Diaphragm muscle

Botulinus toxin comes from Clostridium botulmum, an organism that causes food poisoning. Botulinus toxin prevents the release of ACh from nerve endings by mechanisms that are not clear. Death occurs from respiratory failure caused by the inability of diaphragm muscles to contract. 

Concentration-dependent presynaptic effects of 2-PAM on the release of acetylcholine from terminals of nerves innervating the rat diaphragm muscle were seen at concentrations of 10- -l0" 3 m 2-PAM stimulated the release of acetylcholine higher concentrations led to a total block of the evoked release of acetylcholine.30> 0... 

Hnia K, Hugon G, Rivier F, Masmoudi A, Mercier J, Momet D (2007) Modulation of p38 mitogen-activated protein kinase cascade and metalloproteinase activity in diaphragm muscle in response to free radical scavenger administration in dystrophin deficient Mdx mice. Am... 

Figure i—3. The release of acetylcholine onto the diaphragm muscle causes it to contract and pull air into the lungs (inspiration). The relaxation of this muscle allows air to leave the lungs (expiration). 

A cigarette made from tobacco will contain about 1 to 2 milligrams of nicotine. Because nicotine is quite volatile and heat labile, only about 20% of it is actually inhaled into the body. However, because of its exceptional lipid solubility, at least 90% of the inhaled nicotine is absorbed into the body. Nicotine can also be rapidly absorbed by the mouth or intact skin. Once the smoke is inhaled, absorption via the lungs and transport to the brain occurs within 2 to 7 seconds. This makes smoking tobacco as efficient as an intravenous injection in terms of getting nicotine to its site of action within the brain. This speed of entry into the body may also underlie why nicotine is so toxic. Sixty milligrams is considered a lethal dose for a human death takes only a few minutes to occur and results from a loss of control of the nicotinic receptors on the diaphragm muscles. 

Robert Boyle reported that the volume of a fixed sample of gas is inversely related to pressure, as long as the temperature is constant. As the pressure increases, the volume decreases, and vice versa. This is the basis of breathing. During inspiration, the diaphragm muscle contracts and pulls downward, thereby increasing the volume of the thoracic cavity. The gas pressure in the lungs decreases to less... 

Asthma Users will experience a tightening of the diaphragm muscles, shortness of breath, and other asthma-related problems. Each time this drag or chemical agent is used, make a Fortitude save (DC 15). If the user fails he cannot breathe, and will begin to suffocate unless medical attention is administered (see Suffocation and Drowning on page 213 of the Modern Core Rule book). Frequent users must make a Fortitude save at DC 18 instead. 

Actions Not all muscles are equally sensitive to blockade by competitive blockers. Small, rapidly contracting muscles of the face and eye are most susceptible and are paralyzed first, followed by the fingers. Thereafter the limbs, neck, and trunk muscles are paralyzed, then the intercostal muscles are affected, and lastly, the diaphragm muscles are paralyzed. 

It can be seen that one of the quaternary carbamates has been chosen for this use, mainly because they are safer and also have fewer untoward effects, and since in the early years organophosphate intoxication was considered to be mainly a peripheral breathing problem (paralysis of the diaphragm muscles and edema of the lungs). The realization during the 1980s and 1990s that inhibition of the brain... 

Enzymatic N-demethylation of morphine also occurs in other opioid target tissues such as the GPI and hybrid cell lines but is absent in non-target tissue such as the diaphragm muscle. 

In the rat, the 16S form is found in high concentration at the endplates and it is thought to be involved in neuromuscular transmission (Hall, 1973). The different molecular forms of AChE in SOL and EDL have apparent Km values similar to that previously foimd in the diaphragm muscle (Hall, 1973 Grosswald and Dettbam, 1983a, b). There appears to be no difference between catalytic sites of the molecular forms of AChE in fast EDL and slow SOL muscles, despite the different molecular form patterns and activity in three muscles. 

Gupta et al. (1985, 1986) found the highest number of lesions in all three muscles (diaphragm, SOL, and EDL) of rats within 24 to 48 h after a single injection of DFP (1.5 mg/ kg, S.C.), when the inhibitory effect on AChE activity was also maximal (Table 35.5). The diaphragm muscle had the highest number of lesions, followed by the EDL and SOL. 

Gupta, R.C., Goad, J.T. (2000). Role of high-energy phosphates and their metabolites in protection of carboftiran-induced biochemical changes in diaphragm muscle hy memantine. Arch. Toxicol. 74 13-20. 

Hall, Z.E. (1973). Multiple forms of acetylcholinesterase and their distribution in endplate and nonendplate regions of rat diaphragm muscle. J. Neurobiol. 4 343-61. 

Ah open tube ends on a piece of glassware, except the one used for blowing, should be securely stoppered with cork or asbestos stoppers or rubber plugs. Small leaks must be avoided, as they upset blowing techniques and excessive loss of air can be harmful to the chest and diaphragm muscles. 

Laycock JR, Smith CE, Donati F, Bevan DR. Sensitivity of the adductor pollicis and diaphragm muscles to atracurium in a hemiplegic patient. Anesthesiology 1987 67(5) 851-3. 

Although metalloprotease inhibitors are not constrained by a brief therapeutic window, recovery from BoNT intoxication may stiU be delayed because of the time required to replace cleaved SNARE proteins with intact ones. Estimates from pulse-chase experiments suggest that a halftime of 1 day would be required to replace SNAP-25, 4—5 days to replace synaptobrevin, and 6 days to replace syntaxin, even if no further cleavage were to occur (Foran et al., 2003). Examination of the fraction of total SNARE proteins cleaved by BoNT reveals that a relatively smaU fraction is cleaved at the neuromuscular junction at the time of total muscle paralysis. From local injections of BoNT/A in vivo, Jurasinski et al. (2001) estimated that paralysis requires cleavage of less than 35% of the total SNAP-25. Meunier et al. (2003) reported that isolated diaphragm muscles exposed to 2 nM BoNT/A have only 6.5% of their SNAP-25 in the cleaved form, and suggested that the SNAP-25 relevant to transmitter release must exist in a smaU specialized pool. It is likely that the critical pool of SNAP-25 is even lower than that found by Meunier et al. (2003), since the... 

On the Cover Electron microscopy of neuromuscular junction from diaphragm muscle of rat. Intoxication with Vx. 10 days after treatment with oxime reactivator of ChE. 60 000 x. (Dishovsky, 1975). 

The presence of this enzyme in muscle was first reported in 1958 and has since been investigated by many workers. Villar-Palasi and Lamer demonstrated the conversion of a-D-glucosyl phosphate into glycogen by a uridine-coenzyme-linked reaction in rat skeletal and diaphragm muscle ... 

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