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Paralysis

Crystallizes from water in large colourless prisms containing 2H2O. It is poisonous, causing paralysis of the nervous system m.p. 101 C (hydrate), 189°C (anhydrous), sublimes 157°C. It occurs as the free acid in beet leaves, and as potassium hydrogen oxalate in wood sorrel and rhubarb. Commercially, oxalic acid is made from sodium methanoate. This is obtained from anhydrous NaOH with CO at 150-200°C and 7-10 atm. At lower pressure sodium oxalate formed from the sodium salt the acid is readily liberated by sulphuric acid. Oxalic acid is also obtained as a by-product in the manufacture of citric acid and by the oxidation of carbohydrates with nitric acid in presence of V2O5. [Pg.291]

Carbon disulfide, hydrogen sulfide, and sulfur dioxide should be handled carefully. Hydrogen sulfide in small concentrations can be metabolized, but in higher concentrations it quickly can cause death by respiratory paralysis. [Pg.39]

Approximately 500,000 Americans suffer strokes each year. Many of the 80% that survive suffer paralysis and impaired vision and speech, often needing rehabiUtation and/or long-term care. Hence, whereas treatment using rt-PA is likely to be expensive (costs are 2200/dose for treating heat attacks), the benefits of rt-PA could outweigh costs. In the case of heart attacks, the 10 times less expensive microbiaHy derived streptokinase can be used. There is currentiy no competing pharmaceutical for treatment of strokes (18,19). Consequentiy, the cost of manufacture of rt-PA may not be as dominant an issue as would be the case of other types of bioproducts. [Pg.44]

R = UH3), and morphine (2, R = H), a different derivative of 77 (R = H), ie, (+)-/V-norprotosinomenine (86), serves as the pregenitor of erythraline (87), one of the bases found ia E thnna cristagalli (60). The alkaloids fouad ia all plant parts of E thnna have been iatensively studied because many of them produce smooth muscle paralysis, much like tubocurariae (9). [Pg.545]

Mode of Action. DDT and its analogues specifically affect the peripheral sense organs of insects and produce violent trains of afferent impulses that result in hyperactivity, convulsions, and paralysis. Death results from metaboHc exhaustion and the production of an endogenous neurotoxin. The very high lipophilic nature of these compounds faciUtates absorption through the insect cuticle and penetration to the nerve tissue. The specific site of action is thought to be the sodium channels of the axon, through inhibition of Ca " ATPase. [Pg.276]

Phosphonothioate Esters of Phenols. Phosphonates with a single P—C bond are highly toxic and persistent iasecticides but have not been used extensively because some compounds produce delayed neuropathy leading to irreversible paralysis ia higher animals, including humans. Such compounds specifically inhibit an enzyme, neurotoxic esterase, that is responsible for the growth and maintenance of long nerve axons (31,32). [Pg.284]

The alimentary symptoms may be overshadowed by neuromuscular dysfunction, accompanied by signs of motor weakness that may progress to paralysis of the exterior muscles or the wrist (wrist drop), and less often, of the ankles (foot drop). Encephalopathy, the most serious result of lead poisoning, frequendy occurs in children as a result of pica, ie, ingestion of inorganic lead compounds in paint chips this rarely occurs in adults. Nephropathy has also been associated with chronic lead poisoning (147). The toxic effects of lead may be most pronounced on the developing fetus. Consequendy, women must be particulady cautious of lead exposure (148). The U.S. Center for Disease Control recommends a blood level of less than 10 p.m per 100 mL for children. [Pg.73]

Autoantibodies are directed against nicotinic acetylcholine receptors in myasthenia gravis, resulting in receptor loss, skeletal muscle paralysis, and dysfunction (100). In addition, antibodies directed against voltage-gated Ca " channels produce similar neuromuscular dysfunction of Lambert-Eaton... [Pg.282]

Phenol. Phenol monomer is highly toxic and absorption by the skin can cause severe blistering. Large quantities can cause paralysis of the central nervous system and death. Ingestion of minor amounts may damage kidneys, Hver, and pancreas. Inhalation can cause headaches, dizziness, vomiting, and heart failure. The threshold limit value (TLV) for phenol is 5 ppm. The health and environmental risks of phenol and alkylated phenols, such as cresols and butylphenols, have been reviewed (66). [Pg.302]

The principal arninoglycoside toxicides are neuromuscular paralysis, ototoxicity, and nephrotoxicity. Neuromuscular paralysis is a relatively rare complication resulting from high aminoglycoside concentrations at the neuromuscular junctions following, for example, rapid bolus intravenous injection or peritoneal instillation, rather than the normal intravenous infusion. The mechanism apparentiy involves an inhibition of both the presynaptic release of acetylcholine and the acetylcholine postsynaptic receptors (51). [Pg.482]

The acetylcholinesterase inhibitor tacrine (64) was approved for the treatment of mild-to-moderate SDAT in the United States in 1993 followed by several other countries. The acetylcholinesterase inhibitor galanthamine (65), which has long been in clinical use in Austria for the treatment of indications such as facial neuralgia and residual poliomyelitis paralysis, has also been approved for use in... [Pg.238]

General types of physiological functions attributed to quaternary ammonium compounds are curare action, muscarinic—nicotinic action, and ganglia blocking action. The active substance of curare is a quaternary that can produce muscular paralysis without affecting the central nervous system or the heart. Muscarinic action is the stimulation of smooth-muscle tissue. Nicotinic action is primary transient stimulation and secondary persistent depression of sympathetic and parasympathetic ganglia. [Pg.378]

Health and Safety Factors. Carbonyl sulfide is dangerously poisonous, more so because it is practically odorless when pure. It is lethal to rats at 2900 ppm. Studies show an LD q (rat, ip) of 22.5 mg/kg. The mechanism of toxic action appears to iavolve breakdowa to hydrogea sulfide (36). It acts principally on the central nervous system with death resulting mainly from respiratory paralysis. Little is known regarding the health effects of subacute or chronic exposure to carbonyl sulfide a 400-p.g/m max level has been suggested until more data are available (37). Carbon oxysulfide has a reported inhalation toxicity in mice LD q (mouse) = 2900 ppm (37). [Pg.130]

Enzyme Inhibition. Some materials produce toxic effects by inhibition of biologically vital enzyme systems, leading to an impairment of normal biochemical pathways. The toxic organophosphates, for example, inhibit the cholinesterase group of enzymes. An important factor in thek acute toxicity is the inhibition of acetylocholinesterase at neuromuscular junctions, resulting in an accumulation of the neurotransmitter material acetylcholine and causing muscle paralysis (29) (see Neuroregulators). [Pg.228]

A deficiency of niacin also affects the nervous system. Numbness is initially observed and later, paralysis, particularly in the extremities is common. Severe cases are characteri2ed by tremor and a spastic or ataxic gait and are frequentiy associated with peripheral neuritis. Left untreated, severe thought disorders can ensue (1). [Pg.53]

Pipera2ine causes flaccid paralysis of Jiscaris by blocking the worms abiUty to respond to acetylcholine, thus dislodging the worms from thek... [Pg.245]

For hookworms, treatment is continued for three days. In roundworms, muscle tissue is stimulated continuously, resulting in spastic paralysis. The dmg was introduced in veterinary medicine in 1966 and then appHed to clinical medicine three years later. [Pg.246]

Soluble Compounds. The mechanism of barium toxicity is related to its ability to substitute for calcium in muscle contraction. Toxicity results from stimulation of smooth muscles of the gastrointestinal tract, the cardiac muscle, and the voluntary muscles, resulting in paralysis (47). Skeletal, arterial, intestinal, and bronchial muscle all seem to be affected by barium. [Pg.483]

Ammonia (aqueous) [7664-41-7] M 17.0 + H2O, d 0.90 (satd, 27% w/v, 14.3 N), pK 9.25. Obtained metal-free by saturating distilled water, in a cooling bath, with ammonia (from tank) gas. Alternatively, can use isothermal distn by placing a dish of cone aq ammonia and a dish of pure water in an empty desiccator and leaving for several days. AMMONIA (gas, liquid or aq soln) is very irritating and should not be inhaled in large volumes as it can lead to olfactory paralysis (temporary and partially permanent). [Pg.392]

But probably the most serious barrier has been the paralysis that overtakes the inexperienced mind when it is faced with an explosion. This prevents many from recognizing an explosion as the orderly process it is. Like any orderly process, an explosive shock can be investigated, its effects recorded, understood, and used. The rapidity and violence of an explosion do not vitiate Newton s laws, nor those of thermodynamics, chemistry, or quantum mechanics. They do, however, force matter into new states quite different from those we customarily deal with. These provide stringent tests for some of our favorite assumptions about matter s bulk properties. [Pg.3]

Cattle feeding on herbage containing 25-50 mg/kg (ppm wt) lead develop excitable jerking of muscles, frothing at the mouth, grinding of teeth, and paralysis of the larynx muscles a "roaring" noise is caused by the paralysis of the muscles in the throat and neck. [Pg.122]

Tendency to pulmonary oedema and eventually respiratory paralysis... [Pg.71]

Detectable odour Conjunctivitis Olfactory nerve paralysis... [Pg.124]

Prolonged exposure may cause pulmonary oedema Systemic symptoms may occur in 0.5 to 1 hr Rapid collapse, respiratory paralysis imminent Immediately fatal... [Pg.124]

Atrophy Atrophy is a wasting or decrease in size of a bodily organ, tissue, or part owing to disease, injury, or lack of use. You may have heard this term used in reference to accident or paralysis victims "his muscles atrophied because of nonuse." Exposure to certain chemicals can cause internal organs to degrade, weaken and decrease in size, particularly with chronic (long-term) exposure. [Pg.521]


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Biological agents that paralysis

Biological paralysis

Bladder paralysis

Botulinum toxin causes skeletal muscle paralysis by binding to acetylcholine receptors on the motor end plate

Botulism Flaccid paralysis

Chastek paralysis

Curled toe paralysis

Facial nerve paralysis

Facial paralysis

Flaccid paralysis

Gastric paralysis

Ginger jake paralysis

Ginger paralysis

Hind limb paralysis

Hyperkalaemic periodic paralysis

Hyperkalemic periodic paralysis

Hyperthyroidism paralysis

Hypokalaemic periodic paralysis

Hypokalaemic periodic paralysis thyrotoxic

Hypokalemic periodic paralysis

Hypokalemic thyrotoxic periodic paralysis

Inducing paralysis

Jamaica ginger paralysis

Landry paralysis

Medullary paralysis

Narcolepsy-cataplexy sleep paralysis

Nerve paralysis

Neuromuscular blocking agents paralysis induced

Paralyses, periodic

Paralysis acetylcholinesterase inhibition

Paralysis agitans

Paralysis and

Paralysis botulinum neurotoxins

Paralysis by analysis

Paralysis irreversible

Paralysis nerve agents

Paralysis signs

Paralysis, dietary thiamine deficiency

Paralysis, familial periodic

Paralysis, from biological agents

Paralysis, nerve block

Paralysis, neuromuscular blocking

Paralysis, neuromuscular blocking drugs causing

Paralysis, paresis

Periodic paralysis genetics

Respiratory center, paralysis

Respiratory muscles paralysis

Respiratory paralysis

Respiratory paralysis, neuromuscular

Shock respiratory paralysis

Sleep paralysis

Sleep paralysis, narcolepsy

Spastic spinal paralysis

Strychnine paralysis

Thyrotoxic periodic paralysis

Tick paralysis

Todd’s paralysis

Weakness or paralysis

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