Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The fast-twitch posterior latissimus dorsi muscle of normal and genetically dystrophic chickens was subjected to continuous indirect electrical stimulation at 10 Hz for periods of 4-8 weeks. To sustain this in vivo nerve stimulation an internally implantable miniature stimulator device was designed. This regime of stimulation caused complete fatigue of the normal muscle within 5 min of its initiation. The dystrophic muscles maintained a very small degree of contractile activity during this initial phase. Tangible twitching of the muscle returned in 5 week birds between 3 and 5 days and in 10 week birds between 11 and 16 days after implantation. After 4 weeks of stimulation, no significant change was measured in the time-to-peak of the isometric twitch response, nor in the half-relaxation time. The resistance to fatigue was significantly increased in the stimulated muscles when tested with a series of tetani at 40 Hz. The mean fibre area was decreased, in all muscles stimulated for longer than 3 weeks, in comparison to their contralateral controls, except where fibre splitting in dystrophic birds abnormally reduced the control value. The majority fibre type of the muscle was changed from type IIB to IIA. The histochemical reactions for both NADH-linked oxidation and phosphorylase were distinctly increased in the stimulated muscles. In normal muscle, stimulation increased somewhat the number of nuclei per unit area and changed their intracellular distribution, so that a greater proportion was found adjacent to the sarcolemma. The normal posterior latissimus dorsi muscle responded to chronic stimulation with increases of 3-6-fold in its acetylcholinesterase (AChE) activity. The maximum change in AChE occurred after 2 weeks stimulation; a steady level, 3 times that of the control unstimulated muscle, persisted at later times. Chronic stimulation suppressed the over-production of AChE that is characteristic of dystrophic chicken fast-twitch muscle, to attain a level comparable to the AChE activity in a stimulated normal muscle. Stimulation exerted a strong normalizing influence on dystrophic muscle, as assessed morphologically. The characteristic fibre rounding, fibre hypertrophy and myonuclear proliferation were reduced. This influence was most marked where the stimulation was initiated before the major pathological changes had occurred, but was also significant when commenced in strongly affected birds of 10-11 weeks.
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PMID:Low frequency chronic electrical stimulation of normal and dystrophic chicken muscle. 379 78

We treated a patient with idiopathic fatty liver of pregnancy and a subsequent uncomplicated pregnancy. She experienced general fatigue, nausea, vomiting and jaundice, and renal failure occurred in the third trimester of her first pregnancy. Liver biopsy revealed swollen hepatocytes with microvesicular changes in the cytoplasm. A diagnosis of idiopathic fatty liver of pregnancy was made. Following delivery of a dead fetus, she recovered completely and was discharged on the 30th hospital day. Eighteen months later, she became pregnant again and was delivered of a healthy male baby in the 39th week of gestation. Total bilirubin and transaminase levels were normal, and renal function tests revealed no significant changes during the course of the pregnancy. However, cholinesterase activity increased progressively from the 7th month, thereby suggesting a predisposition to idiopathic fatty liver of pregnancy.
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PMID:Idiopathic fatty liver of pregnancy with a subsequent uncomplicated pregnancy and a progressive increase in serum cholinesterase activity during the third trimester. A case report. 395 27

Ocular myasthenia is a special form of general myasthenia gravis characterized by unilateral or bilateral ptosis and eye muscle pareses of distinct variability, depending on the time of day and the state of fatigue of the patient. Most important for diagnosis is the Tensilon test, which can, however, produce negative results. In such cases a combination of the Tensilon test with electromyography is indispensable. In ocular myasthenia there is not always an increase in the antibody titer against acetylcholine receptors in the blood. The treatment of ocular myasthenia is based on the application of cholinesterase inhibitors. The drug of choice is Mestinon; however, the reaction of the eye muscles to this drug is often unsatisfactory. Local application of cholinesterase inhibitors in the form of Eserine, Prostigmin etc. is an additional important therapy. Also in ocular myasthenia the modern treatment with Cortisone (alternate-day therapy with 100 mg Prednisone every second day) has proved very useful. Another possible method of interfering with the immunological systems of myasthenia is immunosuppression with Azathioprin or Cyclophosphamide. The pathognomonic significance of the thymus in the autoimmune process of myasthenia gravis is demonstrated by the good results obtained by thymectomy, which can also be performed successfully in ocular myasthenia, not only in young patients in whom the condition is severe, but also in older patients in whom it is chronic. Often, the therapeutic measures mentioned have to be tested one after another or in combination in order to achieve an optimal therapeutic effect.
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PMID:[Ocular myasthenia]. 399 98

Cryostat sections from 160 rectal suction biopsies were stained for cholinesterases by the method of Karnovsky and Roots (1964) in an attempt to facilitate the diagnosis of Hirschsprung's disease. The method proved at least as reliable as experienced assessment of paraffin haematoxylin-eosin sections, and appeared to offer the advantages of reduced scanning fatigue and superior demonstration of the increased cholinesterase-positive nerves in Hirschprung's disease. Contrary to the findings of Meier-Ruge (1971) it was not possible to base a diagnosis on mucosal cholinesterase activity.
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PMID:Experience with a cholinesterase histochemical technique for rectal suction biopsies in the diagnosis of Hirschsprung's disease. 483

Using a computer-assisted infrared optometer with a pupillograph, we tried to obtain basic understanding of accommodative disturbance and its by investigating tonic (dark focus) level of accommodation and quasi-static accommodative response. In normal volunteers in whom either visual fatigue, general fatigue, or drunkeness was loaded intentionally, myopic shift of refraction, increased refractive fluctuation, and miosis were induced in all cases but the effect on amplitude of accommodative response was minimal. Subjects that worked at a computer terminal all day for 2 years, but not controls, developed myopic change at a statistically significant level. The effect on tonic level of accommodation of subject age, sustained near-vision tasks, and topical application of autonomic-related drugs was investigated. In subjects with severe eyestrain, myopic shift of tonic accommodation and prominent pupillary unrest were observed, suggesting increased parasympathetic excitation. One patient who was accidentally exposed to diisopropyl fluorophosphate, a potent cholinesterase inhibitor, showed a phenomenon similar to that mentioned above. Chaos attractors based upon the Shil'nikov phenomenon were introduced for evaluation of microfluctuation and pupillary unrest, as first applied by Sumida et al. Topical application of low-dose cyclopentolate hydrochloride was effective for treating accommodative abnormality in professional computed workers, who sometimes develop abnormal parasympathetic excitation. Based on quasi-static accommodation measurements, accommodative abnormality after head and neck injury, including whiplash injury, was divided into two completely different states: accommodative spasm and palsy. Since quasi-static accommodation was greatly affected by satellite ganglion block, sympathetic innervation from cervical ganglions may strongly influence accommodative response. Hyperthyroidism, which may be accompanied by sympathetic hyper-excitation, showed diminished accommodative response. In patients after refractive surgery by excimer laser, there was no difference in accommodative response before and after surgery, although tonic accommodation was slightly unstable after surgery. These findings suggest that the evaluation of tonic level or a similar state of accommodation and pupillary unrest will yield extremely valuable information in regard to various accommodative disturbances.
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PMID:[Pathogenesis and treatment of accommodative disturbance]. 783 69

Acute cholestatic hepatitis developed in two patients, a 58-year-old man and a 54-year-old woman, who had been treated for hypercholesterolaemia with the cholesterol-synthesis inhibitor lovastatin for 3 years and 2 months, respectively. Both of them at first complained only of tiredness and loss of appetite, but then developed jaundice with colourless stool and dark urine. Alkaline phosphatase concentration rose up to maximally 1227 and 569 U/l, gamma-GT to 403 and 410 U/l, respectively. The transaminases and glutamate dehydrogenase were also elevated, while serum cholinesterase had fallen to 2346 and 2418 U/l, respectively. Histological examination of liver biopsies 6 months and 4 weeks, respectively, after onset of jaundice also suggested drug-toxic liver damage. There was no evidence for other causes. After lovastatin had been discontinued the various cholestasis parameters regressed only slowly.
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PMID:[Lovastatin-induced acute cholestatic hepatitis]. 786 82

A 52-year-old woman had a 14-year history of stridor attacks. Pulmonary function tests revealed reversible airway obstruction, and bronchial asthma was diagnosed. She also has bilateral ptosis, diplopia, and moderate weakness of all four limbs; a positive edrophonium test confirmed the diagnosis of myasthenia gravis. Although the parasympathetic system plays an important role in the regulation of bronchial tone, in this patient the edrophonium test did not provoke an asthmatic attack or exacerbate pulmonary function, except for increases in sputum production and in frequency of cough. The general weakness was usually worse in the afternoon. The decrease in grip strength and the shortening of arm elevation time also occurred after asthma attacks, which means that general muscle fatigue was caused by the work of breathing. Furthermore, dyspnea increased and pulmonary function worsened when an anti-cholinesterase inhibitor was discontinued, probably because of respiratory muscle weakness. Accordingly, the clinical status of bronchial asthma seemed to change in parallel with that of the myasthenia gravis.
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PMID:[Bronchial asthma complicated by myasthenia gravis]. 869 67

Chronic neurobehavioral effects of acute sarin poisoning were evaluated in 9 male and 9 female patients who were exposed to sarin poisoning in the Tokyo subway incident in Japan. The investigators used nine neurobehavioral tests, as well as a posttraumatic stress disorder checklist, 6-8 mo after the poisoning occurred. Serum cholinesterase activity in patients on the day of poisoning (i.e., March 20, 1995) ranged from 13 to 131 IU/l (mean=72.1 IU/l). The results of analysis covariance, in which age, education level, alcohol consumption, and smoking status (covariates) were controlled in 18 sarin cases and in 18 controls, showed that the score on the digit symbol (psychomotor performance) test was significantly lower in the sarin cases than in controls. Nonetheless, the scores for the General Health Questionnaires, fatigue of Profile of Mood States, and posttraumatic stress disorder checklist were significantly higher in the sarin cases than controls. The investigators added posttraumatic stress disorder to the covariates, and only the score on the digit symbol test was significantly lower in sarin cases. In addition, the results of stepwise multiple regression analysis in 18 sarin cases revealed that scores for the General Health Questionnaires, fatigue of Profile of Mood States (i.e., fatigue, tension-anxiety, depression, and anger-hostility)-together with the paired-associate learning test-were associated significantly with posttraumatic stress disorder. The association did not remain significant for the digit symbol test score. Perhaps a chronic effect on psychomotor performance was caused directly by acute sarin poisoning; on the other hand, the effects on psychiatric symptoms (General Health Questionnaire) and fatigue (Profile of Mood States) appeared to result from posttraumatic stress disorder induced by exposure to sarin.
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PMID:Chronic neurobehavioral effects of Tokyo subway sarin poisoning in relation to posttraumatic stress disorder. 970 88

During the Persian Gulf War, pyridostigmine bromide (PB), a reversible inhibitor of acetylcholinesterase, was used as prophylaxis against exposure to nerve gas. Exposure to PB has been suggested as a potential cause of the persistent fatigue reported among Gulf War veterans. The aim of this study was to evaluate the effects of acute and continuous exposure to low doses of PB on the neuromuscular junction. Organotypic spinal cord-muscle cocultures were used to examine in vitro the effects of PB under controlled conditions. Acute exposure to PB potentiated neuromuscular activity. Continuous exposure to PB produced a progressive decrease in the contractile activity of muscle fibers. Ultrastructural examination by electron microscopy revealed no abnormalities in the neuromuscular junctions after 1 week of exposure. Nerve terminal degeneration and atrophy of the postjunctional folds were evident after 2-week exposure to low-dose PB. The effects of PB were reversible following withdrawal. The reversibility of the PB-induced changes in vitro suggests that such changes are causally unrelated to the fatigue reported by Persian Gulf War veterans years after exposure to PB.
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PMID:Effects of exposure to low-dose pyridostigmine on neuromuscular junctions in vitro. 1036 19

The purpose of this study was to investigate the functional impact of acute irreversible inhibition of acetylcholinesterase (AChE) on the fatigability of medial gastrocnemius and plantaris muscles of Sprague-Dawley rats. After treatment with methanesulfonyl fluoride (a lipid-soluble anticholinesterase), which reduced their AChE activity by >90%, these muscles were subjected to an in situ indirect stimulation protocol, including a series of isolated twitch and tetanic contractions preceding a 3-min fatigue regimen (100-ms trains at 75 Hz applied every 1.5 s). During the first minute of the fatigue regimen, the effects of AChE inhibition were already near maximal, including marked reductions in peak tension and the force-time integral (area), as well as a decrement of compound muscle action potential amplitudes within a stimulus train. Neuromuscular transmission failure was the major contributor of the force decreases in the AChE-inhibited muscles. However, despite this neuromuscular transmission failure, muscles of which all AChE molecular forms were nearly completely inhibited were still able to function, although abnormally, during 3 min of intermittent high-frequency nerve stimulation.
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PMID:Fatigability of rat hindlimb muscles after acute irreversible acetylcholinesterase inhibition. 1051 78


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