Dexetimide
Maneb
Manganese Poisoning
Zineb
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Manganese
Facilitated Diffusion
Dyskinesias
In vivo imaging of muscarinic cholinergic receptors in temporal lobe epilepsy with a new PET tracer: [76Br]4-bromodexetimide. (1/9)
Muscarinic acetyl cholinergic receptors (mAChRs) may be involved in the pathophysiology of partial epilepsy. Previous experimental and imaging studies have reported medial temporal abnormalities of mAChR in patients with medial temporal lobe epilepsy (MTLE). Suitable radiotracers for mAChR are required to evaluate these disturbances in vivo using PET. Dexetimide is a specific mAChR antagonist that has been labeled recently with 76Br. This first study in humans focused on regional distribution and binding kinetics of [76Br]4-bromodexetimide (BDEX) in patients with MTLE. METHODS: Ten patients with well-lateralized MTLE had combined MRI, 18F-fluorodeoxyglucose (FDG) PET and 76Br-BDEX PET studies. Time-activity curves were generated in PET-defined regions of interest, including the medial, polar and lateral regions of the temporal lobe; the basal ganglia; the external and medial occipital cortex; and the white matter. RESULTS: The highest radioactivity concentration was observed in the basal ganglia and in the cortical regions, whereas radioactivity was lower in the white matter. On late images of PET studies, 76Br-BDEX uptake was statistically significantly decreased only in the medial temporal region ipsilateral to the seizure focus (1.37 +/-0.28, P < 0.01) as determined by FDG PET imaging, anatomic MRI and electroencephalogram correlation, compared with the contralateral medial temporal region (1.46 +/- 0.31). CONCLUSION: 76Br-BDEX concentration is reduced in the temporal lobe ipsilateral to the seizure focus in patients with MTLE. This preliminary study suggests that 76Br-BDEX is a suitable radiotracer for studies of mAChR in humans. Further studies are required to investigate the potential value of 76Br-BDEX PET in other neurological disorders with muscarinic disturbances. (+info)Stereoselective binding in cardiac tissue of the enatiomers of benzetimide, and antimuscarinic drug. (2/9)
1 Benzetimide, possessing two stable enantiomers, dexetimide and levetimide, has been investigated in guinea-pig atria with respect to its atropine-like action and its tissue distribution. 2 The antagonistic potency of dexetimide was found to be over 6000 times higher than that of levetimide, the pA2 values being 9.82 and 6.0 respectively. 3 The tissue accumulation was investigated for both isomers in the concentration range from 1.5 X 10(-9) M to 10(-6) M yielding tissue to medium ratios (T/M) of between approximately 50 and 10. The highest values were found for the lowest concentrations. At any concentration investigated, dexetimide exhibited a higher uptake than the levoisomer. 4 The rate of uptake and washout of dexetimide was extremely slow, that of levetimide being considerably faster at equimolar concentrations. The same pattern held true for the onset and decline of the antagonistic action. 5 The high accumulation was found to be almost entirely due to unspecific binding. Even in the case of dexetimide the relative size of the receptor compartment could not be determined. The unspecific binding sites displayed a certain stereoselectivity but to a much lesser extent than the specific receptor binding sites. (+info)Imaging muscarinic cholinergic receptors in human brain in vivo with Spect, [123I]4-iododexetimide, and [123I]4-iodolevetimide. (3/9)
A method to image muscarinic acetylcholine receptors (muscarinic receptors) noninvasively in human brain in vivo was developed using [123I]4-iododexetimide ([123I]IDex), [123I]4-iodolevetimide ([123I]ILev), and single photon emission computed tomography (SPECT). [123I]IDex is a high-affinity muscarinic receptor antagonist. [123I]ILev is its pharmacologically inactive enantiomer and measures nonspecific binding of [123I]IDex in vitro. Regional brain activity after tracer injection was measured in four young normal volunteers for 24 h. Regional [123I]IDex and [123I]ILev activities were correlated early after injection, but not after 1.5 h. [123I]IDex activity increased over 7-12 h in neocortex, neostriatum, and thalamus, but decreased immediately after the injection peak in cerebellum. [123I]IDex activity was highest in neostriatum, followed in rank order by neocortex, thalamus, and cerebellum. [123I]IDex activity correlated with muscarinic receptor concentrations in matching brain regions. In contrast, [123I]ILev activity decreased immediately after the injection peak in all brain regions and did not correspond to muscarinic receptor concentrations. [123I]IDex activity in neocortex and neostriatum during equilibrium was six to seven times higher than [123I]ILev activity. The data demonstrate that [123I]IDex binds specifically to muscarinic receptors in vivo, whereas [123I]ILev represents the nonspecific part of [123I]IDex binding. Subtraction of [123I]ILev from [123I]IDex images on a pixel-by-pixel basis therefore reflects specific [123I]IDex binding to muscarinic receptors. Owing to its high specific binding, [123I]IDex has the potential to measure small changes in muscarinic receptor characteristics in vivo with SPECT. The use of stereoisomerism directly to measure nonspecific binding of [123I]IDex in vivo may reduce complexity in modeling approaches to muscarinic acetylcholine receptors in human brain. (+info)In vitro and in vivo characterization of 4-[125I]iododexetimide binding to muscarinic cholinergic receptors in the rat heart. (4/9)
4-[125I]iododexetimide binding to muscarinic cholinergic receptors (mAChR) was evaluated in the rat heart. 4-[125I]iododexetimide displayed high in vitro affinity (Kd = 14.0 nM) for rat myocardial mAChR. In vivo, there was high accumulation of 4-[125I]iododexetimide in the rat atrium and ventricle which could be blocked by approximately 60% by preinjection of atropine. In contrast, accumulation of the radiolabeled stereoisomer, 4-[125I]iodolevetimide, was 63% lower than 4-[125I]iodolevetimide and was not blocked by atropine. The blood clearance of 4-[125I]iododexetimide was rapid, providing heart-to-blood ratios of up to 14:1; however, heart-to-lung and heart-to-liver ratios were below unity. The data indicate that 4-[125I]iododexetimide binds potently to rat mAChR. However, since nonspecific binding is relatively high, it is not clear whether iododexetimide labeled with 123I will be useful in SPECT imaging studies of myocardial mAChR. Further studies in humans are indicated. (+info)A human embryonic lung fibroblast with a high density of muscarinic acetylcholine receptors. (5/9)
Binding studies with the radiolabeled muscarinic antagonists dexetimide, quinuclidinyl benzilate and N-methylscopolamine showed that the human embryonic lung fibroblast CCL137 possesses approximately 2 X 10(5) muscarinic receptors/cell, i.e. 2.1 pmol/mg membrane protein. These receptors showed a marked stereoselectivity towards dexetimide and levetimide and only low affinity for another antagonist, pirenzepine. The muscarinic agonist carbamylcholine inhibited forskolin-stimulated adenylate cyclase and induced phosphatidylinositide turnover in the intact cells. Both effects were inhibited by the muscarinic antagonist atropine. Affinity labeling with tritiated propylbenzylcholine mustard revealed a protein of 72 kDa. Finally, down-regulation of the membrane receptors following prolonged treatment with the agonist carbamylcholine was assessed by means of the hydrophilic antagonist N-methylscopolamine. (+info)Axonal transport of muscarinic receptors in vesicles containing noradrenaline and dopamine-beta-hydroxylase. (6/9)
Presynaptic muscarinic receptors labeled with [3H]dexetimide and noradrenaline in dog splenic nerves accumulated proximally to a ligature at the same rate of axonal transport. After fractionation by differential centrifugation, specific [3H]quinuclidinyl benzilate or [3H]dexetimide binding revealed a distribution profile similar to that of dopamine-beta-hydroxylase and noradrenaline. Subfractionation by density gradient centrifugation showed two peaks of muscarinic receptors; the peak of density 1.17 contained noradrenaline and dopamine-beta-hydroxylase whereas that of density 1.14 was devoid of noradrenaline. Therefore the foregoing experiments provide evidence that presynaptic muscarinic receptors are transported in sympathetic nerves in synaptic vesicles which are similar to those containing noradrenaline and dopamine-beta-hydroxylase. This suggests a possible coexistence of receptor and neurotransmitter in the same vesicle. (+info)Purification of muscarinic acetylcholine receptors by affinity chromatography. (7/9)
Calf forebrain homogenates contain 2.8 pM muscarinic acetylcholine receptors per mg of protein. [3H]Antagonist saturation binding experiments under equilibrium conditions revealed a single class of sites with equilibrium dissociation constants of 0.82 nM for [3H]dexetimide and 0.095 nM for [3H]quinuclidinyl benzilate. Displacement binding studies with agonists revealed the presence of low and high affinity sites. Here we describe the solubilization of muscarinic acetylcholine receptors with digitonin and their purification by affinity chromatography using an affinity gel which consisted of dexetimide coupled to Affi-Gel 10 (i.e., carboxy N-hydroxysuccinimide esters linked via a 1 nm spacer arm to agarose beads). Purified proteins were obtained by specific elution with muscarinic drugs, i.e., the antagonist atropine and the irreversible ligand propylbenzilylcholine mustard. SDS-polyacrylamide gel electrophoresis of the radioiodinated purified preparations revealed a major 70-K protein. (+info)Agonist-mediated conformational changes of muscarinic receptors in rat brain. (8/9)
Muscarinic acetylcholine receptors were identified in the microsomal P fraction of rat forebrain by the specific binding of the radiolabeled antagonist [3H]dexetimide. Binding occurred to a single class of noncooperative sites (3.25 mumol/mg protein) with an equilibrium dissociation constant of 1.1 nM. Agonist/[3H]-dexetimide competition binding experiments allowed the distinction between two major muscarinic receptor subpopulations, having respectively high affinity (20% of the total receptor population) and low affinity for agonists, but with the same affinity for antagonists. A 610-fold difference in affinity was calculated for carbamoyl-choline, the agonist extensively investigated in this study. The alkylating reagent N-ethylmaleimide did not affect the total receptor number, antagonist binding to the high-affinity and low-affinity sites, nor agonist binding to the high-affinity sites. The reagent, however, caused a net increase in agonist affinity for the low-affinity sites. This process was dependent on time and dose of N-ethylmaleimide, until a maximal increase in affinity (fourfold increase for carbamoylcholine) was attained. This suggests a quantal conversion of the low-affinity sites by the reagent into an alkylated form, which possesses a higher affinity for agonists but an unchanged affinity for antagonists. The rate of alkylation was enhanced by the presence of agonists but not of antagonists, which is indicative for the ability of agonists to mediate a conformational change of these sites. The close correlation between the N-ethylmaleimide-mediated increase in drug affinity for the low-affinity sites and the ability of the drugs to enhance alkylation of these sites by N-ethylmaleimide can be explained by the ability of (a) muscarinic drugs to interact with the low-affinity sites according to the Monod-Wyman-Changeux 'Plausible Model' and (b) N-ethylmaleimide to freeze these sites in the 'active' conformation by alkylation. (+info)I'm sorry for any confusion, but "Dexetimide" doesn't seem to be a recognized medication or substance in modern medical terminology, at least not in English. It's possible that it might be an obscure or outdated term, or perhaps it's used in a different language or context.
If you have more context or information about where you encountered this term, I might be able to provide a more accurate response. However, without further information, I can't provide a reliable medical definition for "Dexetimide".
Maneb is not a term that has a widely accepted medical definition. However, in the field of agriculture and toxicology, Maneb is a commonly used fungicide to control various plant diseases. It is a complex organometallic compound containing manganese.
In some contexts, Maneb may be mentioned in relation to human health because it has been found to have potential reproductive and developmental effects, as well as being potentially carcinogenic. However, it is not considered a medical term or diagnosis. If you have any concerns about exposure to Maneb or its potential health effects, it would be best to consult with a healthcare professional.
Manganese poisoning, also known as manganism, is a condition that results from excessive exposure to manganese. Manganese is an essential nutrient, but at high levels, it can become toxic to the body. The symptoms of manganese poisoning can be similar to those of Parkinson's disease and may include tremors, difficulty walking, and mood changes. In severe cases, manganese poisoning can lead to irreversible neurological damage. Exposure to manganese can occur through inhalation, ingestion, or skin contact, and is often associated with occupational exposure in industries such as welding, mining, and manufacturing of batteries and fertilizers.
I apologize for any confusion, but "Zineb" is not a medical term or concept that I am familiar with in the field of medicine. Zineb is actually a pesticide that contains the active ingredient ferbam, which is used to control fungi on crops such as grapes, apples, and potatoes. It is not a term used within the context of medical definitions or human health. I hope this clarifies any confusion. If you have any questions related to medicine or healthcare, I would be happy to try and help answer them for you.
An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.
Manganese is not a medical condition, but it's an essential trace element that is vital for human health. Here is the medical definition of Manganese:
Manganese (Mn) is a trace mineral that is present in tiny amounts in the body. It is found mainly in bones, the liver, kidneys, and pancreas. Manganese helps the body form connective tissue, bones, blood clotting factors, and sex hormones. It also plays a role in fat and carbohydrate metabolism, calcium absorption, and blood sugar regulation. Manganese is also necessary for normal brain and nerve function.
The recommended dietary allowance (RDA) for manganese is 2.3 mg per day for adult men and 1.8 mg per day for adult women. Good food sources of manganese include nuts, seeds, legumes, whole grains, green leafy vegetables, and tea.
In some cases, exposure to high levels of manganese can cause neurological symptoms similar to Parkinson's disease, a condition known as manganism. However, this is rare and usually occurs in people who are occupationally exposed to manganese dust or fumes, such as welders.
Facilitated diffusion is a type of passive transport that involves the movement of molecules or ions across a biological membrane with the assistance of a transport protein. Unlike simple diffusion, which occurs spontaneously down a concentration gradient, facilitated diffusion allows for the movement of substances against a concentration gradient, although it does not directly consume energy.
In facilitated diffusion, the transport protein binds to the substance (also known as the solute) on one side of the membrane and then changes shape, releasing the solute on the other side. This process can increase the rate of diffusion by providing a more efficient pathway for the solute to move through the membrane.
Examples of substances that use facilitated diffusion include glucose, amino acids, and ions such as sodium and potassium. These substances are too large or too polar to pass through the hydrophobic interior of the lipid bilayer that makes up the cell membrane, so they rely on transport proteins to help them move across the membrane.
It's important to note that facilitated diffusion is a passive process and does not require energy input from the cell. However, it is a regulated process, as the number of transport proteins in the membrane can be adjusted to control the rate of solute movement.
Dyskinesias are a type of movement disorder characterized by involuntary, erratic, and often repetitive muscle movements. These movements can affect any part of the body and can include twisting, writhing, or jerking motions, as well as slow, writhing contortions. Dyskinesias can be caused by a variety of factors, including certain medications (such as those used to treat Parkinson's disease), brain injury, stroke, infection, or exposure to toxins. They can also be a side effect of some medical treatments, such as radiation therapy or chemotherapy.
Dyskinesias can have a significant impact on a person's daily life, making it difficult for them to perform routine tasks and affecting their overall quality of life. Treatment for dyskinesias depends on the underlying cause and may include medication adjustments, surgery, or physical therapy. In some cases, dyskinesias may be managed with the use of assistive devices or by modifying the person's environment to make it easier for them to move around.
Dexetimide
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Brazilian Controlled Drugs and Substances Act
ATC code N04
C23H26N2O2
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Benzetimide
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164701
- Dexetimide (R 16470) in the control of neuroleptic-induced extrapyramidal side-effects. (wikipedia.org)
Neuroleptic-induced1
- Dexetimide (R 16470) in the control of neuroleptic-induced extrapyramidal side-effects. (wikipedia.org)
Brand1
- Dexetimide (brand name Tremblex) is a piperidine anticholinergic. (wikipedia.org)