Mechanism of injuries

Senaratna, T. McKenzie, B.D. (1986). Loss of desiccation tolerance during seed germination A free radical mechanism of injury. In Membranes, Metabolism and Dry Organisms, ed. A.C. Leopold, pp. 85-101. Ithaca, N.Y. Comstock Publishing Associates. 

A primary mechanism of injury with sepsis is through endothelial cells. With inflammation, endothelial cells allow circulating cells (e.g., granulocytes) and plasma constituents to enter inflamed tissues, which may result in organ damage. 

Function Tissue specificity (e.g., transport characteristics, metabolic pathways) Mechanisms of injury... 

However, although degradation is known to occur under both aerobic and anaerobic conditions, data are not available on the identity of degradation products. Because the limited studies on the mechanisms of injury from di-ra-octylphthalate suggest that mono-n-octylphthalate is the proximate toxicant, it is important to know whether the reduction of di- -octylphthalate is coupled with the accumulation of mono- -octylphthalate. The environmental fate of di-n-octylphthalate and its metabolites is not sufficiently understood to allow assessments of its exposure potential to be made. Additional data are needed on the... 

The toxic effects of ozone in plant systems have been studied for some time, yet the actual mechanisms of injury are not fully understood. In addition to visible necrosis which appears largely on upper leaf surfaces, many other physiological and biochemical effects have been recorded ( ). One of the first easily measurable effects is a stimulation of respiration. Frequently, however, respiration may not increase without concomitant visible injury. Furthermore, photosynthesis in green leaves as measured by CO2 assimilation, may decrease. It is well known that ozone exposure is accompanied by a dramatic increase in free pool amino acids ( ). Ordin and his co-workers ( ) have clearly shown the effect of ozone on cell wall biosynthesis. In addition, ozone is known to oxidize certain lipid components of the cell ( ), to affect ribosomal RNA (16) and to alter the fine structure of chloroplasts (7 ). 

As increases in cardiac troponin detect any form of myocardial injury, nonischemic mechanisms of injury are also responsible for cardiac troponin release from the heart, causing increases in circulating troponin. Table 5-3 shows a list of potential etiologies that have been responsible for increases in non-ischemic damage to the heart. Thus, whenever cardiac troponin is monitored, it is important to follow the serial pattern of a rising or a falling pattern of the biomarker. An increased cTn pattern that remains relatively unchanged and is not indicative of this serial trend is likely not an MI. 

Lopez BD, Ubels JL (1991) Quantitative evaluation of the corneal epithelial barrier effect of artificial tears and preservatives. Curr Eye Res 10(7) 645-656 Rein M (2003) The ocular surface barrier function and mechanisms of injury and repair. In Salem H, Katz S (eds) Alternative Toxicological Methods. CRC Press, New York, pp 89-108... 

This case of heroin myelopathy is similar to other reported cases, except that this case occurred with intranasal rather than intravenous use. The MRI findings were consistent with a transverse myelitis. The authors suggested that hypersensitivity and an immune-mediated attack on the spinal cord was the likely mechanism of injury. 

Discuss fhe classification of explosives and the associated mechanisms of injury. 

Penetrating and blunt traumatic injuries that occur as the result of an explosion are similar to those associated with other mechanisms of injury. Primary blast injuries present unique situations and affect selected body systems. Every body system may be affected following an explosion and subsequent blast wave, the associated injuries and their care are discussed in a head-to-toe manner. 

What are the mechanisms of injury of a blast wave Describe each. 

Borak, J., Diller, W.F. (2001). Phosgene exposure mechanisms of injury and treatment strategies. J. Occup. Environ. Med. 43 110-19. 

Schnellmann RG, Griner RD. Mitochondrial mechanisms of tubular injury. In Mechanisms of injury in renal disease and toxicity. Goldstein RS, Editor.CRC Press Inc, Boca Raton, Florida, USA 1994 p. 247-265. 

Analysis of the etiology of the physical injuries from consumer products includes three components determination of the at-risk population (exposure to hazard), mechanism of injury (consequences of hazard), and characteristics of products (mitigation of hazard). 

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