Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report three cases of poisoning with organic phosphate compounds in children. The first case presented a complex of late signs in the form of toxic polyneuropathy, and two had an acute course. The observation confirmed the view that an at least 7-day hospital stay and 4-week follow-up are necessary in view of great fluctuations in the level of cholinesterase which is often not correlated with the clinical status.
Neurol Neurochir Pol
PMID:[Neurologic complications in organophosphate insecticide poisoning in children]. 314 6

The investigations were carried out on the material taken from four pigs, weight about 35 kg. Ovary ligaments and hilus were taken for these experiments. To trace cholinergic nerves situated in the collected material, Koelle and Friedenwald's thiocholine method in Gomori's modification and Gienc's adaptation was used. To eliminate the possibility of pseudocholinesterase staining in the preparation, Iso-OMPE in dilution 1 X 10(-6) was added to the control material. In the mesovarium of the pig cholinergic nerves have been observed. They can be divided into three groups according to their course and position: 1) paravascular bundles, 2) perivascular plexi and 3) nerve bundles not connected with the vessels.
Pol Arch Weter 1983
PMID:[Cholinergic fibers in the ligament system of the ovary in pigs]. 663 57

Intoxication of rats with single doses of Dichlorvos or Trichlorphon corresponding to 50% of the LD50 led to striking changes of blood plasma phosphatase activities. The complex pattern of these changes was not related to the observed inhibition of plasma cholinesterase. The tested pesticides did not inhibit plasma phosphatases in vitro.
Acta Physiol Pol
PMID:The activity of plasma phosphatases in rats treated with single doses of dichlorvos and trichlorphon. 723 36

Gamma aminobutyric acid injected into the lateral brain ventricle of white rats in doses of 0.6, 0.8 and 1.6 mg raised the level of acetylcholine and in doses of 0.2, 0.4, 0.6, 0.8 and 1.6 mg increased acetylcholine synthesis. The effects were greatest 15 minutes after injection. Gamma aminobutyric acid injected intraventricularly in doses of 0.6 mg increased the activity of choline acetyltransferase but had no effect on the activity of choline esterase.
Acta Physiol Pol
PMID:Gamma aminobutyric acid effect on acetylcholine level and metabolism in rat cerebral cortex. 737 94

Gamma-aminobutyric acid (GABA) injected into the lateral ventricles of rat bran in a dose of 600 microgram raised the level and increased the synthesis of acetylcholine (ACh) raising also the activity of choline acetyltransferase (ChAc) but had no effect on the activity of cholinesterase (AChE) in rat striatum. Bucuculline (Bk) in doses of 10 mirogram i.c.v reduced ACh synthesis and in 50 and 10 microgram doses reduced the activity of ChAc. No Bk effect on AChE activity was demonstrated. The observed effects of GABA were abolished by pretreatment with Bk in doses of 1, 5 or 10 microgram.
Acta Physiol Pol
PMID:Gamma-aminobutyric acid and bicuculline effects on acetylcholine metabolism in the striatum in rats. 744 42

Paraneoplastic Lambert-Eaton myasthenia syndrome is presented in two cases with small cell lung cancer. An increase of serum cholinesterase activity was explained by induced release of biologically active proteins by neoplastic tissue.
Pol Merkur Lekarski 1997 Feb
PMID:[Two cases of Lambert-Eaton syndrome with an increase of serum cholinesterase activity]. 953 60

The last decade brought a considerable progress in pharmacotherapy of addiction. Basing on recently gained knowledge of mechanisms of development of addiction and the physiology of the brain reward system, several therapeutic strategies have evolved. The strategies aimed at targeting the basic mechanisms of addiction rely on the premises that addiction is caused by adaptive changes in the central nervous system and that craving, which is the main cause of relapse, depends on dopaminergic mechanisms and requires high general excitability. The pharmacological approach involves drugs that reduce neuronal adaptability by inhibiting the calcium entry to neurons both through voltage-gated channels (e.g. nimodipine) and NMDA receptors (e.g. memantine), and drugs that stimulate the inhibitory GABAergic system (gamma-vinyl-GABA, baclofen), Particular attention is paid to the compounds that may attenuate dopaminergic hyperactivity, without considerable suppression of tonic activity of dopaminergic neurons (e.g. BP 897, a partial dopamine D3 receptor antagonist). Specific strategies are aimed at interference with the action of particular drugs of addiction. An important group includes the agonistic therapies (known also as substitution or maintenance therapies) in which a long-acting agonist is used in order to reduce the action of the drugs of high addictive potential (e.g. methadone against heroin addiction or vanoxerine (GBR 12909) against psychostimulants). Other specific strategies aimed at reduction of the transport of molecules of addictive substances into the brain: the approaches involve preparation of antibodies that form complexes unable to cross blood-brain barrier or enzymes accelerating the metabolism of the compounds in the blood (e.g. variants of butyrylcholinesterase). A considerable progress has been made in combating the abuse of legal addictive substances, alcohol (naltrexone, acamprosate) and tobacco (bupropion). The prospects for developing effective pharmacotherapies against addiction are bright. Unfortunately, ideological and social implications, as well as the conflict of interest with illegal narcotic manufacturers and distributors, may considerably hamper the progress in combating addiction (e.g. difficulties in introduction of methadone).
Pol J Pharmacol
PMID:Drug addiction. Part III. Pharmacotherapy of addiction. 1199 60

Centrally acting cholinesterase inhibitors (ChEls) improve cognitive functions in Alzheimer's disease (AD) and other forms of dementia. Evaluation of treatment efficacy is based mainly on subjective assessment tools which includes standardized neuropsychological tests. Therefore, an additional objective tool for the evaluation of drug response is necessary. Thirty two patients were treated with ChEls for dementia (tacrine 19, donepezil 5, rivastigmine 8). Cognitive response was assessed before ChEls (baseline) and after 26 weeks, as optimal tolerated doses were achieved and maintained (endpoint). Evaluation included repeated measurements of Mini Mental State Examination (MMSE), ADAS-cog and P300. For statistical analysis we used ANOVA with repeated measures and Pearson correlation coefficient. Results demonstrated improvement of mean ADAS-cog by 2.0 points (from 29.4 to 27.4 p = 0.08) while MMSE remained almost unchanged (20.1 to 19.8). Mean P300 latency reduced significantly by 24 msec (from 383 msec to 359 msec, p = 0.0001) thus reflecting the clinical improvement. However mean amplitudes did not change from baseline to endpoint (13 microvolts). Significant correlation was found between mean ADAS-cog and mean P300 latency at baseline and end-point (R = 0.452 p = 0.014, R = 0.567 p = 0.001 respectively). Strong correlation was found between mean MMSE and P300 latency at Baseline (R = -0.335 p = 0.07), and significant correlation was found at endpoint (R = -0.613 p < 0.001). Our data suggests that P300 is a reliable instrument for assessment of cognitive response to ChEls in demented patients.
Neurol Neurochir Pol 2001
PMID:Evaluation of cholinergic treatment in demented patients by P300 evoked related potentials. 1200 52

Memantine is an NMDA receptor antagonist with moderate affinity, which results in neuroprotective potential due to reducing overstimulation caused by glutamate (excitotoxicity) and simultaneous lack of adverse events (especially psychosis) typical for an antagonist with higher affinity like phencyclidine. In randomized, controlled studies it has been shown that memantine is beneficial in the treatment of moderate to severe dementia of Alzheimer's type and it became the very first compound to be registered for this purpose both in Europe (including Poland) and in the United States. Further investigation require usefulness of memantine in less advanced stages of Alzheimer's disease as well as other types of dementia especially vascular; promising results are shown in dual therapy: memantine + cholinesterase inhibitor.
Psychiatr Pol
PMID:[The clinical relevance of memantine use]. 1530 96

Clinical diagnosis of fronto-temporal dementia (FTD) and its rare variants (semantic dementia and primary progressive aphasia) represents a special challenge bearing in mind its difficulties and is important due to therapeutic differences with the most common Alzheimer's dementia. Of note, cholinesterase inhibitors commonly prescribed in Alzheimer's disease are not effective in FTD and a novel drug, memantine, has not been evaluated as yet. Neuropsychological evaluation is an important add-on to neurological, psychiatric and neuroimaging assessments in the clinical diagnosis of FTD. In this paper, we have described characteristics of neuropsychological deficits observed in FTD (such as attention, language, visuospatial and memory impairments) as well as tools used (tests) in clinical practice. Special attention is paid to the utility of neuropsychological examination in the differential diagnosis of FTD versus Alzheimer's disease, vascular dementia and other, less common forms of dementia.
Neurol Neurochir Pol
PMID:[Neuropsychological assessment in the diagnosis and differential diagnosis of fronto-temporal dementia]. 1635 4


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