Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: EC:3.1.1.8 (cholinesterase)
12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Extracts of Sesbania drummondii administered to chickens by oral intubation are lethal within several days. Effects are dose-dependent; a dose of 1% of body weight is uniformly lethal in 5 days. Signs of poisoning include weakness, depression (CNS), anorexia, diarrhea, ruffled feathers, cold feet, and rapid loss of body weight. Microscopic examination indicates damage to kidney glomeruli and leakage of protein into the kidney tubules. Packed cell volume and plasma glucose concentrations show no difference between controls and treated chickens; however, creatine kinase is increased and plasma cholinesterase and total plasma protein values are severely depressed in poisoned birds. Neither a specific toxin nor a mechanism of action for toxicity has yet been identified.
...
PMID:Determination of the oral toxicity of Sesbania drummondii seeds in chickens. 673 32

In 13 Smooth Fox Terriers with a congenital form of myasthenia gravis, clinical signs included intermittent, progressive muscle weakness that became more pronounced with exercise; muscle wasting; megaesophagus; and aspiration pneumonia. Neurologic abnormalities were apparent only during periods of weakness and included inability to retract the fore- and hindlimbs from painful stimuli. A decrement of the compound muscle action potential was evident during repetitive supramaximal nerve stimulation. Intravenous injection of a short-acting cholinesterase inhibitor evoked immediate improvement of clinical and electromyographic signs. Intracellular microelectrode studies of a biopsied external intercostal muscle revealed reduced amplitude of miniature end-plate potentials, as occurs in acquired myasthenia gravis. However, in contrast to acquired myasthenia gravis, antibodies directed against acetylcholine receptors were not demonstrable in serum and were not bound to acetylcholine receptors in muscle. Despite lack of complexing with immunoglobulin, the amount of acetylcholine receptor protein in biopsied external intercostal muscles from 9 affected pups was less than 25% of the amount in 5 unaffected littermates. The latter finding accounted for the reduction in amplitude of miniature end-plate potential and the failure of neuromuscular transmission. Treatment with a long-acting cholinesterase inhibitor in 6 cases resulted in temporary improvement in muscle strength.
...
PMID:Congenital myasthenia gravis in 13 smooth fox terriers. 684 Dec 51

n-Butyl mercaptan (nBM) is a breakdown product of S,S,S,-tri-n-butyl phosphorotrithioate (DEF) and S,S,S-tri-n-butyl phosphorotrithioite (merphos) in hens and in the environment. n-Butyl disulfide (nBD) is an oxidation product of nBM. A single 500 mg/kg dose of nBM and nBD was administered in gelatin capsules to groups of five 12-month old laying hens. A third group (five hens) was given gelatin capsules. One day after administration, the hens exhibited weakness which progressed to unsteadiness and inability to stand by the third day. These signs were accompanied by a pale comb 18--24 hr after dosing, which changed to dark color at 48 hr. Treated hens improved with time. Heinz bodies and extensive erythrocyte deformation and lysis were observed in blood smears taken from hens 24 and 48 hr after treatment. Hemoglobin concentration, packed cell volume, erythrocytes, and glucose-6-phosphate dehydrogenase activity were significantly lower than controls, while methemoglobin was significantly higher. As the clinical condition of these hens improved, these hematologic changes disappeared. nBM caused an initial increase in plasma butyrylcholinesterase activity which was dose-dependent and returned to normal by the end of the 28-day experiment. Also, brain acetylcholinesterase activity was not different from that of the control at termination.
...
PMID:Heinz body production and hematological changes in the hen after administration of a single oral dose of n-butyl mercaptan and n-butyl disulfide. 687 30

Myasthenia gravis is characterized by variable ocular and skeletal muscle weakness. Peak incidence is in young women and older men. Thymomas are present in 30 percent of myasthenic patients over age 40. Binding of acetylcholine receptors by IgG antibodies may be the mechanism of the neuromuscular disorder. Repetitive nerve stimulation (Jolly test), provocative tests with quinine or curare and the edrophonium test (cholinesterase inhibition) are the diagnostic maneuvers employed.
...
PMID:The neuromuscular junction. Part II: myasthenia gravis. 745 20

Two children, now 5 1/2 and 6 years of age, presented as neonates with hypotonia, multiple joint contractures, ptosis, extraocular weakness, bulbar symptoms, and respiratory distress. Fluctuations and episodic exacerbations of weakness necessitated respiratory support. Both children are developmentally delayed and cannot walk independently, although one child underwent bilateral tenotomies. Biochemical investigations and electromyography, including slow-rate, repetitive nerve stimulation, were normal. Acetylcholine receptor antibodies in serum were absent. Single-fiber electromyography with axonal stimulation revealed prolonged mean jitter in the tibialis anterior and extensor digitorum muscles, with more than 2 abnormal individual jitter values in each muscle. Muscle biopsy demonstrated normal pattern and morphology of muscle fibers; immunohistochemical staining for cholinesterase was positive. Electron microscopy revealed abnormalities in motor endplates: atrophy, flattening of primary synaptic clefts, and paucity of side branches. These findings represent one of the postsynaptic abnormalities (i.e., acetylcholine receptor deficiency or paucity of synaptic folds). Both children improved clinically on pyridostigmine therapy. Arthrogryposis congenital multiplex due to congenital myasthenic syndrome, as diagnosed in our patients, has been reported once before. The diagnosis can be established by clinical history, neurologic examination, and electrophysiologic and pathologic findings. Clinical improvement can be achieved with high-dose anticholinesterase therapy.
...
PMID:Arthrogryposis multiplex congenita due to congenital myasthenic syndrome. 761 91

A patient developed a severe cholinergic syndrome from the use of echothiophate iodide ophthalmic drops, presented with profound muscle weakness and was initially given the diagnosis of myasthenia gravis. Red blood cell and serum cholinesterase levels were severely depressed and symptoms resolved spontaneously following discontinuation of the eye drops.
...
PMID:Cholinergic toxicity resulting from ocular instillation of echothiophate iodide eye drops. 765 Jul 71

Six patients with organophosphorus compound intoxications developed an intermediate syndrome (weakness and fasciculations) and obidoxime was given on eight occasions. The efficacy of the acetylcholinesterase (AChE) reactivator was monitored electrophysiologically by neuromuscular transmission studies using single and repetitive nerve stimulation (20 and 50 Hz) and the activity of the serum (butyryl) cholinesterase (ChE). Dramatic electrophysiologic improvement was seen when obidoxime was given early within 12 h in 3 patients, although evidence of AChE inhibition did not subside completely. When administration of obidoxime was delayed 26 h or more after intoxication on five occasions, electrophysiologic improvement was mild or absent. In one case, 66 h after intoxication with oxydemeton-S-methyl, the neuromuscular block worsened, indicating that aging of the AChE had been completed. The electrophysiologic improvement was always accompanied with better motor function but not necessarily with improvement of the overall clinical status. Serum ChE did not predict the oxime effect at the motor endplate. In humans, the efficacy of oximes in AChE reactivation can be determined rapidly using electrophysiologic studies.
...
PMID:Efficacy of obidoxime in human organophosphorus poisoning: determination by neuromuscular transmission studies. 779 93

A feral Griffon vulture (Gyps fulvus) was found with tremors, weakness, digit and wing flexion, and an inability to fly. A zero blood cholinesterase activity and a favorable response to treatment with pralidoxime hydrochloride indicated exposure to an anticholinergic pesticide. The bird died after 7 d, and traces of the organophosphate insecticide ethyl parathion were found in the liver and from a blue discolored skin area of the neck. Continuous exposure to ethyl parathion through dermal absorption was presumed the cause of death of the vulture.
...
PMID:Percutaneous exposure to ethyl parathion in a feral Griffon vulture (Gyps fulvus). 806 70

Myasthenia gravis (MG) is probably the best studied autoimmune disease caused by autoantibodies against the acetylcholine receptor (AChR) at the neuromuscular junction, subsequently leading to abnormal fatigability and weakness of skeletal muscle. Extraocular muscle weakness with droopy eyelids and double vision is present in about 90% of MG patients, being the initial complaint in about 50%. In approximately 20% of the patients the disease will always be confined to the extraocular muscles. The single most important diagnostic test is the detection of serum antibodies against AChR which is positive in 90% of patients with generalized MG, but only in 65% with purely ocular MG. Electromyographic studies and the Tensilon test are of diagnostic value in clear-cut cases, but may be equivocal in purely ocular myasthenia, especially the latter not rarely producing false-positive results. Treatment response to corticosteroids and anti-cholinesterase agents is satisfactory in many patients with ocular MG, however other immunosuppressive drugs may also be needed. Pathogenetically relevant steps of the underlying autoimmune process have been elucidated during the last few years; nevertheless a number of questions remain open, especially what starts off the autoimmune process, and why are eye muscles so frequently involved in MG?
...
PMID:Ocular myasthenia gravis. A critical review of clinical and pathophysiological aspects. 815 54

Hypothyroidism is associated with muscle weakness and slowed movements. Hormone-deficient muscles do show changes in contractile proteins and sarcoplasmic calcium pumps, however effects on the components of the neuromuscular junction are less clear. In this study, we examined cholinesterase activity in adult fast-twitch muscle from hypothyroid and control rats. Male Holtzman rats underwent thyroidectomy and their age-matched euthyroid controls were simultaneously subjected to sham operation. Thirty days post-operative, animals were sacrificed for anterior tibialis muscles harvest. Muscle cholinesterase isoform activity was measured and compared between experimental treatment groups. Butyrylcholinesterase activities and peak I and III acetylcholinesterase (AchE) activities were similar in euthyroid and hypothyroid groups. However, hypothyroid muscles exhibited half the peak II AchE isoform (G4) activity, as compared to control muscles. Hypothyroidism specifically affects AchE isoform expression in rodent fast-twitch muscle.
...
PMID:Acetylcholinesterase activity in fast-twitch skeletal muscle from thyroidectomized rats. 816 63


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---