Cell death/mortality

Information gained from assays and future potential So far, few field measurements have been made of caspase-like activities (Berman-Frank et al., 2004 Vardi et al., 1999), but the assay methods appear to be sensitive enough to allow use in natural communities. As work using cultures proceeds, and our understanding of cell death processes improves, assays of capase-like activity may offer an important means to distinguish different forms of cell mortality. Aside from bulk in vitro assays, the availability of ceU-permeable substrates, coupled with flow cytometry will provide improved resolution and specificity (e.g. Bidle and Bender, 2008). 

The word cancer covers a diverse array of tumors types that affect a significant number of Americans and are a significant cause of mortality. The term cancer actually refers to more than 100 diseases. What is common to all cancers is the cancerous cell has uncontrolled growth so that it invades tissues and spreads to other parts of the body, called metastasis. In 2005, it is projected that over 1.3 million Americans will be diagnosed with cancer, whereas more than 560,000 Americans will die from the cancer.1 Figure 85-1 reveals cancers by gender, new cases, and deaths. 

In experimental animals the respiratory system is a primary target of acrolein exposure after inhalation, and there is an inverse relationship between the exposure concentration and the time it takes for death to occur." Inhalation LCso values of 327ppm for 10 minutes and 130ppm for 30 minutes have been reported in rats." Of 57 male rats, 32 died after exposure to 4 ppm for 6 hours/day for up to 62 days. Desquamation of the respiratory epithelium followed by airway occlusion and asphyxiation is the primary mechanism for acrolein-induced mortality in animals." Sublethal acrolein exposure in mice at 3 and 6 ppm suppressed pulmonary antibacterial defense mechanisms. A combination of epithelial cell injury and inhibition of macrophage function may be responsible for acrolein-induced suppression of pulmonary host defense. ... 

A follow-up of CMME (BCME) workers found no increased risk of respiratory cancer among those exposed less than 1 year to a 12-fold increase among those exposed 10 years or more. Latency did not appear to be inversely related to dose but, instead, peaked at approximately 20 years from initial exposure. After 30 years of observation 25 of 67 deaths in CMME (BCME)-exposed chemical workers were due to lung cancer (80% small cell carcinoma). Standardized mortality ratios were elevated among the moderately and heavily exposed workers and peaked at 23.1 the first decade and then declined to 7.4 and 7.9 in later decades. ... 

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