Chemical lesions development

We better understand the kinetics of spreading and the histological processes of destruction of the different ocular tissues. The pathophysiology of chemical lesions, in case of an ocular bum, wiU be strongly illustrated, thanks to new technologies which can bring the experimental evidence of the theories developed in the following chapters. 

Modifying effects of various chemicals on preneoplastic and neoplastic lesion development... 

The differential diagnosis of mustard casualties on the battlefield after a known chemical attack is not difficult. The history of a chemical attack is useful, particularly if the chemical agent is known. Simply questioning the casualty about when the pain started—whether it started immediately after the exposure or hours later—is very helpful. Whereas pain from Lewisite (the other vesicant that causes blistering) begins seconds to minutes after exposure, pain from mustard does not begin until the lesion develops hours later. 

On this basis, a versatile even if contradictory role of oxysterols may emerge, which poses the question of how they actually affect the atherosclerotic lesion development and which factors might modulate their behavior. In this connection, how much does it depend on the nature of oxysterols thanselves (e.g., chemical structure, enzymatic or nonenzymatic origin) and how much on extrinsic factors (e.g., stage of disease progression, cell phenotype, presence of other bioactive compounds) ... 

Although Mg is generally considered non-toxic, the inhalation of fumes of freshly sublimed Mg oxide may cause metal fume fever. There is no evidence that Mg produces, true systemic poisoning. Particles of metallic Mg or Mg alloy which perforate the skin of gain entry thru cuts and scratched rilay produce a severe local lesion characterized by the evolution of gas and acute inflammatory reaction, frequently with necrosis. The condition Has been called a chemical gas gangrene . Gaseous blebs may develop within 24 hrs of the injury. The lesion is very slow to heal (Ref 23)... 

Dermal (skin) contact with sulfur mustard agents causes erythema and lesions (blistering), while contact with vapor may result in first and second degree burns contact with liquid typically produces second and third degree chemical burns. Any burn area covering 25 percent or more of the body surface area may be fatal. Respiratory contact is a dose-related factor in the sense that inflammatory reactions in the upper and lower airway begin to develop several hours after exposure and progress over several days. 

If there are any identifiable gross lesions, they often differ between animals that die, and those that survive to the end of the observation period. The reason for these differences is very simple. An animal that dies less than 24 hours after chemical exposure probably has not had sufficient time to develop a well-defined lesion. As mentioned earlier, most deaths occur within 24 hours. Animals that survive for the two-week observation period have probably totally recovered and rarely have apparent lesions. Hence, the animals that provide the best chance to identify test-article-specific lesions are those that die in the region of 24 to 96 hours postdosing. 

In the US-EPA test guidelines for carcinogenicity and combined chronic toxicity/carcinogeni-city (OPPTS 870.4200 and OPPTS 870.4300, respectively), the following definition is provided Carcinogenicity is the development of neoplastic lesions as a result of the repeated daily exposure of experimental animals to a chemical by the oral, dermal, or inhalation routes of exposure. ... 

Useful insights can undoubtedly be obtained by consideration of the likely chemical species present, and their behaviour at varying pH. Saliva is known to be metastable and supersaturated with respect to hydroxyapatite [35], which is further evidence that the purely thermodynamic approach is suspect. It does mean though that there is a significant driving force for remineralisation, as the supersaturated saliva approaches equilibrium with the consequent precipitation of hydroxyapatite. The development or arrest of a carious lesion is therefore dependent on the frequency and duration of the remineralisation and demineralisation processes, and also on their respective rates. These in turn depend on factors such as sucrose consumption, salivary flow, oral hygiene [36] and, of course, fluoride exposure [37]. It is the latter that is of greatest interest in the present chapter, and its role will be considered in detail in the next section. 

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