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)

The microhardness of the surfaces of BISGMA/TEGDMA-polymers decreased after treatment with pork liver esterase for 48 h in concentrations greater than or equal to 0.05 U/ml. This softening effect on BISGMA/TEGDMA-polymer surfaces was also shown as an increased wear rate of the polymers in the presence of esterase measured by a laboratory abrasion method. In this method, polymer cylinders were vigorously shaken in an aqueous slurry containing abrasive particles. The shaking was performed for 3 s followed by a rest period of either 100 or 200 s. This was repeated for 24 h. A greater mean loss of weight of the cylinders was measured when esterase was present in the slurry and the loss of weight increased significantly from 6.7% to 23.8% (P less than 0.001) when the rest period was increased from 100 s to 200 s. The results indicate that enzymatic hydrolytic activity in the mouth will contribute to a breakdown of composite resin fillings.
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PMID:Enzymatic degradation of BISGMA/TEGDMA-polymers causing decreased microhardness and greater wear in vitro. 214 61

The cholinomimetic activities of the antidepressant drug minaprine have been investigated, in vitro and in vivo, in rodents. Minaprine, and its metabolite SR 95070B [3-(2-morpholinoethylamino)-4-methyl-6-(2-hydroxyphenyl) pyridazine hydrochloride] selectively displaced [3H]-pirenzepine from its cortical and hippocampal binding sites, and only weakly inhibited the binding of [3H]-N-methylscopolamine in either the rat cerebellum, heart and salivary glands, or the guinea-pig ileum. In mice, none of these drugs induced the typical cholinergic side-effects up to lethal doses. Minaprine and SR 95070B antagonized rotations induced by an intrastriatal injection of pirenzepine in mice, after intraperitoneal and/or oral administration. Minaprine also antagonized atropine-induced mydriasis in mice. Both minaprine and SR 95070B potentiated the tremorigenic effect of oxotremorine without inducing tremor when injected alone. Finally, minaprine and SR 95070B, after parenteral and/or oral injection, antagonized the scopolamine-induced deficit in passive avoidance learning, and enhanced short-term retention in the social memory test, in rats. The muscarinic agonists arecoline, oxotremorine and RS 86 [2-ethyl-8-methyl-2,8 diazaspiro-4,5 decan-1,3 dion hydrobromide], as well as the acetylcholine esterase inhibitors physostigmine and tacrine were active in most of these models. These results indicate that minaprine, and its metabolite SR 95070B, have cholinomimetic activities which could be, at least in part, mediated by their selective affinity for M1 muscarinic receptors. Thus minaprine could represent a potential useful drug for the treatment of senile dementias and cognitive impairments occurring in elderly people.
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PMID:Cholinomimetic activities of minaprine. 258 34

Alaproclate (10-60 mg/kg) injected i.p. into male mice potentiated and prolonged the oxotremorine and physostigmine-induced tremor in a dose-dependent manner. Atropine completely blocked the tremor caused by oxotremorine or physostigmine both in the presence and absence of alaproclate. Pretreatment with the 5-HT receptor antagonist metitepine completely blocked the enhancement of oxotremorine-induced tremor caused by alaproclate. Biochemical studies indicated that the above effects cannot be explained by assuming that alaproclate a) acts as a cholinergic agonist, b) inhibits the acetylcholine esterase, c) interferes with choline uptake or acetylcholine synthesis, or d) directly potentiates the release of acetylcholine. In ligand binding studies alaproclate was found to be a weak competitive inhibitor of muscarinic antagonist binding to membranes from the rat cerebral cortex, rat striatum, human cerebral cortex and human striatum. (Ki approximately 28-40 microM in all four tissues). The present results suggest that alaproclate may potentiate muscarinic responses by a mechanism involving serotonergic receptor mechanisms rather than by a direct interaction with the muscarinic cholinergic receptors.
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PMID:In vivo and in vitro studies on the potentiation of muscarinic receptor stimulation by alaproclate, a selective 5-HT uptake blocker. 298 30

Tri-o-cresyl phosphate (TOCP), which produces a delayed neurotoxic syndrome in humans and some animal species, was given to Fischer 344 (F344) male (18 week old) rats to determine if it causes biochemical, sensorimotor, and neuropathological effects. Animals were given TOCP by gavage in doses ranging from 10 to 100 mg of TOCP/kg daily for a period of 63 days. The rats were subjected to a series of neurobehavioral tests including fore- and hindlimb grip strength, motor activity, tremor, and latency to respond to a thermal stimulus. Central and peripheral nervous tissues were examined for damage characteristic of organophosphorous compound-induced delayed neurotoxicity (OPIDN). Brain neurotoxic esterase and acetylcholinesterase activities were inhibited in a dose-dependent fashion. A group of three chickens treated with 100 mg of TOCP/kg/day for 18 days was included as the positive control for enzymatic and histopathological alterations associated with OPIDN. Rats showed no consistent neurobehavioral changes or evidence of neuropathological damage in nervous tissues associated with treatment. In contrast, chickens treated with TOCP developed delayed neurotoxicity characterized by ataxia, which progressed to paralysis. These neurological changes included swelling, fragmentation, and degeneration of the axon and myelin in both central and peripheral nervous tissues. This study concludes that the F344 rat is not sensitive to the delayed neurotoxic effects of TOCP. When studying OPIDN in rats, care must be exercised in choosing the experimental animal since some strains, e.g., F344, are not sensitive.
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PMID:Lack of delayed neurotoxic effect after tri-o-cresyl phosphate treatment in male Fischer 344 rats: biochemical, neurobehavioral, and neuropathological studies. 335 6

The dose-effect of oxotremorine upon the onset, duration and magnitude of tremor and salivation was studied in both mice and rats. The threshold doses of oxotremorine (SC) for eliciting tremor were above 50 micrograms/kg in mice and above 150 micrograms/kg in rats and the threshold doses for eliciting salivation were above 75 micrograms/kg in mice and above 200 micrograms/kg in rats. Alaproclate, a nontricyclic 5-HT uptake inhibitor, when injected 30 min prior to the administration of the cholinergic agonist, produced a dose-dependent enhancement of tremor and salivation in both rats and mice. Alaproclate itself did not produce these effects in the absence of a muscarinic cholinergic stimulant such as oxotremorine, arecoline or the acetylcholine esterase inhibitor physostigmine. Both salivation and tremor could be fully blocked by atropine at any dose of the cholinergic stimulant and of alaproclate used. The potentiating effects of alaproclate on salivation and tremor could also be blocked by two serotonin receptor antagonists, metitepine and danitracen, but not by metergoline or cinanserin. Other compounds which inhibit the uptake of 5-HT such as fluoxetine, citalopram, norzimeldine, zimeldine and the non-tricyclic antidepressant, iprindol, did not enhance the cholinergic agonist induced tremor or salivation under the same conditions as did alaproclate. It is suggested that alaproclate exerts the potentiating effect at a hitherto undefined serotonergic receptor site.
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PMID:Serotonergic potentiation of muscarinic agonist evoked tremor and salivation in rat and mouse. 392 96

Many of the interesting functions of human lymphocytes in vitro are known or suspected to be dependent on the presence of monocytes. A practical limiting factor in cell interaction experiments is the ability to separate and recover functional monocytes and lymphocytes rapidly from the same blood specimens. Here we describe a simple, rapid and inexpensive solution to this problem. Incubation at 37 degrees C on Sephadex G-10 columns consistently depleted monocytes to low levels (less than 0.1%) and gave maximum lymphocyte yields (greater than 60%) in a short time. Half the esterase-positive monocytes entering the column may be easily recovered from the beads by a 4 degrees C chilling/shaking technique; by using 0.5% lidocaine, an additional 15% can be recovered. Simultaneously, the G-10-nonadherent lymphocytes are being further separated into T and B cells by E-rosetting. These recovered G-10-adherent cells were above 90% esterase positive, and showed a cell size distribution on the Coulter channelyzer distinctly larger than nonadherent lymphocytes. To illustrate the use of this protocol we present a monocyte titration experiment which demonstrated a plateau of optimal pokeweed mitogen-stimulated Ig production at 5-10% monocytes.
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PMID:Rapid separation of human monocytes and lymphocytes by Sephadex G-10. 660 98

Behavioural changes of medaka (Oryzias latipes) treated with an anticholinesterase insecticide, diazinon (0.1 mg L(-1)), were continuously observed for 4 days in semi-natural conditions. Although variations occurred in individual specimens, the movement tracks appeared differently with typical short-range movement with irregular turns and shaking after the treatments. Eight movement patterns frequently observed before and after the treatments were selected, and the variables characterising the movement patterns were compared quantitatively. The variables were clearly differentiated when the movement patterns were correspondingly matched before and after the treatments (e.g., vertical movements, horizontal movements, etc). Meander and stop duration were highly different among the selected movement patterns. Additionally, different degree of toxic response behaviours could also be detected by quantitative characterisation of the variables. Response behaviour was confirmed with toxicological experiments that show the decrease in the acetylcholine esterase activity in the head and body of specimens. Quantitative investigations on the variables of the movement tracks suggested the usefulness of response behaviour as a monitoring tool for environmental assessment.
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PMID:Movement behaviour of Medaka (Oryzias latipes) in response to sublethal treatments of diazinon and cholinesterase activity in semi-natural conditions. 1573 72

Organophosphates, such as the nerve gas soman, cause inhibition of acetylcholine esterase, accumulation of acetylcholine in synaptic clefts, and excessive activation of cholinergic receptors, causing central nervous symptoms such as tremor and seizures. Soman-poisoned animals have low brain levels of ATP, indicating that energy demand is greater than energy supply. We investigated whether soman poisoning is accompanied by an increased brain metabolism of glucose, as can be inferred from the accumulation of radiolabeled 2-deoxyglucose found in previous studies, or whether soman poisoning entails impairment of cerebral energy metabolism. We performed 13C nuclear magnetic resonance spectroscopy on brain extracts from soman-poisoned mice (160 microg/kg; 1 LD50) that had been dosed with 13C-labeled glucose or pyruvate intravenously. Formation of 13C-labeled glutamate, GABA and glutamine from [1-(13)C]glucose was reduced by approximately 30% in awake, soman-intoxicated animals, but formation of these amino acids from [3-(13)C]pyruvate was not different in soman-intoxicated animals and controls. These results suggest that soman intoxication entails inhibition of glycolysis, but not of tricarboxylic acid cycle activity in the brain. However, when brain metabolism was depressed by a sedative dose of diazepam (5 mg/kg) soman intoxication caused increased metabolism of 13C-labeled glucose. The latter finding shows that the soman-poisoned brain has a high energy requirement even during anticonvulsant therapy. We conclude that metabolic inhibition, as seen in awake, soman-intoxicated animals, may lower seizure threshold and contribute to soman-related neurodegeneration and lethality.
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PMID:Cerebral metabolism of glucose and pyruvate in soman poisoning. A 13C nuclear magnetic resonance spectroscopic study. 1708 95

The present study deals with the isolation of fungi from soil with the ability to degrade polyurethane (PU). A pure fungal isolate was analyzed for its ability to utilize PU as a sole carbon source in shaking culture for 30 days. Incubation of PU with Aspergillus flavus resulted in 60.6% reduction in weight of PU. The scanning electron microscopy and Fourier transform infrared spectroscopy (FTIR) results showed certain changes on the surface of PU film and formation of some new intermediate products after polymer breakdown. Thermogravimetric curves showed changes between the thermal behavior of the samples that were inoculated with A. flavus and control. FTIR spectra showed detectable changes in control and incubated samples, suggesting that degradation occurs, with the decreased intensity of band at 1,715 cm(-1), corresponding to ester linkages. We have identified an extracellular esterase activity which might be responsible for the polyurethanolytic activity.
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PMID:Degradation of polyurethane by Aspergillus flavus (ITCC 6051) isolated from soil. 2236 37

In the present study, we report on enzyme-assisted formation of biomineralized amorphous calcium phosphate nanocomposites (ACP-NCs). About 100-200 nm sizes of the spherical porous enzyme-assisted ACP-NCs were successfully synthesized via double reverse microemulsion, but no ACP-NCs formed without the enzyme. It is believed that the enzyme was used as an organic template or additive that could regulate the biomineralization process. The enzyme-assisted ACP-NCs were well characterized by X-ray diffraction, transmission electron microscopy, scanning electron microscopy, dynamic light scattering, and Brunauer-Emmett-Teller (BET) criteria. The BET surface area, total pore volume, pore size from adsorption, and pore size from desorption of the ACP-NCs were 163 m(2) g(-1) or 0.37 cm(3) g(-1), 8.87 nm, and 7.48 nm, respectively. The enzyme-assisted ACP-NCs retained about 43% of the catalytic activity of free carboxyl esterase. Furthermore, they preserved their bioactivity even after the 10th reuse and were stable over 10 days even under a stringent shaking conditions. The reported method paves the way for novel biomineralization via enzyme molecules to form functional enzymes containing nanocomposites.
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PMID:New functional amorphous calcium phosphate nanocomposites by enzyme-assisted biomineralization. 2327 34


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