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 effects of clomipramine HCl (15 mg kg-1 i.p.) on behaviour, body temperature and brain amines were investigated in rats that had been chronically treated twice daily with increasing doses of delta 9-tetrahydrocannabinol (delta 9-THC, 2-6 mg kg-1 i.v.). delta 9-THC produced a biphasic change in behaviour, stimulation followed by depression, and a pronounced hypothermia. Tolerance developed rapidly to these effects of delta 9-THC. Chronic treatment with delta 9-THC reduced the levels of homovanillic acid, 5-hydroxytryptamine and noradrenaline. The level of dopamine was not altered with chronic treatment and tolerance appeared to develop to the increased levels of 5-hydroxyindoleacetic acid induced by delta 9-THC. Injection of clomipramine, 12-14 h after 2, 5 or 10 days of delta 9-THC treatment induced characteristic changes in the rats behaviour which consisted of writhes, backward kicking, wet shakes, jumps ataxia and front paw and whole body tremor. The severity of the behavioural changes appeared to be dependent on the period of delta 9-THC administration and they were not accompanied by a change in body temperature or consistent changes in brain amines or metabolites. The results indicate that physical dependence on delta 9-THC may occur since clomipramine is able to precipitate changes in behaviour, indicative on an abstinence syndrome, in rats chronically treated with delta 9-THC. It is suggested that tryptaminergic mechanisms are altered during chronic delta 9-THC treatment and that clomipramine induces the behavioural changes by interacting with an altered tryptaminergic system.
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PMID:Time-course of the effects of chronic delta 9-tetrahydrocannabinol on behaviour, body temperature, brain amines and withdrawal-like behaviour in the rat. 612 98

A series of phenylethanolamine derivatives were examined with respect to their bronchospasmolytic effect and their ability to depress the contractions of the soleus muscle in cat and guinea-pig. One group of compounds including D2343 (1-(4-hydroxyphenyl)-2-[1,1-dimethyl-3-(2-methoxyphenyl) propylamino]-ethanol HCl), a new beta 2-adrenoceptor agonist, appeared to be more effective in combating bronchospasm induced by histamine than in depressing the contractions of the soleus muscle in anaesthetized cat. This difference disappeared when serotonin was used to induce bronchospasm. Terbutaline antagonized histamine and serotonin equally well. Experiments in vivo and in vitro with guinea-pigs gave ambiguous results. Slowly developing effects was a common feature of the compounds showing the apparent effect separation. None of the available beta-adrenoceptor agonists appears to distinguish between the adrenoceptors in the airway smooth muscle mediating bronchial relaxation and those in the skeletal muscle associated with tremor.
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PMID:Some problems encountered in the evaluation of new bronchodilating beta-adrenoceptor agonists. 612 71

The frozen tissue was sliced and then homogenized at 20 degree C in LiCl, 2 M; lauryl-trimethyl ammonium chloride (K & K No. 4484), 5%; pronase, B grade (calbiochem), 1 mg/ml and Tris-HCl 10 mM pH 7.5. The homogenate was left to stand 15 min at 20 degree C with occasional shaking. After centrifugation at 35 000 X g for 30 min at 0 degree C, the supernatant containing the crude DNA was purified by filtration on Ultrogel A 2 (LKB, Sweden). The Ultrogel A 2 column (2.5 X 45 cm) was equilibrated with a solution containing NaCl 2 M, EDTA 2.5 mM, Tris-HCl 10 mM pH 7.5. The flow rate was 3 ml cm-2 h-1. Five ml of the supernatant were placed on the column. The first peak contained highly polymerized (as demonstrated by ultracentrifugation) pure DNA (A260/A230 = 3.19; A260/A280 = 1.82). The yield was 2.26 mg of DNA/g of fresh liver.
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PMID:[Simple method for preparation of rat liver DNA]. 617 Dec 20

New oxidimetric titrants, bromamine T, dibromohydantoin, N-bromophthalimide, and N-bromosuccinimide, were applied to the determination of ephedrine.HCl, norephedrine.HCl, and methyldopa. Direct potentiometric and visual indicator titration methods as well as back-titration procedures have been developed for their determination. Oxidation of ephedrine and norephedrine produces benzaldehyde, which is extracted from pH 11.0 phosphate buffer with ether or hexane and determined spectrophotometrically at 242 nm. Beer's law is obeyed in the concentration range from 0.2 to 2 mg ephedrine.HCl and from 0.15 to 1.9 mg norephedrine.HCl. Methyldopa is determined titrimetrically and spectrophotometrically. In addition, this drug acts as a self-indicator: Solutions change from colorless to red, which gradually disappears with continuous addition of brominating agent and shaking. Phosphate buffer is used to produce adrenochrome, characterized by its pink color which can be measured at 485 nm in a working range from 40 to 650 micrograms.
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PMID:Spectrophotometric and titrimetric determination of certain adrenergic drugs, using organic brominating agents. 675 41

Sulfonamide drugs are extracted from feed and feed premixes by shaking with 0.15N HCl in 25% methanol. The extract is diluted, clarified, and chromatographed on a reverse phase C18 column. Mobile phases used are methanol-2% acetic acid (35 + 65) and acetonitrile-2% acetic acid (18 + 82) for sulfamethazine (SMT) and sulfathiazole (STZ), respectively. A solution of dimethylaminobenzaldehyde (DMAB) is added to the column eluate and the resulting sulfonamide-DMAB complex is detected at 450 nm. The method was tested for linearity, recovery, and precision across a broad sample range. Recovery was 100.6 +/- 2.3% and 96.3 +/- 1.6% for STZ and SMT, respectively. Linearity was excellent (r2 = 0.9985 for STZ and r2 = 0.9996 for SMT) as was within-day precision (RSD = 2.00% for STZ and 1.52% for SMT). The method was compared with the Bratton-Marshall colorimetric method. Analysis of 14 STZ and 15 SMT samples failed to detect any bias between the 2 methods. Some practical aspects of the use of this technique are discussed.
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PMID:Use of post-column derivatization in liquid chromatographic determination of sulfamethazine and sulfathiazole in feeds and feed premixes. 711 88

Progressive difficulty in handwriting due to jerking movements precipitated by the act of writing beginning between the ages of 8 to 54 is reported in six patients. There was no rest tremor, but three had mild postural tremor. Specific muscle activity (especially pronation of the wrist or abduction of the fingers) elicited the tremors that persisted as long as the evocative posture or muscle activity was maintained. None had a family history of tremors, but two had a history suggestive of hypoxia at birth. Unlike benign essential tremor, the movements did not respond to propranolol HCl, but most patients were benefited both acutely and chronically by centrally active anticholinergic agents.
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PMID:Primary writing tremor: a selective action tremor. 719 47

1. Two types of nylon-6 supports (small cylinders and a sponge-like derivative) were prepared for immobilizing enzymes. Nylon-6 beads were solubilized by immersion in 80% formic acid and then reprecipitated using two different types of non-solvent solutions (distilled water or a 1:1 acetone:water solution) giving rise to a sponge-like derivative and to a colloidal suspension, respectively. The latter was molded into a thin thread which was cut into small cylinders. 2. Trypsin (EC 3.4.21.4) was covalently bound to glutaraldehyde-activated nylon-6 cylinders as well as to the sponge-like derivative. The maximum (100%) apparent initial enzymatic activity was found for the trypsin bound to small cylinders, while the initial activity of trypsin bound to the sponge-like material was 61% in comparison with that of trypsin-small cylinders, under the same conditions of enzyme immobilization reaction (1 g of nylon support and 5 ml of 1.3 mg/ml trypsin in 0.1 M sodium phosphate buffer, pH 8.5, at 10 degrees C for 18 h) and of enzymatic reaction (1 g of trypsin-nylon in a batch reactor, 2 ml of 0.7% w/v azocasein solution in 50 mM borate buffer, pH 8.5, at 37 degrees C, with shaking, for 1 h). However, the decrease of activity after enzyme immobilization was more conspicuous for the trypsin-small cylinders than for the trypsin-sponge. The former retained approximately 25% of its initial activity, while the latter retained approximately 67% of its initial activity, after seven cycles of utilization for 1 h, pH 8.5, at 37 degrees C and 8 days of storage, pH 8.5, at 4 degrees C in the presence of azocasein. 3. Scanning electron microscopy was performed to visualize the surface of the support after each step of the immobilization process. The electron micrographs show that the two types of nylon supports had a rough surface, which became rougher and full of craters after treatment with 5 N HCl. On the other hand, the partially hydrolyzed nylon surface acquired the appearance of Swiss cheese after treatment with 2.5% glutaraldehyde. After reaction with the enzyme molecules the surface became rougher again.
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PMID:Nylon-6 cylinders and a sponge-like derivative as supports for immobilizing trypsin. 787 18

A field study of 239 horses was conducted to determine the efficacy and safety of clenbuterol HCl, a beta 2-adrenergic bronchodilator, when administered incrementally to effect in the treatment of chronic obstructive pulmonary disease (COPD). The severity of COPD (heaves) and response to treatment was determined by clinical evaluation; an overall 'heaveiness rating' (OHR) was assigned at each observation. The horses were treated orally b.i.d. with clenbuterol (as Ventipulmin Syrup), beginning with the lowest dosage of 0.8 micrograms/kg. On day 10 of treatment at the effective dose (0.8, 1.6, 2.4 or 3.2 micrograms/kg), treatment was either withdrawn (Schedule A) or continued for an additional 20 days (Schedule B). Horses on Schedule A demonstrated a significant improvement in the mean OHR on treatment Day 10 compared to the baseline overall heaveiness rating (BOHR) and a significant increase in the mean OHR (relapse) after the drug was withdrawn. Schedule B horses showed significant improvement (compared to BOHR) on treatment Days 10, 20 and 30. Incremental dosing with clenbuterol provided clinical improvement in 75% of the horses with a lower 95% confidence limit of 71%. Twenty-five percent were nonresponders. A greater percentage of the more severely affected horses required the 3.2 micrograms/kg dosage or were nonresponders compared to horses with a lower BOHR. Side effects of sweating, muscle tremor, and nervousness were of low intensity (mild to moderate) and frequency (< 7% of all observations) due to the regimen of incremental dosing to effect.
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PMID:Clinical efficacy and safety of clenbuterol HCl when administered to effect in horses with chronic obstructive pulmonary disease (COPD). 857 91

We report a right-handed 78-year-old man with early onset parkinsonism. The patient had an onset of micrographia at 23 years of the age in 1939. Seven years later he started to drag his right foot, and at 38 years of age, he walked with small steps with festination. Tremor was also present in his right hand. His daily life was independent as a otorhinolaryngologist. He visited our clinic on March 24, 1977 when he was mentally sound and showed mild parkinsonism consisting of masked face, stooped posture, small step gait, bradykinesia, and right side dominant rigidity and tremor. He showed good response to trihexyphenidyl and amantadine HCl. Two month later, he developed dyskinesia and some worsening of parkinsonism, and was admitted to our hospital for the first time. He was treated with 400 to 600 mg/day of levodopa/ carbidopa. He showed marked improvement, however, dyskinesia remained in his mouth. He was doing well until 77 years of age (June of 1993) when he developed hallucination and motor fluctuations. He was admitted again to our hospital on June 22, 1993. On admission, he was alert and appeared mentally sound. However, Hasegawa dementia scale was 18/30. Upward gaze was slightly restricted (3/5). Voice was somewhat small but no masking was noted. His posture was stooped and the gait was of small step. Dyskinesia was noted during walk. No rigidity nor tremor was noted. Deep tendon reflexes were lost but no sensory loss or motor weakness was noted. Routine laboratory studies were unremarkable. A cranial CT scan revealed only mild to moderate cortical atrophy. Motor and sensory conduction velocities were within normal limits, however, motor action potentials could not be obtained with stimulation to the right common peroneal nerve. He was treated with 600 mg/day of levodopa with carbidopa, 100 mg of amantadine HCl, 300 mg of Dops, and 25 mg of tiapride. He continued to show motor fluctuations, and was discharged on July 23, 1993. Since then his motor functions had become progressively worse with frequent falls, but he was still able to walk without support. On October 3 of 1994, he went to bed as usual. On the next morning, he was found dead in his bed at 9: 30. The patient was discussed in neurological CPC, and the chief discussant arrived at the conclusion that the patient had young-onset Parkinson's disease with Lewy bodies in the substantia nigra. Opinions were divided between Parkinson's disease and Lewy body negative young onset parkinsonism. Postmortem examination revealed obstruction of the trachea by aspirated foods, and the cause of death appeared to have been suffocation by the foods. Macroscopically, the external appearance of the brain was unremarkable except for slight frontal atrophy. The substantia nigra showed depigmentation in the lateral part, but the pigmentation of the medial part was well preserved. Upon histologic examination, the number of pigmented neurons in the dorsomedial part was well preserved. In the lateral part, pigmented neurons were well preserved in the dorsal area, however, in the ventral area, only non-pigmented neurons were seen; they appeared to be neurons in the pars reticulata. No gliosis was seen in any of the nigral areas. No Lewy bodies were seen in the remaining neurons. So-called immature neurons with rounded shape without neuromelanin could not be detected. The locus coeruleus neurons were well preserved. The putamen and the other basal ganglia structures were also intact. Slight myelin pallor was noted in the subcortical white matter, however, otherwise cerebral cortices were normal. The histology of this patient is unique in that only the ventrolateral part of the substantia nigra showed abnormal finding consisting of lack of pigmented neurons without gliosis. It is not clear whether the nigral change represents degeneration or a congenital "hypoplasia'. To our knowledge, such a unique pathology of the substantia nigra has not been reported in the literature. Our patient ma
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PMID:[A 78-year-old man with young onset parkinsonism and sudden death]. 867 9

An autopsy case of pure akinesia (PA) is reported. The patient manifested L-dopa-unresponsive akinesia without accompanying rigidity, tremor, eye movement disorder or dementia from the age of 58 years. Brain magnetic resonance T2-weighted imaging at the age of 63 showed high intensity areas in the subthalamic regions, but brain atrophy was not observed. She received amantadine-HCl and L-threo-3,4-dihydroxyphenylserine (L-DOPS) for 5 years. At the age of 66, she died of the severe illness accompanied by consciousness disturbances, hyperthermia, muscle rigidity, abnormal blood pressure and elevated serum enzymes which were derived from the muscle. We considered her condition to be neuroleptic malignant syndrome (NMS). Pathologically the brain revealed degeneration in the subthalamic nucleus, globus pallidus and substantia nigra. Neurofibrillary tangles were detected in the temporal cortex, hippocampus, amygdaloid body and spinal cord, as well as in the basal ganglia, thalamus and brain stem. These findings were consistent with that of progressive supranuclear palsy (PSP); the change in the ventral pons was insignificant, suggesting that PA may have minimum involvement in the ventral pons. The skeletal muscle showed scattered necrosis that was compatible with NMS. As far as we know, this is the first report of NMS accompanied with PA.
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PMID:Pure akinesia manifested neuroleptic malignant syndrome: a clinical variant of progressive supranuclear palsy. 908 64


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