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)

Benzyl chloride (BCl) is used in the manufacture of basic and acidic dyes, pharmaceutical products, resins, and synthetic tannins. BCl is known to have caused liver malfunctions in some workers exposed to 2 ppm BCl vapors. This study was conducted to investigate the effect of BCl on isolated male rat hepatocytes using several toxicity parameters. The hepatocytes were isolated by a collagenase perfusion technique and were incubated in airtight tubes with 1.8 and 3.6 mM BCl in a shaking water bath at 37 degrees C for 10, 30, 60, and 120 min. Throughout the incubation period the cell viability was determined by trypan blue exclusion and leakage of cytosolic enzymes such as lactate dehydrogenase (LDH), aspartate transaminase (AST), and alanine transaminase (ALT). Exposure to BCl resulted in a significant decrease in cell viability as assessed by trypan blue and significant increase in leakage of these enzymes compared to the controls.
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PMID:Effect of benzyl chloride on rat hepatocytes. 319 58

Amiodarone is a powerful anti-arrhythmic drug. However, its use is somewhat limited by side-effects. No study examining side-effects specifically in elderly patients exists. We have reviewed noncardiac side-effects in 61 elderly patients on long-term oral amiodarone treatment (follow-up 3-66 months). The most troublesome side-effect was hypothyroidism (nine patients, 15%). No cases of frank hyperthyroidism were seen. Elevation of aspartate transaminase (AST) was common (16 patients, 26%), but generally mild and transient. Photosensitivity occurred in six patients (10%). Corneal deposits were common but gave rise to symptoms in only one patient. Two patients reported tremor. Hypothyroidism appeared to be more common and photosensitivity less common than in previously reported series in younger adults. Possible reasons for this are discussed. It is our policy to continue to prescribe amiodarone to elderly patients, regulate monitoring for adverse effects is however mandatory.
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PMID:Noncardiac side-effects of long-term oral amiodarone in the elderly. 336 37

Results of clinical and laboratory examination of animals experimentally infected with Taenia saginata eggs are described. At the early stage of infection, increased temperature, cough, muscle shaking and unstable pace were observed. The locomotive disorders disappeared only on day 50 p.i. Leukocytosis and peripheric eosinophilia were found at the early stage of infection. On days 14-28 p.i. the activity of serum creatine-kinase (CK) significantly increased. The activity of other enzymes (AST, ALT, LD, ALP and ALD) examined was increased only slightly and irregularly. The lipid content in blood serum markedly increased on days 9-16 p.i.
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PMID:Contribution to the symptomatology of experimental bovine cysticercosis. 408 25

Electrophysiological and pharmacological analysis of L-Dopa-induced dyskinesia and tardive dyskinesia (L.DD) due to neuroleptics was performed on 12 patients with Parkinson's disease and on 12 others with psychotic diseases. This analysis included the examination of spinal reflexes, monosynaptic H reflex, polysynaptic cutaneous reflex of the lower limb, muscular responses to passive movement [stretch reflex and shortening reaction (SR)] and the study of the motor response to a dopaminergic stimulus (I.V. injection of Piribedil (PBD), a dopamine agonist). There was no difference in EMG activity between L.DD and TD. Three EMG patterns can be distinguished: anarchic discharge pattern (ADA), tonic grouping discharge pattern (AST) and rhythmic burst pattern (ABR). PBD effects indicate a possible relationship between the EMG patterns and the sensitivity level of the motor dopamine receptors. During L-Dopa dyskinesia and tardive dyskinesia, the same changes in spinal reflexes were observed. Muscle tone tested by muscular responses to passive movement (shortening and myotatic reaction) was normal. Monosynaptic excitability explored by H/M ratio was within the normal range. In contrast, the polysynaptic nociceptive reflex was increased in every case. In Parkinsonian patients with L-Dopa dyskinesia, this pattern of the spinal reflexes was significantly different in comparison to the rigid phase. Intravenous infusion of PBD suppressed tremor and provoked the occurrence of dyskinetic activity in Parkinsonian patients with L-Dopa dyskinesia during the rigid phase. During the dyskinetic phase, as in tardive dyskinesia, PBD increases these phenomena and changes EMG activity in rhythmic pattern. It is suggested that L-Dopa dyskinesia and tardive dyskinesia can be determined by testing EMG activity, spinal reflexes and dopaminergic reactivity. There is evidence to suggest that the various types of involuntary abnormal movement represent a single entity, and that dopamine receptor supersensitivity may be involved.
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PMID:[Electrophysiological and pharmacological analysis of L-dopa-induced dyskinesia and tardive dyskinesia (author's transl)]. 611 68

Haematological and serum biochemical measurements in male spontaneously epileptic rats (SER; double mutants homozygous for zitter and tremor genes) were compared with the values for related rat strains. Some haematological values were low in TRM rats and total leukocyte counts were high in ZI and TRM rats. TRM rats showed higher total cholesterol, phospholipid, high-density lipoprotein cholesterol and calcium values, and lower albumin value than Kyo: Wistar rats. Zitter homozygous rats including SER exhibited low total cholesterol, phospholipid and high-density lipoprotein cholesterol values. The SER showed an increase in urea nitrogen, aspartate aminotransferase and alanine aminotransferase values, and a decrease in glucose value, suggesting deterioration of the whole body with age.
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PMID:Haematological and serum biochemical values in spontaneously epileptic male rats and related rat strains. 958 5

We present the first reported study of Ruta graveolens toxicity in 7-8-month-old Nubian goats. Oral administration of 5 g/kg bw per day of R. graveolens leaves caused tremor, dyspnoea, frequent urination, incoordination of movement, ataxia and recumbency, with death after 1-7 days. In goats receiving oral doses of 1 g/kg bw per day of the leaves, the course of toxicity was prolonged and the animals had pallor of the visible mucous membranes and loss in condition; one died on day 17, the others being slaughtered on days 41 and 46. The clinical effects were correlated with pathological changes in various organs, alterations in serum aspartate transaminase, creatine kinase, total protein, cholesterol, urea and other serum constituents, haematological values and the concentrations in the tissues of copper, iron, zinc, manganese, calcium and phosphorus.
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PMID:Preliminary observations on experimental Ruta graveolens toxicosis in Nubian goats. 1216 28

Valproic acid (VPA) is an antiepileptic drug widely used and well-tolerated by most of patients. Its non-dose-dependent side effects seen mostly are the temporary gastrointestinal disturbances including anorexia and nausea, and hepatoxicity. As to its dose-dependent side effects are the weight loss, tremor, skin eruption and the alopecia. In this study we aimed to put forward the biotinidase deficiency considered as a possible cause of alopecia in the rats administered with valproic acid, and the correlation between liver and serum biotinidase enzyme activities (BEA) and transaminases, albumin and serum valproic acid levels. In our study, 4 groups of which one of them was a control group, each consisting of 15 male Wistar rats was organized. 200, 400, and 600 mg/kg/day of VPA, and distilled water, two divided doses per day, were administered per orally to VPA-1, VPA-2, VPA-3, and control group, respectively, in 60 days. Their serum and liver biotinidase enzyme activities, serum AST, ALT, albumin, and valproic acid levels were measured. Alopecia was seen in the subjects of 6.6% of VPA-1, 13.3% of VPA-2, and 26.6% of VPA-3. Significant difference in the liver tissues BEA was noted only between VPA-3 and the control group. Reductions were observed both in the liver tissues BEA and the serum BEA levels, which are inversely proportional to the VPA doses. A positive correlation between the liver biotinidase enzyme activities and the serum valproic acid levels, and the negative correlation between the liver tissues biotinidase activities and the serum valproic acid levels were noted, respectively. As a conclusion, the partial alopecia which is an initial symptom of reduced biotinidase activity may also be created depending on the reduction of biotinidase activity during valproic acid therapy. The alopecia which may further be observed in the patients receiving valproic acid therapy may be prevented by means of administration of biotin in a dose of 10 mg/day.
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PMID:Serum and liver tissue biotinidase enzyme activity in rats which were administrated to valproic acid. 1668 56

A 58-year-old woman complaining of finger tremor was referred to our hospital. The diagnosis of Graves' disease was made based on increased free triiodothyronine (18.88 pg/ml) and free thyroxine (7.47 ng/dl), low TSH (<0.005 microIU/ml) and increased TSH receptor binding antibody activity (70.9%). Serum level of AST (62 U/l) and ALT (93 U/l) were increased and liver biopsy revealed linkage of adjacent portal areas by lymphoplasmacytic infiltrates and fibrosis with piecemeal necrosis. Although antinuclear antibody was negative, these findings indicated that she had autoimmune hepatitis (AIH) according to the criteria of the International Autoimmune Hepatitis Scoring System. Slowly progressive type 1 diabetes mellitus (DM) was confirmed by a diabetic response pattern due to 75 g-oral glucose tolerance test, and seropositivity towards anti-glutamic acid decarboxylase (725 U/ml) and islet cell (80 JDF Units) antibodies. This case exhibited an extremely rare combination of three different autoimmune diseases, including Graves' disease, slowly progressive type 1 DM and AIH, and had no known sensitive human leukocyte antigen (HLA) typing or haplotype for these disorders. Although it is common for patients with Graves' disease to exhibit abnormal liver function, it is important to make an accurate diagnosis of AIH because of this life-threatening disorder.
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PMID:A case of polyglandular autoimmune syndrome type III complicated with autoimmune hepatitis. 1694 65

How to effectively mix small volumes of liquids within microplate wells is a still underestimated and often neglected challenge. The method the authors introduce here relies on violent turbulent motion within a liquid caused by spotting an organic solvent drop onto its surface. The amount needed, less than 1 to 3 microL, is generally small enough not to alter bioactive molecules. Moreover, a solvent may be selected for its compatibility with assay components. The method was tested with layers of aqueous liquids that differ in pH and concentration of a pH-dependent dye, allowing mixing to be monitored optically. Rapid mixing was caused by spotting drops of alcohols, acetone, acetonitrile, and aqueous solutions of these, as long as the difference of surface tension between the drop and the uppermost layer of the bulk liquid surpassed 30 dynes/cm. Along with this difference, position and velocity of spotting, as well as viscosity and geometry of the bulk liquid volume, may influence the turbulence evoked. No significant difference was found for the activity of aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase when measured after mixing by shaking and after mixing by spotting 1 microL of methanol onto assays within 96-well microplates.
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PMID:Turbo-mixing in microplates. 1725 92

Sodium azide poisonings occur very rarely. The mechanism of sodium azide toxic effect has not yet been fully explained. Despite the lack of an explicit procedure for the cases of sodium azide poisonings, in vitro tests and rare case reports suggest that treatment with antidotes for cyanide poisoning victims can be effective. This study describes two cases of suicidal sodium azide ingestion. Case 1. 30-year-old male ingested ca. 180 mg of sodium azide. On admission to hospital, within 4 hours from poisoning, the man complained of dizziness and anxiety. Physical examination revealed horizontal nystagmus, flapping tremor, HR 135/min. In laboratory tests, higher blood concentration of lactates (3 mmol/l) was detected, as well as lower potassium concentration (3.4 mmol/L) and increased transaminase activity (ALT 74 U/l, AST 90 U/l). Electrocardiographic tests showed a negative T wave in limb lead III. Other results were within normal. As the patient ingested a toxic dose of sodium azide, he was treated according to the therapy prescription for cyanide poisoning (amyl nitrite inhalation followed by intravenous administration of sodium nitrite and sodium thiosulphate). ECG record of the last day of hospitalization (7th day of treatment) showed negative T waves in lead III, V4-V6. He was discharged from hospital in good condition. Case 2.23-year-old male ingested 10 g of sodium azide 1.5 hours prior to admission to hospital. At the beginning, the patient's condition was good, but it changed to critical state within the first hours of hospitalization. He developed a deep coma, respiratory and circulatory insufficiency, metabolic acidosis, cardiac dysrrhythmias and anuria. Cardiac activity monitoring showed alternating tachycardia (140 beats per minute) and bradycardia (48 beats per minute), numerous additional supraventricular and ventricular extrasystoles and sinus dysrrhythmia. Cardiac arrest (asystolia) occurred twice, the second incident with fatal outcome. The patient received supportive therapy, he was also treated according to the therapy prescription for cyanide poisoning. Circulatory disturbances observed in both cases have been described in literature as symptoms of sodium azide poisoning. However, available literature data are scarce and lack systematization, most of them coming from several decades ago. The lack of patient's consent for detailed examination of circulatory system and liver made it impossible to gather further knowledge on the subject. The efficacy of treatment with antidotes for cyanide poisoning has not been unequivocally determined for this kind of intoxication.
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PMID:[Sodium azide--clinical course of the poisoning and treatment]. 1772 2


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