Knapton RW & Mineau P. (1995). Effects of granular formulations of terbufos and fonofos applied to cornfields on mortality and ...
Knapton RW & Mineau P. (1995). Effects of granular formulations of terbufos and fonofos applied to cornfields on mortality and ...
Fluenetil Fluorine Fluoroacetamide Fluoroacetic acid Fluoroacetyl chloride Fluoroantimonic acid Fluorouracil Fonofos ...
dichlorvos dimethoate fenthion fenitrothion fonofos [16] methamidophos methidathion parathion mevinphos monocrotophos naled ...
... fonofos MeSH D02.705.539.500 --- leptophos MeSH D02.705.539.639 --- malathion MeSH D02.705.539.746 --- parathion MeSH D02.705. ... fonofos MeSH D02.886.309.500 --- leptophos MeSH D02.886.309.639 --- malathion MeSH D02.886.309.746 --- parathion MeSH D02.886. ...
Fonofos: O-Ethyl S-phenyl ethylphosphonothiolothionate N,N-Dialkyl (Me, Et, n-Pr or i-Pr) phosphoramidic dihalides Dialkyl (Me ...
Fonofos je organsko jedinjenje, koje sadrži 10 atoma ugljenika i ima molekulsku masu od 246,329 Da. ... Преузето из „https://sr.wikipedia.org/w/index.php?title=Fonofos&oldid=8981266" ...
... , alanwood.net Fonofos, Pesticide Information Profile, Extension Toxicology Network Appendix A List of Extremely ... Fonofos is an organothiophosphate insecticide primarily used on corn. It is highly toxic and listed as an extremely hazardous ...
... is a widely used, broad-spectrum benzimidazole fungicide and a metabolite of benomyl. It is also employed as a casting worm control agent in amenity turf situations such as golf greens, tennis courts etc. and in some countries is licensed for that use only.[2] The fungicide is used to control plant diseases in cereals and fruits, including citrus, bananas, strawberries, pineapples, and pomes.[3] It is also controversially used in Queensland, Australia on macadamia plantations.[4] A 4.7% solution of carbendazim hydrochloride, sold as Eertavas, is marketed as a treatment for Dutch elm disease. Studies have found high doses of carbendazim cause infertility and destroy the testicles of laboratory animals.[5][6] Maximum pesticide residue limits (MRLs) have reduced since discovering its harmful effects. The MRLs for fresh produce in the EU are now between 0.1 and 0.7 mg/kg with the exception of loquat, which is 2 mg/kg.[7] The limits for more commonly consumed citrus and pome fruits are ...
While botulinum toxin is generally considered safe in a clinical setting, there can be serious side effects from its use. The use of botulinum toxin A in cerebral palsy children is safe in the upper and lower limb muscles.[5][6] Most commonly, botulinum toxin can be injected into the wrong muscle group or with time spread from the injection site, causing temporary paralysis of unintended muscles. Side effects from cosmetic use generally result from unintended paralysis of facial muscles. These include partial facial paralysis, muscle weakness, and trouble swallowing. Side effects are not limited to direct paralysis however, and can also include headaches, flu-like symptoms, and allergic reactions.[41] Just as cosmetic treatments only last a number of months, paralysis side-effects can have the same durations.[citation needed] At least in some cases, these effects are reported to dissipate in the weeks after treatment.[citation needed] Bruising at the site of injection is not a side effect of the ...
GV (IUPAC name: 2-(Dimethylamino)ethyl N,N-dimethylphosphoramidofluoridate) is an organophosphate nerve agent. GV is a part of a new series of nerve agents with properties similar to both the "G-series" and "V-series". It is a potent acetylcholinesterase inhibitor with properties similar to other nerve agents, being a highly poisonous vapour. Treatment for poisoning with GV involves drugs such as atropine, benactyzine, obidoxime, and HI-6.[1][2] ...
The four-membered ring in α-pinene 1 makes it a reactive hydrocarbon, prone to skeletal rearrangements such as the Wagner-Meerwein rearrangement. For example, attempts to perform hydration or hydrogen halide addition with the alkene functionality typically lead to rearranged products. With concentrated sulfuric acid and ethanol the major products are terpineol 2 and its ethyl ether 3, while glacial acetic acid gives the corresponding acetate ester 4. With dilute acids, terpin hydrate 5 becomes the major product. With one molar equivalent of anhydrous HCl, the simple addition product 6a can be formed at low temperature in the presence of ether, but it is very unstable. At normal temperatures, or if no ether is present, the major product is bornyl chloride 6b, along with a small amount of fenchyl chloride 6c.[5] For many years 6b (also called "artificial camphor") was referred to as "pinene hydrochloride", until it was confirmed as identical with bornyl chloride made from camphene. If more HCl is ...
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... is extracted from Huperzia serrata.[2] It is a reversible acetylcholinesterase inhibitor[6][7][8][9] and NMDA receptor antagonist[10] that crosses the blood-brain barrier.[11] Acetylcholinesterase is an enzyme that catalyzes the breakdown of the neurotransmitter acetylcholine and of some other choline esters that function as neurotransmitters. The structure of the complex of huperzine A with acetylcholinesterase has been determined by X-ray crystallography (PDB code: 1VOT; see the 3D structure).[12] For some years, huperzine A has been investigated as a possible treatment for diseases characterized by neurodegeneration, particularly Alzheimer's disease.[2][13] A 2013 meta-analysis found that huperzine A may be efficacious in improving cognitive function, global clinical status, and activities of daily living for individuals with Alzheimer's disease. However, due to the poor size and quality of the clinical trials reviewed, huperzine A should not be recommended as a treatment for ...
When used in the central nervous system to alleviate neurological symptoms, such as rivastigmine in Alzheimer's disease, all cholinesterase inhibitors require doses to be increased gradually over several weeks, and this is usually referred to as the titration phase. Many other types drug treatments may require a titration or stepping up phase. This strategy is used to build tolerance to adverse events or to reach a desired clinical effect.[12] This also prevents accidental overdose and is therefore recommended when initiating treatment with drugs that are extremely potent and/or toxic (drugs with a low therapeutic index). ...
... can be broadly categorized as a cholinergic physiological antagonist, because it reduces the apparent activity of cholinergic neurons, but does not act at the postsynaptic ACh receptor. Vesamicol causes a non-competitive and reversible block of the intracellular transporter VAChT responsible for carrying newly synthesized ACh into secretory vesicles in the presynaptic nerve terminal. This transport process is driven by a proton gradient between cell organelles and the cytoplasm. Blocking of acetylcholine loading leads to empty vesicles fusing with neuron membranes, decreasing ACh release. ...
... s are a group of highly conserved G-protein coupled receptors from the adhesion G protein-coupled receptor family. These receptors were originally identified based on their ability to bind the spider venom alpha-latrotoxin.[1] This conserved family of membrane proteins has up to three homologues in chordate species, including humans.[2] The precise functions of latrophilins remain unknown.[2] Genetic defects in latrophilin genes have been associated with diseases such as attention-deficit hyperactivity disorder and cancer.[3] ...
... ( anticholinergic agent) is a group of substances that blocks the action of the neurotransmitter acetylcholine (ACh) at synapses in the central and the peripheral nervous system, and, in broad terms, neuromuscular junction.[1][2] These agents inhibit parasympathetic nerve impulses by selectively blocking the binding of the neurotransmitter acetylcholine to its receptor in nerve cells. The nerve fibers of the parasympathetic system are responsible for the involuntary movement of smooth muscles present in the gastrointestinal tract, urinary tract, lungs, and many other parts of the body;[3] cholinergic process otherwise by enhancing ACh function.[3] In broad terms, anticholinergics are divided into two categories in accordance with their specific targets in the central, peripheral nervous system and neuromuscular junction:[3] antimuscarinic agents, and antinicotinic agents (ganglionic blockers, neuromuscular blockers).[4] In strict terms, anticholinergic only comprises ...
InChI=1S/C28H32O8/c1-24(2)10-9-22(29)26(4)27(24,31)12-11-25(3)28(26,32)15-17-20(36-25)14-19(35-23(17)30)16-7-8-18(33-5)21(13-16)34-6/h7-10,13-14,31-32H,11-12,15H2,1-6H3/t25-,26+,27-,28-/m1/ ...
... is an alkaloid found in Corydalis (Papaveraceae) and Dicentra, plants in the family Fumariaceae that can cause fatal poisoning in sheep and cattle.[citation needed] It has been shown to act as an acetylcholinesterase inhibitor,[1] and inhibits biosynthesis of dopamine via inhibition of the enzyme tyrosine hydroxylase.[2][3] Like apomorphine, it is reported to be an inhibitor of amyloid beta protein (Aβ) fiber formation, whose presence is a hallmark of Alzheimer's disease (AD). Bulbocapnine is thus a potential therapeutic under the amyloid hypothesis.[4] According to the Dorlands Medical Dictionary, it "inhibits the reflex and motor activities of striated muscle. It has been used in the treatment of muscular tremors and vestibular nystagmus".[5] A psychiatrist at Tulane University named Robert Heath carried out experiments on prisoners at the Louisiana State Penitentiary using bulbocapnine to induce stupor.[6] This work at Tulane inspired, and was continued parallel to, experiments ...
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