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)

1. Increasing the concentration of dissolved urate promotes the crystallization of calcium oxalate from urine. The possibility was investigated that this effect may be caused by heterogeneous nucleation of calcium oxalate by particles of crystalline urate. 2. Urine samples were collected from 10 healthy men, centrifuged and filtered, and a solution of sodium urate was added to increase the medium urate concentration from 2.2 to 5.6 mmol/l. Calcium oxalate crystallization was induced by the addition of oxalate, followed by incubation for 90 min in a shaking waterbath at 37 degrees C. The crystalline material was filtered out and the urate concentration was determined in the filtrate. 3. No difference in the urate concentration before and after induction of calcium oxalate crystallization was observed. These findings were confirmed by infra-red spectroscopy, X-ray powder diffraction and ultraviolet wet chemical analysis with detection limits of 5-10, 1.0 and 0.055%, respectively; urate was not detected in the calcium oxalate crystals. 4. In addition, three urine samples were collected and passed through 10 kDa ultrafiltration membranes to remove any colloidal particles which might have been present. The urate concentration was increased and an oxalate load was added as before, prior to incubation at 37 degrees C in a shaking water bath for 5 min, followed by passage through 10 kDa ultrafiltration membranes. Scanning electron microscopy revealed no particles on the membranes thereby indicating that colloidal or crystalline urate was not formed early in the crystallization experiments.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dissolved urate promotes calcium oxalate crystallization: epitaxy is not the cause. 840 2

An improved method for isolation of human and Rhesus monkey band-3 separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) is described. Purified band-3 was obtained from human hemoglobin-free ghosts (Hb-free ghosts) after SDS-PAGE by chemical elution+sonication (CE+S). The section of the gel corresponding to the antigen was cut out, mechanically disrupted and incubated in 1% NaHCO3 containing 1% SDS, for 2 h, with shaking, at room temperature, followed by overnight incubation at 4 degrees C. The preparation was subsequently sonicated and clarified by centrifugation. Supernatants were dialyzed against distilled water, their protein contents were measured, and the presence of purified band-3 was demonstrated by SDS-PAGE. A calibration curve was developed for assay of CE+S material using densitometric evaluation of the protein profile on SDS-PAGE. An amount of 37.5 mg of Hb-free ghosts gave 3.15 mg of purified band-3 after CE+S, corresponding to an 8.4% yield. Rabbits were immunized with 50 micrograms CE+S antigen. Sera were collected and assayed by Western blot analysis against its proteolytic fragments, which were obtained from packed red blood cells by treatment with protease type VI from Streptomyces griseus (1 h at 37 degrees C), followed by extensive washing and hypotonic lysis. Specific antibodies recognized band-3 and its proteolytic fragments 60 and 63 kDa in human ghosts obtained from different blood donors, confirming the genetic polymorphism. Analogous serum obtained against the Rhesus monkey band-3 proteolytic fragment 63 kDa recognized the human antigen and its respective fragments. These results indicate the existence of similarities between these two species of band-3, suggesting the potential use of this technique in taxonomic and phylogenetic studies. Purification by CE+S is an efficient and rapid method for isolation of band-3 and its fragments with satisfactory yields and maintenance of both their immunogenic and antigenic properties.
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PMID:An improved method for the isolation of erythrocyte antigen band-3. 858 Aug 81

To observe the incidence of complications in severely hyponatraemic hospitalized patients and relate outcome to rate of correction, all patients admitted to a tertiary referral hospital in New York City, USA or a group of hospitals in Oxford, UK with a sodium < or = 120 mmol/l were studied. Review of the notes and prospective evaluation were used to ascertain cause of hyponatraemia, method of management and outcome. There were 84 episodes in New York and 100 in Oxford, over 9.5 months and one year, respectively; 79% had chronic hyponatraemia ( > 3 days duration). During hyponatraemia, 76% of patients had clouding of consciousness with 11% in coma. Other hyponatraemic complications included long track signs (including hemiparesis) (6.0%), seizures (3.3%), hallucinations (0.5%), tremor (1.0%), intellectual impairment without clouding of consciousness (0.5%), and acute psychosis (0.5%). 4.3% died as a direct result of their electrolyte disturbance. After correction, central pontine myelinolysis (0.5%), post-correction seizures (1.0%), intellectual impairment (2.2%), tremor (0.5%), paraesthesiae (0.5%), and striatal syndrome (0.5%) were observed. Correction of hyponatraemia was started in 158 patients, and the mean maximum rate of correction in 24 h was 8.4 mmol/l (SD 5.6, range 2-42). The maximum rate of correction was higher in those who developed neurological sequelae (12.1 mmol/l/24 h vs. 8.2 mmol/l/24 h; p = 0.0125, t-test, separate variance, two-tail). Neurological sequelae were associated with faster rates of correction, and correction of chronic severe hyponatraemia should be < 10 mmol/l in 24 h.
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PMID:Severe hyponatraemia: complications and treatment. 859 51

In microscopic sections of the rodent brain the dorsal fascia dentata frequently shows perineuronal swelling and neuronal swelling and shrinkage. Factors influencing the occurrence of such changes, which may mimic excitotoxic effects, have been examined using various schedules of anaesthesia and perfusion fixation. Laboratory mice anaesthetized with a low dose of sodium pentobarbital manifested prolonged excitation in comparison to those anaesthetized with a high dose: the occurrence of tremor and convulsions, however, was not related to the morphological changes in the fascia dentata. The changes were diminished by increasing the perfusion pressure (from 80 to 120 mmHg), by reducing the duration of the wash-out period with buffer (from 45 to 15 seconds) and by prolonging the perfusion time (from 7 to 15 minutes). They were abolished when 5% solution of glutaraldehyde was used instead of a 2.5%. The results show that the quality of brain fixation may be best assessed according to the morphology of the dorsal fascia dentata, and that the occurrence of acute swelling and shrinkage in this area should not be mistaken for pathological changes.
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PMID:The dorsal fascia dentata as a probe of fixation quality in the rodent brain. 859 47

1. The neuroleptic malignant syndrome (NMS) may occur, occasionally, in Parkinson's disease (PD) after withdrawal of antiparkinsonian drugs. However, the circumstances in which the NMS occurs and the pathophysiologic mechanisms remain uncertain. 2. The authors studied a woman with PD, who developed hyperthermia, increased muscular tone, tremor, signs of autonomic dysfunction and stupor as symptoms of acute hyponatremia due to gastrointestinal loss of sodium in excess of water. 3. The correction of hyponatremia led to a complete recovery after about 6 hours. During this period the antiparkinsonian therapy was not modified. 4. An acute imbalance of sodium in the central nervous system may play a role in the pathophysiology of NMS.
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PMID:Acute hyponatremia and neuroleptic malignant syndrome in Parkinson's disease. 877 7

We found that 1-(3,4-dimethoxyphenethyl)-4-(3-phenylpropyl) piperazine dihydrochloride (SA4503), a potent and selective sigma 1 receptor agonist, significantly enhanced the cerebral acetylcholine (ACh) release in the rat using in vivo brain microdialysis technique. Interestingly, the significant enhancement of ACh release elicited by SA4503 was observed in the rat frontal cortex and hippocampus, although the striatal ACh release was unchanged. This cortical ACh release was fully reversed by haloperidol, a prototype sigma receptor antagonist, or by N, N-dipropyl-2-(4-methoxy-3-(2-phenylethoxy)phenyl)ethylamine monohydrochloride, a putative sigma 1 receptor antagonist. In addition, this enhanced ACh release by SA4503 was inhibited by tetrodotoxin, a Na+ channel blocker. However, tetrahydroaminoacridine, an acetylcholinesterase inhibitor, significantly increased the extracellular ACh level in the rat frontal cortex and weakly increased the hippocampal level. This compound also showed the significant increase of extracellular ACh level in the rat striatum. Moreover, tetrahydroaminoacridine markedly produced cholinomimetic side-effects, such as hypothermia, tremor, miosis and lacrimation. However, SA4503 did not produce these cholinomimetic side-effects. These findings suggest that SA4503 enhances the ACh release that is mediated through a novel mechanism, namely sigma 1 receptor subtype. Furthermore, SA4503 has regional differences in the enhancement of cerebral ACh release, and did not produce cholinomimetic side-effects. These profiles are different from tetrahydroaminoacridine.
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PMID:Enhancement of acetylcholine release by SA4503, a novel sigma 1 receptor agonist, in the rat brain. 885 82

Protein containing quality control (QC) material in ampoules for blood gas, pH and electrolyte analysers has been manufactured using buffered protein (Bovine Serum Albumine, BSA) solution with sodium bicarbonate and chloride salts. For comparison a similar QC material but without protein was manufactured. Results obtained with ampouled QC material depend on pre-analytical effects, on matrix effects and on the stability of the material. Pre-analytical variation occurs with closed and/or opened ampoules. The shaking rate of the ampoule must be high (vortexing) and the duration of shaking long enough (15 seconds) to give good reproducibility. Temperature coefficients of protein containing controls are equal to those of protein free controls when incubated at different temperatures. Vigorously shaking of the ampoule gives a protein foam layer resulting in stable values for pH, pCO2 and pO2 during maximally 6 minutes after opening of the ampoule. Concerning matrix effects the CO2 buffer capacity of protein containing QC material is slightly higher compared to that of protein free QC materials as determined by tonometry with CO2/air gas mixtures and measuring pH and plotting log pCO2 vs. pH. The O2 buffer capacity measured as the bias on a properly functioning blood gas analyser is smaller than the bias of protein free QC material. The protein containing quality control is stable for at least 12 months when stored refrigerated at 2-6 degrees C and 28 days at room temperature.
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PMID:Evaluation of protein containing quality control materials for blood gas analysis. 886 21

A 40-year-old female receiving divalproex sodium (VPA) monotherapy for epilepsy developed a tremor secondary to the drug. Propranolol treatment was initiated. While receiving propranolol 40 mg, VPA clearance was reduced from 1.66 L/hr to 1.19 L/hr and dropped to 1.08 L/hr on propranolol 80 mg. The mechanism of this interaction is unknown. To evaluate the potential for a drug interaction between these two agents, 12 patients on VPA monotherapy, ages 19-55, were studied. The subjects were maintained on a constant dose of VPA. Each was then randomly assigned to receive placebo, or long-acting propranolol 60 mg/day or 120 mg/day. Mean VPA serum concentrations did not change among the three groups. Plasma half-life of VPA ranged from 7.3-18 hours and did not change with coadministration of propranolol. We concluded that VFA metabolism is not affected by coadministration of propranolol in this group of patients.
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PMID:A pharmacokinetic study to determine the drug interaction between valproate and propranolol. 894 79

Lamotrigine (LTG) inhibits repetitive high frequency firing in depolarised neurones by selectively prolonging slow inactivation of the sodium channel, thereby suppressing the release of excitatory amino acids. It has been shown to be effective in 11 pivotal double-blind add-on trials in patients with refractory partial seizures with or without secondary generalisation. Subsequent anecdotal data support its efficacy for typical and atypical absences, myoclonic jerks, tonic or clonic seizures, Lennox-Gastaut syndrome and infantile spasms. Most recently LTG has been compared with carbamazepine and phenytoin in double-blind trials in patients with newly diagnosed partial and primary and secondary generalised tonic-clonic seizures. At the doses used, its efficacy was similar to the older agents for all seizure types, but LTG was better tolerated than both of the older agents. The commonest side-effects with LTG include headache, nausea, diplopia, dizziness, ataxia and tremor. Rash occurs in fewer than 5% patients. Its incidence can be reduced by starting treatment with a low dose, particularly in patients receiving concomitant sodium valproate which inhibits LTG metabolism. Enzyme inducers, such as carbamazepine, phenytoin and phenobarbital, accelerate its elimination, but LTG itself has no effect on hepatic metabolic processes. A pharmacodynamic interaction with carbamazepine necessitates a dosage reduction in some patients when LTG is introduced. LTG is a new antiepileptic agent with a long elimination half-life, a broad spectrum of activity, and a wide therapeutic ratio.
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PMID:Lamotrigine--an update. 895 Dec 13

Phenobarbital (phenobarbitone) and phenytoin are the most useful anticonvulsants in neonates because adverse effects are most readily reversed when these drugs are used. Most anticonvulsants are very rarely associated with haematological adverse effects. Platelet function is particularly vulnerable to valproic acid (sodium valproate) therapy. Barbiturates and phenytoin can precipitate metabolic bone disease. Although very infrequent, lymphadenopathy is most common with phenytoin, and lupus-like illnesses with ethosuximide. Valproic acid may precipitate underlying metabolic disorders. Nephrolithiasis can occur with topiramate. Liver disease is most likely with felbamate or valproic acid, but can occur with other anticonvulsants. Valproic acid and ethosuximide are the main precipitants of gastrointestinal symptomatology; while valproic acid and vigabatrin are frequently associated with excessive bodyweight gain. Rash is most likely to occur with barbiturates, but there is a high risk of this adverse effect if large doses of lamotrigine are given with valproic acid. Adverse cosmetic effects are most likely with phenytoin, but valproic acid may cause alopecia. All anticonvulsants may cause unwanted neurological effects: when they occur, diplopia is usually precipitated by carbamazepine; tremor by valproic acid; and other motor disturbances are probably most common with phenytoin. Most anticonvulsants can cause drowsiness. Phenobarbital leads anticonvulsants as a cause of behavioural difficulties. Effects of anticonvulsants on cognitive function are difficult to assess, but subtle changes have been reported for all anticonvulsants in use up to the 1980s. Compared with other anticonvulsant drugs, phenytoin and felbamate are more often discontinued as a result of unwanted effects.
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PMID:A comparative review of the adverse effects of anticonvulsants in children with epilepsy. 896 93


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