactic dehydrogenase were lost from the cells, but subsequent enzyme leakage was low. Leakage increased with shaking, incubation at 37 degrees C, or increasing the oxygen tension of the suspending medium, but was minimal when the Na(+):K(+) ratio in the medium was 8:1 and the osmolarity was high. Losses of particulate enzyme activities were negligible. Respiration was constant for up to 4 hr and was insensitive to calcium, bicarbonate, oxygen tension, and pH. It was inhibited by cyanide and iodoacetate and varied with the Na(+):K(+) ratio of the extracellular fluid and the structural integrity of the cells. All preparations concentrated potassium and excluded sodium, but lost this ability if ouabain was added or cells were broken. Potassium-42 uptake was also sensitive to temperature, ouabain, and structural integrity. The preparations are being used to study cell metabolism in the intestinal epithelium.
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PMID:Studies on epithelial cells isolated from guinea pig small intestine. 500 Jan 70

Duerre, John A. (University of North Dakota, Grand Forks), and Patrick J. Buckley. Pigment production from tryptophan by an Achromobacter species. J. Bacteriol. 90:1686-1691. 1965.-A microorganism was isolated from the soil near the University of North Dakota. Biochemical and morphological characteristics indicated that this organism would best be classified as a member of the family Achromobacteraceae, genus Achromobacter, species unknown. The organism produced a red pigment when grown in a medium containing yeast extract and tryptophan. The pH optimum for pigment production was about 8.0 and the optimal temperature was 25 C. During a study of the nutritional requirements for growth and pigment production, it was found that the organism would grow and produce pigment in a medium containing tryptophan and nucleosides, but the rate of both growth and pigment formation in this medium was slower than that observed with tryptophan and yeast extract. The organism grew well in the presence of acid-hydrolyzed casein and nucleosides without producing pigment, indicating that the pigment is not necessary for growth. Resting-cell experiments definitely established tryptophan as the sole exogenous requirement for pigment production. The pigment was extracted from yeast extract-tryptophan medium with chloroform. Thin layer chromatographic analysis of the crude pigment extracted from this medium revealed the presence of two other pigments in addition to the major red pigment. One of these was a highly fluorescent orange pigment and the other a pink pigment. Only the red pigment was produced by resting cells in the presence of tryptophan alone. This pigment served as an electron acceptor when coupled with formic dehydrogenase, indicating its possible function as an oxidation-reduction pigment. The oxidized pigment had absorption peaks at 506 and 304 mmu. The peak at 506 mmu disappeared upon reduction with sodium sulfite. Shaking the reduced pigment in air proved to be an unsatisfactory method for returning the reduced pigment to the oxidized, colored state.
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PMID:Pigment production from tryptophan by an Achromobacter species. 585 90

In 70-80% of asthmatic patients, an attack of asthma will follow 6-10 min of strenuous exercise. The increase in airway resistance is accompanied by hyperinflation and arterial hypoxemia and makes it difficult to continue or resume exercise. The past 10 yr have seen major advances in the prevention and treatment of exercise-induced asthma (EIA). The beta-sympathomimetic drugs, when administered as aerosols, have been shown to be most effective in reversing the airway obstruction, hyperinflation, and exercise-induced hypoxemia in patients with asthma. When administered as aerosols prior to exercise, the increase in airways resistance, hyperinflation, and hypoxemia are blocked in about 90% of patients. In addition to the sympathomimetic agents, sodium cromoglycate will also ameliorate or prevent EIA in 60-70% of patients. Oral administration of beta-sympathomimetics or methylxanthines is less efficacious in the prevention or treatment of EIA. Delay in absorption from the gastrointestinal tract requires at least 1-2 h before a significant response is observed. Prevention of EIA requires an adequate blood level, possibly because a high concentration of the drug does not reach the airway when the drug is given by the oral route. More importantly, aerosol administration prevents EIA at a fraction of the dose required orally. The side effects, such as nausea, tachycardia, and skeletal muscle tremor commonly observed following oral bronchodilator administration are rare with aerosol therapy.
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PMID:Drugs affecting the respiratory system with particular reference to asthma. 611 44

Administration of thyroliberin (TRH) to reserpinized mice causes tremor and counteracts the hypothermia in a dose-dependent fashion. The thyroliberin response is inhibited by gamma-hydroxybutyric acid (GHB) and baclofen, but not by other, more specific GABA-ergic agents, such as THIP, gamma-acetylenic GABA, and sodium valproate. Picrotoxin neither potentiates nor inhibits the thyroliberin actions. Nor are the thyroliberin effects dependent on cholinergic, monoaminergic or histaminergic mechanisms. The results repudiate a current hypothesis, that the peptide actions may be mediated by GABA-ergic pathways in the brain.
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PMID:Thermic and tremorogenic effects of thyroliberin (TRH) in reserpine-treated mice--the non-involvement of GABA-ergic mechanisms. 611 36

The mutual enhancement of the side effects of muscular tremor and rigidity caused by lithium and neuroleptic drugs should be recognised. However, at present the 'case' for a neuroleptic-lithium interaction producing severe organic brain syndrome is arguably weak; in the absence of standardised sampling for monitoring lithium serum concentrations such reports may simply reflect 'pure' lithium intoxication rather than a drug interaction. Certainly it seems unwarranted in this connection to ascribe specific properties to haloperidol. A potentially high risk of interaction should be recognised between lithium and natriuretic diuretics, and other drugs and therapeutic measures affecting sodium balance. Such interactions may disturb stable treatment monitoring and give rise to the start of self-increasing lithium intoxication. The practical clinical importance of lithium interactions with neuromuscular blocking agents, phenytoin, carbamazepine, iodide salts and methyldopa is only weakly supported by the data available at this time. However, if simple prophylactic measures are available when such drugs are to be used in patients receiving lithium, for example temporary withdrawal of lithium, it may be prudent to take such steps.
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PMID:Lithium and drug interactions. 612 49

The interactions of anaesthetics and other drugs with high pressure suggest that protection against the high pressure neurological syndrome (h.p.n.s.) can no longer be considered in terms of generalized non-specific mechanisms. The evidence from our work shows that anaesthetics may either protect, have no effect, or potentiate h.p.n.s. Structural analogues of the steroid anaesthetic Althesin have a protective effect against high pressure tremors in spite of the fact that they have no anaesthetic effects. Low doses of flurazepam are effective against tremor but can be antagonized by Ro 15-1788, which implies in this case a role for the benzodiazepine receptor complex. Pressure interactions with other drugs have included the classic anticonvulsants--which, in general, were relatively ineffective--and various agents perturbing the balance of specific neurotransmitter systems. Representative examples from different studies include 6-hydroxydopamine, muscimol, and sodium valproate. Finally, the potent protection against h.p.n.s. by 2-amino-phosphonoheptanoic acid, an antagonist with preferential action against excitation produced by aspartate and N-methyl-D-aspartate, provides the first evidence that enhanced excitatory amino acid neurotransmission may have an important role in the h.p.n.s.
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PMID:Specific effects of drugs at pressure: animal investigations. 614 82

Since we have demonstrated that ATPase system was sensitive to chlordecone, it was decided to examine the relationship between physiological and biochemical responses to this neurotoxin. Male Sprague-Dawley rats were fed with chlordecone by gastric intubation at 10, 25 and 50 mg/kg/day for three days. Control rats received 0.3 ml of corn oil. Complete body movements (including tremors) were monitored for a period of 12 hr at 24, 48 and 72 hr after treatment by a piezoelectric crystal attached to the bottom of a plastic rodent cage. The output of the crystal was recorded by a Grass model of EEG machine and magnetic tape. For biochemical study chlordecone treated rats were killed, the brain synaptosomes were prepared and Na+-K+ ATPase, oligomycin-sensitive and insensitive Mg2+ ATPases were determined. Rats receiving chlordecone showed an increased tremor activity which was significant and dose- dependent with a correlation coefficient of the regression line of 0.96. The onset of tremors was evident as early as 2 hr in 50 mg/kg dosed rats. Behavioral abnormalities include startling response to external stimuli like sound, etc. The brain synaptosomal Na+-K+ and oligomycin-sensitive Mg2+ ATPases were significantly decreased in chlordecone treated rats as compared to controls and the decrease was dose-dependent. A linear relationship was observed between the decreases in ATPase activities and physiological (tremor) activity with an r value of 0.96. These results suggest that the inhibition of ATPase system in brain may be related to the production of the neurotoxic symptoms.
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PMID:Acute chlordecone toxicity in rats: a relationship between tremor and ATPase activities. 617 57

From the analysis of 115 cases of primary generalized epilepsies treated for a mean duration of 43 months with sodium valproate as sole therapy, it appears that: the mean effective daily dosage is 21 mg/kg; the efficacy of valproate proved excellent in 82.6% of cases (seizures fully controlled: 74%, seizures occurring exceptionally: 9%); a loss of activity was never observed; in these circumstances of prolonged administration of the drug, no signs of major intolerance were seen; side-effects occurred in 29% of cases, including 20% long-term effects (weight gain, essential tremor); 64 series of laboratory tests including 15 parameters made it possible to evaluate the hematological, hepatic and pancreatic tolerance of valproate: the majority of the tests were normal. The authors believe that during long-term therapy with valproate, monitoring does not need to include the routine performance of liver function tests, but that it would be more advisable, should a suggestive clinical sign be noted, to investigate the platelet count, coagulation (partial activated thromboplastin time) and protein synthesis (fibrinogen).
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PMID:[Monotherapy with sodium valproate in generalized primary epilepsy. 2d phase: Study of long-term efficacy and tolerance]. 619 93

Phosphorylated proteins may play an important role in regulating the metabolism or function of rod photoreceptors. In mammalian retinas, a photoreceptor protein of 33 000 (33K) molecular weight is phosphorylated in a cyclic nucleotide dependent manner in vitro. Since light initiates the activation of a photoreceptor-specific phosphodiesterase and a rapid reduction in guanosine cyclic 3',5'-phosphate concentration, phosphorylation of the 33K protein may be modulated by light in situ. In order to test this possibility, dark-adapted rat retinas were incubated for 30 min in the dark in phosphate-free Kreb's buffer containing [32P]orthophosphate. Following incubation, rod outer segments were detached by shaking, and the 32P-labeled rod outer segment proteins were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, detected by autoradiography, and quantitated by densitometric scanning. The incorporation of radioactivity (32P) into the 33K protein was higher than into any other rod outer segment protein, and the amount of 32P-labeled 33K protein in the detached rod outer segments remained unchanged during 10 additional min of darkness. The addition of isobutylmethylxanthine to the incubation medium enhanced the incorporation of 32P into 33K protein to about 400% of the original level. Exposure of freshly detached rod outer segments to room light for 90 s decreased the amount of labeled 33K protein to 45% of its original level. The dephosphorylation of labeled 33K protein continued, reaching 12% of the original dark value 10 min after the previously illuminated sample was returned to darkness. Light initiated the phosphorylation of rhodopsin, and rhodopsin phosphorylation continued during the postillumination period of darkness.
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PMID:Light-induced dephosphorylation of a 33K protein in rod outer segments of rat retina. 620 20

Nifedipine and verapamil injected into the cerebral ventricles of unanaesthetized cats produced a longlasting rise in the body temperature. The hyperthermic effect of nifedipine and verapamil were not dose-dependent. The hyperthermic effect of verapamil was preceded by a shortlasting fall in the body temperature, which was not dose-dependent. Calcium antagonists, nifedipine and verapamil also produced mydriasis, tachypnoea, dyspnoea, ataxia, tremor and muscular weakness. These symptoms were inconsistent and of slight intensity. In agreement with the theory of ionic set point controlling the body temperature, the most probable explanation is that calcium antagonists, nifedipine and verapamil produced changes in the body temperature by acting on sodium and calcium fluxes in the posterior hypothalamus.
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PMID:[Effects of nifedipine and verapamil on body temperature in cats]. 624 Oct 13


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