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Latent period

The long latent periods involved in development of cancers make correlation of chemical exposures and disease extremely difficult. This can be countered pardy with tests on naturally short-Hved animals. Tests on bacteria, eg, the Ames test, may permit rapid detection of cancer potential, although there is no direct relationship between the results of bacterial tests and the effects of the tested chemicals on humans (56). [Pg.96]

After a latent period of 2 to 24 hours, the subject complains of burning in the throat and chest, shortness of breath and increasing dyspnea Where the exposure has been severe, the development of pulmonary edema may be so rapid that the subject dies within 36 hours after ex-... [Pg.727]

Figure 2. Muscle stimulation, a) a single nerve impulse (stimulus) causes a single contraction (a twitch). There is a small delay following the stimulus before force rises called the latent period, b) A train of stimuli at a low frequency causes an unfused tetanus. Force increases after each progressive stimulus towards a maximum, as calcium levels in the myofibrillar space increase. But there is enough time between each stimulus for calcium to be partially taken back up into the sarcoplasmic reticulum allowing partial relaxation before the next stimulus occurs, c) A train of stimuli at a higher frequency causes a fused tetanus, and force is maximum. There is not enough time for force to relax between stimuli. In the contractions shown here, the ends of the muscle are held fixed the contractions are isometric. Figure 2. Muscle stimulation, a) a single nerve impulse (stimulus) causes a single contraction (a twitch). There is a small delay following the stimulus before force rises called the latent period, b) A train of stimuli at a low frequency causes an unfused tetanus. Force increases after each progressive stimulus towards a maximum, as calcium levels in the myofibrillar space increase. But there is enough time between each stimulus for calcium to be partially taken back up into the sarcoplasmic reticulum allowing partial relaxation before the next stimulus occurs, c) A train of stimuli at a higher frequency causes a fused tetanus, and force is maximum. There is not enough time for force to relax between stimuli. In the contractions shown here, the ends of the muscle are held fixed the contractions are isometric.
The incidence of liver tumors due to morpholine and nitrite was reduced from 65% in the absence of to 49% in the presence of sodium ascorbate, and the latent period was nearly doubled, from 54 to 93 weeks, indicating in vivo nitroso-morpholine (NMOR) production was probably about 50% inhibited (10). [Pg.195]

Diborane heated at 105-165°C with oxygen detonates after a latent period. [Pg.170]

Cancer is the major latent harmful effect produced by ionizing radiation and the one that most people exposed to radiation are concerned about. The ability of alpha, beta, and gamma radiation to produce cancer in virtually every tissue and organ in laboratory animals has been well-demonstrated. The development of cancer is not an immediate effect. In humans, radiation-induced leukemia has the shortest latent period at 2 years, while other radiation induced cancers have latent periods >20 years. The mechanism by which cancer is induced in living cells is complex and is a topic of intense study. Exposure to ionizing radiation can produce cancer at any site within the body however, some sites appear to be more common than others, such as the breast, lung, stomach, and thyroid. [Pg.309]

Delayed - usually 4-6 h until first symptoms appear. Latent periods of up to 24 h have been observed, however, and in rare cases of up to 12 days. [Pg.4]

Two types of OPIDN have been described in animals (Abou-Donia and Lapadula 1990). Type I is produced by compounds with a pentavalent phosphorus (like TOCP), and Type II is produced by compounds with a trivalent phosphorus. Characteristics used to differentiate between the types of OPIDN include species selectivity, age sensitivity, length of latent period, and morphology of neuropathologic lesions. Thus, at doses that did not produce death due to acetylcholinesterase inhibition, TOCP (a Type I compound) produced lesions in the spinal cord of rats without producing ataxia. In contrast, triphenyl phosphite (a Type II compound) produced delayed (1 week) ataxia in the rat and a distribution of spinal cord lesions distinct from those produced by TOCP (Abou-Donia and Lapadula 1990). [Pg.184]

The eclipse is the period during which the stages of virus multiplication occur. This is called the latent period, because no infectious virus particles are evident. Finally, maturation begins as the newly synthesized nucleic acid molecules become assembled inside protein coats. During the maturation phase, the titer of active virus particles inside the cell rises dramatically. At the end of maturation, release of mature virus particles occurs, either as a result of cell lysis or because of some budding or excretion process. The number of virus particles released, called the burst size, will vary with the particular virus and the particular host cell, and can range from a few to a few thousand. The timing of this overall virus replication cycle varies from 20-30 minutes in many bacterial viruses to 8-40 hours in most animal viruses. We now consider each of the steps of the virus multiplication cycle in more detail. [Pg.123]

Bacteriophage T7 Bacteriophage T7 and its close relative T3 are relatively small DNA viruses that infect Escherichia coli. (Some strains of Shigella and Pasteurella are also hosts for phage T7.) The virus particle has an icosahedral head and a very small tail. The virus particle is fairly complex, with S different proteins in the head and 3-6 different proteins in the tail. One tail protein, the tail fiber protein, is the means by which the virus particle attaches to the bacterial cell surface. Only female cells of Escherichia coli can be infected with T7 male cells can be infected but the multiplication process is terminated during the latent period. [Pg.140]

Typically, there is a latent period with no visible effects between the time of exposure and the sudden onset of symptoms. This latency can range from 1 minutes to 18 hours and is affected by such factors as the amount of agent involved, the amount of skin surface in contact with the agent, and the area of the body exposed (see Liquids). Moist, sweaty areas of the body are more susceptible to percutaneous penetration by solid nerve agents. [Pg.6]

Information on the latency of this class of agents is unavailable. However, based on animal studies, there does not appear to be a significant latent period for convulsive effects. However, effects from subconvulsive doses may not be immediately obvious. [Pg.222]

There is no antidote for exposure to these agents. Enforce rest as even minimal physical exertion may shorten the clinical latent period. Asymptomatic individuals suspected of exposure to pulmonary agents should be monitored for possible complications caused by... [Pg.271]

Rey and coworkers78 reported methyltin intoxication in six chemical workers exposed to Me2SnCl2 and MesSnCI. After a latent period of 1 -3 days, the first symptoms occurred, including headache, tinnitus, deafness, impair of memory, disorientation, aggressiveness, psychotic behavior, syncope, loss of consciousness and, in the most severe cases, respiratory depression requiring ventilatory assistance. Increased tin excretion was detected in the urine of all patients, particularly those most ill. The patient with the highest tin levels died 12 days after the initial exposure. [Pg.891]

Interestingly, many forms of partial epilepsy are characterized by a seizure-free interval lasting months to years between the occurrence of the causative insult and the emergence of epilepsy termed the latent period , this provides a valuable window of opportunity during which pharmacologic intervention might be implemented in high-risk individuals so that development of epilepsy could be prevented. [Pg.633]

Peripheral pathogenesis involves the lymphoreticular system. Although the pathological consequences of prion infection occur in the central nervous system, and experimental transmission of these diseases is most efficiently accomplished by intracerebral inoculation, most natural infections do not occur by these means. Indeed, administration to sites other than the central nervous system is known to be associated with much longer incubation periods, which may extend to 20 years or more [5,12]. Experimental evidence suggests that this latent period is associated with clinically silent prion replication in... [Pg.794]

Diazinon exerts its toxic effects by binding to the neuronal enzyme acetylcholinesterase (AChE) for long periods after exposure. Diazinon, in turn, is converted to diazoxon, which has a higher affinity for AChE (and thus greater toxicity) than the parent compound. There is a latent period in... [Pg.976]

A latent period was evident between exposure and signs of intoxication. [Pg.1434]


See other pages where Latent period is mentioned: [Pg.66]    [Pg.498]    [Pg.236]    [Pg.1139]    [Pg.351]    [Pg.271]    [Pg.204]    [Pg.363]    [Pg.176]    [Pg.432]    [Pg.439]    [Pg.445]    [Pg.445]    [Pg.456]    [Pg.458]    [Pg.68]    [Pg.131]    [Pg.136]    [Pg.6]    [Pg.144]    [Pg.153]    [Pg.154]    [Pg.380]    [Pg.413]    [Pg.456]    [Pg.1178]    [Pg.1416]    [Pg.1419]    [Pg.1435]    [Pg.1440]   
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See also in sourсe #XX -- [ Pg.5 ]

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